Localisation of Spinal Cord Lesions

AUSTRALIAN VETERINARY ASSOCIATION PROCEEDINGS 2009

Richard A. LeCouteur, BVSc, PhD, DACVIM (Neurology), DECVN University of California, Davis, CA, USA
20183730

The ability to complete and interpret results of a neurological examination, compile a list of differential diagnoses, and understand the available diagnostic procedures and current treatment recommendations, is essential in the management of spinal cord disorders of animals. This lecture outlines a diagnostic approach to diseases of the spinal cord. Motor, sensory, reflex, and sphincter abnormalities may be used to determine the location of a lesion within one of four major longitudinal divisions of the spinal cord. The divisions are cervical (C1 to C5 spinal cord segments), cervical enlargement (C6 to T2), thoracolumbar (T3 to L3), and lumbar enlargement (L4 to Cd5). It is essential to remember that these divisions refer to spinal cord segments, not vertebrae, and that spinal cord segments do not correspond exactly with vertebrae of the same number. Some variations may be encountered due to slight differences between animals in segments that form cervical and lumbar enlargements. A disorder of each of the four regions of the spinal cord results in a combination of neurological signs that is specific for the region involved. Recognition of these clinical signs allows accurate localization of a spinal cord lesion. The presence of neurological deficits indicative of involvement of more than one region of the spinal cord is highly suggestive of multifocal or disseminated spinal cord disease. The functional differences between upper motor neurons (UMNs) and LMNs may be used to localize lesions to one of the functional regions of the spinal cord. Cell bodies of spinal cord LMNs are located in the spinal cord gray matter. Their axons leave the spinal cord via the ventral nerve roots to become part of a peripheral nerve, and to terminate in a muscle. The LMNs of the thoracic limb have their cell bodies in C6 to T2 spinal cord segments that form the cervical enlargement, while LMNs of the pelvic limb arise from the L4 through Sl spinal cord segments of the lumbar enlargement. Anal and urethral sphincter LMNs originate from S1 through S3 spinal cord segments. Signs of LMN dysfunction, which in diseases affecting the spinal cord reflect damage to the spinal cord segment(s) from which LMNs originate, are decreased or absent voluntary motor activity, decreased or absent muscle tone, normal, decreased or absent segmental spinal reflexes, and rapid, severe atrophy of an affected muscle due to denervation. Upper motor neurons arise from cell bodies located in the brain. Their axons form descending pathways of the spinal cord and terminate on interneurons that in turn synapse with LMNs. Lesions affecting UMNs result in UMN signs. These UMN signs result from an increase in the excitatory state of LMNs. Upper motor neuron signs include depression or loss of voluntary motor activity, normal or exaggerated segmental spinal reflexes, appearance of abnormal spinal reflexes (e.g., crossed extensor reflex), increased muscle tone, and muscle atrophy due to disuse. Unilateral signs resulting from spinal cord disease are unusual; however, signs frequently are asymmetric. In the majority of cases, a lesion resulting in asymmetric signs is located on the side of greater motor and sensory deficit.

CERVICAL (C1 TO C5)

Fatal respiratory paralysis resulting from interruption of descending respiratory motor pathways or damage to motor neurons of the phrenic nerve (C5 to C7 spinal cord segments) occurs in a complete transverse myelopathy. Lesions that are less than complete may not affect respiration, and in such cases other signs may be detectable. Ataxia and paresis of all four limbs usually are seen. Tetraplegia rarely is seen, as lesions of sufficient severity to cause tetraplegia also produce respiratory paralysis. Hemiparesis occasionally may be present in association with a cervical lesion. Lesions of the cervical spinal cord may result in paraparesis with minimal neurologic deficits in thoracic limbs. The reasons for this are poorly understood.

Spinal reflexes and muscle tone are intact in all limbs, and may be normal or exaggerated. Muscle atrophy generally is not present. However, disuse atrophy may develop in cases that have a chronic course. Anal reflexes are intact and anal tone usually is normal. Bladder dysfunction may occur due to detrusor muscle areflexia, with normal or increased urinary sphincter tone, and loss of voluntary control of micturition. Reflex dyssynergia may also be seen. Although voluntary control of defecation may be lost, reflex defecation occurs when feces are present in the rectum. Horner's syndrome (ptosis, miosis, and enophthalmos) rarely may be present in an animal with a severe destructive cervical lesion. Proprioceptive positioning and other postural reactions usually are depressed or absent in all limbs. Complete loss of proprioceptive positioning may occur without detectable loss of pain perception. Cervical hyperesthesia ("spasms," apparent pain on palpation, cervical rigidity, and abnormal neck posture) may be seen in some animals with cervical myelopathy. It should be noted that apparent cervical pain may also be seen in association with lesions affecting the brain stem and cerebrum. Occasionally an animal may hold a thoracic limb in a partially flexed position, a posture that may be consistent with Cl to C5 nerve root or spinal nerve entrapment ("root signature"), although this posture is seen more commonly with a disorder affecting the cervical enlargement. Disorders that affect the cervical region of the spinal cord must be differentiated from brain lesions that result in tetraparesis. This may be accomplished by doing a complete neurologic examination; however, occasionally this distinction may be difficult. In most circumstances a cervical lesion does not result in neurologic deficits attributable to involvement of the medulla oblongata; however, there are several notable exceptions to this rule. Positional strabismus, resulting from loss of the vertebral joint proprioceptive input to the attitudinal reflexes, may be seen in association with a cranial cervical lesion (Cl to C3 spinal cord segments). A cranial cervical lesion may also cause facial hypesthesia as a result of involvement of the spinal nucleus and tract of the trigeminal nerve. Cranial cervical trauma often results in clinical signs referable to injury to the caudal brain stem (head tilt, pharyngeal paresis, facial paresis) or cerebellum. The Schiff-Sherrington sign (syndrome or phenomenon) consists of hypertonicity of thoracic limb muscles and hyperextension of the neck, and is seen in association with spinal cord lesions caudal to the cervical enlargement. It is essential to differentiate this sign from thoracic limb hypertonicity resulting from a cervical lesion.

CERVICAL ENLARGEMENT (C6 TO T2)

Ataxia and paresis of all four limbs usually are present. Occasionally paresis of thoracic limbs and paralysis of pelvic limbs may be seen. Spinal reflexes and muscle tone may be normal or decreased in thoracic limbs, and normal or exaggerated in pelvic limbs. The nature of thoracic limb reflex alterations depends on the exact craniocaudal location of a lesion within this region. Muscle atrophy often is severe in thoracic limbs. Panniculus reflex may be depressed or absent unilaterally or bilaterally due to interruption of the LMNs involved in this reflex (C8 and Tl spinal cord segments). If bladder dysfunction occurs, it is similar to that observed with a lesion in the cervical region, with loss of voluntary control of urination. Anal reflexes and anal tone most often are normal although voluntary control of defecation may be absent. Unilateral Horner's syndrome is commonly observed with a spinal cord lesion of the cervical enlargement, particularly a lesion involving Tl to T3 spinal cord segments or nerve roots. Proprioceptive positioning and other postural reactions usually are depressed in all four limbs. Alterations in these functions may be more pronounced in the pelvic limbs than in thoracic limbs. Occasionally, proprioceptive positioning is absent only in a thoracic and pelvic limb on the same side. Severe depression or loss of pain perception rarely is seen in association with a lesion of the cervical enlargement, except in intrinsic myelopathies (e.g., ischaemic myelopathy). There may be hyperesthesia at the level of a lesion of the cervical enlargement, thoracic limb lameness, or apparent neck pain.

THORACOLUMBAR (T3 TO L3)

The majority of spinal cord lesions of dogs or cats occur in this region. Typically thoracic limb gait is normal, and paresis and ataxia, or paralysis, are seen in pelvic limbs. Thoracic limb spinal reflexes are normal. Pelvic limb spinal reflexes and muscle tone are normal to exaggerated, depending on the severity of the lesion. Muscle atrophy is not seen in thoracic limbs. Pelvic limb muscle atrophy, if present, is the result of disuse and is seen in animals with a severe, chronic lesion. Anal reflexes and anal tone usually are normal or exaggerated. Voluntary control of defecation may be lost. Reflex defecation occurs when the rectum is filled with feces; however, it may not be at an appropriate time or place. Degree of bladder dysfunction varies depending on the severity of a spinal cord lesion. There may be loss of voluntary control of urination, detrusor muscle areflexia with normal or increased urinary sphincter tone, or reflex dyssynergia in which initiation of voiding occurs and is stopped by involuntary contraction of the urethral sphincter. The bladder can be manually expressed in some animals, but not in others due to increased tone of the urinary bladder sphincter. This is often referred to as a "UMN bladder". Although "overflow" incontinence may occur with lesions of the spinal cord in this region secondary to overfilling of the bladder, detrusor muscle tone and urinary sphincter tone are present, distinguishing this type of incontinence from that due to lesions of the lumbar enlargement and cauda equina ("LMN bladder"). Proprioceptive positioning and other postural reactions are normal in the thoracic limbs, and depressed or absent in the pelvic limbs. Pain perception is normal in the thoracic limbs and may be normal, depressed, or absent in the pelvic limbs. Panniculus reflex may be reduced or absent caudal to a lesion. In the lumbar region the panniculus reflex may be present in lesions caudal to L3 due to the pattern of cutaneous innervation of lumbar spinal nerves. There may be an area of hyperesthesia at the level of a lesion. The Schiff-Sherrington sign may be seen with a lesion in this region. Usually it is an indication of an acute and severe spinal cord lesion, although such a lesion may be reversible.

LUMBAR ENLARGEMENT (L4 TO CD5) AND CAUDA EQUINA

Involvement of this region by a pathologic process results in varying degrees of pelvic limb paresis and ataxia, or paralysis, and is often accompanied by dysfunction of bladder and by paresis or paralysis of anal sphincter and tail. Thoracic limb function is normal. Pelvic limb reflexes and muscle tone are reduced or absent. Muscle atrophy often is present in pelvic limbs. Conscious proprioception and other postural reactions may be reduced or absent in pelvic limbs. Anal tone and anal reflexes are reduced or absent. The rectum and colon may become distended with feces, and fecal incontinence, with continual leakage of feces, is often seen. Constipation may result from the inability to void feces. Paresis or paralysis of the urethral sphincters and detrusor muscle result in overfilling of the bladder and "overflow" incontinence. Affected animals have a large residual volume of urine in the bladder, and the bladder is easily expressed manually ("LMN bladder"). The Schiff-Sherrington sign occasionally may be seen with an acute lesion affecting this region of the spinal cord. The term cauda equina is used to describe the lumbar, sacral, and caudal nerve roots and spinal nerves as they extend caudally from the caudal tip (conus medullaris) of the spinal cord within the vertebral canal. Lesions that affect cauda equina result in clinical signs that are indistinguishable from lesions that affect the spinal cord segments from which the nerves of the cauda equina arise (L6 to Cd5).

Table 1. Diseases affecting the cervical region (spinal cord segments C1-C5) (common causes are included in italics).
Hereditary/congenital Atlantoaxial subluxation Congenital vertebral anomalies

Syringomyelia/hydromyelia Myelodysplasia Spina bifida Pilonidal sinus/epidermoid cyst/dermoid cyst Spinal stenosis Degenerative Intervertebral disc disease (Type I/II) Cervical spondylomyelopathy Spondylosis deformans Synovial cyst Inflammatory/infectious Diskospondylitis Corticosteroid responsive meningitis-arteritis Distemper myelitis FIP meningitis/myelitis Bacterial/fungal/rickettsial/protothecal myelitis Protozoal myelitis Spinal nematodiasis Neoplastic Neoplasia Traumatic Spinal cord trauma Vascular Ischaemic myelopathy Progressive hemorrhagic myelomalacia Hemorrhage Vascular malformations & benign vascular tumors Nutritional Hypervitaminosis A in cats Idiopathic Spinal intra-arachnoid cysts Osteochondromatosis Calcinosis circumscripta

Table 2. Diseases affecting the cervical enlargement (spinal cord segments C6-T2) (common causes are included in italics).
Hereditary/congenital Congenital vertebral anomalies Spina bifida Myelodysplasia Syringomyelia/hydromyelia Pilonidal sinus/epidermoid cyst/dermoid cyst Degenerative Intervertebral disc disease Type I/II Cervical spondylomyelopathy

Spondylosis deformans Synovial cyst Inflammatory/infectious Diskospondylitis Distemper myelitis FIP meningitis/myelitis Protozoal myelitis Granulomatous meningoencephalomyelitis Spinal nematodiasis Neoplastic Neoplasia Traumatic Spinal cord trauma Vascular Ischaemic myelopathy Progressive hemorrhagic megalomaniac Vascular malformations & benign vascular tumors Nutritional Hypervitaminosis A in cats Idiopathic Spinal intra-arachnoid cysts Osteochondromatosis

Table 3. Diseases affecting the thoracolumbar region (spinal cord segments T3-L3) (common causes are included in italics).
Hereditary/congenital Congenital vertebral anomalies Spina bifida Myelodysplasia Syringomyelia/hydromyelia Pilonidal sinus/epidermoid cyst/dermoid cyst Spinal stenosis Degenerative Intervertebral disk disease Type I/II Degenerative myelopathy Spondylosis deformans Synovial cyst Diffuse idiopathic skeletal hyperostosis Inflammatory/infectious Diskospondylitis Distemper myelitis FIP meningitis/myelitis Bacterial/fungal/Rickettsial/protothecal myelitis Protozoal myelitis Spinal nematodiasis

Granulomatous meningoencephalomyelitis Neoplastic Neoplasia Traumatic Spinal cord trauma Vascular Ischemic myelopathy Progressive hemorrhagic myelomalacia Hemorrhage Vascular malformations & benign vascular tumors Idiopathic Osteochondromatosis Spinal intra-arachnoid cyst Calcinosis circumscripta

Table 4. Diseases affecting the lumbar enlargement (spinal cord segments L4-CD5 and cauda equina) (common causes are included in italics).
Hereditary/congenital Spina bifida Sacrocaudal dysgenesis Congenital vertebral anomalies Myelodysplasia Syringomyelia/hydromyelia Pilonidal sinus/epidermoid cyst/dermoid cyst Spinal stenosis Degenerative Intervertebral disk disease Type I/II Lumbosacral vertebral canal stenosis Spondylosis deformans Diffuse idiopathic skeletal hyperostosis Synovial cyst Inflammatory/infectious Diskospondylitis Protozoal myelitis Distemper myelitis FIP meningitis/myelitis Bacterial/fungal/Rickettsial/protothecal myelitis Spinal nematodiasis Granulomatous meningoencephalomyelitis Neoplastic Neoplasia Traumatic Spinal cord trauma Vascular Ischemic myelopathy

Progressive hemorrhagic myelomalacia Hemorrhage Vascular malformations & benign vascular tumors Idiopathic Osteochondromatosis Spinal intra-arachnoid cyst

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Richard A. LeCouteur, BVSc, PhD, DACVIM (Neurology), DECVN University of California Davis, CA, USA

Intervertebral Disc Disease: Old and New Tips to Localise the Lesion WSAVA/FECAVA/BSAVA World Congress 2012 Daisuke Ito, DVM, PhD Nihon University, Fujisawa, Kanagawa, Japan
23011742

Intervertebral disc disease is one of the most common disorders in dogs (but rare in cats), and symptomatic disease can arise at any site where there is an intervertebral disc, but there are specific predilection sites. To perform proper treatment, especially surgical intervention, localising the lesion is important. The fundamental method to localise the spinal cord lesion including intervertebral disc disease is to localise the lesion into one of following spinal cord segments: cervical (C15), cervicothoracic (C6T2), thoracolumbar (T3L3) and lumbosacral (L4S3). Using the information associated with clinical signs, postural reactions and LMN (lower motor neuron) and UMN (upper motor neuron) signs of the four limbs obtained by neurological examination, the examiner can localise the lesion. Spinal Cord Dysfunction and Neurological Signs Cervical Spinal Cord (C15) A lesion in this spinal cord segment can cause hemiparesis, hemiplegia, tetraparesis or tetraplegia. However, some cases only show neck pain without proprioceptive or gait deficits. Clinical signs are typically ipsilateral to the lesion. Patients with lesions in this area may show decreased or absent postural reactions in four limbs. A C15 lesion might cause UMN signs to both the thoracic limbs and pelvic limbs but is not always apparent. Cervicothoracic Spinal Cord (C6T2) Similar to C15 lesion, the patients with C6T2 spinal cord lesion might show similar gait abnormalities with decreased or absent postural reactions on neurological examination. The absolute difference of neurological disorders between cervical and cervicothoracic lesions is the reflexes in the four limbs. A C6T2 lesion typically causes LMN signs to the thoracic limbs (if the lesion involves the grey matter or nerve roots) and UMN signs to the pelvic limbs. Thoracolumbar Spinal Cord (T3L3) Clinically the patients with this lesion typically show symmetric/asymmetric paraparesis or paraplegia. In neurological examination, the thoracic limbs have normal postural reactions and spinal reflexes, and the pelvic limbs have decreased or absent postural reaction with UMN signs of spinal reflex. Lumbosacral Spinal Cord (L4S3) Lesions in this spinal cord segment cause signs of LMN dysfunction in pelvic limbs and/or bladder function with symmetric/asymmetric paraparesis or paraplegia. L46 lesions cause signs of LMN dysfunction in the pelvic limbs with decreased to absent patellar reflex and intact

withdrawal reflex, because the neurons of the femoral nerve are in this area. L7S3 lesions cause signs of LMN dysfunction in the area which innervates the sciatic nerve (decreased to absent withdrawal reflex and gastrocnemius reflex), the pudendal nerve (decrease to absent perineal reflex) and the pelvic nerve (LMN bladder dysfunction). Spinal Radiography Survey radiographs of vertebrae are often performed at the suspected area of the lesion during the diagnostic evaluation. However, the limitation is that the spinal cord and non-mineralised intervertebral disc material cannot be seen on these radiographs. Therefore spinal radiographs often cannot reveal any abnormal findings of soft tissue spinal compressive disease such as Hansen type I disc extrusion. The survey radiographic findings to suggest intervertebral disc extrusion are: Wedging or collapse of the intervertebral disc space Decrease in the articular facet joint space dimensions Thinning or alteration in the intervertebral foramen (shaped like horse's head) Radio-opaque disc material apparently within the spinal canal (Figure 1) To evaluate these findings on spinal radiographs, it is important that the spine should be straight and the radiographic beam centred directly over the suspected area to avoid misinterpretation of vertebral alignment, intervertebral foraminal size and intervertebral disc space. In addition, the presence of these findings does not always provide accurate lesion and definitive diagnosis. Therefore an advanced imaging modality that can describe intervertebral disc protrusion/extrusion and compression of the spinal cord, such as myelography, computed tomography (CT) scanning and magnetic resonance imaging (MRI) must be performed for accurate localisation. Figure 1. Survey spinal radiograph (lateral view).

Mineralised intervertebral disc material is apparently seen within the spinal canal (arrow) with collapse of intervertebral disc space (arrowhead). Myelography During the past two decades, myelography has been most commonly used to diagnose and localise the lesion of intervertebral disc disease. Myelography provides a white parallel outline of the spinal cord through an injection of radio-opaque contrast medium into the subarachnoid space (Figure 2). This technique can be used to detect intervertebral disc material compressing the spinal cord by observing the absence of the contrast medium in the sub-arachnoid space. Herniated disc material is usually seen ventral or lateral to the spinal cord, but is sometimes found dorsally. The disadvantages of myelography are: Invasiveness because the spinal needle enters the spinal cord in close proximity to the filum terminale and the spinal cord (for lumbar myelography) to inject contrast medium into ventral arachnoid space. It is difficult to localise the lesion when the spinal cord swelling occurs.

Figure 2. Myelography (healthy dog).

Computed Tomography CT is also useful to detect herniated/protruded intervertebral disc material in the spinal canal. The degenerated disc material is seen with a hyperdensity (white). The advantage of CT is that images can be reconstructed on computer and several views including sagittal, transverse and horizontal images can be made to evaluate the lesion site (Figure 3). However it is very difficult to assess the spinal cord itself because it is poorly distinguished from other soft tissue within the vertebral canal. In addition, it is difficult to distinguish herniated disc material and haemorrhage because both lesions show hyperdensity on CT images. Therefore CT myelography, CT with a subarachnoid injection of the contrast medium, might be needed for further evaluation. Figure 3. Reconstructed CT images (sagittal view, top; transverse view, bottom).

A hyperdense lesion can be seen on both the sagittal (arrow) and transverse (arrowhead) views. Magnetic Resonance Imaging (MRI) Because of its efficient ability to reveal the localisation of intervertebral disc disease and the condition of the spinal cord, MRI is rapidly becoming the gold standard imaging modality. MRI allows concise localisation of extruded or protruded disc material including the affected area (right or left, ventral or dorsal) and extent of extruded disc material by evaluating multiple planes. The MR images are usually collected at least in sagittal and transverse T1-weighted, T2weighted and contrasted T1-weighted images. Sagittal planes are important for understanding anatomical structures of the affected region of the intervertebral disc and the spinal cord, and transverse images are important to know the exact location of any compressive material surrounding the spinal cord in a cross-sectional plane (Figure 4). Hence these two different views

are important to recognise the location of the lesion especially if surgical intervention is to occur. Additional views such as dorsal (coronal) images might be helpful to understand the location of the lesion and anatomical variations. However, we would recommend other types of image using FE3D sequence (TR 45.9 ms, TE 6.8 ms) to reveal the nerve roots called a 'nerve root image', and MR myelography using fast spin echo single shot (TR 6000 ms, TE 1000 ms) to describe the line of cerebrospinal fluid (CSF) in preference to taking simple dorsal images. The nerve root image can show accurate localisation of herniated disc material in association with nerve root (Figure 5, arrow). MR myelography can describe the lesion by detecting disappearance of CSF line (Figure 5, arrowhead). Figure 4. MR images (midsagittal T2-weighted image, above and transverse T2weighted image, left).

An extruded intervertebral disc material compresses the spinal cord (arrow and arrowhead respectively). Figure 5. MR nerve root image (left) and MR myelography (right).

Herniated disc material is compressing the spinal cord (white arrow) and the nerve root adjacent to the disc material is apparent (black arrow). Disappearance of CSF line can be seen on MR myelography (arrowhead).

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Daisuke Ito, DVM, PhD Nihon University Fujisawa, Kanagawa, Japan

The Neurological Examination British Small Animal Veterinary Congress 2007 J. Penderis, BVSc, MVM, PhD, CertVR, DECVN, MRCVS Senior Lecturer in Veterinary Neurology, Institute of Comparative Medicine, Faculty of Veterinary Medicine, University of Glasgow Glasgow, UK
18273874

Before embarking on the neurological examination it is essential to always first obtain a good history and perform a detailed clinical examination. In part this is to exclude the possibility of non-neurological disease, but in forebrain disease the major clinical sign is often altered behaviour. What are we trying to achieve by performing a neurological examination: Establish if there is a neurological lesion. Problems that may mimic a neurological lesion include metabolic problems (e.g., hepatic encephalopathy) and bilateral orthopaedic problems. Localise the lesion Determine the severity of the lesion Establish possible causes Establish a prognosis How Do We Perform the Actual Neurological Examination? We first start with the hands-off examination, where we assess the animal as it walks around and interacts with its surroundings (usually the consulting room) Then start with the hands-on localisation (involving pinpointing the lesion to a smaller and smaller area) We also assess for signs of intracranial or cranial nerve disease Hands-Off Examination It is essential to watch the animal walk and interact with the surroundings. Some abnormalities (for example a high stepping gait) are only apparent when the animal walks, and the animal may appear normal at rest. Certain abnormalities may suggest that the problem actually lies within the brain (or cranial nerves) and not the spine, for example circling or a head tilt. The hands-off examination allows evaluation of: posture (e.g., head tilt, wide-based stance), gait (e.g., ataxia, circling) and mental status (e.g., alert, depressed).

Hands-On Localisation The idea of the hands-on localisation is to pinpoint stepwise the lesion to a progressively smaller area. Summary of the basic steps of the hands-on examination: Determine which limbs are affected Does the lesion affect the reflex arcs to the limbs (i.e., upper motor neuron or lower motor neuron)? Are the tail, bladder and anus affected (i.e., the sacral segments)? Accurate localisation to specific spinal cord segments (e.g., by focal pain or panniculus reflex) Determine the severity of the lesion Determine Which Limbs are Affected Not all spinal cord pathways are equally susceptible to injury and therefore when deciding whether a limb is affected we use that function that is lost first, i.e., proprioception and evaluating for weakness: Evaluating the animal walking has already partly assessed proprioception and weakness Paw position response--tests conscious proprioception Hopping--allows you to assess for weakness in each individual limb Based on which limbs are affected some information about the localisation should be apparent: All four limbs affected: lesion is likely to be from the brain to the cervical enlargement (cranial to T3 spinal cord segment) or a polyneuropathy/polymyositis

If the pelvic limbs are affected and the thoracic limbs are normal, this indicates a spinal cord lesion behind the cervical enlargement (caudal to T3), or a pelvic limb peripheral nerve or muscle lesion

If just one thoracic limb is affected the lesion is likely to be on that side in peripheral supply to that limb Does the Lesion Affect the Reflex Arcs (upper motor neuron or lower motor neuron)? If the reflex arcs to the limbs are involved then one or more of the abnormalities in Figure 1 may be present. Spinal reflexes which are routinely assessed include the extensor carpi radialis (may be hard to elicit in cats and small dogs), patellar reflex and withdrawal reflex (pedal or flexor reflex). Figure 1. Upper motor neuron or lower motor neuron lesions. Factors evaluated Resting muscle tone Limb flexion and extension Spinal reflexes Muscle atrophy UMN lesion Normal Slight resistance Normal to exaggerated Little and late (disuse) LMN lesion Normal to decreased Decreased resistance Normal, decreased or absent Early and severe (neurogenic)

Are the Tail, Bladder and Anus Affected (i.e., the sacral and caudal segments)? Assess the anal reflex, bladder function and tail function. If bladder function is impaired then it is important to ascertain whether there is increased sphincter tone (with urinary retention and overflow) or decreased sphincter tone (with a half full, flaccid bladder, which is very easy to express).

Based on the examination so far the lesion should localise to (unless multifocal or extensive) one of the areas illustrated in Figure 2. Figure 2. Localisation of lesions.

Accurate Localisation to Specific Spinal Cord Segments If the lesion is focal then it may be further pinpointed by evaluation for: Focal pain LMN lesion: assess which muscle groups are affected Panniculus reflex: allows accurate localisation in the T3-L3 region of the spinal cord and assesses the brachial plexus (outflow of the panniculus reflex) Determining the Severity of the Lesion Due to varying susceptibility of different spinal pathways injuries can usually be graded. The critical prognostic feature is the presence or absence of conscious pain in the affected limbs.

Grade 0 Normal 1 Pain: not severe enough to result in any neurological dysfunction 2 Paresis with or without pain 3 Plegia: total loss of voluntary movement in the affected limbs (and/or tail) 4 Plegia with loss of voluntary urinary function 5 Plegia with loss of voluntary urinary function and loss of deep pain Syndrome Approach to Intracranial and Cranial Nerve Lesions If the lesion could involve the brain then a simple method of localising intracranial and cranial nerve (CN) lesions is to try and group them in one of three 'syndromes' or regions of the brain. The neurological deficits are described and an attempt is made to fit the neurological abnormalities into one of the three syndromes. Multifocal lesions may affect more than one region. The syndromes include: The forebrain and/or the associated cranial nerves I and II The cerebellum The brainstem and/or the associated cranial nerves III to XII Clinical Signs of Forebrain Lesions Seizures Altered behaviour (e.g., loss of house training, loss of obedience training, uncharacteristic behaviour) Circling: in the majority of cases this is towards the lesion, but can be away from the lesion Head turn (the head is not tilted: the ears are still horizontal): usually towards the lesion Conscious sensory deficits opposite to the lesion. This includes decreased facial sensory awareness, conscious proprioceptive deficits and the so-called 'hemi-neglect' or 'hemi-inattention' syndrome Blindness opposite to the lesion (central blindness, i.e., with intact pupillary light reflexes) Decreased levels of consciousness, typically to the level of a stupor An important differential diagnosis of diffuse and symmetrical cerebral lesions is the presence of a metabolic or toxic cause, e.g., hypoglycaemia or hepatic encephalopathy. Clinical Signs of Cerebellar Disease

The cerebellum has an important function in controlling and moderating movements of the limbs, body and head and in the unconscious maintenance of balance. Diffuse cerebellar lesions will therefore result in a loss of this moderating influence and interfere with the unconscious maintenance of balance, with clinical signs of: Symmetrical ataxia with no loss of strength Dysmetric gait (altered rate, range or force of movement), usually with an exaggerated limb movement (hypermetria) but in some instances decreased limb movements (hypometria) Truncal ataxia and even a truncal sway Head tremor Muscle hypertonia Bilateral menace response deficits in the presence of intact vision and facial nerve function Unilateral cerebellar lesions will usually result in deficits on the same side as the lesion. Clinical Signs of Brainstem Disease The brainstem, as the continuation of the spinal cord tracts and the site of numerous tightly packed cranial nerve nuclei, is an extremely important region of the brain. Damage to the brainstem will usually result in damage to numerous adjacent brainstem structures. These include: Ascending afferent pathways (primarily the proprioceptive tracts) Descending efferent pathways (primarily the motor tracts, but rarely the sympathetic pathways) Brainstem nuclei of cranial nerves III to XII Brainstem nuclei controlling (amongst others) motor function and the vital functions (respiration and cardiac function). Interference with the vital brainstem functions will usually result in rapid death due to failure of respiratory function Alteration in mentation. The observed clinical spectrum varies from depression to stupor to coma The important cranial nerves in clinical practice associated with the brainstem: III oculomotor nerve, IV trochlear nerve and VI abducent nerve Most important function: motor to the extraocular muscles and pupil constrictor

Lesion: dilated pupil and/or abnormal eye position or paralysis of the extraocular muscles V trigeminal nerve Function: motor to the masticatory muscles and sensation to the face and eyeball Lesion: dropped jaw (bilateral motor lesion). Unilateral masticatory muscle atrophy (unilateral motor lesion). Loss of sensation to face, cornea or nasal mucosa (sensory lesion). VII facial nerve Most important function: motor to the muscles of facial expression Lesion: look for drooping lip or ear with drooling saliva from affected side of mouth, inability to blink, deviation of the face to the unaffected side and/or dry eye and nose in combination VIII vestibulocochlear nerve Function: hearing and balance Lesion: ipsilateral deafness and ipsilateral vestibular dysfunction XI hypoglossal nerve Function: motor to the tongue muscles Lesion: bilateral lesion--tongue paralysis. Unilateral lesion--unilateral tongue atrophy and protrusion of tongue to affected side, although in some cases the tongue can deviated towards the unaffected side. Author Information (click the author's name to view other papers and abstracts submitted by this author) Jacques Penderis, BVSc, MVM, PhD, CertVR, DECVN, MRCVS Institute of Comparative Medicine, Faculty of Veterinary Medicine University of Glasgow Glasgow, UK

Localising Neurologic Lesions Using the NeuroMap: Brain World Small Animal Veterinary Association World Congress Proceedings, 2013 Christine E. Thomson, BVSc (Hons), DACVIM (Neurology), DECVN, PhD VetLearn, New Zealand Veterinary Association, Massey University, Palmerston North, New Zealand
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This talk follows on from the previous talk, so please refer to those notes prior to reading this. The NeuroMap and accompanying table are designed to help you localise neurological lesions; this is the first and most fundamental step in managing a neurological case. Once you've localised the lesion, then you can list the possible causes and make a diagnostic plan. The NeuroMap is based on mapping the main neural functions on a diagram of the nervous system. If a lesion is in a particular area, you can read from the NeuroMap which neural functions could be disrupted and conversely, which neural functions will be normal. Or, given a set of clinical signs (normal and abnormal), you can work out from the NeuroMap where the lesion is likely to be located. The NeuroMap depicts the location of the main neural functions tested in the neurological examination, including: behaviour and arousal; ascending sensory systems (tactile, proprioception and nociception); motor function (posture and gait); cranial nerve function; and spinal reflexes. In this session, we'll discuss further the components evaluated in a neurological examination and add them to a BrainMap (see Figure 1), from which is constructed a ready reference table (Table 2) that can be used in conjunction with the BrainMap for localizing lesions. Functional Brain Divisions Functionally, there are three main regions of the brain - the forebrain, brainstem (midbrain, pons and medulla oblongata), and the cerebellum. Each region is associated with characteristic neurological signs, so we talk about animals having a region-specific localisation - e.g., forebrain disease, brainstem disease, or cerebellar signs. Functions Assessed During the Neurological Examination 1. Behaviour is primarily associated with the forebrain (limbic system). However, it can only be expressed if other neural functions (e.g., awareness and motor function) are normal. 2. Awareness and arousal (consciousness) are dependent on the function of the ascending reticular activating system (ARAS). This is located in the brainstem and has diffuse projections throughout the forebrain. Thus, decreased arousal can occur with focal lesions in the brainstem (e.g., tumour) or diffuse lesions of the cerebrum (e.g., encephalitis). In veterinary medicine, it is useful to talk about five different arousal levels.

Table 1. Arousal level Normal Obtunded Stuporous Comatose Description Bright, alert and responsive Dull; tends to fall asleep if left undisturbed, but can be aroused by non-noxious stimuli Somnolent; requires a noxious stimulus to arouse it Unconscious; cannot be roused by even a noxious stimulus

Brain dead No cerebrocortical electrical activity, no brainstem reflex function Note: 'Depressed' is a psychological term and is inappropriate. 3. Proprioception is awareness of body position (see previous session notes). Input from the limbs and body is via spinal nerves and the spinal cord travelling to the ipsilateral cerebellum (subconscious proprioception) or the contralateral forebrain (conscious proprioception). Head proprioception arises from the vestibular apparatus in the inner ear, travels to the brainstem and then cerebellum (SCP) or forebrain (CP). 4. Motor function in quadrupeds is controlled by motor centres in the brainstem (for semiautomatic activities such as locomotion) and from the motor cortex in the contralateral cerebrum for voluntary motor activity (learned, skilled). Therefore, brainstem lesions can severely perturb gait (paresis), while forebrain lesions usually have minimal effect on gait but will affect learned movements, e.g., cat playing with a feather. Upper motor neurons (UMN or 'central MN') arise from both motor centres and influence brainstem and spinal cord lower motor neurons (LMN or peripheral MN). The cerebellum functions to coordinate the activity of extensor and flexor muscles to achieve the correct tone in opposing muscles for sustaining posture and smoothing movement. Dysfunction of agonist-antagonist contraction causes tremor. Loss of subconscious proprioceptive input to the cerebellum results in ataxia (incoordinated movement). The cerebellum uses SCP input to influence the output from the UMN centres, thereby ensuring that movement occurs with the correct rate, range, and force of movement. This is called metria. Overall, the output from the cerebellum is inhibitory; thus, cerebellar dysfunction can cause hypermetria and spasticity. A specific region of the cerebellum processes vestibular input; lesions in that region can cause vestibular signs (nystagmus, head tilt). 5. Cranial nerves are primarily associated with the brain; therefore, animals with spinal cord lesions have intact cranial nerve function. As specific cranial nerves are associated with different areas of the brain, cranial nerve signs can be quite localising, e.g., strabismus may suggest a rostral brainstem lesion, as that is the site of attachment of CNN III and IV, innervating extraocular muscles.

6. Reflexes involving both spinal and cranial nerve reflexes are tested during the neurological examination. Those reflexes involving cranial nerves may be compromised with brain lesions, but not spinal cord lesions. Conversely, spinal cord reflexes, but not cranial nerve reflexes, may be compromised with spinal cord lesions. The NeuroMap Figure 1 depicts the location of the main neural functions tested in the neurological examination. If you cover a region of the brain on the NeuroMap (e.g., with a coin) representing a lesion, you will be able to see which neurological functions will be compromised and which will still function normally. Conversely, if you have a case with specific neurological deficits, identify the pathways associated with each deficit and see where they coincide - that is likely to be the location of the lesion. If you cannot account for all signs with a single lesion, then the animal may have multifocal disease, which is associated with specific aetiologies (e.g., inflammation or tumour). For example, consider an animal that is obtunded, blind in the right eye, and knuckles (CP deficit) on the right side. Identify the CP pathway on the NeuroMap: the lesion could be in the spinal cord or forebrain (contralateral). Vision is also associated with the forebrain (primarily contralateral); thus, the left forebrain is likely to be involved. Obtundation can occur with diffuse lesions of the forebrain, too, so the lesion is probably quite large. If the function of other cranial nerves (IIIXII), and general locomotion, coordination, and spinal reflexes are intact, then this also supports a lesion in the forebrain and not the brainstem, cerebellum, or spinal cord. Thus, both the signs of dysfunction and signs of normal function have helped you localise the lesion.

Figure 1. The NeuroMap of the brain

Roman numerals refer to cranial nerves. Table 2. Summary of neural signs that can occur with lesions in different parts of the brain Function Conscious proprioception Subconscious Proprioception Nociception Motor systems Forebrain Yes, sensory cortex No Yes Yes No Yes Brainstem Yes Yes, caudal brainstem Cerebellum No Yes Spinal cord Yes Yes

Yes, important for Yes, major site of planning motor UMN nuclei in

Yes, for motor Yes coordination, but UMN tracts

function and voluntary movement Motor cortex (UMN), functions in voluntary motor activity, but has a minor role in gait. No LMNs. Behaviour, emotion and memory Arousal Yes Limbic system Yes, the ARAS projects to widespread areas of forebrain CN I, II

quadrupeds; important in posture and locomotion. Cranial nerves have LMNs innervating head and neck muscles

no UMNs (no weakness)

LMNs innervating neck, body, limbs and tail

No

No

No

Yes (the ascending reticular activating system (ARAS) CN IIIXII

No

No

Cranial nerves

CN VIII head and eyeball positionb Intact

Noa

Spinal reflexes

Intact

Intact

Could be reduced/lost

a = Part of CN XI (accessory nerve) arises from the cervical spinal cord, but it is hard to see signs of its dysfunction with lesions in this area of spinal cord. b = Important links between the cerebellum and vestibular system mean that some vestibular signs may occur with lesions in certain parts of the cerebellum. Note: Seizures will only occur with forebrain disease. Figure and tables reprinted with permission from: Thomson C, Hahn C. Veterinary Neuroanatomy: A Clinical Approach. Elsevier Health Sciences; 2012. ISBN 9780702034824. References 1. Thomson C, Hahn C. Veterinary Neuroanatomy: A Clinical Approach. Elsevier Health Sciences; 2012. ISBN 9780702034824. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. Thomson, BVSc (Hons), DACVIM (Neurol), DECVN, PhD VetLearn, New Zealand Veterinary Association Massey University Palmerston North, New Zealand

The Neuromap: A Simple Guide to Localizing Neurological Lesions - The Brain and Cranial Nerves ACVIM 2012 Christine E. Thomson, BVSc(Hons), DACVIM(Neurology), DECVN, PhD Palmerston North, New Zealand
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This session follows on from Session 35, The NeuroMap: A Simple Guide to Localizing Neurological Lesions - Spinal Cord and Peripheral Nervous System. It uses the same key concepts discussed in Session 35 as follows: 1. The NeuroMap, in which the five main neural functions tested in the neurological examination are mapped onto a diagram of the brain. These functions are behaviour and arousal; ascending sensory systems (tactile, proprioception and nociception); motor function (posture and gait); cranial nerve function, and spinal reflexes. Spinal sensitivity (hyperpathia) can further localise the lesion in spinal cord cases. 2. Using the neurological examination to identify both the neural functions that are normal and those that are abnormal (dysfunctional). See Figure 1, Session 35. 3. Using the battery and light bulb analogy to remember that signs of dysfunction can be due to a lesion located anywhere along the neural pathway - at the origin, middle of the pathway or at the pathway termination. 4. Remembering the NeuroRAT (Session 35, Figure 2 & Table 1) to help differentiate between lesions affecting upper (central) motor neurons (UMNs) and lower (peripheral) motor neurons (LMNs). See Session 35 re 'central' and 'peripheral' MNs. 5. A reflex has three parts to it - input from a sensory receptor in the periphery, a central connection in the CNS (brain or spinal cord, for reflexes involving the cranial and spinal nerves, respectively) and a LMN that connects back to the muscle via a neuromuscular junction. Damage to any one of those components will cause reduction/loss of the reflex. Localising the neurological lesions can be challenging, particularly if it is not something you do frequently. The NeuroMap is a simple, visual aid that can help with localizing lesions in the nervous system. It is accompanied by a ready reference table. A key feature about the NeuroMap is that you don't need a degree in neuroanatomical-ese (terminology) to get a basic understanding of what could be happening in the nervous system of your patient. The NeuroMap is based on mapping out the location of the main functions of the nervous system. Thus, it can be seen from the NeuroMap what neural functions may be disrupted with a lesion in a certain area and conversely, what neural functions will be normal. In this session we'll draw a NeuroMap (see Figure 1) to help with localizing brain lesions and from that construct a ready reference table (Table 2) that can be used in conjunction with the BrainMap.

Functional brain divisions: Functionally, the brain can be divided into three main regions: the forebrain, brainstem (midbrain, pons and medulla oblongata) and the cerebellum. Because clinical signs of brain disease are characteristic for each region, then we talk about animals having a region-specific localization (e.g., forebrain disease, or brainstem disease or cerebellar signs). Neurological Functions Assessed During the Neurological Examination Behaviour is primarily associated with the forebrain (limbic system), but its expression is dependent on other neural functions being normal. Awareness and arousal are associated with the ascending reticular activating system (ARAS) of the brain stem and its diffuse projections into the cerebrum. Clinically, decreased consciousness can be due to focal lesions involving the brainstem or diffuse lesions of the cerebrum. One of the best ways to determine arousal levels is by observation. What is the animal's awareness like when it is left quietly in the environment? As soon as you start handling the animal it will be stimulated, so subtle changes in arousal might be missed. In veterinary medicine, five different levels of arousal can be described. Note: the commonly used term 'depressed' is a psychological term and is inappropriate: 1. Normal - bright, alert and responsive 2. Obtunded - dull, tends to fall asleep if left undisturbed, but can be aroused by non-noxious stimuli 3. Stuporous - somnolent; requires a noxious stimulus to arouse it 4. Comatose - unconscious; cannot be roused by even a noxious stimulus 5. Brain dead - no cerebrocortical electrical activity, no brainstem reflex function Proprioception from the limbs and body travels cranially along the spinal cord. Subconscious proprioception projects to the ipsilateral cerebellum, whereas conscious proprioception projects to the contralateral forebrain (somatosensory cortex) (see session 35 notes). Proprioception for the head is from the vestibular apparatus in the inner ear. Motor function: Upper (central) motor neurons in quadrupeds originate in the forebrain (motor cortex) and brainstem motor nuclei. UMNs influence lower (peripheral) motor neurons that exit the CNS in cranial and spinal nerves, from brainstem and spinal cord, respectively. The motor cortex of the forebrain functions primarily to direct voluntary, learned movements in the head, body, limbs and tail. The motor cortex influences LMNs in the brainstem that give rise to cranial nerves, and LMNs that exit the spinal cord as spinal nerves. The tracts passing into the spinal cord are called pyramidal UMNs as they pass through the structures in the caudal brainstem called the 'pyramids'. In quadrupeds, the brainstem UMN centres are important for posture and locomotion and semi-automatic activities such as chewing and swallowing. Brainstem UMN centres give rise to extrapyramidal UMNs (tracts do not pass through the pyramids) influencing

LMNs in cranial and spinal nerves. Thus, brainstem lesions can severely perturb gait (paresis), while forebrain lesions usually have minimal effect of gait. The cerebellum's job is to coordinate motor function to achieve posture, and the correct rate, range and force of movement ('metria'). It also coordinates the contraction/relaxation of agonist/antagonist muscles acting around the joint. To coordinate motor function, it has to know where the body parts are located in space, so it must constantly receive proprioceptive information from the limbs, body and head (subconscious proprioception). Thus, cerebellar disease can result in altered posture, ataxia (incoordinated gait), hypermetria and tremor. As the cerebellum has a calming down (inhibitory) effect on motor function, cerebellar dysfunction can result in excess motor function; characteristically this causes spasticity. Cranial nerves: Noting cranial nerve dysfunction can be quite localising. Specific cranial nerves are associated with each region of the brain, but clinically they are not associated with spinal cord function. Therefore, an animal with spinal cord disease should have intact cranial nerve function (identifying normal function is just as important as identifying those neural functions that are abnormal in lesion localisation). Conversely in an animal with purely brain disease, the spinal reflexes should be intact. An animal that has multiple cranial nerve signs (e.g., cannot blink and has a droopy ear, has a head tilt, has reduced facial sensation and cannot swallow) probably has brainstem disease affecting cranial nerves VII, VIII, V, IX and X. Such a brainstem lesion will probably have compromised other functions in the brainstem (e.g., mentation, cranially directed proprioceptive tracts and UMN centres). Testing the function of cranial nerves is outlined in Table 1. Reflexes: Both spinal and cranial nerve reflexes are tested. Spinal reflexes should be intact (present) in animals with brain lesions, as the wiring of their reflex arc is intact. Cranial nerve reflexes may be compromised if the cranial nerve, or the region of the CNS associated with the reflex has been damaged. Table 1. Testing the function of cranial nerves. Head function Olfaction Vision

Innervation Ia IIa

Clinical testing

Dysfunction

Observation, odourant such Dysosmia as food Maze test Menace response - IIa & VIIe Pupillary light reflex - IIa & IIIe (parasympathetic) Blindness, dilated pupil Note: mydriasis can also be due to primary ophthalmic disease or CN III dysfunction Anisocoria, Mydriasis ( CN II (input) or CN III parasympathetic output) Miosis ( sympathetic

Pupil size

IIa, IIIe Pupillary light reflex parasympathetic, e Pharmacological testing sympathetic, e

innervation). (Note cerebellar lesions and primary ophthalmic lesions can also affect pupil size) Eyeball position VIIIa IIIe, IVe, VIe Visual tracking of moving objects Eyeball position in different head positions Vestibulo-ocular reflex VIIIa & IIIe, IVe, Vie Tactile stimulation Va different regions of the face - muzzle and ventral eyelid, dorsal eyelid, mandible Palpebral reflex - Va & VIIe (dorsal eyelid ophthalmic br. ventral eyelid - maxillary br) Auriculo-palbebral reflex Va & VIIe (stimulate just in front of the external ear canal) Jaw tone Assess the bulk of the masticatory muscles e.g., temporalis and masseter muscles Strabismus - static (LMN affecting cranial nerves III, IV or VI), - dynamic (vestibular) Facial hypoalgesia - ipsilateral with brainstem disease - contralateral with forebrain disease

Facial sensation

Va - all three branches (ophthalmic, maxillary, mandibular)

Mastication

Ve - mandibular

Muscle atrophy Dropped jaw if bilateral

Facial expression

VIIe

Facial symmetry Facial paresis/paralysis Palpebral reflex Va & VIIe Auriculo-palbebral reflexes Va & VIIe Movement of muzzle, external nares, eyelids, ears Symmetry of position of lip commissures when head is held up vertically. Head position Eyeball position (also involves III, IV, VI) Vestibulo-ocular reflex (VIIIa & IIIe, IVe, VIe) Gait and movement Head tilt, circling, rolling Spontaneous nystagmus; abnormal vestibule-ocular reflex Strabismus Deranged body posture and ataxia

Vestibular function

VIIIa

Pharyngeal function Laryngeal function

IX & X, a & e

Gag reflex (IXa, Xa & IXe, Dysphagia Xe) Salivation Swallowing Phonation Respiration Dysphonia Respiratory stridor laryngeal obstruction, Aspiration Atrophy, paresis/paralysis unilateral or bilateral

X & XI, a & e

Tongue

XIIe

Observation - LMN signs, usage Withdrawal from tactile stimulus

a = afferent (input); e = efferent (output) The NeuroMap (Figure 1) depicts where the main neural functions tested in the neurological examination are located. If you cover a region of the brain on the NeuroMap, representing a lesion in it, you will be able to see which neurological functions will be compromised and which will still function normally. Conversely if you have an animal with particular signs, e.g., blindness in the right eye, knuckling on right forepaw and hind paw, relatively normal gait, and obtundation, you can identify on the NeuroMap where the wiring for one of the functions is, e.g., vision (forebrain). What other functions are passing through this region? Sensory input from both the pelvic and thoracic limbs and arousal are associated with the forebrain. That all fits. The right side of the body is affected. Both vision and conscious proprioception are received in the contralateral forebrain - thus the lesion must be in the left forebrain. As cranial nerves (IIIXII) are functioning normally, and the animal has intact subconscious proprioception, reasonable gait (UMN from the brainstem) then the lesion is not in the brainstem or the cerebellum. Thus, both the signs of dysfunction and signs of normal function have helped you localise the lesion.

Figure 1. The NeuroMap of the brain. Roman numerals refer to cranial nerves.

Table 2. Summary of neural signs that can occur with lesions in different parts of the brain. Function Proprioception a) Conscious b) Subconscious Nociception Yes, somatosensory cortex No Yes Yes Yes, caudal brainstem Yes Yes, major site of UMN nuclei in quadrupeds, important in posture and locomotion. Cranial nerves No Yes No Yes, for motor coordination, but no UMNs (no weakness) Yes Yes Yes Yes UMN tracts LMNs innervating neck, body, limbs and tail Forebrain Brainstem Cerebellum Spinal cord

Motor systems Yes, important for planning motor function and voluntary movement Motor cortex (UMN), functions in voluntary motor

activity, but has a minor role in gait. No LMNs. Behaviour, emotion and memory Arousal Yes Limbic system Yes, the ARAS projects to widespread areas of forebrain

have LMNs innervating head and neck muscles No No No

Yes (the No ascending reticular activating system (ARAS) CN IIIXII CN VIII head and eyeball positionb Intact

No

Cranial nerves CN I, II

Noa

Spinal reflexes Intact

Intact

Could be reduced/lost

a=Part of CN XI (accessory nerve) arises from the cervical spinal cord, but it is hard to see signs of its dysfunction with lesions in this area of spinal cord. Note: seizures will only occur with forebrain disease. b=important links between the cerebellum and vestibular system means that some vestibular signs may occur with lesions in certain parts of the cerebellum References Figures and tables reprinted with permission from Veterinary Neuroanatomy: A Clinical Approach by Christine Thomson and Caroline Hahn, Elsevier Health Sciences, May 2012, ISBN 9780702034824.

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. Thomson, DACVIM Massey University Palmerston North, AL, New Zealand

The Neurological Exam British Small Animal Veterinary Congress 2010 Laurent S. Garosi, DVM, DECVN, MRCVS, RCVS & European Specialist in Veterinary Neurology Davies Veterinary Specialists, Manor Farm Business Park, Higham Gobion, UK
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Introduction The lack of initial thoughts as to where exactly the problem might be within the nervous system and what kind of disease processes may be there is the most common cause of failure in the diagnosis of neurological condition in dogs or cats. Even without specialist facilities for definitive diagnosis, a great deal of information can be gained from the neurological examination with some basic knowledge and a logical stepwise approach. What Are the Goals of the Neurological Examination? The aims of the neurological evaluation are to answer the following questions: Do the clinical signs observed refer to a nervous system lesion? What is the location of this lesion within the nervous system? What are the main types of disease process that can explain the clinical signs? How severe is the problem? The first two questions are answered by performing a general physical and neurological examination and aim to determine the anatomical diagnosis (location and distribution of the lesion within the nervous system). The third question is answered by compiling the information on the patient signalment and history of the problem with the anatomical diagnosis to determine the differential diagnosis. Disease severity helps to determine prognosis of the differential diagnoses. Diagnostic tests are then carried out to investigate the differential diagnosis. The choice and interpretation of these tests must rely on a clear knowledge of the anatomical diagnosis and the expected disease processes. Are You Dealing With a Nervous System Lesion? A number of non-neurological conditions may mimic a nervous system lesion. Orthopaedic problems, cardiorespiratory diseases or metabolic disturbances, to name a few, can easily mimic some common neurological presentations such as gait abnormality, neuromuscular weakness or collapse. Furthermore, some inflammatory, infectious or neoplastic diseases of the nervous system may also affect other body systems. A detailed clinical examination should therefore be performed before embarking on the neurological examination. Why Should You Attempt to Localise the Problem Within the Nervous System?

The purpose of the neurological examination is to determine the neurological abnormalities and, based on that, the location of the lesion or lesions responsible for causing these abnormalities. The location is the anatomical diagnosis. Narrowing down to which part(s) of the nervous system may be affected can undeniably present a number of advantages. From a diagnostic point of view, the differential diagnosis is entirely dependent on the anatomical diagnosis. Aside from determining which part of the nervous system is affected, localising the lesion also involves determining whether the problem is focal, multifocal (i.e., affecting multiple parts of the nervous system) or diffuse (i.e., affecting globally and symmetrically one or more parts of the nervous system). Such information can then be used to narrow down the differential list even further (see section on how to establish a differential diagnosis list). Furthermore, a number of disease processes may only be diagnosed by exclusion of other causes mimicking a similar clinical history and presentation. This process of exclusion implies evaluating the correct part of the nervous system to confidently rule out these mimics. If there is failure to localise the lesion, the interpretation of any diagnostic test results can be a very challenging task for the clinician in the face of negative findings (as seen with some vascular or degenerative diseases of the central nervous system) or findings that do not match the clinical history. Finally, running a limited number of investigations aimed at narrowing down the differential list to a specific part of the nervous system can only be good as it should result in less cost for the owners and less time taken to reach a diagnosis, for the clinician. What Are the Principles of Lesion Localisation? Before rushing into the specifics of the neurological examination, attention should be focused on what questions you want answered: Is there any neurological abnormality detected? Which part(s) of the nervous system may be involved to explain these abnormalities? Is the lesion localisation focal, multifocal or diffuse? The first question does not require any detailed knowledge of neuroanatomy or neuroanatomical pathways. By simple observation and testing a number of reflexes and responses, the clinician should be able to determine whether or not the animal is neurologically sound. The neurological examination aims to test the integrity of these various components of the nervous system and, if present, detect any functional deficit. Normal findings are as important as the abnormal ones in localising the lesion. Neurological abnormalities detected on examination should be listed and added to the list of abnormal findings collected from the history. Each of these abnormal findings should then be correlated to a specific region or to specific pathways within the peripheral and/or central nervous system. Attempts should then be made to explain all the abnormal findings by a single lesion within one of the following regions of the nervous system: focal forebrain; brainstem; cerebellum; C1-C5 spinal cord segments; C6-T2 spinal cord segments; T3-L3 spinal cord segments; L4-L6 spinal cord segments; L7-S3 spinal cord segments; peripheral nerve; neuromuscular junction; muscle. Lesions within these regions of the nervous system result in predictable and specific neurological signs. Note that in localising a lesion, it is not necessary

that all the clinical signs referable to one location or syndrome be present. If a single lesion cannot explain all the listed abnormal findings, the lesion localisation is considered as multifocal or diffuse. How to Practically Localise the Problem Within the Nervous System The neurological examination can be divided into two main parts. Hands-Off Examination The first step in the neurological examination should focus on evaluating the animal's state of consciousness, awareness of its environment and attitude to being handled. Posture evaluation helps to appreciate the general symmetry of the animal and its balance while standing. It can also reveal abnormal postures such as head tilt (associated with vestibular disorder), head turn (associated with ipsilateral forebrain lesion), ventroflexion of the neck (associated with neuromuscular disorder or severe cervical spinal cord grey matter lesion) and spinal curvature (kyphosis or lordosis). Evaluation of the gait should be done with the aim of determining whether the patient is ataxic (uncoordinated), paretic (weak) or lame (from either neuromuscular disease or an orthopaedic disorder) and which limb(s) are involved. A normal gait requires intact function of the brainstem, cerebellum, spinal cord and sensory and motor peripheral nerves, neuromuscular junction and muscles. Hands-On Examination The primary aim of postural reaction testing is to detect subtle deficits that were not obvious on gait evaluation. These reactions test the animal's awareness of the precise position and movements of parts of its body, especially the limbs, as well as the animal's ability to generate movement in the part tested. The reactions commonly tested are the paw replacement (or 'knuckling' response), hopping, visual or tactile placing response. Spinal reflex evaluation should be considered as a continuation of the evaluation of the gait and postural reactions and not as a sole entity. Spinal reflex evaluation helps to narrow down further the lesion localisation by testing the integrity of the C6-T2 and L4-S3 intumescences as well as respective segmental sensory and motor nerves that form the peripheral nerves and the muscles innervated. Spinal reflexes are segmental. They only evaluate the spinal segment(s) within the intumescences corresponding to the stimulated nerve. They do NOT require consciousness. Lesions at the level of these intumescences result in loss of segmental spinal reflexes as well as reduced muscle tone and size. Cranial nerve examination helps to evaluate functions such as balance, vision, the pupils' reaction to light, swallowing, jaw and tongue function and command of the muscles of facial expression. How to Establish a Differential Diagnosis List The differential diagnosis list is entirely dependent on the location of the lesion within the nervous system. Determination of a differential diagnosis list is essential in choosing and interpreting any diagnostic test however sophisticated they may be. The aim of performing such diagnostic tests should only be to confirm or exclude the differentials in the list and not replace

the clinical evaluation. The differential diagnosis list can be developed taking into account signalment, historical data (mode of onset and evolution of the condition, presence of asymmetry...) and neurological findings (location and distribution of the disease within the nervous system). Disease processes that can affect the nervous system are classically categorised according to the mnemonic VITAMIN D: Vascular Inflammatory/Infectious Traumatic/Toxic Anomalous Metabolic Idiopathic Neoplastic/Nutritional Degenerative Each of these disease processes has a typical signalment, onset and progression as well as distribution within the nervous system. What To Do Next? With a clear understanding of the region of nervous system involved and the differential list reduced to no more than three or four disease processes, consideration should only be given to diagnostic tests that help to narrow down the list further and to those that can be afforded by the client. These tests should ideally be run from the least invasive (and least expensive) to the more invasive test. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Laurent S. Garosi, DVM, DECVN, MRCVS, RCVS & European Specialist in Veterinary Neurology Davies Veterinary Specialists Higham Gobion, Hertfordshire, UK

The NeuroMap: A Simple Guide to Localizing Neurological Lesions - Spinal Cord and Peripheral Nervous System ACVIM 2012 Christine E. Thomson, BVSc(Hons), DACVIM(Neurology), DECVN, PhD Palmerston North, New Zealand
23241060

The aim of the neurological examination is to determine whether neurological dysfunction is present and, if so, where the lesion causing the dysfunction is located in the nervous system. Once the lesion is localised, the possible causes can be listed and an appropriate diagnostic and subsequent treatment plan can be implemented. Whenever possible, we try to see if the signs can all be accounted for by a single lesion. If not, then the animal is considered to have a multifocal lesion, which makes certain diseases more likely. Localising neurological lesions can be challenging, particularly if it is not something you do frequently. The NeuroMap is a simple visual aid that has been designed as a ready reference guide to assist you in localising lesions. It is accompanied by a ready reference table. A key feature about the NeuroMap is that you don't need a degree in neuroanatomical-ese (terminology) to get a basic understanding of what could be happening in the nervous system of your patient. The NeuroMap is based on mapping out the location of the main functions of the nervous system. You can read from the NeuroMap what neural functions may be disrupted with a lesion in a certain area and conversely, what neural functions will be normal. Two key concepts underlie lesion localization: 1) you need to note both the neural systems that are functioning normally, as well as those that are dysfunctional (Figure 1); 2) it doesn't matter where a lesion is sited along the neural pathway (origin, middle or termination), the clinical signs of dysfunction will be similar. This is analogous to a battery (origin), wire (middle) and light bulb (termination). If there is a problem with any component, the light won't work. For example, an animal has a proprioceptive deficit and is standing on top of its paw (knuckling). The lesion could be in the sensory receptor (origin), the peripheral nerve or spinal cord pathway or brainstem (middle), or the sensory cortex of the forebrain (termination). The neurological examination involves evaluating five neural functions: behaviour and arousal; ascending sensory systems (tactile, proprioception and nociception) motor function; cranial nerve function; and spinal reflexes. Spinal sensitivity (hyperpathia) may further localise a spinal cord lesion. Based on the results of the tests, the clinician determines whether the animal has neurological deficits and if so, which parts of the nervous system are functioning normally and which parts are functioning abnormally. Using the NeuroMap, the clinician can see where each of the neural functions being tested is located in the nervous system. Can a single lesion account for all the observed signs - both the normal and abnormal? A number of functions are associated with most regions of the nervous system, either because neural pathways begin or end there, or are passing through it. If a lesion is in a particular region, then it could damage pathways in that region and cause signs of dysfunction. However, if a neural function is not associated with that region, then it will not be affected. Identifying the

neural pathways that are functioning normally indicates to the examiner that the lesion is probably not located in the region that those systems occupy. Figure 1. Normal AND abnormal function in the nervous system helps to localise a lesion.

Consider the animal knuckling on its hindpaws - this indicates a conscious proprioception deficit (see later text) and can be represented by pathway B in Figure 1. The animal also has loss of the withdrawal reflex in that limb (pathway A), but the cutaneous trunci reflex (pathway C) is intact. The proprioceptive pathway (B) begins in the foot and travels up specific nerves to the spinal cord, along the spinal cord to the brainstem where it crosses sides and travels rostrally to the sensory cortex of the forebrain. The lesion could be anywhere along that pathway, but we know that A is also compromised and C is functioning normally. Thus the lesion must be at X and not Y. In this instance, X represents the lumbosacral spinal cord. Therefore that which is NORMAL (C), is just as important to identify as that which is ABNORMAL for localising the lesion. Upper and lower motor neurons: UMN = upper motor neuron - you could also think of it as a 'central motor neuron' as the neuron is confined to the central nervous system (CNS = brain and spinal cord). LMN = lower motor neuron - you could also think of it as a 'peripheral motor neuron' as although the neuronal cell body is found in the CNS, the axon is largely in the periphery. LMNs supply striated muscle (e.g., limbs) and autonomic LMNs supply smooth muscle (e.g., the urinary bladder). UMN disease damages UMNs (motor neurons in the brain or spinal cord), while LMN disease damages LMNs (motor neurons that are mainly in the peripheral spinal and cranial nerves.

Figure 2 and Table 1. The NeuroRAT - reflexes, atrophy and tone.

To help remember how to differentiate between lesions affecting upper (central) motor neurons and lower (peripheral) motor neurons - think of the Neuro RAT. R = Reflexes, A = Atrophy (of muscles), T = Tone. The table lists the changes that may be present caudal to the lesion. UMN disease (damage to the UMNs) LMN disease (damage to the LMNs) Decreased to absent

Sign

Reflexes Normal to increased

Atrophy Disuse: Mild, generalised Neurogenic: severe, specific muscles Tone Normal to increased Decreased to absent

A spinal cord segment is a region of spinal cord to which is attached a pair of dorsal (sensory) nerve roots and a pair of ventral (motor) nerve roots. The dorsal and ventral roots fuse to form a spinal nerve; spinal nerves attach bilaterally to each spinal cord segment. These segmental spinal nerves form much of the peripheral nervous system (PNS) of the body and limbs; they may remain discrete (e.g., C3 spinal nerve), or spinal nerves may fuse in a plexus to form specific named nerves (e.g., brachial plexus giving rise to the radial nerve). Functional regions of the spinal cord are based around where the limb innervation attaches. For the dog, this creates the regions: cervical (C15: neck), cervical intumescence (C6T2: thoracic limbs), thoracolumbar (T3L3: trunk), lumbosacral intumescence (L4S3: pelvic limbs and viscera) and caudal segments (Cd15: tail). Because clinical signs of spinal cord disease are characteristic for each region, then we talk about animals having a region-specific localisation e.g., thoracolumbar disease.

Reflexes: A reflex has three anatomical parts to it: input from a sensory receptor in the periphery, a central connection in the CNS (brain or spinal cord, for reflexes involving the cranial and spinal nerves, respectively) and a lower (peripheral) motor neuron that connects back to the muscle via a neuromuscular junction. Damage to any one of those components will cause reduction/loss of the reflex. The main reflexes used to assess limb innervation are the patellar and withdrawal reflexes in the pelvic limbs and the withdrawal reflex in the thoracic limbs. The perineal and the cutaneous trunci reflexes are also used to evaluate sacral and thoracolumbar spinal cord function, respectively. UMN versus LMN disease: If an animal has a lesion at one of the intumescences (cervical or lumbosacral), where the limb innervation originates, then it is likely to compromise the lower (peripheral) motor neurons innervating that limb resulting in LMN signs: reduced Reflexes, Atrophy of specific muscles within that limb and reduced muscle Tone. These signs are quite localising and the clinician can tell which specific nerves, or which specific spinal cord segments, have been compromised. If an animal has a lesion cranial to the intumescence (e.g., thoracolumbar or cervical lesion), then the reflex arc and its LMN and the neuromuscular junction will be intact; the muscle will still be innervated. Thus, in the case of thoracolumbar disease, the pelvic limbs will have intact reflexes, and as the muscles still have their LMN innervation, they will have tone and any muscle atrophy will be mild due to disuse. As the upper (central) motor neuron has been compromised, the animal is described as having UMN signs to the pelvic limbs. Note: an animal will have UMN signs to the pelvic limbs if the lesion is located anywhere in the spinal cord cranial to L4. Thus UMN signs are not nearly as localising as LMN signs. If the lesion was in the cervical intumescence, the UMN supplying the pelvic limbs have been compromised, the LMN to the thoracic limbs will also be compromised. Thus in this example, the animal will have UMN signs to the pelvic limbs, but LMN signs to the thoracic limbs. A C1C5 lesion will result in UMN signs to both the pelvic and thoracic limbs. Continence can also be affected (see below). Increased muscle tone and reflexes: UMNs can facilitate or inhibit LMNs. Loss of facilitatory UMNs can result in paresis (decreased movement). Loss of inhibitory UMNs can result in excess LMN activity and reflex function. As the LMNs supplying extensor (antigravity) muscles dominate those supplying flexor muscles, loss of inhibitory UMN may result in increased extensor tonus (spasticity). Sensory function and proprioception: Also remember that it is not just motor neurons that will be compromised by a lesion in the spinal cord, but the sensory innervation will also be affected from the body caudal to the lesion. This includes sensory information about body position (proprioception), about the external environment (tactile, thermal and noxious stimuli) and the internal environment (e.g., viscera such as the fullness of the urinary bladder). There are two kinds of proprioception: 1) subconscious proprioception - the information that is projected to the ipsilateral cerebellum; 2) conscious proprioception - this information is projected to the contralateral forebrain for conscious awareness. Subconscious proprioception is particularly important for posture and locomotion; it's the sort of information that is used to keep the limbs located under the body's centre of gravity, both at rest and during movement. It originates in receptors in muscles and tendons. This information is projected to the cerebellum which then uses it to modulate motor function associated with postural and locomotory muscles.

Subconscious proprioception will be compromised in an animal with cerebellar disease (affecting pathway termination). It may not know where its limbs are with respect to its centre of gravity, so it may stand base-wide or base-narrow, or cross its feet when ambulating. It will probably have ataxia (incoordination of gait). Conscious proprioception is important for awareness of movement, particularly movement that is voluntary and learned (e.g., the kitten patting at a feather). Tactile input is a key component of this. An animal that has forebrain disease will still have good posture and locomotion (subconscious proprioception is intact), but the information from tactile receptors (e.g., from the paw) will not be received. Thus, the animal may stand on top of its foot ('knuckling'). [Copies of subconscious proprioceptive information is sent to the forebrain too (kinaesthesia) so the animal can be consciously aware of posture and locomotion.] Note: As both conscious and subconscious proprioceptive tracts travel up the spinal cord, spinal cord lesions often affect both types of proprioception; the parts of the body caudal to the lesion are often ataxic or the limbs have a stumbling gait, and the animal may stand on the top of its paw(s). Nociception involves the transmission of noxious (tissue-damaging) stimuli by spinal nerves to the spinal cord where it stimulates local reflex function (e.g., withdrawal reflex) or is projected to the forebrain for conscious perception. It travels to the forebrain in many pathways distributed across the transverse area of the spinal cord. Thus, to lose conscious perception of a noxious stimulus requires that the spinal cord has been extensively damaged. In an animal with a transected thoracolumbar spinal cord, the reflex arc for the withdrawal reflex will still be present in the pelvic limbs, but the cranially directed nociceptive tracts will be interrupted. Thus, when a noxious stimulus is applied to the hind foot, the animal will still pull its foot away, but it will not be able to consciously perceive the noxious stimulus. This implies severe spinal cord damage. Innervation of the urinary bladder and anal sphincter: Sensory input from the bladder wall, urinary sphincter and perineum travels to the sacral spinal cord (S13). Cranially directed pathways convey information about the fullness of the bladder and rectum to the brain for conscious perception. The sacral spinal cord (S13) is the origin of LMNs supplying the bladder wall smooth muscle (parasympathetic innervation - this stimulates detrusor muscle contraction during voiding) and the striated muscle of the urinary and anal sphincters (contraction maintains continence). Sympathetic LMNs arise from the cranial lumbar spinal cord and stimulate contraction of smooth muscle at the neck of the bladder and relaxation of bladder wall muscle for urine storage. The LMNs innervating the bladder wall and the sphincters result in muscle tone and are necessary for reflex function. Thus, lesions affecting the sacral spinal cord will result in LMN signs with reduced detrusor muscle tone and perineal reflex, and poor tone in the anal sphincter. The bladder will be large, floppy, and because of poor tone in the striated sphincter, it will be easy to express and the animal will probably be dribbling urine. Similarly, the anal sphincter may be dilated and the animal will be faecally incontinent. If the lesion is cranial to the sacral spinal cord, then the LMNs supplying the bladder wall and the striated muscle of the urinary and anal sphincters will be intact. Thus, the bladder will be full, turgid and difficult to express; the latter sign occurs because of loss of UMN inhibition to the LMNs innervating the urinary sphincter. Spinal cord disease often affects both urinary and faecal continence; uncommonly one elimination system only may be affected.

Using the NeuroMap: If you cover a region of the spinal cord in the NeuroMap (representing a lesion in it), you will be able to see which neurological functions will be compromised and which will still function normally. Conversely, if you have an animal with particular signs (e.g., tetraparesis, knuckling on all four limbs, loss of thoracic limb reflexes), but with intact pelvic limb reflexes, you can identify on the NeuroMap where the wiring is for one of those functions [e.g., the thoracic reflexes, (C6T2)]. What other functions are passing through this region? Yes, UMN to the pelvic limbs and sensory input from both the pelvic and thoracic limbs. That all fits. The pelvic limb reflexes are intact implying that their LMN are intact - yes, that is possible with a lesion in the C6T2 region. Thus, both the signs of dysfunction and signs of normal function have helped you localise the lesion. Figure 3. The NeuroMap for the spinal cord and spinal nerves.

Table 2. Summary of effect of lesions in different areas of the spinal cord. Loss of Presence of Presence of LMN proprioception and UMN signs to limbs; Loss sensory input signs of other reflexes TL and PL both affected

Location of lesion Cervical C15

Loss of urinary and faecal continence

TL and PL No LMN signs in TL UMN bladdera both and PL. Cutaneous Faecal incontinencec affected trunci and perineal reflexes intact

Cervical intumescence C6T2 Thoracolumbar T3L3

TL and PL both affected

PL only

TL, loss of cutaneous UMN bladder trunci reflex if lesion Faecal incontinencec in C8T2. Perineal reflex intact No LMN signs in TL UMN bladder or PL Faecal incontinence Cutaneous trunci reflex lost caudal to lesion, perineal reflex intact LMN signs in PL UMN bladder Cutaneous trunci Faecal incontinence reflex intact, perineal reflex intact LMN signs to pelvic viscera. Loss of perineal reflex LMN signs to tail LMN bladderb LMN anal sphincter (dilated anus), faecal incontinence Normal continence

PL only affected (TL normal)

PL only (TL normal)

Cranial lumbosacral L4S1 Caudal lumbosacral S1S3 Caudal nerves Cd15

PL only affected (TL normal)

No UMN signs to limbs No UMN signs to limbs No UMN signs to limbs

TL normal, PL probably normald

Decreased tail sensation

TL = thoracic limb, PL = pelvic limb. a = UMN bladder - turgid, full, difficult to express. b = LMN bladder - flaccid, distended, easy to express, dribbling urine; c = animal will deposit faeces with good emptying of colon, but may not be aware that it is defaecating. d = may see some proprioceptive deficits or paresis with an S1S3 lesion as S1 and S2 make variable contributions to the sciatic nerves. Note: whether or not all signs are present, depends on lesion severity. References Figures and tables reprinted with permission from Veterinary Neuroanatomy: A Clinical Approach by Christine Thomson and Caroline Hahn, Elsevier Health Sciences, May 2012, ISBN 9780702034824.

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. Thomson, DACVIM Massey University Palmerston North, AL, New Zealand

Peripheral or Central Vestibular Disease: Yes, It Matters WSAVA/FECAVA/BSAVA World Congress 2012 Daisuke Ito, DVM, PhD Nihon University, Fujisawa, Kanagawa, Japan
23011746

Functional Neuroanatomy of the Vestibular System The vestibular system is a special proprioception system responsible for the proper maintenance of posture, orientation and balance of the head and trunk, and position of the eyes in relation to head position or movement. In addition this system coordinates activity with portions of the cerebellum. Neuroanatomically and functionally, the vestibular system can be divided into peripheral and central components. Peripheral Component The membranous labyrinth and the vestibular portion of the vestibulocochlear nerve are the peripheral vestibular components in the inner ear. The membranous labyrinth is a series of fluidfilled chambers and tubes, including the cochlea, which manages auditory function, and the utricle, saccule and semicircular canals, which manage vestibular function. The vestibulocochlear nerve comprises sensory neurons of the 8th cranial nerve (CN VIII). CN VIII has bipolar neurons; those functioning in the vestibular system are located in the vestibular ganglion and those functioning in the auditory system are located in the spiral ganglion. These ganglia are located within the bony labyrinth of the petrous temporal bone close to the facial nerve (CN VII) and sympathetic innervation to the face. The function of the utricle and saccule is to detect gravity and linear acceleration and that of the semicircular canals is to detect head rotation. Central Component The central part of the vestibular system includes structures within the brainstem and cerebellum. The vestibular portion of CN VIII connects to the vestibular nuclei sited in the medulla oblongata of the brainstem, and to neurons in the rostral portion of the cerebellum. The vestibular nuclei are connected to the nuclei of the oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves and aid in control of eye movements. The vestibular nuclei are also connected to the neurons in the spinal cord via descending pathways which adjust tone in the muscles of the neck, trunk and limbs to oppose gravity to maintain posture. The first step to diagnose cases with vestibular system abnormalities is localisation of the lesion: determining whether the lesion is in the peripheral or central vestibular system is critically important for making differential diagnosis and predicting prognosis. Coordination of Eye Movements In the healthy animal, head rotation induces a compensatory eye movement in the opposite direction to the initial head movement. This coordination of eye and head movement is called the

vestibulo-ocular (or oculo-cephalic) reflex, and stimulated from information acquired in the semicircular canals. Information then enters the appropriate motor nuclei of the CN III, IV and VI to control the extraocular muscles. For example, if the head of the animal is turned to the left, movement of the endolymph in the left horizontal semicircular canal increases the activity of the hair cells; in contrast the endolymph activity in the right horizontal semicircular canal is decreased. These responses result in movements of the eyes toward the right and are termed the slow phase of the vestibulo-ocular reflex. If the head is further turned continuously after initiating the slow phase, this slow phase is interrupted by corrective fast movement of the eyes in the same direction of head turning (the 'fast phase' of the vestibulo-ocular reflex). Following the fast phase, the slow phase is resumed. A series of slow and fast phases is called nystagmus. Clinical Signs of Vestibular Disease Damage to either the peripheral or central vestibular system leads to various vestibular dysfunctions including head tilt, nystagmus, strabismus, ataxia and gait disturbance. Head Tilt Head tilt is a condition of loss of antigravity muscle tone on one side of the neck, usually due to unilateral vestibular dysfunction. As a result, the head tilts towards the loss of muscle tone. In cases with peripheral vestibular lesion, head tilt is towards the side of the lesion. For example, left inner ear disease (i.e., otitis media interna) causes left head tilt. A unilateral central vestibular lesion can cause a head tilt to either side. Bilateral vestibular lesions usually do not cause a head tilt; however, because of the loss of antigravity muscle tone on both sides the affected animal may not be able to hold the neck in a normal position. Nystagmus A series of slow and fast phase of the rhythmical eye movement is called nystagmus. Several variations of direction including horizontal, vertical and/or rotational nystagmus can be observed. The direction of nystagmus is defined as the direction of fast phase. Physiological nystagmus describes the normal vestibulo-ocular reflex. In contrast, pathological nystagmus occurs in animals with vestibular disease and can be classified into spontaneous nystagmus and positional nystagmus. Spontaneous nystagmus is the nystagmus which occurs when the head is in a normal stationary position. The direction of spontaneous nystagmus in animals with acute unilateral peripheral vestibular lesion is horizontal or rotational nystagmus. The fast phase is directed opposite to the side of lesion. For example, if the animal had left vestibular disease, the animal may show fast eye movement towards the right, and this is called nystagmus to the right side. Nystagmus of peripheral origin often disappears a few days after its appearance because of compensation by other balance systems (cerebellum, vision), but sometimes it can be induced by altering the head position. Nystagmus of central vestibular origin may be vertical, horizontal or rotational. Therefore spontaneous vertical nystagmus suggests that the lesion is in the central nervous system. Positional nystagmus can be seen when the head is placed in unusual positions, such as upside down. Therefore the examiner should try to induce positional nystagmus by positioning animals in lateral and dorsal recumbency. It is impossible to localise the lesion by assessment of positional nystagmus, although the direction of nystagmus sometimes changes in

direction in animals with a central lesion. Usually bilateral vestibular diseases do not show spontaneous and positional nystagmus. Ataxia and Gait Disturbance Either peripheral or central vestibular dysfunction can be the cause of ataxia and gait disturbance. Strabismus Strabismus is an abnormal position of the eyes. Ventral or ventolateral strabismus can be seen in animals with vestibular disease when the head is raised and the neck is extended (positional strabismus), or spontaneously. Usually strabismus is seen on the same side as the lesion. Vomiting and Salivation Some animals show vomiting and salivation secondary to vestibular diseases. Clinical Localisation of Peripheral Versus Central Vestibular Disease From the clinical signs mentioned above, it may be difficult to localise the vestibular lesion because most of the clinical signs can be seen in association with lesions affecting either the peripheral or central components. The most important key to determine the lesion location is to identify other clinical signs as compatible with only components of the peripheral vestibular system or that could only be explained by a central lesion (see Figure 1). An accurate history and physical and neurological examination are essential to success. Figure 1. Neurological signs of peripheral vs central vestibular dysfunction. Clinical signs Head tilt Nystagmus Peripheral lesion Towards the side of the lesion Horizontal or rotational; the fast phase is directed opposite to the side of lesion Yes Yes Facial nerve paresis to same side as lesion Possible to same side No Central lesion To either side Horizontal, rotational or vertical; the fast phase to either side; may change the direction with head position Yes Yes Cranial nerves V, VI, VII, IX, X or XII might be affected; same side of lesion Rarely seen Yes (possible), usually same side as

Ataxia and gait disturbance Strabismus Cranial nerve deficits Horner's syndrome Postural

reaction deficits Mental status Signs of cerebellum deficits Normal No

lesion Depressed, stuporous or comatose Possible; dysmetria or intentional tremor

Peripheral Vestibular Lesion Near the peripheral vestibular system, there are CN VII and sympathetic innervations. Therefore key clinical signs in animals with peripheral vestibular diseases may be facial nerve paresis and/or Horner's syndrome (ptosis, enophthalmos, miosis and protrusion of the third eyelid) ipsilaterally to the clinical signs of vestibular dysfunction. Animals do not show proprioceptive deficits due to peripheral vestibular dysfunction. Central Vestibular Lesion The single strongest sign of central vestibular disease is the presence of conscious proprioceptive deficits. The examiner must be cautious not to mistake ataxia for proprioceptive deficits, and to perform an accurate neurological examination. In addition, central vestibular lesions may cause neurological signs and cranial nerve deficits other than deficits of CN VII and CN VIII, such as abnormal mental status including depression, stupor or coma; cerebellum deficits including intentional tremor and dysmetria (hypermetria); behavioural changes and seizure; other cranial deficits. One specific clinical sign of central vestibular disease in association with vestibular function is vertical nystagmus. Peripheral Vestibular Diseases Otitis media-interna. Otitis is the most common cause of peripheral vestibular disease in the dog and also common in cats. Bacteria themselves may cause dysfunction and toxin produced by the bacteria may affect to the inner ear. Idiopathic vestibular syndrome. The second most common cause of peripheral vestibular disease in dogs, and is also well recognised in cats. There is no age tendency in cats, but dogs tend to be older (~12 years old). Therefore sometimes the disease is known as idiopathic geriatric vestibular disease. Diagnosis of idiopathic vestibular syndrome is by exclusion of other diseases. Proprioception and other cranial nerves should be normal. Nasopharyngeal polyps. Inflammatory polyps derive from the lining of the tympanic cavity or auditory tube and are commonly seen in cats aged 15 years old. Central Vestibular Diseases Any diseases, including neoplastic, inflammatory, toxin ingestion and miscellaneous, which involve the brainstem or cerebellum have the potential to cause vestibular dysfunction.

Differential diagnosis should be made according to other clinical signs, including age and speed of onset of the clinical signs.

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Daisuke Ito, DVM, PhD Nihon University Fujisawa, Kanagawa, Japan

The Emergency Head Tilt (V195) Western Veterinary Conference 2009 Simon R. Platt Department of Small Animal Medicine & Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA
18668729

Introduction The onset of a head tilt is a cardinal sign of vestibular disease. It is the most consistent sign of unilateral vestibular dysfunction, which occurs as a result of the loss of anti-gravity muscle tone on one side of the neck. Bilateral vestibular disease may also cause a head tilt if the disease process is not symmetrical but usually does not cause such a sign. The vestibular system has two functional components; the peripheral component is located in the inner ear and the central component is located in the brain stem and cerebellum. Unfortunately, a head tilt is not specific for a brainstem or a peripheral vestibular system lesion localisation, nor does it indicate a specific aetiology. Generally, central vestibular disease is associated with different aetiologies and a worse prognosis than peripheral vestibular disease. Therefore, it is essential to approach these cases aiming to primarily further localise the neurological lesion. Clinical signs due to disease of the peripheral vestibular system: Head tilt, circling, falling or rolling toward the side of the lesion If nystagmus is present it is horizontal or rotatory with the fast phase away from the side of the lesion May have concurrent facial nerve paralysis (CN VII) and Horner's syndrome (ptosis, miosis and enophthalmos) with middle and inner ear lesions Clinical signs due to disease of the central vestibular system: Head tilt, circling, falling, or rolling toward or away from the side of the lesion Conscious proprioceptive deficits, hemiparesis or hemiplegia on the side of the lesion if unilateral or worse on one side if bilateral Nystagmus may be horizontal, rotatory or vertical if present May be depressed or stuporous May have facial paralysis (CN VII) but Horner's syndrome is rare Diagnostic Plan for Patient with Vestibular Dysfunction

Obtain a comprehensive history of the onset of the disease. Information regarding previous systemic disease, previous ear disease, previous medication administration (both topical and systemic), travel history, the possibility of toxin exposure and head trauma is important. Perform a complete neurological examination. There are several very important components of the examination that can assist with the lesion localisation. In addition to the head tilt, the other signs of vestibular disease include pathologic nystagmus, positional strabismus and ataxia characterized by a base-wide stance and swaying of the trunk and head. Pathological nystagmus can be spontaneous or positional. Spontaneous nystagmus is nystagmus that occurs when the head is not moving and is in the normal position. A unilateral acute peripheral lesion often causes spontaneous nystagmus with horizontal and rotational components. The fast phase is directed away from the side of the lesion. Spontaneous nystagmus resulting of central origin can be purely vertical, horizontal or rotational. Positional nystagmus refers to nystagmus that is present only when the head is placed in an unusual position, for example upside down. There are less specific neurological signs that may be associated with vestibular dysfunction that include; conscious proprioception deficits (indicative of brainstem disease); Horner's syndrome (usually indicative of peripheral disease); cranial nerve deficits (multiple cranial nerve dysfunction usually indicates central disease, but facial nerve paresis can occur with central or peripheral disease); head tremor (indicating cerebellar disease) and an altered level of consciousness (indicative of central disease). The differentials for peripheral and central vestibular disease are discussed below. The next steps may be determined by the lesion localisation. A minimum data-base should be performed on all cats which should include haematology, serum chemistry, urinalysis and thoracic radiographs. If toxicity is suspected due to antibiotic administration (metronidazole and aminoglycosides), I would recommend immediate withdrawal of the medication. In most cases, there is resolution of the vestibular abnormality. In the absence of a systemic health concern, a practical approach can be taken with peripheral vestibular disease cats. Ancillary tests for patients with peripheral disease include otoscopic examination; imaging of the tympanic bullae with radiography, computed tomography (CT), or magnetic resonance (MR) imaging; and thyroid function testing. A brainstem auditory evoked response (BAER) test may be of value in examining the auditory portion of cranial nerve VIII (vestibulo-cochlear nerve) as well as potentially assisting in localising the disease to the peripheral or central components. Diagnosis of central disease is based upon CT or MR imaging of the brain and analysis of cerebrospinal fluid (CSF). Causes of Peripheral Vestibular Disease Idiopathic vestibular syndrome is a common cause of peripheral vestibular disease in the dog and cat. The onset of the vestibular disease may be so acute that is accompanied by vomiting, but this is not specific for this aetiology. Postural reactions are normal in this disease, and cats do not have facial paresis or Horner's syndrome. This can be only by diagnosed by ruling out the other causes, however, it is the only differential of peripheral disease that will start to improve in 72 hours with no specific treatment. If the patient is closely monitored over this time course, marked resolution of the nystagmus can be seen. This will be followed by improved gait over a 7-day

period and improvement of the head tilt over a 2-month period. The head tilt may never completely resolve. If there is evidence of facial nerve involvement or Horner's syndrome further ancillary tests should be considered. Otitis media-interna. Up-to 50% of cases of peripheral vestibular disease are due to otitis media-interna. Infection of the middle ear can cause vestibular disease due to the production and spread of bacterial toxins into the inner ear. The infection can directly damage the inner ear with spread to the labyrinth. The bacteria commonly responsible for this disease are Staphylococcus spp., Streptococcus spp., E. coli and Pseudomonas spp. If the culture results are negative but bacterial otitis interna is suspected, then oral enrofloxacin 5 mg/kg every 12 hours for dogs or cats or a combination of oral trimethoprim sulfadiazine (TMP-SDZ) 15-30 mg/kg orally every 12 hours and oral cephalexin 22 mg/kg every 8 hours may be administered. Antibiotic therapy should be continued for 6-8 weeks. Tear production should be monitored to detect sicca associated with facial nerve (CN 7) involvement or antibiotic therapy and artificial tears administered if necessary to prevent keratitis and corneal ulceration. Aminoglycosides are contraindicated in otitis interna/media. In cases of concurrent otitis externa and media with a ruptured tympanic membrane, the external and middle ears are gently flushed with saline or a 2.5% acetic acid solution and caustic ear cleaning substances are avoided if possible. Diluted ear cleaning solutions may be necessary in some cases for debris that cannot be cleared by other means, but thorough rinsing is essential so residual cleaning solution does not irritate the vestibular labyrinth. Topical treatment of the external ear canal with small amounts of low residue non-irritating antibiotic solutions for a few days may be given but the accumulation of greasy ointments in the middle ear should be avoided. The vestibular signs may resolve in 1-2 weeks but if antibiotics are prematurely discontinued, the clinical signs and infection recur and can be more difficult to treat. Corticosteroids are usually not required and are avoided if osteomyelitis is present. In acute cases oral prednisone 0.25 mg/kg once daily for 1-3 days is sometimes given to reduce inflammation and swelling of the vestibular labyrinth. In animals with recurring otitis, underlying dermatologic problems such as atopy or hypothyroidism should be investigated and treated. Ear hygiene should be monitored but care should be taken when cleaning the external ear canals. Surgical intervention: External ear canal ablation and bulla osteotomy in refractory cases. Nasopharyngeal polyps. Polyps are pedunculated masses, which arise from the lining of the tympanic cavity, eustachian tube, or nasopharynx. Non-septic otitis media/interna may occur secondary to occlusion of the eustachian tube due to a nasopharyngeal polyp and polyps may occur as a result of chronic middle ear infection or from ascending infection from the nasopharynx. Diagnosis may require advanced imaging if physical examination and skull radiographs are not helpful. Neoplasia. Neoplasia of the structures of the ear includes squamous cell carcinoma, ceruminous gland adenocarcinoma and lymphoma. Ototoxicity. There are many drugs listed as being ototoxic and can potentially cause both vestibular dysfunction and deafness. The deafness caused by such drugs is often permanent

whereas the vestibular disease may resolve or at least the dog may compensate for the abnormality. The most common topical drug implicated in this scenario is chlorhexidine. Trauma. Head trauma may cause the onset of vestibular disease, which may be peripheral or central depending upon the severity of the trauma. Middle ear haemorrhage subsequent to a trauma may cause peripheral vestibular disease seen with or without facial paresis and Horner's syndrome. Congenital disease. Peripheral vestibular disease may be evident in young animals and attributed to a congenital malformation or degeneration of the inner ear structures. If the abnormality is bilateral, these animals may not have a head tilt or nystagmus; however, they will frequently have a symmetrical ataxia, a wide-based stance, and a side-to-side movement of the head in the horizontal plane. They may also be deaf. Numerous breeds have been associated with congenital vestibular disease (German shepherd, Doberman, English Cocker, Beagle, Siamese, Burmese, Tonkinese). Clinical signs usually begin around 3-4 weeks of age (when the animal begins to ambulate) and may consist of a head tilt, nystagmus, strabismus, ataxia, circling, falling, rolling, and abnormal head movements. Many learn to compensate by 2-4 months of age but some will remain permanently affected. Recurrence can occur. With bilateral disease, there is usually no abnormal nystagmus and normal nystagmus cannot be elicited. Causes of Central Vestibular Disease Inflammatory disease. The common infectious diseases responsible for inflammation of the brain and its structures are canine distemper, feline infectious peritonitis (FIP), Toxoplasma, bacteria and Cryptococcus. Whilst all the above infections can cause vestibular disease, they often have a multifocal central nervous system distribution and may also cause profound systemic abnormalities. The prognosis for each patient not only depends on the infectious etiology but also on the severity of the presenting signs, neurological as well as systemic. There are several inflammatory diseases of unknown aetiology and presumed immune-mediated. These include granulomatous meningoencephalomyelitis (GME) and necrotizing meningoencephalitis and can both affect the central vestibular system as part of a multifocal disease. Neoplasia. The most common tumours to cause central vestibular disease in cats are meningiomas and lymphomas located at the cerebello-medullary pontine angle. Tumors of the forebrain can also cause central vestibular disease due to caudal transtentorial herniation with secondary compression of the brain stem. Metronidazole toxicity. Dosages greater than 30mg/kg/day can result in vestibular disease. The onset is acute and usually occurs when animals receive high doses for a long duration (e.g., after being on high doses for 7 to 12 days). Dose reductions need to be made in patients with liver and kidney disease as the drug is metabolized and excreted by these organs, respectively. Clinical signs may include generalized ataxia, nystagmus, anorexia, and vomiting. In severe cases, altered mental status, seizures, and opisthotonus may be present. Removal of the drug and supportive care (IV fluid diuresis) usually results in quick recovery. Occasionally, deficits are permanent.

Cerebrovascular disease. Cerebrovascular disease (CVD) may cause a peracute onset of central vestibular signs. Ischemia may be embolic or thrombotic and is the most common form of CVD; its causes may be due to sepsis, neoplasia, endocrine disease, hypertension or may commonly be idiopathic. In some areas of the country this can result from aberrant parasite migration through the nervous system. Non-traumatic hemorrhage, the other form of CVD, is bleeding into the parenchyma of the brain that may extend into the ventricles. Recovery from this disorder can be complete but can depend on the underlying disorder. References 1. Evans J, Levesque D, Knowles K, et al. Diazepam as a treatment for metronidazole toxicosis in dogs: a retrospective study of 21 cases. J Vet Intern Med 2003;17(3):304-310. 2. Garosi LS, Dennis R, Penderis J, et al. Results of magnetic resonance imaging in dogs with vestibular disorders: 85 cases (1996-1999). J Am Vet Med Assoc 2001;218(3):385-391 3. Sturges BK, Dickinson PJ, Kortz GD, et al. Clinical signs, magnetic resonance imaging features, and outcome after surgical and medical treatment of otogenic intracranial infection in 11 cats and 4 dogs. J Vet Intern Med. 2006;20(3):648-656. 4. Troxel MT, Drobatz KJ, Vite CH. Signs of neurologic dysfunction in dogs with central versus peripheral vestibular disease. J Am Vet Med Assoc. 2005;227(4):570-574. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN University of Georgia, College of Veterinary Medicine Dept. of Small Animal Medicine & Surgery Athens, GA, United States

Vestibular Disease in Dogs and Cats

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2008
Simon Platt, BVM&S, DACVIM (Neurology), DECVN, MRCVS Department of Small Animal Medicine & Surgery, College of Veterinary Medicine, University of Georgia Athens, GA, USA
18293641

The onset of a head tilt is a cardinal sign of vestibular disease. It is the most consistent sign of unilateral vestibular dysfunction, which occurs as a result of the loss of anti-gravity muscle tone on one side of the neck. Bilateral vestibular disease may also cause a head tilt if the disease process is not symmetrical but usually does not cause such a sign. The vestibular system has two functional components; the peripheral component is located in the inner ear and the central component is located in the brain stem and cerebellum. Unfortunately, a head tilt is not specific for a brainstem or a peripheral vestibular system lesion localisation, nor does it indicate a specific aetiology. Generally, central vestibular disease is associated with different aetiologies and a worse prognosis than peripheral vestibular disease. Therefore, it is essential to approach these cases aiming to primarily further localise the neurological lesion.

DIFFERENTIATION OF VESTIBULAR LESIONS

Clinical Signs Due to Disease of the Peripheral Vestibular System
Head tilt, circling, falling or rolling toward the side of the lesion If nystagmus is present it is horizontal or rotatory with the fast phase away from the side of the lesion May have concurrent facial nerve paralysis (CN VII) and Horner's syndrome (ptosis, miosis and enophthalmos) with middle and inner ear lesions

Clinical Signs Due to Disease of the Central Vestibular System

Head tilt, circling, falling, or rolling toward or away from the side of the lesion Conscious proprioceptive deficits, hemiparesis or hemiplegia on the side of the lesion if unilateral or worse on one side if bilateral Nystagmus may be horizontal, rotatory or vertical if present May be depressed or stuporous May have facial paralysis (CN VII) but Horner's syndrome is rare

DIAGNOSTIC PLAN FOR PATIENT WITH VESTIBULAR DYSFUNCTION

1. Obtain a comprehensive history of the onset of the disease. Information regarding previous systemic disease, previous ear disease, previous medication administration (both topical and systemic), travel history, the possibility of toxin exposure and head trauma is important. 2. Perform a complete neurological examination. There are several very important components of the examination that can assist with lesion localisation. In addition to the head tilt, the other signs of vestibular disease include pathologic nystagmus, positional strabismus and ataxia characterized by a base-wide stance and swaying of the trunk and head. Pathological nystagmus can be spontaneous or positional. Spontaneous nystagmus is nystagmus that occurs when the head is not moving and is in the normal position. A unilateral acute peripheral lesion often causes spontaneous nystagmus with horizontal and rotational components. The fast phase is directed away from the side of the lesion. Spontaneous nystagmus resulting of central origin can be purely vertical, horizontal or rotational. Positional nystagmus refers to nystagmus that is present only when the head is placed in an unusual position, for example upside down. There are less specific neurological signs that may be associated with vestibular dysfunction that include: conscious proprioception deficits (indicative of brainstem disease); Horner's syndrome (usually indicative of peripheral disease); cranial nerve deficits (multiple cranial nerve dysfunction usually indicates central disease, but facial nerve paresis can occur with central or peripheral disease); head tremor (indicating cerebellar disease); and an altered

level of consciousness (indicative of central disease). The differentials for peripheral and central vestibular disease are discussed below. The next steps may be determined by the lesion localisation. 3. A minimum database should be performed on all cats which should include haematology, serum chemistry, urinalysis and thoracic radiographs. If toxicity is suspected due to antibiotic administration (metronidazole and aminoglycosides), I would recommend immediate withdrawal of the medication. In most cases, there is resolution of the vestibular abnormality. In the absence of a systemic health concern, a practical approach can be taken with peripheral vestibular disease cats. 4. Ancillary tests for patients with peripheral disease include: otoscopic examination; imaging of the tympanic bullae with radiography; computed tomography (CT), or magnetic resonance (MR) imaging; and thyroid function testing. A brainstem auditory evoked response (BAER) test may be of value in examining the auditory portion of cranial nerve VIII (vestibulo-cochlear nerve) as well as potentially assisting in localising the disease to the peripheral or central components. Diagnosis of central disease is based upon CT or MR imaging of the brain and analysis of cerebrospinal fluid (CSF).

CAUSES OF PERIPHERAL VESTIBULAR DISEASE

Idiopathic Vestibular Syndrome
Idiopathic vestibular syndrome is a common cause of peripheral vestibular disease in the dog and cat. The onset of the vestibular disease may be so acute that is accompanied by vomiting, but this is not specific for this aetiology. Postural reactions are normal in this disease, and cats do not have facial paresis or Horner's syndrome. This can be only by diagnosed by ruling out the other causes; however, it is the only differential of peripheral disease that will start to improve in 72 hours with no specific treatment. If the patient is closely monitored over this time course, marked resolution of the nystagmus can be seen. This will be followed by improved gait over a 7-day period and improvement of the head tilt over a 2-month period. The head tilt may never completely resolve. If there is evidence of facial nerve involvement or Horner's syndrome further ancillary tests should be considered.

Otitis Media-Interna
Up-to 50% of cases of peripheral vestibular disease are due to otitis media-interna. Infection of the middle ear can cause vestibular disease due to the production and spread of bacterial toxins into the inner ear. The infection can directly damage the inner ear with spread to the labyrinth. The bacteria commonly responsible for this disease are Staphylococcus spp., Streptococcus spp., E. coli and Pseudomonas spp. If the culture results are negative but bacterial otitis interna is suspected, then oral enrofloxacin 5 mg/kg every 12 hours for dogs or cats or a combination of oral trimethoprim sulfadiazine (TMP-SDZ) 15-30 mg/kg orally every 12 hours and oral cephalexin 22 mg/kg every 8 hours may be administered. Antibiotic therapy should be continued for 6-8 weeks. Tear production should be monitored to detect sicca associated with facial nerve (CN 7) involvement or antibiotic therapy and artificial tears administered if necessary to prevent keratitis and corneal ulceration. Aminoglycosides are contraindicated in otitis interna/media. In cases of concurrent otitis externa and media with a ruptured tympanic membrane, the external and middle ears are gently flushed with saline or a 2.5% acetic acid solution and caustic ear cleaning substances are avoided if possible. Diluted ear cleaning solutions may be necessary in some cases for debris that cannot be cleared by other means, but thorough rinsing is essential so residual cleaning solution does not irritate the vestibular labyrinth. Topical treatment of the external ear canal with small amounts of low residue non-irritating antibiotic solutions for a few days may be given but the accumulation of greasy ointments in the middle ear should be avoided. The vestibular signs may resolve in 1-2 weeks but if antibiotics are prematurely discontinued, the clinical signs and infection recur and can be more difficult to treat. Corticosteroids are usually not required and are avoided if osteomyelitis is present. In acute cases, oral prednisone 0.25 mg/kg oncedaily for 1-3 days is sometimes given to reduce inflammation and swelling of the vestibular labyrinth. In animals with recurring otitis, underlying dermatologic problems such as atopy or hypothyroidism should be investigated and treated. Ear hygiene should be monitored but care should be taken when cleaning the external ear canals

Surgical intervention: External ear canal ablation and bulla osteotomy in refractory cases.

Nasopharyngeal Polyps
Polyps are pedunculated masses which arise from the lining of the tympanic cavity, eustachian tube, or nasopharynx. Non-septic otitis media/interna may occur secondary to occlusion of the eustachian tube due to a nasopharyngeal polyp and polyps may occur as a result of chronic middle ear infection or from ascending infection from the nasopharynx. Diagnosis may require advanced imaging if physical examination and skull radiographs are not helpful.

Neoplasia
Neoplasia of the structures of the ear includes squamous cell carcinoma, ceruminous gland adenocarcinoma and lymphoma.

Ototoxicity
There are many drugs listed as being ototoxic and can potentially cause both vestibular dysfunction and deafness. The deafness caused by such drugs is often permanent whereas the vestibular disease may resolve or at least the dog may compensate for the abnormality. The most common topical drug implicated in this scenario is chlorhexidine.

Trauma
Head trauma may cause the onset of vestibular disease, which may be peripheral or central depending upon the severity of the trauma. Middle ear haemorrhage subsequent to a trauma may cause peripheral vestibular disease seen with or without facial paresis and Horner's syndrome.

Congenital Disease
Peripheral vestibular disease may be evident in young animals and attributed to a congenital malformation or degeneration of the inner ear structures. If the abnormality is bilateral, these animals may not have a head tilt or nystagmus; however, they will frequently have a symmetrical ataxia, a wide-based stance and a side-to-side movement of the head in the horizontal plane. They may also be deaf. Numerous breeds have been associated with congenital vestibular disease (German shepherd, Doberman, English cocker, beagle, Siamese, Burmese, Tonkinese). Clinical signs usually begin around 3-4 weeks of age (when the animal begins to ambulate) and may consist of a head tilt, nystagmus, strabismus, ataxia, circling, falling, rolling, and abnormal head movements. Many learn to compensate by 2-4 months of age but some will remain permanently affected. Recurrence can occur. With bilateral disease, there is usually no abnormal nystagmus and normal nystagmus cannot be elicited.

CAUSES OF CENTRAL VESTIBULAR DISEASE

Inflammatory Disease
The common infectious diseases responsible for inflammation of the brain and its structures are canine distemper, feline infectious peritonitis (FIP), Toxoplasma, bacteria and Cryptococcus. Whilst all the above infections can cause vestibular disease, they often have a multifocal central nervous system distribution and may also cause profound systemic abnormalities. The prognosis for each patient not only depends on the infectious etiology but also on the severity of the presenting signs, neurological as well as systemic. There are several inflammatory diseases of unknown aetiology and presumed immune-mediated. These include granulomatous meningoencephalomyelitis (GME) and necrotizing meningoencephalitis and can both affect the central vestibular system as part of a multifocal disease.

Neoplasia
The most common tumours to cause central vestibular disease in cats are meningiomas and lymphomas located at the cerebello-medullary pontine angle. Tumors of the forebrain can also cause central vestibular disease due to caudal transtentorial herniation with secondary compression of the brain stem.

Metronidazole Toxicity
Dosages greater than 30 mg/kg/day can result in vestibular disease. The onset is acute and usually occurs when animals receive high doses for a long duration (e.g., after being on high doses for 7 to 12

days). Dose reductions need to be made in patients with liver and kidney disease as the drug is metabolized and excreted by these organs, respectively. Clinical signs may include generalized ataxia, nystagmus, anorexia, and vomiting. In severe cases, altered mental status, seizures, and opisthotonus may be present. Removal of the drug and supportive care (IV fluid diuresis) usually results in quick recovery. Occasionally, deficits are permanent.

Cerebrovascular Disease
Cerebrovascular disease (CVD) may cause a peracute onset of central vestibular signs. Ischemia may be embolic or thrombotic and is the most common form of CVD; its causes may be due to sepsis, neoplasia, endocrine disease, hypertension or may commonly be idiopathic. In some areas of the country this can result from aberrant parasite (Cuterebra) migration through the nervous system. Non-traumatic hemorrhage, the other form of CVD, is bleeding into the parenchyma of the brain that may extend into the ventricles. Recovery from this disorder can be complete but can depend on the underlying disorder

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Simon Platt, BVM&S, DACVIM (Neurology), DECVN, MRCVS Department of Small Animal Medicine & Surgery, College of Veterinary Medicine University of Georgia Athens, Georgia, U

Localization of Brain Lesions

VETERINARY NEUROLOGY SYMPOSIUM 2005
Dr. Peter Dickinson, BVSc, PhD, Diplomate ACVIM (Neurology)
18285591

Clinical neurology is based on a sound understanding of neuroanatomy, neurophysiology, and the recognition of clinical signs resulting from loss of function of specific areas of the nervous system. The nervous system is logically arranged, and the use of a systematic and logical approach to examination, allows the clinician to localise diseases to specific parts of the brain.

WHY IS LOCALISATION SO IMPORTANT?

1. Together with history and signalment, determining the location of a lesion and whether it is solitary or multifocal/diffuse enables the clinician to form a differential list of the most likely diseases. Based on this differential list a logical diagnostic plan can be formed leading, hopefully, to a diagnosis. (eg localization of multifocal disease would be more typical of infectious or inflammatory disease rather than primary brain neoplasia) 2. Localisation allows accurate choice and "targeting" of appropriate diagnostics (eg CT may be more appropriate when imaging the bony structures of the middle ear in peripheral vestibular disease versus MR imaging of the brainstem for central disease) 3. The significance of lesions defined by diagnostic tests (eg MRI) is determined in part by the correlation of their location with the clinical localisation. Contrary to what most neurophobic clinicians believe, a detailed knowledge of all the specific tracts and structures within the brain is not necessary to do basic localization of intracranial disease! Understanding the major areas of the brain, how they interact and what their major functions are at a fairly simplistic level is all that is required.

BASIC ANATOMY

Neurological examination: A complete neurological examination should be done on all animals suspected of having neurological disease. The examination should allow the determination of: 1. The presence of neurological disease Not all animals that appear to have neurological disease do so. Animals with severe orthopedic disease, profound metabolic abnormalities or cardiovascular disease may be unable or unwilling to walk, or may have changes in behavior that may mimic neurological disease. In some cases animals with neurological disease (e.g. idiopathic epilepsy) may have a normal neurological examination. History is especially important in this regard.

2. The localisation of the problem(s) grossly- Brain? Spinal cord? or Neuromuscular? And subsequently to more specific areas. 3. The severity of the problem

NEUROLOGICAL EXAMINATION: SUMMARY

Below is a summary of the components of a neurological examination. For each section there will be a discussion of the sorts of abnormalities that may be found with intracranial disease, whether they are specific localisers of intracranial disease, and how they help in neurolocalisation.

Mentation/behaviour: *****
Altered mentation /behaviour is almost always associated with intracranial disease. Spend time just watching the animal in the examination room. Does the animal respond appropriately to its environment and external stimuli? Inappropriate or compulsive behaviour such as pacing, head pressing, aggression etc suggests brain disease, usually affecting the forebrain. Decreased mentation may be associated with diffuse cerebral disease or brain stem disease due to disruption of the reticular activation system. It is important to distinguish between animals that truly have decreased levels of mentation and animals that are "quiet" due to generalised systemic disease or pain. In some cases this can be difficult and may require repeat examinations. For example a dog with brain disease and obtundation may not bother to look around when a new person enters the room (inappropriate), however a dog with significant cervical pain due to a herniated disc may also not look around either, which is appropriate in this circumstance. Decreasing level of mentation Normal Obtunded Stuporous Comatose Normal response to stimuli Decreased response to normal stimuli. Responds only to abnormal stimuli (e.g. painful stimuli). No response to any stimuli.

Posture:
Again, observe the animal in the examination room, or outside. Look for abnormal positions of the head, trunk and limbs with respect to gravity. Abnormalities of the vestibular system (CN VIII) are a common cause of abnormal posture particularly head tilt, leaning, tilting to one side. Animals with bilateral vestibular disease will often have a wide based stance although this may also be seen with neuromuscular weakness. Severe damage to the brainstem may result in a decerebrate posture with opisthotonus (extension of the neck and limbs). Extension of the thoracic limbs may also be seen with cerebellar disease (decerebellate). However postural abnormalities are not restricted to intracranial disease. Animals with spinal cord disease may also have abnormal postures particularly if they have spinal pain resulting in low, stiff neck carriage or hunched postures. Rigid extension of the thoracic limbs may be seen with severe (T3-L3) spinal cord lesions. (Schiff-Sherrington sign) Neuromuscular weakness may also result in postural signs such as cervical ventroflexion, especially in cats.

Gait:
Paresis - Decreased voluntary movement (mono, para, hemi, tetra/quadri) Paralysis/plegia - Absence of voluntary movement (mono, para, hemi, tetra/quadri) Ataxia - Incoordination of voluntary movement Dysmetria - Inappropriate force or range of movement (hyper/hypo) Abnormalities of gait may be the result of disease in many areas of the nervous system (cerebrum, brainstem, cerebellum, spinal cord and neuromuscular system) as well as resulting from nonneurological disease such as orthopaedic, cardiovascular and metabolic disease.

Neurological causes may result from loss of sensory perception of limb /body position, loss of motor pathways, or loss of cerebellar "regulation" of movement.

Paresis
The dog and cat have 2 major areas of motor neurones in the brain, the motor cortex and the basal nuclei (which are located along the length of the brainstem). The important things to remember are: Dogs and cats essentially walk on their brainstems (red nucleus in the mid brain is V important) therefore cortical lesions rarely cause profound paresis but brainstem lesions or spinal cord lesions do. Motor pathways cross over at the level of the midbrain so that lesions cranial to this point cause contralateral deficits, lesions caudal cause ipsilateral deficits.

Ataxia
Ataxia (uncoordinated movement) may be seen with cerebellar, vestibular or spinal cord disease

Dysmetria
Lesions involving the cerebellum (sometimes spinal cord pathways to the cerebellum) can result in gaits where there are movements that are too long (goose stepping)(hypermetria) or too short (hypometria). There may also be overshooting of head movements and tremors.

Circling ****
Circling is nearly always a reflection of intracranial disease. Tight circles are usually caused by vestibular disease whereas wider circling is often the result of forebrain disease. Circling usually occurs towards the side of the lesion.

Postural reactions:
Tests aimed at assessing an animals ability to maintain an appropriate posture include tests of conscious proprioception (CP) such as the paw position test and reflex stepping, and as part of the assessment of motor strength, hopping, wheel barrowing and hemiwalking. All of these tests require the integration of both sensory information from the limbs (touch, pressure, muscle spindle and golgi tendon ) and body, as well as appropriate motor responses. For a normal CP in the pelvic limb, sensory information must pass from the toe, up the spinal cord and brainstem to the thalamus, and finally to the sensory motor cortex. Once the abnormal foot position is recognised, the motor response must travel all the way back down again to the limb to correct the abnormality. A lesion anywhere in this pathway can cause A CP deficit. Postural reactions are therefore very sensitive indicators of neurological disease, but poor localisers! Contralateral CP deficits may be the only signs seen with cortical brain lesions, since motor deficits are often minimal.

Cranial nerve examination:

Abnormalities of cranial nerves are one of the most important indicators of intracranial disease. Because the cranial nerve cell bodies (nuclei) and peripheral nerves are located in specific areas of the brain, they are extremely useful for localising lesions. A basic understanding of anatomy and function is all that is required. Some of the major functions and more common clinical findings are listed below. I. (Olfactory) limited clinical use. II. (Optic) see below III. (Oculomotor) Location: MIDBRAIN, Functions: Extraocular eye muscles (most), Constriction of the pupil (parasympathetic) Signs: Loss of eye movement, loss of pupillary light response (PLR) IV. (Trochlear) limited clinical use Location: MIDBRAIN Functions: Extraocular eye muscle (dorsal oblique)

V. (Trigeminal) Location: PONS (motor) PONS-C1 (sensory) Functions: Facial sensation, Masticatory muscles Signs: Loss of palpebral reflex, Loss of facial sensation, Atrophy of temporal/masseter muscles (enophthalmos due to atrophy of pterygoid muscle) VI. (Abducens) limited clinical use Location: Medulla (rostral) Functions: Extraocular eye muscles (lateral rectus, retractor bulbi) VII. (Facial) Location: Medulla (rostral) Functions: Muscles of facial expression, lacrimation, salivation (parasympathetic) Signs: Facial droop, lip droop, loss of palpebral reflex and menace response, dry eye VIII. (Vestibulocochlear) Location: Peripheral receptors in temporal bone; Central nuclei medulla (rostral) + cerebellum Functions: Maintenance of balance/posture, hearing Signs: Ataxia, head tilt/leaning/circling, nystagmus, strabismus, vomiting, deafness IX/X/XI. (Glossopharyngeal/Vagus/Accessory) Location: Medulla (caudal) Functions: Pharyngeal/laryngeal muscles, (parasympathetic to heart viscera) Signs: Dysphagia, decreased gag, laryngeal paralysis, megaloesophagus XII. (Hypoglossal) uncommonly involved clinically Location: Medulla (caudal) Function: Tongue muscles (intrinsic) Signs: Deviation/atrophy of tongue, dysphagia Some important anatomy Cranial nerves V,VII,VIII. arise from the brain stem very close together in the region of the cerebellar pontine angle and are often affected at the same time. The facial nerve and sympathetic nerves to the eye pass through the middle ear and may be involved in otitis media/interna and vestibular disease.

Vision/PLR
Assuming that animals have normal ophthalmological examinations, loss of vision and PLR is often associated with intracranial disease. Loss of vision may be determined by loss of the menace response and watching an animal in its environment (negotiating obstacles). Pupil size is determined by parasympathetic (CNIII) and sympathetic input. Parasympathetic input is most important for resting pupil size and results in pupil constriction. Loss of parasympathetic innervation - mydriasis (dilation) Loss of sympathetic innervation - miosis (constriction) /ptosis/enophthalmos (Horner's syndrome) Mydriatic pupils usually localise to intracranial disease due to loss of either the stimulus to cause pupil constriction (optic nerve/chiasm/optic tract) or loss of CN III (midbrain). Miotic pupils (Horner's syndrome) more commonly reflects disease outside the brain, since the sympathetic pathway is more complex and passes from the brainstem to the thoracic spinal cord (nerve roots T1-T3) then back up the neck via the cervical sympathetic trunk and the middle ear before reaching the eye! Because part of the visual pathway is necessary to stimulate the PLR, this can be used to further localise lesions. Lesions resulting in loss of PLR and vision usually affect the common pathway ie optic nerve/chiasm/ optic tract.

Lesions resulting in loss of vision alone must be distant from these common pathways and usually involve damage to the visual cortex in the occipital lobe(s) at the caudal aspect of the brain (or the projections to the cortex)

Spinal reflexes:
Most important for localising spinal cord disease. Reflexes may be increased in nature with lesions

Muscle/spinal palpation
Muscles of mastication (temporalis/masseter), paraspinal, and limb muscles should be palpated to assess muscle atrophy. Profound and rapid (1-2 weeks) atrophy is seen with lower motor neuron lesions. Less severe, gradual disuse atrophy may be seen following UMN lesions. Localised masticatory muscle atrophy may be associated with trigeminal nerve deficits, but can also be found with extracranial disease such as masticatory muscle myositis. Although cervical spinal pain is usually associated with cervical disease, it may also be seen with intracranial disease such as large space occupying masses or infectious/inflammatory disease.

Other findings:
Seizures arise from the cerebral cortex and are a specific indicator of cerebral dysfunction. It is important however to remember that the underlying cause may be within the cortex itself (eg tumour) or extracranial, resulting in cortical dysfunction (eg hypoglycaemia secondary to an insulinoma) Lesions affecting the brainstem/cerebellum will often result in significant clinical signs because there are a lot of important structures in a fairly limited space. It is not uncommon however to have quite large lesions affecting the cerebrum with minimal or no obvious clinical signs. Signs may be subtle and involve changes in behaviour, particularly interactions with the owner. Always listen to the owner regarding such changes.

NEUROLOGICAL EXAMINATION - CONCLUSIONS:

Signs resulting from intracranial disease are not always specific for disease affecting the brain. However by knowing which ones are specific for intracranial disease, and by combining findings from multiple abnormalities we can usually determine whether the neurological abnormalities are due to intracranial disease and if so where specifically the abnormalities are located.

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Peter Dickinson, BVSc, PhD, Diplomate ACVIM (Neurology)

Understanding Vestibular Disease British Small Animal Veterinary Congress 2010 Jon Wray, BVSc, DSAM, CertVC, MRCVS, RCVS-Recognised Specialist in Small Animal Medicine (Internal Medicine) Dick White Referrals, Station Farm, Six Mile Bottom, Suffolk, UK
19885011

Relevant Anatomy The role of the vestibular apparatus is to assist balance by integration of sensory detection of position, gravity, acceleration and rotation with position of the eyes, trunk and head. The vestibular apparatus comprises: A 'peripheral portion' consisting of sensory receptors to detect gravity and linear acceleration (within the saccule and utricle) and rotational movement (within the semicircular canals) housed within the membranous labyrinth of the inner ear in the petrous temporal bone A 'central portion' comprising the vestibular nuclei of the medulla oblongata in the brainstem (from which pathways project to the nuclei of cranial nerves III, IV and VI, which are principally concerned with eye movement, and to the spinal cord) and projections to the flocculonodular lobe of the cerebellum Axons connecting the two areas Traditionally and logically it is useful to categorise vestibular disease as affecting either the peripheral or central neuroanatomical segment of the vestibular apparatus Clinical Signs of Vestibular Disease The cardinal clinical signs of vestibular disease are of head tilt and jerk nystagmus. Loss of balance associated with vestibular disease frequently causes nausea in acute cases and vomition may be marked in some dogs. Head tilt, or rotation of the head along its central axis so that one ear is held lower than the other, should be differentiated from head aversion and it should be borne in mind that disorders causing aural or dental pain may also be associated with apparent head tilt. Nystagmus is an oscillatory movement of the eyes and jerk nystagmus refers to this oscillation being slow in one direction and more rapid in the other (as opposed to pendular nystagmus seen in Siamese, Birman and Himalayan cats due to a congenital disorder of the visual pathway). The direction of nystagmus is named after the direction in which the fast phase occurs. In vestibular disease, nystagmus may be horizontal, vertical or rotary. Nystagmus occurring when the head is in a static position is termed 'spontaneous nystagmus' whereas nystagmus only induced by altering head position (for example by positioning the animal in dorsal recumbency) is termed 'positional nystagmus'. In addition to the above finding, animals with vestibular disease may display an ataxic, rolling gait with wide-based stance, falling or circling towards the side of the head tilt, variable changes in proprioceptive positioning and additional cranial nerve deficit; these last are useful in differentiating lesion localisation. Initial Assessment A thorough history should precede clinical examination and should include dietary, environmental, vaccination/worming, family and in-contact animal, previous medical and therapeutic assessment. A general physical examination is mandatory even though the examiner may be immediately suspicious of disease localised to the vestibular system. The key component of the initial assessment is a carefully performed neuroophthalmic examination with the aim of

identifying whether the animal with vestibular disease has changes which are focally affecting the vestibular apparatus (or whether, for example, multifocal disease may be present), and to determine whether there is evidence of peripheral or central involvement. Whilst the neuroophthalmic examination should be complete in every way, the key components are a very thorough assessment for evidence of aural disease, assessment for conscious proprioceptive deficits, and careful identification of other cranial nerve abnormalities. The facial nerve (CN VII) due to the position of its nucleus within the rostral medulla and course via the petrous temporal bone may be concurrently affected in both peripheral and central vestibular disease causing loss of tone in muscles of facial expression and absent blink/menace. Similarly the sympathetic innervations of the eye and face may be affected by lesions within first-order neurons as they course through the brainstem but also (and more commonly) within the third-order neuron which courses adjacent to the tympanic bulla, causing Horner's syndrome (miosis, enophthalmos, third eyelid protrusion). Other cranial nerve deficits, particularly of cranial nerves V-XII, strongly suggest brainstem involvement in the disease process and implicate central vestibular disease. Although ataxia may be severe with either, ipsilateral (i.e., on the same side) proprioceptive loss implies central vestibular disease. Nystagmus has a fast (corrective) phase and a slower (pathological) phase. In most circumstances the fast phase occurs away from the side of the lesion. Whilst vertical nystagmus and positional nystagmus are seen only with central vestibular lesions, the presence of horizontal or rotary nystagmus may be seen with either peripheral or central vestibular disease. Paradoxical vestibular disease may occur with central lesions of the cerebellum or caudal cerebellar peduncle. In this situation the head tilt and circling occur away from the side of the lesion, but proprioceptive deficits occur ipsilateral to it. Occasionally animals may be encountered with bilaterally symmetrical vestibular disease. These patients are characterised by severe ataxia accompanied by a low laterally 'swinging' head carriage. Clues to help differentiate central from peripheral vestibular disease are listed in Figure 1. Figure 1. Clues to Differentiate Central from Peripheral Vestibular Disease. Central vestibular disease Nystagmus Proprioceptive loss Altered level of consciousness Peripheral vestibular disease

Vertical, rotary or horizontal. Rotary or horizontal May alter with head position Possible, ipsilateral to lesion No Possible No

Other cranial nerve deficits May affect cranial nerves V- Cranial nerve VII only XII Horner's syndrome Differential Diagnoses Possible but uncommon Possible

Principal differential diagnoses of peripheral and central vestibular disease are listed in Figure 2. Figure 2. Differential Diagnoses of Central and Peripheral Vestibular Disease. 'Vitamin-D' mnemonic V--Vascular I--Idiopathic T--Toxic, traumatic Metronidazole toxicity Trauma Central vestibular disease Ischaemic or haemorrhagic vascular disease Idiopathic peripheral vestibular disease Ototoxicity caused by a range of topical products Trauma Congenital peripheral vestibular disease Hypothyroidism Meningoencephalitis: --Infectious --Non-infectious (unknown aetiology) Thiamine deficiency Tumours of the brainstem/ cerebellopontine angle Neurodegenerative disorders and storage diseases Otitis media-interna Labyrinthitis Polyps Tumours of the middle/inner ear Peripheral vestibular disease

A--Anomalous, anatomical Chiari-like malformation M--Metabolic I--Inflammatory

N--Nutritional, neoplastic

D--Degenerative

Further Investigation Further investigation is best guided by the clinical history and lesion localisation based on neuroophthalmic examination. No investigation may need to be undertaken, for instance if the clinical history or patient records indicate the strong possibility of peripheral disease caused by topical ototoxicity or where central disease is caused by metronidazole toxicity, in which discontinuation of the agent will usually result in recovery. Peripheral vestibular disease is most commonly seen with topical ototoxic agents, idiopathic vestibular disease, otitis media-interna and sometimes in association with hypothyroidism. A rational approach once toxic causes have been excluded is for a thorough evaluation of the external ear canal and tympanic membrane (usually best performed under general anaesthesia and is significantly enhanced by magnifying equipment such as video-otoscopy) and evaluation of the tympanic bulla and bony labyrinth by diagnostic imaging. Samples of fluid from the tympanic bulla may be collected via myringotomy for cytology and culture. Radiography, provided that images are taken with meticulous attention to positioning, may be very valuable, though superimposition of bony structures renders radiography inferior to more advanced (and expensive) techniques such as computed tomography (CT) and magnetic resonance imaging

(MRI). The pharynx should also be evaluated for polyps. Assessment of thyroid function should be performed but results may be difficult to interpret. Central vestibular disease is usually investigated by assessment of structural abnormalities of the brainstem and cerebellum by neurodiagnostic imaging, and assessment of cerebrospinal fluid (CSF) usually via cisternal puncture. CSF is assessed for cytology, protein content and for evidence of infectious organisms by cytology and polymerase chain reaction (PCR) analysis; it is best performed after neurodiagnostic imaging as this may detect evidence of raised intracranial pressure, in which case collection may risk brain herniation. Neurodiagnostic imaging by MRI or CT is invaluable provided that such images are collected with meticulous positioning and thorough understanding of neuroradiology. Some rarer nutritional and metabolic causes of central vestibular disease are best delineated by magnetic resonance sequences, which may not be appreciated by individuals without expertise in this area. If neurodiagnostic imaging is performed consideration should be given as to who is to perform and interpret such images as well as the simple availability of equipment. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Jon Wray, BVSc, DSAM, CertVC, MRCVS, RCVS-Recognised Specialist in SA Medicine (Internal Medicine) Dick White Referrals Station Farm Six Mile Bottom, Suffolk, UK

Where is the Lesion? Localizing Spinal Lesions British Small Animal Veterinary Congress 2009 Rita Gonalves, DVM, DECVN, MRCVS Faculty of Veterinary Science, The University of Liverpool, Liverpool
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The neurological examination aims to determine whether the underlying cause of the patient's clinical signs is indeed due to a lesion in the nervous system and, if so, where that lesion localizes to and how severe it is. This information along with the history (most importantly the speed of onset, progression of the signs and presence or absence of pain) and signalment allows for establishment of a shortlist of possible differential diagnoses and guides the diagnostic investigation. A thorough history should be collected, and initial examination starts with simple observation of the patient, assessing the animal's mentation, body posture and, most importantly in spinal disease, the gait. Gait Ataxia simply means uncoordinated gait. Ataxia can be due to cerebellar lesions (often associated with hypermetria, wide-based stance, intentional tremors--drunken gait), vestibular disease (commonly with leaning and falling to the side of lesion, head tilt, nystagmus--it looks like the animal is off balance) and spinal or less commonly peripheral nerve disease (due to decreased proprioceptive information arriving from the limbs--this is more subtle). Paresis is weakness of the gait, reduced voluntary movement. One can often see excessive wearing of the nails and hear scuffing of the feet during movement. Paresis can be classed as ambulatory or non-ambulatory (when the animal still has voluntary motor function but cannot ambulate unaided). Paralysis is complete loss of voluntary movement. Both paresis and paralysis (-plegia) can be used to describe the deficits in only one limb (monoparesis/plegia), in the pelvic limbs (paraparesis/plegia), in all four limbs (tetraparesis/ plegia) or on one side of the body (hemiparesis/ plegia). Neurological Examination of the Spine The aims of the hands-on examination are to determine which limbs are affected and to classify the lesion as affecting the upper motor neuron (UMN) or lower motor neuron (LMN). The LMN is the efferent neuron that connects the central nervous system with the effector organ (muscle or gland). The cell body is in the spinal cord grey matter or within the nucleus of a cranial nerve and its axon becomes the peripheral nerve. The UMN is the efferent neuron that originates in the brain and synapses (indirectly through an interneuron) with a LMN, modulating its activity. With a lesion affecting the LMN, flaccid paresis/paralysis with reduced muscle tone and reflexes and muscle atrophy is expected. In contrast, an UMN lesion results in spastic paresis/paralysis with normal to increased muscle tone and reflexes due to loss of its inhibitory effect over the LMN.

Functionally, the spinal cord can be divided into four areas: C1-C5, C6-T2, T3-L3 and L4-S3. The LMNs for the thoracic limbs are located in the cervical intumescence (C6-T2) and the LMNs for the pelvic limbs are in the lumbosacral intumescence (L4-S3). Lesions at these segments of the spinal cord result in LMN signs in the corresponding limbs (Figure 1). Assessment includes: Paw position, hopping and placing responses--test the awareness of the position and movement of the limbs. These tests confirm the presence of a neurological disorder and can detect subtle dysfunction, helping identify which limbs are affected. Usually they remain intact in muscular disease and junctionopathies (like myasthenia gravis) Muscle bulk and tone--both are reduced in LMN lesions and normal to increased with UMN disease Spinal reflexes--the easiest and most reliable are the patellar reflex in the pelvic limbs and the withdrawals in both the pelvic and the thoracic limbs. Don't forget to examine the tail and anus (perineal reflex). Reduced reflexes in a limb identify a LMN lesion in that limb, whilst normal or increased reflexes localize the lesion to the UMN Cutaneous trunci reflex (panniculus)--helps narrow down lesion localization in the thoracolumbar region. After pinching the skin, the sensory information enters the spinal cord approximately two vertebral spaces cranially, ascends the spinal cord to the level of C8-T1 where bilateral synapse occurs with the motor neurons of the lateral thoracic nerve, which then course through the brachial plexus and innervate the cutaneous trunci muscle, resulting in bilateral contraction of these muscles. Normally, this reflex is present from T2 to about L4-L5 and a cut-off in this region suggests a spinal cord lesion just cranial to the cut-off level. Loss of the cutaneous trunci reflex can also be due to a brachial plexus lesion, in which case it will be completely absent on the side of the lesion and normal on the contralateral side Pain sensation--the spinal pathways that carry pain sensation are located deep in the spinal cord so only a severe lesion will impair pain perception (making this an important prognostic factor). For conscious perception of pain, manifested by vocalization and/or turning the head and trying to bite, the information needs to be recognized by the sensory nerve, travel up the entire spinal cord cranial to that area and be interpreted by the brain. It is important to differentiate a pain response from a local withdrawal reflex (which should be present if both the peripheral nerve and spinal cord segment of the stimulated peripheral nerve are intact), in which case the limb will be retracted but no signs of conscious awareness of the pain will be evident. Pain sensation is tested by applying heavy pressure with haemostats to the bones of the digits (don't forget to test different digits) or to the long bones of the limbs Spinal palpation--looking for areas of hyperaesthesia or deformities. Pressure is applied to the spinous and transverse processes of the vertebrae in all spinal segments. Manipulation of the neck in all directions is also very helpful in identifying cervical pain

Other clues: cranial nerve examination may reveal Horner's syndrome if the lesion is in the cervical spinal cord. Shiff-Sherrington posture (hyperextension of thoracic limbs, which maintain voluntary movement, and normal conscious proprioception and paralysis of the pelvic limbs) can be seen with acute severe thoracolumbar lesions but does not have prognostic significance Figure 1. Lesion location and signs in limbs. Lesion location C1-C5 C6-T2 T3-L3 L4-S3 Polyneuropathies Severity of Disease Motor function--if the animal is non-ambulatory, support the animal's weight and check whether there is any voluntary movement present (better prognosis if there is) Deep pain perception--this is the most important prognostic factor. If absent, it is of great importance to determine when it was lost (if deep pain perception is absent for longer than 24-48 hours then there is a poor prognosis for recovery) Prognosis The prognosis mostly depends on the underlying aetiology of the neurological deficits (e.g., spinal neoplasia vs. minor contusive injury). One of the most common conditions seen causing spinal disease is degenerative intervertebral disc disease. It is important to know the prognosis for recovery with either surgical or conservative treatment for the different degrees of severity of the signs so appropriate clinical decisions can be made. The reported success rates vary widely and Figure 2 is a amalgamation of several study results that can be used as a guideline. Figure 2. Guide to prognosis of spinal injuries. Adapted from Sharp, NJH; Wheeler, SJ (2005). Grades Grade 1 Grade 2 Grade 3 Grade 4 Clinical signs No deficits, just pain Paresis, ambulatory Paralysis Prognosis with Prognosis with conservative treatment surgical treatment 100% 84% 81% 97% 95% 93% 95% Thoracic limbs UMN LMN Normal Normal LMN Pelvic limbs UMN UMN UMN LMN LMN

Paresis, non-ambulatory 84%

Grade 5 Recurrence References

No pain sensation

7% ~35%

60% Ascending myelomalacia in 5-10% dogs ~10-20%

1. Braund KG. Clinical neurology in small animals: localization, diagnosis and treatment. Ithaca, New York: International Veterinary Information Service, 2003. 2. Garosi L. The neurological examination. In: Platt, SR; Olby, N. eds. BSAVA manual of canine and feline neurology (third edition). Gloucester: BSAVA Publications, 2005; 1-23. 3. Garosi L. Lesion localisation and differential diagnosis. In: Platt, SR; Olby, N. eds. BSAVA manual of canine and feline neurology (third edition). Gloucester: BSAVA Publications, 2005; 24-34. 4. Sharp NJH, Wheeler SJ. Thoracolumbar disc disease. In: Small animal spinal disorders: diagnosis and surgery (second edition). Philadelphia: Elsevier Mosby, 2005. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Rita Gonalves, DVM, DECVN, MRCVS Faculty of Veterinary Science The University of Liverpool Liverpool, UK

Nursing and Management of Dogs with Weak Pelvic Limbs British Small Animal Veterinary Congress 2011 Joan R. Coates, BS, DVM, MS, DACVIM (Neurology) Clydesdale Hall, Department of Veterinary Medicine, College of Veterinary Medicine, University of Missouri, Columbia, MO, USA
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Introduction Management of the weak (paretic) or recumbent dog is contingent upon a team approach that begins with patient evaluation, pain management, bladder assessment and supportive care. The veterinary practitioner and technician work with the pet owner to tailor the appropriate care that enables the animal to return to activity. Increased access to dedicated facilities specific for animal rehabilitation and physical rehabilitation has become an important component in the care of animals with neurological disease. Patient Evaluation Nursing and management of a dog with neurological-related weakness in the pelvic limbs begins with obtaining a comprehensive history and patient examination. Patient examination requires a physical, neurological and orthopaedic examination. Often, aged and large-breed dogs have concurrent medical or orthopaedic conditions. For example, it will be more of a challenge for a dog that has concurrent intervertebral disc herniation and severe hip osteoarthritis to regain ambulatory status. A thorough patient history will evaluate the owner's expectations for outcome and abilities to care for their pet at home. It is important to question the owner about their pet's living environment with respect to flooring, ability to navigate indoor versus outdoor access and about the temperament of their pet, which may play a role as to which treatments and exercises are realistic. During the evaluation process, an assessment will be made to determine whether the owner is capable of following through with rehabilitation exercises and at-home patient care or prefers in-patient or out-patient therapy for their pet. Neurological Assessment Neurological assessment is key to documenting lesion localisation, severity of lesion and prognosis. The neurological examination will closely assess ambulatory status and motor function, integrity of spinal reflexes, bowel and bladder function and ability of the patient to perceive pain. Neuroanatomical localisation will provide an assessment of whether the weakness is upper motor neuron (UMN) or lower motor neuron (LMN) (see Figure 1). This will guide the veterinary surgeon and technician for appropriate neurodiagnostic testing and also with patient management. For example, an animal with LMN signs will be predisposed to decubitus ulceration from loss of muscle mass over bony prominences. Animals with only pelvic limb paresis have neurological disease caudal to the second thoracic spinal cord segment. Lesions in the region of T3L3 produce general proprioceptive (GP) ataxia (loss of coordination) and UMN paraparesis. The pelvic limb LMNs, located in segments L4S2, remain intact and are capable of reflex motor activity; however, voluntary motor control from the

brain is lost because the motor pathways in the spinal cord are damaged. The spinal reflexes are normal or exaggerated. Exaggerated reflexes result when UMN inhibitory influence on the LMNs is lost. Similarly, extensor hypertonus or spasticity also may develop. Ataxia results from damage to the spinal cord's general proprioceptive pathways, which transmit position sense signals from receptors in the pelvic limbs to the brain. Anaesthesia caudal to the lesion results from disruption of pain pathways from the pelvic limbs to the brain. Pain perception (nociception) is lost only if the lesion is bilateral and severe. Voluntary visceral functions such as micturition may be lost when UMN or sensory pathways in the spinal cord are damaged. Muscle atrophy from disuse will develop with time. In summary, spinal cord lesions in the region of T3 L3 segments result in: Paresis GP ataxia Decreased or absent postural reactions Normal reflexes or hyperreflexia Impaired micturition Variable degrees of sensory loss caudal to the lesion Lesions in the area of L4S2 or those that involve the cauda equina (the L7 and S1S2 spinal nerve roots and spinal nerves) produce pelvic limb paresis of the LMN type. Lesions involving spinal cord segments of L4S2 injure the motor neurons that form the lumbosacral plexus. Abnormalities related to femoral, sciatic, pudendal and pelvic nerves are encountered in these patients. Pelvic limb reflexes are depressed or absent and the muscles may be hypotonic. Neurogenic muscle atrophy develops. Sensory dysfunction results from an injury to the sensory neurons and nerve fibres located in this region of the spinal cord. Abnormalities of visceral function result from an injury to the motor and sensory neurons that innervate the bladder and the anus. Lesions involving the caudal segments of the spinal cord and the cauda equina damage nerve fibres that form the sciatic, pudendal, pelvic and caudal nerves. Because the femoral nerve is spared, the animal is able to support weight on the pelvic limbs but will have a plantigrade posture or stance. The patellar reflex is normal and pain perception is perceived from the medial aspect of the first digit and the thigh. The clinical signs are related to motor and sensory dysfunction of the involved nerves. Figure 1. Neurological examination findings for UMN and LMN signs. Upper motor Lower motor neuron neuron signs (T3L3) signs (L4S2) Muscle tone Increased (spasticity) Decreased (flaccidity)

Muscle atrophy Weakness (paresis) Spinal reflexes Pain Perception

Slow - disuse

Rapid and severe neurogenic Present Decreased to absent

Present Normal to exaggerated

Presence of pain perception is the most important prognostic indicator. In general, loss of pain perception as a result of spinal cord injury indicates severe spinal cord injury and a guarded prognosis. Dogs with intervertebral disc extrusions that have surgical decompression within 24 hours from time of injury have a 60% chance of recovery to ambulatory function. However, a dog with a spinal fracture and complete loss of pain perception has a poor to hopeless prognosis. Moreover, a dog that recovers pain perception within 2 weeks after surgery has a better chance of recovering ambulatory function. When assessing pain perception a noxious stimulus should be applied to the digits using a haemostat while taking care not to damage the skin. The patient is observed for vocalisation, turning towards and trying to escape from the stimulus or other behavioural responses that indicate cortical perception. Withdrawal of the limb by itself during the stimulus does not indicate deep pain perception. Each limb is assessed individually along with the tail. Pain Management An effective treatment plan for pain management provides acceptable analgesia with few side effects. In veterinary medicine, this may include clinical interventions and pharmacological and rehabilitative approaches singly or in combination. Goals are to reduce pain and improve function as much as possible. Efficacy, tolerability, cost and safety need consideration with any type of pharmacological therapy. Routes of administration may factor into effective pain control. Considerations should also be given for short-term and long-term therapeutic regimens. Recognition of different pain types (e.g., inflammatory versus neuropathic; acute versus chronic) assist with development of a pain management protocol. Opioid analgesics are classified into various groups based on their pharmacological activity, potency and clinical use. Type and dosage of opioid selection varies upon severity of pain. Opioid analgesics modify pain perception and behavioural reactions, and relieve anxiety and distress. Effectiveness of pharmacological opiates may vary with route of administration: parenteral, epidural, rectal, oral and transdermal (fentanyl patch) drug delivery. Direct delivery of opioids to the spinal cord (epidural anaesthesia) is used to produce effective anaesthesia for surgical procedures. Opioids are more effective for postsurgical and traumatic pain and considered less effective for neuropathic pain. Opioids that are pure agonists may provide more effective pain control than agonist-antagonist opioids. Tolerance to opiate effects may develop during repeated and chronic administration. Side effects may include altered consciousness, including dysphoria and respiratory depression.

The plethora of different non-steroidal anti-inflammatory drugs (NSAIDs) available for use in dogs and cats provides the practitioner with a choice for the most appropriate NSAID which will best complement pain management while minimising patient side effects. Response to specific NSAIDs may vary with each individual patient and the type of pain. If one NSAID does not appear to remedy the pain, an alternative NSAID or adjunctive use of a different class of analgesic needs consideration. Concurrent use of more than one NSAID or of an NSAID with glucocorticoids should be avoided. A 'washout' period (4872 hours) should be allowed before administering a different NSAID. NSAIDs appear to have synergistic effects with opioids and may allow for lower dosage of both. Inflammatory pain also can be alleviated through anti-inflammatory actions of glucocorticoids. Specific disease processes vary widely in optimal corticosteroid usage. It is important to obtain a confirmatory diagnosis before glucocorticoid usage. Initial rapid improvements without a differential diagnosis can be misleading. Moreover, chronic use of corticosteroids without monitoring can lead to deleterious side effects. For compressive spinal cord disease, dexamethasone or prednisone have been administered at anti-inflammatory doses to control inflammatory response and pain and to reduce spinal cord oedema. Concurrently, strict cage rest is important to prevent excessive activity in animals with spinal disease. Only a short-term antiinflammatory regimen of prednisone is recommended. Bladder Function Until proven otherwise, it should be assumed that animals with spinal cord disease are unable to voluntarily urinate or complete the micturition process. Risks associated with urine retention include developing urinary tract infection (UTI), bladder overdistention and damage to the kidneys. Dogs with neurogenic-related urine retention and intermittent and/or indwelling urinary catheters have potential risks for UTI. A prospective study determined that the prevalence of UTIs in dogs with thoracolumbar and lumbar intervertebral disc disease (IVDD) was 30% with a higher incidence in dogs that were female and those that had a lower intraoperative body temperature. The most common cause of voiding problems in the neurosurgical patient is urinary retention secondary to the underlying neurological disease. UMN bladder dysfunction occurs with lesions between the pons of the brain stem and L7 spinal cord segment. With an UMN bladder both the motor and sensory pathways of the detrusor reflex are affected. The bladder becomes large and firm and the urethral sphincter tone is increased. The bladder is difficult to express manually. Secondary overflow incontinence occurs when bladder pressure exceeds urethral pressure. LMN bladder dysfunction occurs with a lesion within the sacral spinal cord and nerve roots, and the pelvic plexus. A lesion in this area will abolish the detrusor reflex. The detrusor muscle becomes flaccid (detrusor atony) as a result of over-distension secondary to absent detrusor contraction and external sphincter tone is lost. The internal sphincter is innervated by the hypogastric nerve and remains intact. This may actually make bladder expression difficult. Animals with LMN bladder dysfunction also will lose their perineal reflex and sensation. Trauma is the most common cause for this type of dysfunction.

Bladder atony from overdistension can result from non-neurogenic or neurogenic causes. Nonneurogenic bladder atony is secondary to urinary obstruction and disruption of the tight junctions of the detrusor myofibres. Overdistention also can result from pelvic fractures and recumbency, itself. Urinary bladder emptying can be done by manual expression that can be facilitated using pharmacological therapies or by use of catheters (intermittent, indwelling). Basic principles need to be followed to prevent bladder overdistension in animals with urinary retention. Urinalysis and urine culture should be periodically performed to monitor for UTI. Manual bladder expression is indicated if the bladder is easily expressed, but residual urine should be periodically monitored by ultrasonography or urinary bladder catheterisation. Urinary bladder expression can be difficult in dogs with UMN disease or obesity and is considered a painful procedure in dogs that have recently had spinal surgery. Residual urine after expression is a potential source of infection and can lead to overflow incontinence and detrusor atony. Intermittent urinary bladder catheterisation often is indicated and has a lower risk of inducing a urinary tract infection over indwelling closed-system urinary catheterisation techniques. If an indwelling system is selected, minimising the duration is important. Pharmacological therapies for urine retention include drugs that improve bladder contraction and relax the urethral sphincters (Figure 2). Figure 2. Drug therapies to assist with urinary bladder emptying in dogs. Drug Mechanism of action Dosage Side effect

Decrease urethral sphincter tone Prazosin Phenoxybenzamine Diazepam Alpha-adrenergic agonist Alpha-adrenergic agonist Centrally acting skeletal muscle relaxant 1 mg/15 kg orally q1224h 0.250.5 mg/kg orally q1224h 0.52 mg/kg orally q68h Hypotension, tachycardia Hypotension, tachycardia Sedation, excitation

Increase detrusor muscle contraction Bethanecol Cholinergic 2.525 mg /dog orally q8h (start at low dose) 0.5 mg/kg orally q8h Gastrointestinal, bradycardia, dyspnoea Gastrointestinal

Cisapride

Increase acetylcholine release

Supportive Care Supportive care to improve psychological and physical well-being is especially important in the recumbent patient. Bedding should be supportive enough to evenly distribute the patient's weight

especially over bony prominences to prevent decubitus ulcers. Absorbent materials (lamb's wool, diaper pads) need to cover supportive materials (air, foam mattresses). The patient will need to be turned on a frequent basis (every 4 hours). Cleanliness and dryness are critical to prevent faecal and urine scalding. Cryotherapy of the surgical incision to reduce inflammation, pain and swelling is applied for the first 4872 hours or until the incision is no longer warm to touch. An ice pack covered with a towel to protect the skin is applied for 1020 minutes three times daily. Hydrotherapy also can play a role in increasing circulation of the limb vasculature and prevention of decubitus ulcers. Having the pet owner and technicians intimately involved with the postoperative care is important in the patient's overall wellbeing and quality of life. Physical Rehabilitation Physical rehabilitation is integral in management of neurological diseases and enhancement of neuroregenerative processes. Disuse and immobilisation can cause loss of muscle mass and debilitating joint contracture. Physical rehabilitation during recovery from neurological disorders is important not only for strengthening and increasing flexibility but also for pain reduction and improvement in quality of life. Elements to implement early in the recovery process include standing exercises, range of motion (ROM), hydrotherapy and basic supportive care. Rehabilitation in immediate postoperative and recumbent patients begins with massage and passive ROM. Massage is used in the beginning to relax the patient and loosen the muscles, thus reducing damage to muscles during exercise. Neuromuscular electrical stimulation is applied to selected muscle groups that undergo disuse atrophy, which assists with preservation of muscle strength. During passive ROM, joints of limbs are extended and flexed through normal ROM 510 minutes several times a day. Toe pinch exercises that use the flexor reflex will activate muscle contraction as well as providing resistance with the limb in extension. Animals with LMN weakness may only show muscle fasciculation or contraction rather than complete limb flexion. In these cases, the limb will need assistance in flexing. Active ROM includes swimming and standing exercises. Underwater treadmill therapy is most effective as the animal is beginning to regain the ability to ambulate. While non-ambulatory outside of the treadmill, the animal may first begin to show motor function while in the underwater treadmill. Water buoyancy helps in rehabilitation of weak muscles and painful joints by minimising the amount of weightbearing on joints while generating the gait cycle. The goal is to have the limbs in a normal position while bearing only a portion of the body weight. With the paraplegic or paraparetic patient in the underwater or land treadmill, a gait pattern can be established. It is important, though, during these exercises to allow adequate rest periods of 2 minutes between the walking periods. Superficial and deep heat therapy can further reduce muscle spasm and improve circulation. As the patient begins to ambulate, therapeutic exercising includes standing and more dynamic ambulation activities, which serve to enhance ROM, muscle strength, balance and overall daily

function. This process can be initiated with assistive walking devices and during hydrotherapy. Static and mechanical forms of stretching techniques are performed in conjunction with ROM exercises to prevent fibrosis and contracture of joints and muscles. Gait training exercises encourage more ambulation to affected limbs. Sling-assisted walking, cavaletti rails and physioroll or ball balancing are all useful for developing strength and coordination. Proprioceptive neuromuscular training using a mattress or balance boards improves the awareness and use of limbs at rest and in motion. As the strength improves with neurological recovery, exercises will then include stair or hill climbing, pulling weights, walking on mattresses, open water swimming, sit to stand and weaving. Repetitions of 10 of 23 sets at one to three times a day are guided by whether the patient fatigues. In disorders such as degenerative myelopathy, it will be important to avoid fatigue and further muscle injury. Leg weights are used when one leg is weaker. Other modalities of physical therapy and supplemental therapies that complement mobility therapies include thermal, electrical stimulation, massage, ultrasonography, acupuncture and weight loss. Muscle or joint contracture is difficult to overcome but therapeutic ultrasound may reverse or lessen tendon, joint and ligament contractures. In summary, rehabilitation protocols are individually tailored to meet patient's needs during the recovery process. References 1. Millis DL. Physical therapy and rehabilitation of neurologic patients. In: Bonagura JD, Twedt DC. eds. Kirk's Current Veterinary Therapy XIV. St. Louis: Saunders Elsevier, 2008; 1131 1135. 2. Olby N, Halling KB, et al. Rehabilitation for the neurologic patient. Veterinary Clinics of North America: Small Animal Practice 2005; 35: 13891409. 3. Sherman J, Olby NJ. Nursing and rehabilitation of the neurological patient. In: Platt SR, Olby NJ. eds. BSAVA Manual of Canine and Feline Neurology. Quedgeley: British Small Animal Veterinary Association, 2004; 394407. 4. Steiss JE, Levine D. Physical agent modalities. Veterinary Clinics of North America: Small Animal Practice 2005; 35: 13171333. 5. Stiffler KS, Stevenson M, et al. Prevalence and characterization of urinary tract infections in dogs with surgically treated type I thoracolumbar intervertebral disc extrusion. Veterinary Surgery 2006; 35: 330336. Joan R. Coates , BS, DVM, MS, DACVIM(Neurology) Department of Veterinary Medicine, College of Veterinary Medicine University of Missouri Columbia, MO , USA

Video Tour of the Neurological Examination (V196) Western Veterinary Conference 2009 Simon R. Platt Department of Small Animal Medicine & Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA
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The neurological examination is performed to determine if a neurological problem is present, where it is located in the nervous system and how severe it might be. The neurological examination starting from the front to back of the animal may be divided into the evaluation of the head, gait, neck and thoracic limbs, back, pelvic limbs, anus and tail. The Hands-Off Evaluation Mentation--can be observed while collecting the initial history. The owner's opinion of any behavior changes is important to note. A depressed animal is quiet but appropriate. A demented animal is awake but dull and inappropriate. Lesions of the cerebrum and diencephalon (thalamus) produce dementia, delirium, rage, stupor and coma. Lesions of the midbrain can produce stupor and coma. Posture--a head tilt (the ear on one side closer to the ground) is associated with a unilateral lesion of the CN VIII. Head incoordination and tremors may be observed when animals lift their heads or attempt to drink and eat and indicate a lesion of the cerebellum. Gait--a normal gait requires proper function of all sensory and motor peripheral nerves and tracts through the spinal cord and brainstem and the cerebellum. The cerebrum is less important in animals and lesions there may cause only temporary alterations in gait. Circling or pacing may be observed and indicate a lesion of the cerebrum or diencephalon. Animals usually circle toward the side of the lesion. Ataxia is an uncoordinated gait and may be due to sensory peripheral nerve (rare), spinal cord, brainstem or cerebellar lesions. Ataxia with limb paresis (weakness) may be due to peripheral nerve, spinal cord or brainstem lesions. Paresis is not seen with cerebellar lesions. Paresis can be mild, moderate and severe. With severe paresis the animal is unable to stand but still has some voluntary movement. Paralysis is the total loss of all voluntary movement--indicates brainstem or spine disease. The Hands-on Evaluation A. The Cranial Nerve Examination

Olfactory nerves (CN I)--tested by blindfolding the animal and offering food to observe if they can find the food with their sense of smell. Optic nerves (CN II)--evaluated using the menace response, general visual capabilities, the pupillary light reflex and pupil size. The menace response evaluates CN II and the Facial nerves (CN VII) and their connections through the brainstem, brain and cerebellum--tested by advancing the hand or fingers toward the eye and observing the animal blink the eyelids or retract the globe. Vision is the function of CN II, the diencephalon and occipital lobes of the cerebrum--tested by observing the animal walk around an unfamiliar environment to see if they bump into objects, or throwing cotton balls. The pupillary light reflex evaluates CN II and the Oculomotor nerves (CN III)--tested by shining a light into the pupil and observing pupillary constriction in the eye tested (the direct response) and the opposite eye (the indirect response). Pupil size is observed in normal room light. Pupils may be large with lesions of CN II or CN III or midbrain. Pupils may be small with lesions of the sympathetic innervation to the pupil, which ascends up the neck from the vagosympathetic trunk and produces a Horner's syndrome. Oculomotor nerves (CN III)--tested by the pupillary light response, eyeball position, and eyeball movement. Eyeball position--a true strabismus occurs when the eyeball is deviated into an abnormal position when the head is in the normal position. Ventrolateral strabismus occurs with lesions of CN III, a contralateral dorsolateral strabismus is seen with lesions of CN IV, and a medial strabismus is seen with lesions of CN VI. Trochlear nerves (CN IV)--tested by eyeball position and eyeball movement. Trigeminal nerves (CN V)--tested by evaluation of temporal and masseter muscle size and tone as well as facial sensation, which is evaluated with the palpebral reflex and the aural and buccal reflexes. Temporal and Masseter muscle atrophy is observed by palpation and is associated with lesions of CN V and primary muscle diseases of the head musculature. Jaw tone and motion is observed by manipulation opening and closing the mouth. Loss of jaw tone is usually associated with bilateral lesions of CN V and restricted range of motion is often due to primary muscle diseases of the head musculature. The palpebral reflex is elicited by touching the medial and lateral canthi of the eyes and observed as the eyelids closing; evaluates CN V and CN VII.

The aural and buccal reflexes are elicited by touching or pinching the ear or lip respectively and observing movement of these; evaluates CN V and CN VII. Abducent nerves (CN VI)--tested by evaluation of eyeball position and eyeball movement (lateral and retraction). Facial nerves (CN VII)--tested by evaluation of facial symmetry, palpebral, aural and buccal reflexes and by Schirmer tear tests. Vestibular nerves (CN VIII)--tested by evaluation of head posture (tilt with disease), spontaneous and physiological nystagmus, positional strabismus, gait (dysequilibrium with disease) and hearing ability. Positional strabismus is an abnormal eyeball position when the head is placed in abnormal positions but not at resting posture. This is different than true strabismus as eyeballs are not paralyzed in abnormal positions. As the head is moved both eyeballs move to the same degree. Positional strabismus most commonly occurs with a lesion of CN VIII or the vestibular regions of the cerebellum. The eyeball on the affected side drops more than the eyeball on the normal side as the nose is elevated. Physiological nystagmus is observed when the head is moved and the eyes move slowly (slow phase) away from the direction of head movement then rapidly snap back (fast phase) toward that side. These eye movements are repeated several times when the head is moved side to side or up and down and require the integrity of the CNs III, IV, VI and VIII. Pathological nystagmus may occur without head movement with lesions of the CN VIII, the rostral medulla oblongata or cerebellum. Nystagmus has a fast and slow phase. Nystagmus may be horizontal, vertical or rotary. The nystagmus is named by the direction of the fast phase. Hearing is grossly tested by observing a response to a noise such as whistling. Glossopharyngeal nerves (CN IX), Vagus nerves (CN X) and Spinal Accessory nerves (CN XI)--these nerves are often evaluated together by evaluation of the animal's swallowing ability, upper respiratory tract and esophageal function. Swallowing is observed by applying pressure to the hyoid bones or stimulating the pharynx with a finger. Stridor or increased respiratory noise through the larynx may be due to unilateral or bilateral laryngeal paresis or paralysis and may be heard with the bare ear or a stethoscope. Dysphonia may be observed or noted in the history. Regurgitation may be observed or noted in the history and may be due to megaesophagus most commonly secondary to esophageal muscle disease and less commonly from lesions of CN X.

Hypoglossus nerves (CN XII)--evaluated by examination of tongue size and function. B. Postural Reaction Examinations Not all necessary but can be very helpful in 1) confirming a neurological deficit and 2) determination of asymmetry. Wheel-barrowing can detect deficits not appreciated during the gait evaluation. In tetraparetic animals, this test may be performed to determine if the thoracic limbs are more involved than the pelvic limbs. Hopping is evaluated by lifting the opposite thoracic or pelvic limb and both pelvic limbs or thoracic limbs and pushing the animal forward and laterally to observe their ability to walk or hop on each thoracic or pelvic limb independently. Equal responses should be seen on both sides. Conscious proprioception when performed correctly can be a very important tool to detect subtle dysfunction. The animal is supported slightly, the paw is then turned so standing is on the dorsal surface. The animal should return the paw to the correct position within a few seconds. The animal should not be leaning against the examiner nor should the examiner be supporting the animal's weight. C. The Reflex Examination Spinal cord reflexes pass through specific peripheral nerves and spinal cord segments, so if a spinal reflex is depressed or absent the lesion is localized to that specific site. These tests will determine if the lesion is lower motor neuron (LMN) or upper motor neuron (UMN). Factors evaluated UMN Lesion Resting muscle tone Spinal reflexes Normal Normal to exaggerated LMN Lesion Normal to decreased Usually normal to decreased (or even absent), but may be increased (pseudo-hyperreflexia) Early and severe muscle atrophy (neurogenic)

Muscle atrophy

Little and late muscle atrophy (chronic stages: disuse atrophy)

Thoracic limb spinal reflexes: The Biceps tendon reflex (C6-8 spinal cord segments) The Triceps tendon reflex (C7-T2 spinal cord segments) The Extensor carpi radialis muscle reflex (C7-T2 spinal cord segments)

The Flexor withdrawal reflex also referred to as toe pinch reflex (C7-T2 spinal cord segments) Pelvic limb spinal reflexes: The Patellar reflex (L4-5 spinal cord) Gastrocnemius muscle reflex (L6-S2 spinal cord) The Cranial tibial muscle reflex (L6-S2 spinal cord) The Flexor withdrawal reflex (L6-T2 spinal) The Crossed extensor reflex occurs if the opposite limb extends when the flexor reflex of the other limb is elicited. The presence of an obvious crossed extensor reflex usually indicates a lesion above spinal cord segment L4. The Anal reflex (S1-3 spinal cord segments). The perineal area on each side is pinched with hemostatic forceps and the anus muscle will contract. If a reduced reflex is suspected, a gloved finger should be inserted into the anus and strong anal muscle contraction should be felt if normal. The Tail reflex (S1-Cd5 spinal cord). As the perineal area is stimulated with forceps or a finger the tail will contract toward the anus. Panniculus reflex. Allows accurate localisation in the T3 to L3 UMN region of the spinal cord, and assesses the C8 to T1 region of the brachial plexus (outflow of the panniculus reflex). In the occasional normal animal the panniculus is either unreliable or totally absent. D. Pain Evaluation Focal pain--palpate down the spine feeling for focal pain, muscle spasm and heat. If the dog does not react to light palpation then moderate pressure is applied. Flex the neck from side-toside, dorsally and ventrally. Extend and flex the lumbosacral junction while trying not to flex other joints. The presence of pain implies pathology of the meninges, nerve roots, vertebral joints, spinal muscles or discs. Pathology of the spinal cord itself is not painful unless it involves the meninges as well. Deep pain--is tested by applying pressure to one of the digits with hemostatic forceps and observing a behavioral response. Withdrawal of the toes is only the flexor reflex. If no deep pain is observed on one digit, all digits should be tested. A complete loss of deep pain signifies a severe spinal cord lesion and a grave prognosis. Based on the above tests the lesion should be localised to one of the following areas (unless multifocal or extensive):

1. Forebrain (cerebrum / diencephalon) 2. Cranial nerves (peripheral or central {brainstem}) 3. C1 to C5: UMN to all limbs 4. C6 to T2: LMN to thoracic limbs and to UMN pelvic limbs 5. T3 to L3:Thoracic limbs are normal and UMN to pelvic limbs 6. L4 to S1:Thoracic limbs are normal and LMN to pelvic limbs 7. S1 to S3All limbs normal, but LMN to bladder, perineum and/or tail 8. Polyneuropathy/polymyopathy: LMN to all four limbs

References 1. Glass EN, Kent M. The clinical examination for neuromuscular disease. Vet Clin North Am Small Anim Pract 2002;32(1):1-29 2. Thomas WB. Initial assessment of patients with neurologic dysfunction. Vet Clin North Am Small Anim Pract 2000;30(1):1-24 Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN University of Georgia, College of Veterinary Medicine Dept. of Small Animal Medicine & Surgery Athens, GA, United States

Diagnostic Approach to Canine and Feline Neuromuscular Disease ACVIM 2006 Kate E. Chandler, BVetMed, DECVN, PhD, MRCVS London, UK
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Introduction Neuromuscular diseases in dogs and cats are a diagnostic challenge. The key to success with investigating these conditions is to start with a thorough history and detailed physical and neurological examination. As with all neurological problems, neuroanatomical localization of the lesion by performing a full neurological examination is absolutely vital in order to correctly identify the patient with a neuromuscular disorder. Neuromuscular conditions include diseases of the peripheral nervous system (PNS), neuromuscular junction (NMJ) and muscle. They can be focal or generalized. How can the clinician determine that these systems are dysfunctional? Historical Findings in Neuromuscular Disease Generalized Neuromuscular Disease Owners may report signs of generalized weakness (paresis). In dogs, the most common clues include: exercise intolerance, collapse, short choppy strides that gradually get shorter until collapse, flaccid paralysis, generalized muscle loss (which might be reported as weight loss), inability to get into the car, go upstairs or jump. In cats, owners may notice a reduced level of activity, weight loss, and neck ventroflexion. Pain can also be a characteristic of muscle disease, particularly if it is inflammatory in nature. Muscle pain can be difficult to localise since it is often diffuse and the owner may report that the animal vocalizes when handled or seems generally painful. Focal Neuromuscular Disease Common focal cranial nerve signs include a lip droop in facial nerve paralysis, a voice change (e.g., high pitched bark) in recurrent laryngeal nerve dysfunction, or lameness or paresis affecting isolated limbs in isolated peripheral nerve lesions. Focal muscle atrophy is also possible, for example masticatory muscle myositis may lead to bilateral masticatory muscle atrophy, which owners sometimes report as an abnormal head shape. Brachial plexus lesions could lead to atrophy of specific muscle groups in the thoracic limb. Physical and Neurological Findings in Neuromuscular Disease Generalized Neuromuscular Disease When faced with the tetraparetic animal, lesion localization can be difficult. A C1-5 or C6-T2 spinal cord lesion such as disc herniation, polyneuropathy, or a junctionopathy such as myasthenia gravis may cause motor deficits in all four limbs (Olby, 2004). However, there a number of key clinical findings that can differentiate between neuromuscular disease and other

causes of tetraparesis. The concept of upper motor neuron and lower motor neuron disease is extremely helpful in this situation. A C1-C5 spinal cord lesion will cause upper motor neuron weakness in all four limbs whereas a generalized neuromuscular disease such as a polyneuropathy will lead to lower motor neuron signs in all four limbs. Upper motor neuron paresis is characterized by normal to exaggerated spinal reflexes, normal to increased tone in the musculature, and absence of atrophy. The most useful spinal reflexes are the patellar reflex and withdrawal reflexes. Triceps, biceps, gastrocnemius and extensor carpi radialis reflexes are unpredictable in normal dogs and are particularly difficult to elicit in cats. Lower motor neuron paresis is characterized by reduced spinal reflexes (again, the patellar and withdrawals are the easiest to interpret), reduced muscle tone and neurogenic atrophy. It is also important to remember that spinal reflex deficits occur commonly in polyneuropathies however in myasthenia gravis, a disorder of the neuromuscular junction, spinal reflexes are usually normal. Similarly, generalized muscle disease such as polymyositis usually leaves the spinal reflexes intact unless there has been profound muscle atrophy or fibrosis. Gait Dogs and cats with both upper motor neuron weakness and neuromuscular deficits may both have a weak (paretic) gait. However spinal cord lesions that cause paresis are also associated with ataxia and have significant conscious proprioceptive deficits, as well as having upper motor neuron signs depending on the site of the lesion. Generalized muscle disease tends to cause a stiff, short-strided, choppy gait with an absence of proprioceptive ataxia, since the proprioceptive pathways are not affected. However, in neuropathies with a sensory component, decreased pain response (hypalgesia) or sensation (hypaesthesia), abnormal sensation (paraesthesia) and conscious proprioceptive deficits may also be seen. Animals with myasthenia gravis tend to have a short strided gait which gets progressively gets worse during attempted exercise and then improves after rest. Patients with polyneuropathy tend to have a more flaccid paralysis. Focal Neuromuscular Disease Signs of focal cranial nerve deficits may be detected on cranial nerve examination. Some of the most common cranial neuropathies are facial nerve paralysis and trigeminal nerve paralysis. Other examples of focal neuromuscular signs are specific atrophy of muscle groups, for example, a brachial plexus tumour (malignant peripheral nerve sheath tumour) may cause focal atrophy of specific muscle groups in the thoracic limb. Autonomic neuropathies additionally may exhibit signs of anisocoria or dilated pupils, decreased tear secretion , decreased salivation and bradycardia (Harkin et al., 2002; Cave et al., 2003). Once a neuroanatomical localisation has been achieved, a list of differential diagnoses needs to be determined. A thorough list of differentials for neuromuscular diseases has been provided by Braund (2003). Examples of Common Differential Diagnoses of Peripheral Nervous System Disease Degenerative

Several breed associated neuropathies have been reported e.g., Rottweiler distal sensimotor polyneuropathy Anomalous Storage diseases, e.g., fucosidosis Metabolic Hypothyroidism, hyperadrenocorticism, chronic hypoglycaemic neuropathy, diabetic neuropathy Neoplastic Paraneoplastic neuropathy, peripheral nerve tumours Inflammatory Polyradiculoneuritis Idiopathic Facial nerve paralysis Traumatic Brachial plexus avulsion Toxic Toxic neuropathies, e.g., vincristine, organophosphates Vascular Ischaemic neuromyopathy Examples of Common Differential Diagnoses of Muscular Disease Degenerative Labrador Retriever hereditary myopathy, congenital muscular dystrophy Anomalous Storage disorders, e.g., glycogenosis Metabolic

Hyperadrenocortical (Cushing's) myopathy, hypokalemic myopathy, hypothyroid myopathy, malignant hyperthermia Neoplastic Paraneoplastic myositis, skeletal muscle tumors Inflammatory Polymyositis, protozoal disease, e.g., Neospora caninum, Toxoplasma gondii Idiopathic Facial nerve paralysis Traumatic Fibrotic myopathy Toxic Toxic myopathy, e.g., monensin Vascular Ischaemic neuromyopathy Diagnostic Work-Up Once history, physical and neurological examination has determined the presence of neuromuscular dysfunction, a differential diagnosis list will be selected depending on signalment, history, clinical findings and localisation. A diagnostic plan then needs to be instigated depending on the differential diagnosis list. Haematology and biochemistry are important to determine signs of metabolic, electrolyte disorders or multisystemic disease. Creatine kinase needs to be carefully noted, as this may increase markedly if there is significant muscle involvement. Endocrine tests such as TSH and T4, ACTH stimulation and low dose dexamethasone tests may need to be performed to look for underlying endocrinopathy. Serology may need to be performed for suspected infectious agents e.g., Neospora caninum, Toxoplasma gondii. Acetylcholine receptor antibody testing may be indicated. Radiographs and ultrasound may need to be used to detect any signs of neoplasia or multisystemic disease. Magnetic resonance imaging is indicated in some situations, for example if a brachial plexus tumour is suspected. Cerebrospinal fluid analysis may detect abnormalities if nerve roots are inflamed e.g., polyradiculoneuritis, or if there is also central nervous system involvement e.g., protozoal disease. Clinical electrophysiological techniques including electromyography and nerve conduction studies will be extremely useful to further localise the extent of any neuromuscular disease and to confirm sites of abnormality prior to other diagnostic tests. These methods are

discussed in detail by Poncelet (2004). Lastly, nerve and muscle biopsy are indicated depending on the results of electrophysiological testing and other clinical findings. The nerves and muscles to be biopsied should be selected on the basis of clinical signs and electrophysiological testing. The most commonly biopsied nerves include the peroneal and tibial branches of the sciatic nerve because both are commonly involved in polyneuropathies and are easy to surgically approach. Nerve and muscle histopathology should be performed by a specialist neuromuscular laboratory in order to obtain the most information from the sampled tissue. Summary History, physical and neurological examination are the most important steps in investigating a neuromuscular condition. Correct and precise neuroanatomical localisation will greatly assist in drawing up a list of differential diagnoses. It may be possible to differentiate between peripheral nerve, NMJ, and muscular disease. This will then be helpful in selecting the most appropriate diagnostic tests. Unfortunately, there are still many neuromuscular diseases in dogs and cats that are not fully understood and treatments are limited in some situations. However, many specific neuromuscular conditions can be treated such as the endocrinopathies and inflammatory conditions. It is therefore worthwhile pursuing a full diagnostic work-up to achieve a definitive diagnosis, in order to provide the most appropriate treatment and to give an accurate prognosis for the owner. References 1. Braund K. Braund's Clinical Neurology in Small Animals: Localization, Diagnosis and Treatment 2003 online at www.ivis.org. Cave TA et al., Vet Rec. 2003;153(13):387. 2. Harkin KR et al., J Am Vet Med Assoc. 2002;220(5):633. 3. Olby NJ, Chapter 14. In: BSAVA Manual of Canine and Feline Neurology 3rd Edition. Ed. By SR Platt and NJ Olby. 4. Poncelet L, Chapter 4. In: BSAVA Manual of Canine and Feline Neurology 3rd Edition. Ed. By SR Platt and NJ Olby. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Kate Chandler, BVetMed, DECVN, PhD, MRCVS The Queen Mother Hospital for Animals The Royal Veterinary College Hatfield, Great Britain

Localising Neurologic Lesions Using the NeuroMap: Spinal Cord World Small Animal Veterinary Association World Congress Proceedings, 2013 Christine E. Thomson, BVSc (Hons), DACVIM (Neurology), DECVN, PhD VetLearn, New Zealand Veterinary Association, Massey University, Palmerston North, New Zealand
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The first step in neurology cases is to localise the lesion, but that can be challenging, particularly if it is not something you do frequently. The NeuroMap and associated table are simple aids that have been distilled from years of clinical practice and can assist you in localising lesions. As diseases are often location-specific, once you've localised the lesion, then you can list the possible causes and make a diagnostic plan. The NeuroMap is derived from mapping the main neural functions on a diagram of the nervous system. If a lesion is in a particular area, you can read from the NeuroMap which neural functions could be disrupted and, conversely, which neural functions will be normal. Key point: Identifying both the neural functions that are disrupted and those functions that are still normal are essential in lesion localisation. Clinical signs of dysfunction indicate that a lesion is disrupting that neural system. However, if a neural system is functioning normally, that suggests the lesion is not in the region of the nervous system housing that neural system. The Neurological Examination The following neural functions are assessed in the neurological examination: 1. Behaviour and arousal (awareness) 2. Ascending sensory systems (tactile, proprioception, and nociception) 3. Motor function 4. Cranial nerve function 5. Spinal reflexes Spinal sensitivity/pain may help to further localise a spinal cord lesion. By noting from these test results which systems are functioning normally and which are abnormal, then by referring to the NeuroMap (and accompanying table), you can determine where the lesion is likely to be cited. Can a single lesion account for all the observed signs (normal and abnormal)? If not, then the animal may have a multifocal lesion, indicating specific aetiologies. Functional Regions of the Spinal Cord These are based around where the innervation to the limbs connects; they comprise specific spinal cord segments. In the dog, these are: cervical (C15: neck), cervical intumescence (C6 T2: thoracic limbs), thoracolumbar (T3L3: trunk), lumbosacral intumescence (L4S3: pelvic

limbs and pelvic viscera), and caudal segments (Cd15: tail). As the clinical signs of spinal cord disease are characteristic for each of these regions, animals are considered to have a regionspecific localisation: e.g., thoracolumbar disease. Upper and Lower Motor Neurons A UMN is confined to the central nervous system (CNS = brain and spinal cord), thus it might help to think of it as a 'central motor neuron.' An LMN has its cell body in the CNS, but the bulk of the cell (the axon) is in the periphery, thus it might help to think of it as a 'peripheral motor neuron.' Reflexes A reflex comprises three parts: sensory input from a peripheral receptor; a central connection in the brain or spinal cord for reflexes involving the cranial and spinal nerves, respectively; and output via a lower (peripheral) motor neuron that connects to the muscle via a neuromuscular junction. Damage to any one of those components will result in a reduction or loss of the reflex. Damage to LMNs results in reduced/lost reflexes, but when UMNs are damaged, reflexes will still be present; they may even be increased due to loss of inhibitory UMN influence. UMN versus LMN Disease When a lesion affects an intumescence (cervical or lumbosacral), it can damage cell bodies of the lower (peripheral) motor neuron cell bodies supplying the limbs, resulting in LMN signs such as reduced/lost Reflexes, Atrophy of specific muscles innervated by those LMNs, and reduced muscle Tone. Conversely, when the lesion is cranial to the intumescence, then the LMNs to that limb will be intact (good tone and intact reflex arcs); the animal is described as having UMN signs to the limbs as the upper (central) motor neuron has been compromised. Table 1. Differentiating between UMN and LMN lesions Sign UMN disease LMN disease Decreased to absent Neurogenic: severe, specific muscles Decreased to absent

Reflexes Normal to increased Atrophy Disuse: Mild, generalised Tone Normal to increased

Figure 1. The Neuro RAT (Reflexes, Atrophy, Tone)

The Neuro RAT is a useful mnemonic to help differentiate between the signs of UMN disease and LMN disease. Sensory Function and Proprioception Spinal cord lesions can also compromise sensory function caudal to the lesion. This can cause reduced/lost proprioception, and sensory input from the external (tactile, thermal and noxious stimuli) and the internal environment (e.g., viscera such as the distension of the urinary bladder or rectum). Proprioception is awareness of body position. Subconscious proprioception projects to a subconscious area of the brain - the cerebellum. SCP is used to keep the limbs located under the body's centre of gravity and is particularly important for setting posture both at rest and during locomotion. Thus, an animal with deficits in subconscious proprioception may stand basewide or base-narrow, or cross its feet when ambulating, resulting in an ataxic (incoordinated) gait. Input from muscle and joint receptors is important in SCP. Conscious proprioception (CP) is projected to the sensory cortex of the contralateral forebrain and is used by the animal for voluntary or skilled motor function, e.g., the dog lifting paw to 'shake hands.' Tactile input is a key component of CP. An animal with deficits in CP may stand on top of its foot ('knuckling'). However, animals with spinal cord disease usually have both conscious and subconscious proprioceptive deficits, as both types of information travel up the spinal cord. Note: Normal proprioceptive reactions require both sensory and motor functions to be intact. Nociception Noxious (tissue-damaging) stimuli travel via spinal nerves into the spinal cord. There they can stimulate local reflex function (e.g., withdrawal reflex). The nociceptive information is also projected to the forebrain for conscious perception. There are many nociceptive pathways travelling to the brain, bilaterally; thus only severe spinal cord lesions, compromising the width of the cord, will result in loss of nociception. If such a lesion is cranial to an intumescence, then the withdrawal reflex to that limb will still be intact, but there will be no conscious perception of the stimulus. But if the lesion is in the intumescence, both the withdrawal reflex and conscious perception will be lost. Innervation of the Urinary Bladder and Anal Sphincter

The innervation of the urinary bladder, rectum, anal sphincter and perineum is associated mainly with the sacral spinal cord (S13). It receives sensory input from pelvic viscera and perineum and gives rise to parasympathetic LMNs supplying the bladder wall (for detrusor muscle tone and its contraction in urination) and somatic LMNs supplying the striated urinary and anal sphincters (urine and faecal retention). Sympathetic fibres originate from the cranial lumbar spinal cord; they stimulate contraction of smooth muscle at the neck of the bladder and relaxation of bladder wall muscle for urine storage. Sensory input synapses in the sacral spinal cord triggering reflex activity (e.g., perineal reflex) and also projects cranially to the brain, conveying information about the distension of the bladder and rectum for conscious perception. When LMNs originating in the sacral cord are damaged, there is reduced or lost muscle tone (bladder wall and sphincters) and reflexes. Such an animal will have a bladder that is large, flaccid, and easy to express; it may dribble urine. Loss of LMN supplying the anal sphincter may lead to a dilated sphincter and faecal incontinence; the perineal reflex will also be compromised. Conversely, with UMN lesions cranial to the sacral spinal cord, LMN innervation will be intact, and the bladder wall and striated urinary and anal sphincters will still have tone - thus, the bladder will be full, turgid, and difficult to express; the perineal reflex will also be intact. Using the NeuroMap If you cover a region of the NeuroMap with your finger or a coin (representing a lesion in it) you will be able to see which neurological functions will be compromised and which will still function normally. Conversely, if you have an animal with particular signs, you can use the NeuroMap to help localise the lesion. For example, consider an animal that is tetraparetic, with proprioceptive deficits in all four limbs and intact reflexes in all limbs. Identify on the NeuroMap where the wiring is for one of those functions. Where would a lesion have to be to compromise the proprioceptive tracts for all four limbs? C15 or C6T2. Would that cause the tetraparesis? Yes. But as the thoracic reflexes are intact, then the lesion can't be at C6T2. That makes it likely that it is a C15 lesion. That all fits. The pelvic limb reflexes are intact, implying that their LMN are intact - yes, that is possible with a lesion in the C15 region. Thus, both the signs of dysfunction and signs of normal function have helped you localise the lesion.

Figure 2. The NeuroMap for the spinal cord and spinal nerves

Table 2. Summary of effects of lesions in different areas of the spinal cord Presence of LMN Loss of Presence of signs to limbs sensory input UMN signs Loss of other reflexes TL, trunk, PL, TL and PL tail both affected TL, trunk, PL, PL only tail

Location of lesion Cervical C15

Loss of urinary and faecal continence

No LMN signs in TL UMN bladdera and PL. Faecal incontinencec Cutaneous trunci and perineal reflexes intact TL, loss of cutaneous UMN bladder trunci reflex if lesion in Faecal incontinencec C8T2. Perineal reflex intact

Cervical intumescence C6T2 Thoracolumbar T3L3

Trunk (caudal PL only No LMN signs in TL UMN bladder to lesion), PL, (TL normal) or PL Faecal incontinence tail Cutaneous trunci reflex lost caudal to lesion, perineal reflex intact PL, tail No UMN signs to limbs No UMN signs to LMN signs in PL UMN bladder Cutaneous trunci reflex Faecal incontinence intact, perineal reflex intact LMN signs to pelvic viscera. LMN bladderb LMN anal sphincter

Cranial lumbosacral L4S1 Caudal lumbosacral

Tail, PL probably

S1S3 Caudal nerves Cd15

normald Tail

limbs No UMN signs

Loss of perineal reflex LMN signs to tail

(dilated anus), faecal incontinence Normal continence

TL = thoracic limb, PL = pelvic limb a = UMN bladder - turgid, full, difficult to express b = LMN bladder - flaccid, distended, easy to express, dribbling urine c = Animal will deposit faeces with good emptying of colon, but may not be aware that it is defaecating. Note: Whether or not all signs are present depends on lesion severity. References 1. Thomson C, Hahn C. Veterinary Neuroanatomy: A Clinical Approach. Elsevier Health Sciences; 2012. ISBN 9780702034824.

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. Thomson, BVSc (Hons), DACVIM (Neurol), DECVN, PhD VetLearn, New Zealand Veterinary Association Massey University Palmerston North, New Zealand

Brain Cases: Understanding the Signs Part 1 & 2. Where's The Problem?-Localising Brain Lesions ACVIM 2003 Dr. Christine Thomson, BVSc (Hons), MRCVS, PhD, DACVIM (Neurol), Dip ECVN Glasgow, Scotland, UK
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What is required to localise a brain lesion? 1. Ability to perform a standard neurological examination 2. Ability to recognise both normal function as well as neurological dysfunction 3. A brain map From these three items, most neurological lesions can be localised and with that knowledge a list of likely diseases can be drawn up and diagnostic strategies determined. NOTE: you do not need to know the names of all the pathways and anatomical structures involved! INTRODUCTION Localising the lesion is essential in clinical neurology as different neurological locations are susceptible to different diseases. Successful localisation is half the battle in the diagnosis of a clinical neurology case. These seminars are aimed at helping you to understand the reasons why 'brain cases' present as they do. Once you have established where you think the lesion is located then the diagnostic procedures and case management follow logically. Lists of likely diseases are found in any good general or specialist neurology text book. 1) THE GENERAL NEUROLOGICAL EXAMINATION In the general neurological examination of any animal, the following functions are tested and evaluated. 1. sensory-proprioception, pain, tactile 2. motor 3. mentation and behaviour 4. cranial nerves 5. spinal reflexes

Once this information has been obtained and evaluated then the examiner should be able to determine whether 1. The lesion is based in the nervous system (NS) or another system e.g., orthopaedic 2. If the lesion is neurological whether it is localised to the a. Peripheral NS (PNS) including the neuromuscular components and cranial nerves (CN) I-XII b. Central NS (CNS) i. Spinal cord-C1-5, C6-T2, T3-L3, L4-S3, caudal segments ii. Brain-forebrain, brain stem or cerebellum 3. Whether it is focal, multifocal or diffuse NOTE: signs of peripheral and cranial nerve dysfunction can occur with either central (CNS) or peripheral (PNS) pathology. Main Anatomical Areas of the Brain For clinical testing, the brain can be subdivided usefully into the following areas based on similarity of function of the neural structures within those areas. The aim is to localise the lesion to one of these areas, or to determine that it is in more than one of these areas-i.e., multifocal/diffuse disease. 1. Forebrain-cerebral hemispheres and diencephalon (thalamus and associated structures) 2. Brain stem-midbrain, pons, myelencephalon/medulla oblongata 3. Cerebellum The 5 functions outlined in the general neurological examination are tested when examining for brain disease NOTE: Naming of neural tracts-prefix = origin of the tract and suffix = destination of the tract e.g., vestibulospinal-vestibular nucleus to the spinal cord, e.g., spinothalamic-spinal cord to thalamus. The names of the main tracts are provided in case you want to cross reference your information. Neurological Function and Dysfunction in the Brain 1. Sensory

a) Proprioception is the sensation of body position; it may be perceived at the conscious level (forebrain) or the unconscious level (cerebellum). This is conscious (CP) and unconscious proprioception (UCP), respectively. In a nutshell, CP is required for complex voluntary movement, UCP is required for basic posture and gait. Proprioceptive sensory information is conveyed on long neural tracts from receptors in the limbs and trunk to ipsilateral cerebellum and the contralateral cerebrum. The input from the muscle, tendons and joints mainly goes to the cerebellum and conveys information about body posture, muscle tension and length, joint angle etc. The information to the sensory cortex of the forebrain is more concerned with the precise knowledge of where and how the limbs are positioned e.g., that the foot is weight bearing on its palmar/plantar surface. Conscious proprioception (CP) Conscious proprioception is the sensory information that the forebrain receives and uses in the planning and execution of motor activity that is more complex than basic posture and gait e.g., dog catching a Frisbee, cat playing with a mouse. Pathway - peripheral receptors (touch, pressure, joint receptors), project through peripheral nerves, then spinal cord (fasciculus gracilis and cuneatus) through the brainstem, where it crosses to the opposite side, to terminate in contralateral cerebrum. NEx - primarily paw position/knuckling, hopping, tactile placing Deficits - stumbling, knuckling Brain areas involved - brainstem, forebrain Unconscious proprioception (UCP) Unconscious proprioception is the sensory information that the cerebellum receives and uses to coordinate motor function to maintain appropriate posture during sitting, standing and basic ambulation (walk, trot, canter etc) Pathway - peripheral receptors (muscle spindles, joint and tendon receptors) project through peripheral nerves, then spinal cord (spinocerebellar tracts) to terminate in the ipsilateral cerebellum. NEx- - postural observation during rest and motion-the animal's feet should be in an appropriate position under its body to bear weight e.g., not base-wide or base-narrow. The feet should track efficiently during movement; they should not go too wide or too narrow or get caught up on each other. The trunk and neck should be held in an appropriate position; not too high/low and with sufficient lateral truncal tone to stop the animal falling to either side. NEx- - hip sway, reflex stepping/sliding paper test, hopping Deficits - sensory ataxia (incoordination of movement), abnormal posture (at rest and during motion, may fall to the side)

Brain areas involved - brainstem (caudal), cerebellum b) Pain Pathway - peripheral receptors, peripheral nerves, spinal cord (spinothalamic tract) to the contralateral sensory cortex of the forebrain. It is also projected to the reticular formation (ARAS-see below) of the brain stem. The information that arrives at the reticular formation is relayed diffusely to the cerebral hemisphere; this is what causes normal, generalised arousal/alertness. NEx - superficial pain = pinprick, deep pain = bone-crushing pain Deficit - hypo/anaesthesia Brain areas involved - brainstem, forebrain 2. Motor In quadrupeds, the main motor centres are located in the brainstem, thus forebrain disease has minimal effect on gait, whereas in humans and primates, the motor cortex of the forebrain is of much greater importance. Pathway - brainstem motor initiating centres, pathways (upper motor neuron-UMN tracts) project through brainstem to CN nuclei and through the spinal cord to terminate on lower motor neurons (LMN). These UMN tracts may stimulate or inhibit LMN. The cerebellum coordinates motor activity by projecting to the motor centres of the brainstem. Note: LMN are found in both the cranial nerves and the peripheral nerves. Facilitatory function - Extensors: UMN tracts facilitating extensors-primarily run in the ventral white matter of the spinal cord (e.g., vestibulospinal tract). Flexors: UMN tracts facilitating flexors-primarily run in the lateral white matter of the spinal cord (e.g., rubrospinal and corticospinal tracts). Inhibitory function - one of the UMN tracts in particular, (medial medullary reticulospinal) has a massive inhibitory influence on LMN, hence disruption to this tract may result in the classical UMN signs of increased muscle tone and spinal reflexes. UMN signs more likely to occur with spinal cord lesions than brain lesions. NEx- - observation of stance and gait, hopping, wheelbarrowing, extensor postural thrust Deficits- - ataxia, weakness/paresis. Cerebellar disease can cause ataxia, tremor, spasticity, hypermetria and vestibular signs. Brain areas involved - brainstem disease -> weakness, whilst cerebellar disease -> incoordination of movement, but not weakness. Forebrain disease may lead to clumsy fine motor skills e.g., cat batting at a ball, dog catching a Frisbee, but not overt weakness

NOTE: ataxia is incoordination of gait and can be sensory and/or motor in origin NOTE: When evaluating motor function such as gait, you will be assessing proprioception as well as the motor function. 3. Mentation and behaviour a) Mentation - Awareness/consciousness is associated with ascending reticular activating system/formation (ARAS) function. This diffuse network of neurons is located throughout the brain stem. Incoming sensory information is projected to both precise brain areas (e.g., visual cortex, sensory cortex, auditory areas) and to the ARAS. This information stimulates the ARAS, which in turn diffusely stimulates the entire cerebral cortex causing awareness and arousal. The respiratory, cardiac and vomiting centres are also associated with the reticular formation. Signs of decreased mentation are obtundation, stupor and coma, (death!). Obtundation (somnolence)-the animal tends to sleep when left undisturbed, but can be aroused by a nonnoxious stimulus e.g., noise. Stupor-the animal sleeps/is unconscious, and can only be aroused by a noxious stimulus such as pain e.g., hard pinching of the toe. Coma-the animal is unconscious and cannot be aroused by any form of stimulus. NEx-observation of animal's interaction with the environment, response to non-noxious and noxious stimuli (as indicated) Brain areas involved - brainstem and forebrain. Decreased consciousness can occur with focal lesions in the brain stem affecting the ARAS, or it can occur with diffuse forebrain disease. b) Behaviour - Behaviour is both instinctive and learned from experience thus requiring intact memory Behaviour and memory circuits are located in the forebrain and particularly involve the limbic system and hippocampus. NEx - owner's history and observation (owner and clinician) Deficits - loss of house-training, change in animal's character e.g., bold animal becoming timid etc, failure of recognition of animate/inanimate objects Brain areas involved - forebrain, but remember that intact brainstem motor function is required to perform the behaviour 4. Cranial nerves The twelve pairs of CN are numbered with Roman numerals and are sequentially ordered from rostral to caudal.

I and II-are associated with the forebrain III and IV-midbrain V-XII-pons and myelencephalon, CN VIII-although it attaches to the brainstem, it also requires an intact cerebellum for correct function. The CN are the peripheral nerves of the head region, but they may also extend into the body (e.g., CN X and XI). Some of them supply striated muscle and damage will result in signs of LMN disease (Atrophy (severe), Reflexes , Tone - ART). NEx- - see table 3. Some of the CN are involved in reflexes, which consequently have afferent, central and efferent components similar to that of spinal segmental reflexes. For example-the palpebral reflex: touching the margins of the palpebral fissure, stimulates reflex blinking-CN V afferent, CN VII efferent portion of the reflex arc to the facial muscles. Deficits - see table 3 Brain areas involved - forebrain (I, II), brainstem (III-XII), cerebellum (VIII) 5. Segmental spinal reflexes The spinal reflex pathways are restricted to the spinal cord. Brain disease could cause UMN signs due to damage to descending inhibitory motor pathways; however, this is less likely than with spinal cord lesions (q.v.). 2) INTERPRETING THE NEUROLOGICAL EXAMINATION General principle for localisation: Neural pathways can be affected anywhere along their length-origin/receptor, middle, termination. Similar signs of dysfunction can result regardless of where the pathway is interrupted by disease. So, how do you know where a lesion is located along the length of a pathway, to produce the signs? All pathways and neural structures are closely surrounded by other neural structures. So you look to see whether nearby neural structures are also affected. Figure 1. Localising a lesion in a long neural pathway

Example - signs of disease affecting pathway A are present in an animal. This pathway travels for a long distance. For part of that distance, pathways B and C are located nearby in different regions of A. Pathway B is functioning normally, but there are signs of dysfunction in pathway C. Therefore, it is likely that pathway A has been affected by a disease in the region in which it lies close to pathway C. Note that identifying both normal function (pathway B) and abnormal function (pathway C) have contributed to the neuro-anatomical diagnosis on pathway A. Identifying both normal and abnormal functioning of the nervous system is important in the neurological exam. 3) THE BRAIN MAP The following diagrams show the location of the neural structures associated with the functions previously discussed. Using these diagrams and table 1, it should be relatively easy to predict the signs that you would expect with disease located in each of the three main functional areas of the brain. Conversely, in cases presenting with a certain set of brain/CN signs you should be able to localise the lesion to one of these areas. Figure 2. The three main functional areas of the brain, forebrain, brainstem and cerebellum

Table 1. Table summarising where each function is located in the brain and spinal cord (see also figures 3a and b) Function Motor Mentation Behaviour Forebrain Minimal Brain stem CP and UCP Major initiating centres None Cerebellum UCP Coordination, not initiation None None Spinal cord CP and UCP Motor tracts None None

Proprioception CP

Diffuse areas ARAS Major centres

CN

I,II

III,IV (midbrain) V-XII

(VIII)

None

Spinal reflexes None

?UMN influence

None

UMN & LMN signs

CP = conscious proprioception, UCP = unconscious proprioception, UMN/LMN = upper/lower motor neuron, ARAS = ascending reticular activating system Note: CP crosses sides in the brain stem so that the left side of the body will be perceived in the right forebrain and vice versa. UCP terminates in the ipsilateral cerebellum so that the left side of the body projects to the left side of the cerebellum Figure 3a. Location of proprioceptive pathways and areas associated with mentation in the brain

Figure 3b. Location of motor areas, behaviour and cranial nerve attachments in the brain.

Based on the above diagrams mapping the main functional areas of the brain, you can determine what functions could be compromised with pathology in each of the different brain areas. Table 2. Clinical signs that are likely to occur with disease in different areas of the brain. Neurological exam Proprioception CP UCP Motor function Forebrain disease CP deficits Knuckling, stumbling, gait is reasonable UCP - OK Minimal effect Brainstem disease CP deficits Cerebellar disease CP-OK

UCP deficits-if caudal brain UCP deficits-ataxia, stem lesion postural deficits Weakness-can be severe Incoordination spasticity and tremor, but not weakness Mentation-OK

Mentation

Decreased mentation Decreased mentation with with diffuse forebrain focal brainstem disease disease Altered

Behaviour

No direct effect, but Behaviour-OK damage to motor/mentation can preclude normal behaviour III-XII can be affected (see table 3) Normal Normal Can see vestibular signs

Cranial nerves

I, II-visual disturbances most likely Normal

Spinal reflexes

Note: Forebrain disease can also cause circling (usually to the side of the lesion) andseizures: Seizures or fits, only occur with forebrain disease. Causes of Diseases affecting the brain and cranial nerves-DAMNIT! After localising the lesion based on your neurological examination, then the aim is to list the most likely diseases that could be causing the problem. From that, a diagnostic plan is formulated. I try to list the top three likely diseases in order of priority. Identifying which diseases are likely, takes into account the history and signalment of the animal as well as the results of the physical and neurological examinations and the localisation of the lesion. There are many, many diseases and rather than learning them by rote, I use the mnemonic 'DAMNIT' to help remember the sorts of diseases that can affect the nervous system (NS).

D A

Degenerative Anomalous (congenital), Angiomatous (we use this term 'cos we could not find a better word for vascular-based conditions!)

M N I

Metabolic including endocrine Neoplastic Nutritional Inflammatory/Infectious/Immune-mediated Idiopathic Iatrogenic

Toxin Trauma

EXAMPLES OF CLASSICAL CASES Forebrain (FB) 1. Focal lesion, e.g., tumour: aimless walking possibly circling, gait is reasonable but some stumbling might be noted, contralateral CP deficits, contralateral visual deficits, animal may "forget" to use the contralateral limbs in voluntary movement. Mentation, maybe a bit dull, +/seizures 2. Diffuse lesion: (bilateral forebrain), CP deficits on both sides, stumbling, decreased awareness to coma, +/- seizures Brainstem lesion (Bst) CP deficits, weakness, multiple CN deficits (e.g., vestibular signs and facial paresis), decreased mentation to coma Cerebellar lesion UCP deficits, spasticity, tremor, ataxia and UCP deficits, BAR, possibly vestibular signs Multifocal disease E.g., seizures (FB), decreased mentation (FB or BSt), multiple CN signs (III-XII). E.g., visual deficits (FB) and vestibular (BSt or cerebellum) signs. Note: Vestibular signs could be due to pathology in the inner ear, brain stem or cerebellum. How would you differentiate the location of the pathology?

Table 3. The cranial nerves, testing and signs of dysfunction; a = afferent, e = efferent Head function Olfaction Vision Innervation Ia IIa Clinical testing Observation, food Maze test Menace response-IIa & VIIe PLR-IIa & IIIe (parasympathetic) Pupil size IIa, IIIe PLR (parasympathetic) Pharmacological testing Sympathetic -e (Cerebellum) Eyeball position IIIe, IVe, VIe (also VIIIa) Visual tracking Eyeball position in different head positions Strabismus-constant position (LMN of CN III, IV, VI), changing position (UMN/central). Anisocoria, mydriasis, miosis +/- other signs of Horner's syndrome Dysfunction Dysosmia-difficult to prove clinically Blindness, dilated pupil (although this can be due to just CN III dysfunction)

Vestibulo-ocular reflex VIIIa & Loss of vestibulo-ocular reflex IIIe,IVe,VIe Facial sensation Va-all three branches Touch Palpebral reflex-Va & VIIe (medial and lateral canthus) Auriculo-palbebral reflex Va & VIIe (just in front of ear for V) Mastication Ve-mandibular Jaw tone Masticatory muscle bulk Facial expression VIIe Facial symmetry Palpebral reflex Va & VIIe Auriculo-palbebral reflex Va & VIIe Muzzle movement, Ear Muscle atrophy Dropped jaw-only if bilateral Facial paresis/paralysis Loss of blink and ear reflex twitching Facial hypalgesia Loss of blink and ear reflex twitching

movement Lip commisure symmetry Vestibular function VIIIa Head position, Eyeball position Head tilt, circling, rolling (also involves III, IV, VI) Vestibulo-ocular reflex (VOR) (VIIIa & IIIe, IVe, VIe) Gait and movement Pharyngeal IXe and Xe function Laryngeal function Xe and XIe Gag reflex (IXa & IXe,Xe), Swallowing Voice Respiration Tongue XIIe Spontaneous nystagmus, Strabismus Deranged body posture and ataxia Dysphagia, Salivation, Aspiration Dysphonia Respiratory stridor-laryngeal obstruction

Observation-LMN signs, usage Atrophy, paresis/paralysis-uni or bilateral Withdrawal

NOTE: the menace response is a learned RESPONSE not a hard-wired reflex. It is a response as it has to be learnt, it is absent in young animals-typically appearing in kittens and puppies between 8-16 weeks of age Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. Thomson, BVSc (Hons), MRCVS, PhD, DACVIM (Neurol), Dip ECVN SACS University of Glasgow Veterinary School Bearsden Rd. Glasgow, G61 1QH SCOTLAND

Cervical Vertebral Stenotic Myelopathy I & II (V462, V463) Western Veterinary Conference 2005 Stephen M. Reed, DVM, DACVIM The Ohio State University , Columbus, OH, USA279239 The recognition and diagnosis of disease involving the nervous system in the horse is often a multiple step process. The neurological examination helps to provide a neuroanatomic localization of the problem and helps to determine which diagnostic tests are indicated, such as radiography, myelography, electromyography and cerebrospinal fluid analysis. Many central nervous system (CNS) diseases can result in similar clinical signs, making the specific cause difficult to determine. A diagnosis rests on identifying the specific neurological functions, which are deranged, and associating them with the anatomical regions of the nervous system, which are damaged. It should include a careful and complete musculoskeletal examination. The neurologic examination of the horse should proceed from the head caudally, and should be consistent and systematic in order to reduce the likelihood of omitting parts. The neurologic examination begins with an observation of the animal at rest and should include its mental attitude, level of consciousness, head, neck, trunk and limb posture, as well as for signs of abnormal behavior. A closer examination of the head for cranial nerve deficits should be performed. Examination of the eyes includes the blink response, its ability to negotiate in a strange environment and an ophthalmologic exam. If a horse has a lesion in the eye or optic nerve, it will have ipsilateral blindness. A contralateral blindness would indicate a lesion in the optic tract or lateral geniculate nucleus. The pupil size is under control of the autonomic nervous system and is affected by the level of environmental light and the level of fear or excitement. To test the pupillary light response, a light should be directed in each eye and an observation of pupil constriction should be noted. Injury to the 3rd, 4th or 6th cranial nerves results in a deviation of the eye. The trigeminal nerve is a large nuclei, which contains both sensory and motor branches. Injury to this nerve results in a dropped jaw and loss of sensation to the face and nares. The seventh nerve supplies motor innervation to the ears, eyelids and nose. If the seventh nerve is injured, a droopiness of the ear or eyelid will result along with deviation of the face to the unaffected side. With injury to the vestibulocochlear nerve, the horse often has a head tilt toward the affected side and nystagmus with the fast phase away from the site of the lesion. Damage to the nerves which supply the muscles of the larynx and pharynx will result in difficulty with swallowing, breathing and vocalization. When signs of damage to these nerves are present, the examiner should carefully check for guttural pouch infection, a caudal brainstem lesion, or injury to the nerve somewhere along its course from the brainstem to the appropriate muscle. The head and neck should be manipulated to check for signs of pain and to determine the range of motion. Symmetry of the neck and forelimbs is then evaluated. This may involve palpation as well as observation. Normal animals stand with their legs about shoulder and hip width, with the weight equally distributed on all four legs. A base wide stance may be seen with spinal cord, cerebellar or vestibular disease. It often indicates a loss of proprioception or balance. If a horse has a "knuckled" or non-weight bearing limb, it may be a result of loss of proprioception or paralysis in that limb that may be due to a peripheral nerve, spinal cord or brainstem lesion. If the limb appears painful, close examination for musculoskeletal disease is indicated.

The gait, which is predominately controlled by the forebrain, brainstem, spinal cord, peripheral nerve and muscle function, should be examined thoroughly. Gait abnormalities include weakness, ataxia, dysmetria and spasticity. Weakness is often seen as dragging of the toes and stumbling when walking, or trembling and lack of support at rest. Signs of weakness may be seen with cerebral, brainstem and spinal cord lesions, as well as with peripheral nerve, neuromuscular junction, and muscle lesions. With a brainstem or spinal cord lesion, weakness is present in all limbs caudal to the lesion. Ataxia often denotes a proprioceptive deficit and is characterized by poor coordination of movements. The lesion causing an ataxic gait may be located in the cerebellum, vestibular system, spinal cord, brain stem or peripheral nerve. Ataxia includes abnormal foot placement, crossing of the limbs, circumduction of a limb when circling and stepping on other feet. Severely ataxic horses will often pace. Spasticity is best described as a "tin soldier" gait--the animal showing very little flexion of its joints when moving. Dysmetria is best described as an inability to regulate the rate and direction of motion. In contrast to a spastic gait that has a decreased range of joint movement, the motions in animals with dysmetria often appear exaggerated. Gait deficits are graded with zero as normal or no gait deficit and a 5 as a recumbent animal. A grade 1 deficit is very subtle, grades 2 and 3 are obvious on initiation of movement and a horse with grade 4 deficits may fall or nearly fall when moving. If no head, neck or forelimb neurologic deficit is identified, abnormalities in the trunk and hindlimbs must be explained by a lesion between T2 and S2. The final segment of the neurologic examination is the finding of the explanation for any deficits of the tail, anus and other structures innervated by the sacral and coccygeal spinal cord segments. This can be accomplished by determining whether the horse can lift or move its tail, has good anal tone and normal reflex. The pathogenesis of CVSM is unknown but appears to be multifactorial. Etiologic factors such as genetic predisposition, hormonal changes, nutrition, trauma, and exercise are the most investigated. Early on, a genetic predisposition to CVSM in horses was suspected based on the frequency of this problem in certain families of Thoroughbreds, however, lack of many close relationships in a group of 47 horses with CVSM gave rise to thoughts on other etiologic factors. Although some investigators have failed to demonstrate genetic determination of CVSM, others believe that genetic factors that determine the length of the neck, cervical vertebral biomechanics, and body size play a significant role in the development of CVSM. In the most recent investigation of the heritability of CVSM, the author suspects that a genetic predisposition, wherein horses inherit increased sensitivity to environmental factors affecting cartilage growth, is likely. On postmortem examination of 30 horses with CVSM, the authors demonstrated narrowing of the vertebral canal and noticed that commonly these horses had bony changes characteristic of degenerative joint disease, including osteoarthritis and malformation of the articular processes. In this study the importance of nutrition in the development of CVSM was suggested. Mayhew et al (1978) found that horses with CVSM, to a far greater extent than control horses, had decreased differentiation of cartilage and osteopetrosis sometimes associated with osteonecrosis and osteoclasia. These degenerative changes in the cervical vertebral articular processes and costochondral junctions of horses with CVSM were associated with osteochondrosis dissecans. He proposed CVSM to be a "performance" or "production" disease with a multifactorial etiology, comprised of genetic predisposition, overnutrition, and environmental and iatrogenic modifying factors. Similar to these findings were histopathology results of vertebrae involved in

myelocompressive lesions, indicating that the lesion was an osteochondrotic type defect (Stashak et al. 1985). Osteochondrotic lesions are the result of abnormal endochondral ossification, and osteochondrosis of the articular processes may result in instability and malalignment of adjacent vertebrae, secondary osteoarthritis of the articular processes, and hypertrophy of soft tissue structures. All of these may contribute to spinal cord compression. Multiple investigators have shown that horses with CVSM have an increased incidence and severity of degenerate joint changes in the axial skeleton (Dimock and Errington 1939; Binkhorst 1976; Mayhew et al. 1978; Stewart et al. 1991) and Wagner et al (1985) demonstrated that, although offspring from horses with CVSM did not develop myelocompressive lesions themselves, this group did have a high incidence (45%) of osteochondrotic lesions in both the axial and appendicular skeleton. There has not been general agreement on the importance of degenerative joint disease of the cervical vertebrae in the pathogenesis of CVSM. Rooney (1969) has proposed that malformation of the articular processes is the predisposing lesion and, thus, is essential in the pathogenesis of CVSM. Binkhorst (1976), however, found only 8% correlation between lesions of the articular processes and histologic changes in the spinal cord, and similar to Binkhorst's findings, Stewart et al (1991) reported that the site of the most severe osteochondrotic lesions did not always correlate with the site of vertebral stenosis. This suggests that osteochondrosis of the articular processes is not the direct cause of CVSM, but that the primary predisposing factor in the pathogenesis of CVSM is the insufficient diameter of the cervical vertebral canal at the site where spinal cord compression occurs. This is why Hurtig and Pool (1996) suggest CVSM is a manifestation of developmental orthopedic disease, but does not belong in the osteochondrosis syndrome. The positive correlation between osteochondrosis and CVSM, however, may indicate that the pathogenesis of both conditions is similar and may respond to the same preventive and therapeutic measures (Stewart et al. 1991; Reed 1997). In contrast to young horses in which the role of degenerative joint disease in the pathogenesis of CVSM appears controversial, in older horses (> 4 years) CVSM is generally associated with significant arthropathies of the caudal cervical articular processes. In these horses the compression of the spinal cord can be attributed to the bony and soft tissue proliferation at the affected articular processes. This finding is supported by the improvement most of these horses show following medical and surgical treatment with subsequent radiographic evidence of reduction of the bony proliferation. The genesis of the degenerative joint disease in older horses with CVSM is speculative, however, currently the role of external trauma is thought to be the most important (Mayhew 1999). The effects of trauma and exercise in predisposed animals are hypothesised to contribute to the development of osteochondrosis and CVSM (Donawick et al. 1989), but controversy exists on this statement (Savage 1998) as well as on the role of numerous dietary factors in the development of these diseases. The accelerated rate of gain, not of growth, has been related to osteochondrosis and CVSM in horses, however, controlled investigations have failed to confirm this relationship (Knight et al. 1990). Nutritional factors that have been associated with the incidence of developmental orthopedic disease are a dietary imbalance in the calcium/phosphorus concentration, copper deficiency, excess zinc, excess protein, and excess

carbohydrate. The three most important nutritional factors appear to be excessive dietary digestible energy, excessive dietary phosphorus, and dietary copper deficiency (Savage 1998). Carbohydrate excess in the diet is thought to contribute to developmental orthopedic disease through an endocrine imbalance involving elevation of serum insulin concentrations and decreased serum thyroxine concentrations, resulting in a lack of cartilage maturation (Glade and Belling Jr. 1984; Glade and Luba 1987). Based on this hypothesis a "paced growth" program for the prevention and therapy of CVSM has been recommended in order to slow down body growth in height and weight (Donawick et al. 1989). Savage et al (1993a) demonstrated that high digestible energy diets, composed of both carbohydrates and corn oil components caused osteochondrotic lesions in foals, but that these are not solely due to an excessive average daily weight gain. It is suggested that feeding high digestible energy diets result in endocrinologic alterations that mediate local cartilaginous factors and selectively activate genes that cause a specific alteration in matrix phenotype (Savage 1998). A dietary calcium/phosphorus imbalance has been implicated in CVSM (Binkhorst 1976) and particularly excessive phosphorus (388% of the requirements) appears to be correlated with an increased incidence and severity of osteochondrotic lesions in foals (Savage et al. 1993b). Copper deficiency leads to defective lysyl oxidase, which is a copper-dependent enzyme required for proper maturation of connective tissues. A low copper diet (15 ppm) produced 3 times as many osteochondrotic lesions of the appendicular and 7 times as many osteochondrotic lesions of the axial skeleton, as compared to foals fed a high copper (55 ppm) diet (Knight et al. 1990), however, copper supplementation did not eliminate developmental orthopedic disease, supporting the presence of other etiologic factors. Similar results were obtained when foals fed 7 ppm of copper had a much higher incidence of macroscopic osteochondrosis than foals fed 30 ppm of copper (Hurtig et al. 1993). Zinc has an antagonistic effect to copper and it has been postulated that diets excessive of zinc could cause secondary copper deficiency (Knight et al. 1985), but this has not been proven in the horse. Conclusion CVSM is the most common non-infectious cause of spinal cord ataxia in the horse. Stenosis of the cervical vertebral canal and subsequent myelocompression is the cause of this neurologic disease. Although the etiology of CVSM is not fully understood, diagnostics and therapeutic options for affected horses have improved over the last years. The specificity and sensitivity of predicting CVSM from survey radiographs using the sagittal ratio method is high, however, myelography remains necessary for localisation of compressive lesions. Further research is required in the field of antemortem diagnostics, i.e., defining criteria to evaluate myelograms and evaluating the use of computed tomography. Ventral interbody fusion has been proven an effective surgical procedure, however, complete recovery does not occur in all horses, and risks associated with post-operative performance must be carefully considered by the owners. Stephen M. Reed, DVM, DACVIM The Ohio State University Columbus, O

Acute Neurological / Spinal Injury

AUSTRALIAN COLLEGE OF VETERINARY SCIENTISTS SCIENCE WEEK 2005
Simon LeMin1, BVSc, MACVSc; Jason Mouatt2, BVSc, FACVSc 1 Animal Emergency Centre; 2Veterinary Specialist Service, Underwood, QLD, Australia18
279665

Patients with acute collapse and spinal dysfunction can be challenging, emotional and urgent cases. Signs are often severe and sudden. Affected animals often present in distress, as do their owners. However, the majority of these acute spinal cases carry a good prognosis if adequate treatment is given in a timely manner. The initial assessment and management are often a key step in successful recovery. An understanding of the possible causes, options for treatment and likely outcomes will often greatly influence the treatment and the owners' willingness to treat their pets.

PART 1. ASSESSING THE ACUTELY COLLAPSED PATIENT

There are a wide range of potential causes of acute collapse in dogs and cats. This presentation will deal mostly with spinal causes, however it is important to have a systematic approach to collapsed patients to allow differentiation between neurological and other causes of collapse (e.g., toxic, musculoskeletal, metabolic, respiratory causes) As always, a thorough history and clinical examination are essential with all patients. The clinician should consider the possibility of other causes of acute collapse including: Metabolic--e.g., Addison's disease, DKA, hypoglycaemia Respiratory--laryngeal paralysis , brachycephalic airway disease Cardiac disease / syncope, acute haemorrhage Heat stress Toxins--Tick paralysis, Snake bite Generalised LMN disease--myasthenia gravis, polyradiculoneuropathy Orthopaedic disease--bilateral cruciate rupture, bilateral tibial crest avulsions Blood biochemistry and CBC are often indicated to assess for concurrent disease and electrolyte abnormalities. Neurological cases are usually differentiated on clinical and neurological examination well before xrays or further tests are done. The initial neurological assessment should include: Signalment--breed, age, sex History--Time of onset, Rate of progression, inciting factors, mental changes Distant examination / Posture--mono-, hemi- , para-, quadra paresis or paralysis, back arching, head position, etc Gait analysis--ataxia, hypermetria, short stepping, "lameness", circling, etc Close examination--Muscle wasting, toe scuffing, self trauma The neurological examination can essentially be broken into a few questions or steps: 1. Is this case neurological 2. Lesion localisation 3. Differential diagnosis list 4. Further diagnostic tests The major differentiating factor in patients with spinal disease (compared to other causes of collapse) will be the lack of conscious proprioception. This is most easily tested with knuckling tests of

each paw, but hopping, wheelbarrowing hemi-walking and placing responses are also tests of proprioception that can be used. It must be remembered that some very painful, ill or mentally depressed patients will not respond normally to tests for proprioception. Supporting the patient's weight when testing proprioception will provide a more reliable response in some of these patients. Presence of seizures or cranial nerve deficits will usually also suggest neurological brain) disease. Lesion localisation allows the clinician to develop a list of differential diagnoses and therefore provide a diagnostic and treatment plan, and some sort of prognosis. Presence of seizures or cranial nerve deficits suggests brain or multifocal disease. Spinal lesion localisation is achieved with: Spinal reflexes Hyperpathia / pain focus Superficial pain dermatomes (for some LMN lesions) Spinal reflexes allow localisation to a smaller segment of the spinal cord. It is essential to understand the interpretation of these reflexes. A reduced reflex suggests damage to the lower motor neuron motor arc. This can occur anywhere in the peripheral nerve or the spinal cord segment that the nerve comes from. (LMN changes = reduced or absent reflex). If the reflex is not reduced in a neurologically affected limb, then the reflex arc and associated spinal segment must be intact, meaning the spinal lesion is proximal to the spinal segment tested by that reflex. These Upper motor neuron spinal lesions (UMN) cause normal or increased reflexes. Forelimb tests include withdrawal (flexor reflex), Biceps, triceps and extensor carpi radialis reflexes. Withdrawal is very reliable however the other reflexes can be difficult to elicit and are often therefore unreliable. Hindlimb reflexes include withdrawal, patella reflex, cranial tibial, sciatic and gastrocnemius reflexes. Withdrawal (Sciatic nerve) and Patella reflex (Femoral nerve) are more reliable than the others and test the 2 major nerves in the hindlimb. Use of these reflexes usually allows localisation to one of 4 spinal segments--C1-5 (UMN to fore and hind); C6-T2 (LMN fore, UMN hind); T3-L3 (no deficits in fore, UMN hind); L4-S3 (no deficits in fore, LMN in hind) Panniculus reflex is a useful localising tool if there is a definite cut off. Panniculus is usually not present caudal to L4. Testing should begin caudally and work cranially 1 vertebrae at a time. A distinct cut-off point (i.e., present cranial, but absent caudal to a specific point) will usually indicate a spinal dysfunction 1-2 vertebrae cranially. Unilateral panniculus is pathognomonic for a high thoracic (T1-3) or brachial plexus injury. Complete absence of panniculus is non diagnostic. Normal panniculus does not rule out a spinal dysfunction. Presence of a pain focus is usually very helpful, both in localising the disease and developing a differential diagnosis list. Neck manipulation should be done slowly and carefully, particularly in compromised patients where there is the possibility of a traumatic injury or vertebral instability. The neck should be isolated into cranial and caudal parts and each section flexed laterally, dorsally and ventrally. A normal dog should be able to touch the tip of the nose to the iliac crest without pain. Deep palpation of the ventral wings of the vertebrae may also elicit pain. Thoracic, lumbar and sacral vertebrae should all be deeply palpated slowly and deliberately. The chest and abdomen should be supported with the other hand when palpating, as most dogs will drop down with unsupported thoracolumbar or lumbosacral pain. Painful neurological disease is consistent one of 5 things-- IVDD, neoplasia, trauma, meningitis or discospondylitis. Non painful spinal disease is more commonly associated with parenchymal disease such as vascular accidents, intramedullary neoplasia, and degenerative disease. Schiff Sherrington syndrome--this describes a severe extensor rigidity of the forelegs associated with a high to mid thoracic spinal dysfunction due to compromise of the border cells and ascending inhibitory tracts to the forelegs. This sign has often been described as a poor prognostic sign, however

this is not always the case and prognosis depends more on the cause and severity of signs rather than just the presence of Schiff Sherrington posture. Deep pain assessment is a critical prognostic aid with spinal dysfunction and collapse. Generally speaking, patients that have not lost motor function should still have deep pain. Deep pain tests the deepest white matter tracts of the spinal cord and compromise to these tracts usually represents severe cord trauma. Loss of deep pain does not necessarily indicate a hopeless prognosis, although it certainly makes the outlook more guarded. Rather it suggests aggressive, rapid therapy is indicated to provide the best chance of a good outcome. Deep pain DOES NOT equal withdrawal--remember withdrawal of a limb is a reflex and will occur even after spinal transection. Deep pain requires a conscious response from the patient (cry, turning around, biting etc).

PART 2. NEUROLOGICAL CAUSES OF ACUTE COLLAPSE

The major differential diagnoses include:

1. Intervertebral disc disease(IVDD)

IVDD is the most common cause of acute collapse seen in veterinary medicine, and may be chronic to peracute in onset. Affected patients are mostly painful and usually have no history of recent severe trauma associated with onset. Occasionally acute traumatic disc extrusion can occur following a severe external force. In non chondrodystrophic dogs, this often causes cord concussion but minimal ongoing compression and surgery may not benefit. Chondrodystrophic dogs usually cause a marked continued compressive lesion of the cord. Myelography, CT or MRI is required to differentiate these two situations. IVDD usually occurs in either the cervical or thoracolumbar region with each having differing signs Cervical IVDD Predominantly a small breed / chondrodystrophic dog disease. Occurs usually in dogs over 2 years of age (mostly middle aged dogs). Most dogs show screaming pain with variable neurological compromise ranging from none, to severe hemi- or quadriparesis. C2-3 is the most common site and the incidence reduces at each more caudal space. Therefore most dogs with neurological signs will show conscious proprioceptive deficits in fore and hind legs, and in theory UMN reflexes in all legs (although this is sometimes inconsistent in the forelegs). Pain is evident on careful neck palpation, lateral flexion and dorsal and ventral neck flexion. Some dogs will show a "root signature" due to nerve root compression within the canal. Radiographs of the neck are often difficult to interpret but narrowed IV spaces of mineralisation in the canal may be suspicious. Myelography is required for definitive diagnosis. Clinical cervical disc disease is rare in cats. Thoracolumbar IVDD Predominantly chondrodystrophic dogs, with peak incidence between 3-6 years. Larger dogs have a lower incidence and usually occurs in middle aged to older dogs. Majority (75%) of IVDD cases are between T11-12 and L1-2. Occasionally affects mid to caudal lumbar vertebrae. Rarely affects cranial to T10. Often mild cases confused with abdominal pain (usually without GIT signs). Most affected dogs will have focal pain on spinal palpation. Many will have panniculus cutoff. Hind leg ataxia/paralysis usually with CP deficits and UMN reflexes (if lesion above L4). Forelegs should be "normal".

Cats--IVDD much less common, but does occur, usually in middle aged to older cats with similar signs to dogs (pain, HL ataxia / paralysis). Deep pain presence is major prognostic sign.

2. Fibrocartilagenous embolism (FCE)

Occurs mostly in large breed, non chondrodystrophic breeds. About 80% of cases occur between 3 and 6 yrs of age. Exact cause is still controversial but essentially involves infarction of a spinal segment following embolism of a piece of fibrocartilagenous tissue. This tissue is hypothesised to come from the nucleus pulposus. Affected dogs often have a history of high exertional exercise at onset, and often are reported to scream out at the time of collapse. Onset is usually instantaneous and severe. Over half show asymmetric signs initially, progressing to bilateral signs. Maximal signs occur within 24 hours. Affected dogs are NON PAINFUL after 10-60 minutes. May produce UMN or LMN signs depending on area of cord affected. Radiographs are normal. Myelogram is normal or may suggest mild cord swelling. CSF analysis is often normal or shows subtle changes only. MRI will show a transverse myelopathy with oedema (hyperintense T2 signal) at the affected site.

3. "Wobbler" Syndrome
Dogs with caudal cervical spondylomyelopathy / disc associated wobbler syndrome usually show a slow chronic weakness. However, occasionally dogs with mild or no clinical disease can have acute collapse episodes. The exact cause for this is unknown, but may be due to sudden cord concussion from the unstable thickened dorsal annulus, vascular compromise of a chronically compromised spinal cord, or exacerbation by acute disc protrusion. Most patients show evidence of chronic disease on radiographic and myelographic examination. Affected dogs may or may not have neck pain +/- root signature. They are usually quadraparetic, with some forelimb extensor rigidity and UMN hindlimb reflexes. Most dogs are aged Dobermans or Doberman crosses, but other large breeds can be affected C6-7, C5-6 and C4-5 most commonly. Diagnosis requires cervical myelography with traction views.

4. Neoplasia
Neoplasia may originate from the spinal cord, meninges, nerve roots, tissues of the vertebral canal, or as a secondary metastasis from elsewhere in the body. In dogs, bone tumours (osteosarcoma, chondrosarcoma, fibrosarcoma) and nerve sheath tumours are most common. In cats, lymphosarcoma is most common. Clinical signs depend on the site affected--in many signs are progressive (as expected with a slow growing mass), however between 25 and 40% of cases will have an acute and severe onset (presumably due to vascular compromise or pathological fracture). Pain is variable--intramedullary tumours are not painful, however tumours compressing meninges or nerve root are often painful. Diagnosis may require radiographs (bony destruction), myelography, CT scan or MRI. Definitive diagnosis and histopath usually requires surgical exploration.

5. Trauma
Fractures may be pathological (developmental e.g., atlantoaxial instability, bone neoplasia, discospondylitis, etc) or traumatic. Traumatic injuries usually have a history to suggest possible injury.

Vertebral damage reflects severity of the lesion and the direction of force. 2 radiographic views are essential for diagnosis-look for damaged vertebral bodies, displacement, narrowing or widening of vertebral spaces. Clinical / neurological examination provides a better assessment of severity of the cord compromise than the radiographic picture.

6. Meningitis, Brain Disease

There are a wide range of inflammatory diseases than can be highly variable in their presentation. Meningitis often shows generalised or multifocal spinal pain, mental dullness, etc suggesting a more generalised problem. However, it may also show signs consistent with a focal spinal disease (especially GME). Diagnosis involves ruling out other causes of spinal pain (i.e., radiographs / myelogram), CSF analysis and perhaps advanced imaging.

7. Discospondylitis
Infection of 1 or more intervertebral discs. Usually bacterial (Staph intermedius most commonly) but may be fungal. Most common sites are C6-7, T5-6, T13-L1 and L7-S1, but can be anywhere. Most patients show weight loss, lethargy, intermittent pyrexia, and spinal pain. Occasionally see acute neurological condition--often associated with the bacterial waste products and toxins affecting cord function and not necessarily to the degree of cord compression. May also see acute vertebral instability secondary to bone lysis. Diagnosis on lateral spinal radiographs--lytic area around disc with surrounding sclerosis and possibly new bone production. Myelography rarely necessary. Urine and blood cultures may allow growth and sensitivity of causative agent.

PART 3. EMERGENCY MANAGEMENT OF THE ACUTE SPINAL PATIENT

1. Systemic Stabilisation
It is important to thoroughly assess all patients. Trauma patients may have multiple other injuries. It is a basic tenet of emergency medicine to "treat the most life threatening condition first"--remember that a severed spinal cord in a veterinary patient is life threatening as in most cases it will lead to euthanasia. Deal with other problems (haemorrhage, respiratory, cardiovascular, head trauma etc) but if spinal dysfunction may be present it is important to recognise early. Maintain spinal cord perfusion--the normal spinal cord has an autoregulatory ability which ensures adequate vascularity during mild hypotension. A damaged cord however loses this ability, therefore prolonged hypotension will lead to decreased blood flow to the cord, cord hypoxia and further associated injury. Therefore IV fluids are strongly advised in the compromised spinal patient. Avoid medications that may severely drop blood pressure unless absolutely necessary. Analgesia--many acute spinal conditions are extremely painful and can lead to patients being stressed, aggressive, difficult to settle, etc. Analgesia may allow a painful animal to relax and stay restricted more easily. Attempt neurological assessment prior to use of analgesics.

2. Prevention of further damage

Trauma--rigidly restrain patient--If there is a risk of unstable vertebral fracture/s the patient should be stopped from excessive movement and further vertebral displacement. This is best done by taping or strapping the patient in lateral recumbency to a board or table prior to any radiographs or major manipulation. Straps should be very firm and be placed across the head, shoulders, midbody (caudal ribs) and pelvis. In many cases patients may need chemical restraint. Any patient transport or diagnostics (e.g., radiographs) should be performed with the patient attached to the board / table until unstable vertebral injury can be ruled out.

Suspect IVDD cases should be strictly confined to reduce movement-strict cage rest should be enforced. If early improvement is seen, do not allow increased exercise as further nuclear extrusion is common and may cause further cord compromise. Medications--There is always dispute over medication use with acute spinal injury. However the fact remains that few drugs have consistently shown statistical improvement in outcomes of spinal patients. Methyl prednisolone sodium succinate (MPSS--Solu-Medrol)-this has been shown to improve clinical outcomes in people and some animal studies. This occurs mostly by blocking free radical peroxidation and destruction of the white matter tracts. The general guidelines are: Do not use unless within 8 hr of initial injury (if not sure, do not use) 30mg/kg SLOW IV Follow with 15mg/kg at 2 and 6 hr later; or 15mg/kg q6hr; or 2.5-5mg/kg/kr for 23 hrs Do not exceed 24 hours use Higher doses (60-90mg/kg) are detrimental Use after 8 hrs may increase neural necrosis Dexamethasone--HAS NO PROVEN BENEFIT in acute spinal trauma. Use of high doses is CONTRAINDICATED. Dexamethasone is very ulcerogenic and side effects often severely complicate spinal management (i.e., diarrhoea, sepsis, death). Low (antiinflammatory) doses of 0.1-0.2mg/kg may reduce some cord oedema, however oral prednisolone (0.5mg/kg) may provide a similar benefit in non surgical cases with less side effects.

3. Initial Diagnostics
Radiographs--important to rule out overt fractures, vertebral luxation or subluxation, obvious neoplasia and discospondylitis. Intervertebral disc disease and vertebral canal neoplasia can rarely be definitively diagnosed on radiographs, but disc space narrowing and vertebral foramen clouding/opacity may provide suspicion of IVDD. Where possible, general anaesthesia should be used, as poorly positioned radiographs and tense animals often cover up lesions. Take 2 views where possible. Repeated neurological assessment--watch for changes in neurological grade.

4. General management
Regular assessment. Bladder management--Neurologically affected dogs often don't or can't urinate. Regular (every 4 hours) expression or placement of an indwelling urinary catheter and closed collection system should be started early in the management to avoid detrusor atony, urine scalding and urinary tract infection. Good padded bedding. Regular turning, repositioning if the vertebral column is stable.

5. Further diagnostic Tests

Myelogram--essential in assessment of potential IVDD and neoplasia cases. Generally not indicated unless it will change the treatment, therefore mostly indicated if owners are prepared to consider surgical intervention. CSF analysis--should be collected if meningitis is high on the differential list. Preferably collect prior to administration of any corticosteroids. Advanced imaging--CT / MRI--sometimes useful for assessment of IVDD, neoplasia and (especially cervical) fracture cases.

6. Early Referral if surgery is indicated

PART 4. TREATMENT OPTIONS AND OUTCOMES

1. IVDD
Treatment essentially can be surgical or medical. Medical management is indicated for IVDD on the initial occurrence that shows only pain or mild neurological signs. Patients with acute collapse have a superior outcome if treated with surgery at an early stage by an experienced surgeon. Cervical IVDD--is usually treated with ventral slot surgery to allow removal of extruded nucleus from the spinal canal, however dorsal laminectomy, hemilaminectomy and ventral fenestration are all described. Surgery is indicated in all patients with severe or recurrent pain not responsive to medical therapy, those with marked neurological signs, or those with progressive signs. Seim and Prata (1982) reported on 54 patients undergoing ventral slot--within 48 hours all with neck pain, 12/14 with neurological dysfunction and 6/7 plegic dogs had improved and by 12 months post-op all by one dog had completely recovered. Smith el al (AVP 1997,p 58) reported a 29.8% resolution rate and 49.5% improvement rate by the time of discharge from hospital. They also suggested a poorer level of pre and postoperative neurological condition in those with more caudal cervical lesions. Fitch et al (JAHAA 2000, p68) suggested C2-3 and C3-4 lesions carried a significantly better prognosis than those more caudal. A 4.9% occurrence of post-operative respiratory difficulty has been described with cervical surgery requiring ventilation post-op. 10/13 ventilated patients survived and 9/10 recovered neurologically. Gill et al (JAAHA 1996) reported on 30 dogs undergoing dorsal laminectomy for IVDD with 69% normal 2 weeks after surgery and al dogs clinically normal at long term follow-up. Thoracolumbar IVDD--Hemilaminectomy is the treatment of choice for grade 2 and worse cases. Conservative management (strict rest) provides up to 90% recovery in grade 1-3 cases, although this can be slow and uncomfortable and recurrence is not uncommon. About 50% of grade 4 lesions will recover and a 7% recovery rate with grade 5 (loss of deep pain) lesions. Conservative management generally requires longer recovery times. Overall recovery in large and small breed dogs appears to be about 85%. In patients with deep pain present success (return to normal or near normal pain free function) is 90% or above. Loss of deep pain has been widely discussed and carries a poorer prognosis. Gambardella et al (Vet Surg 1980) found a 56% rate of recovery rate if surgery done within 12 hours of deep pain loss, a 25% recovery within 12-36 hours and <5% recovery after 48 hours. In contrast, Scott and McKee (JSAP 1999, p 417) presented a 62% recovery rate in patients with no deep pain. They suggested the rate of loss of deep pain was more prognostic, and that those with peracute loss of deep pain had a far poorer prognosis than those with gradual loss. Length of deep pain loss was not quite as significant in this study.

2. FCE
There is little specific treatment available for FCE cases. Surgery provides minimal assistance and medication appears also to provide little change in the course of the disease. Therefore patients require adequate nursing and time. Recovery depends on the severity of the spinal damage. Those with deep pain carry a poorer, but not hopeless prognosis. There is no difference in the recovery rate in those with UMN or LMN changes, however loss of deep pain with LMN signs is generally a poor sign. Generally recovery takes from 1-6 weeks, and some residual deficits may remain. However the large majority of suspected cases show some improvement within 5-10 days and the majority of those cases will go on to good function.

3. Wobbler syndrome

Treatment for acute collapsed wobbler patients generally requires surgery, although some will recover in the short term with conservative management. A range of surgeries to decompress or stabilise the affected vertebrae have been described and a recent report suggested that there is no obvious statistical difference between published results of various techniques. About an 80% success rate is seen with surgery. There is debate as to whether acutely collapsed patients truly carry a poorer prognosis, however it appears their recovery is slower and more difficult than that of ambulatory patients. However a significant number of patients still improve.

4. Neoplasia
The prognosis with neoplastic lesions is generally very guarded. Dernell et al (JAAHA 2000, p245) described 20 vertebral body tumours with various treatmentsPrognosis is generally poor--MST was 135d and OYS was 10%. Multimodal therapy including radiation appears to offer an improved outcome perhaps. Intramedullary tumours provide a hopeless prognosis. Levy et al (JAAHA 1997,p307) described outcomes in 37 dogs. Median survival with nerve sheath tumours was 180d. Median survival with Meningioma was over 1400 days. survival with lipoma was 2520d. Survival with Myxoma / myxosarcoma was 570 and 1080d. Survival with Osteosarcoma was 31 and 300d. The message is that with surgery, most patients recover well and some will have prolonged good recovery. Tumour type often can not be determined until surgical biopsy.

5. Trauma
Conservative management is indicated in patients with mild clinical signs and stable vertebrae and clinical signs. This involves 3-6 weeks of splinting and rest. Cervical lesions often respond well to good padded neck support with 89% recovery reported in one study. Thoracic and lumbar lesions can be supported by a dorsal back splint taped from the shoulders to the pelvis (+ cage rest). Severe neurological status, severe vertebral instability or deteriorating neurological status or uncontrollable pain warrant surgery. There are a number of surgical options for both cervical and thoracolumbar stabilisation. Adequate stabilisation provides a guarded to good prognosis in patients with deep pain. Cervical surgery has been reported to have a 36% perioperative death rate. Loss of deep pain at the time of the injury carries a poor prognosis generally.

6. Discospondylitis
Most patients respond well to appropriate antibiotic therapy, rest, NSAIDs and time. Treatment often takes 3-6 months, but clinical signs should improve rapidly after beginning treatment. Fungal discospondylitis carries a very guarded prognosis. In German Shepherd dogs this is usually a systemic disease. Patients with severe vertebral instability or acute deterioration may warrant myelography to assess cord compression, and possibly surgery to stabilise the vertebral bodies. The placement of implants in an infected site is not ideal and if possible should be avoided. Acute deterioration however often does not correlate to obvious spinal compression and therefore surgery may not be beneficial and may actually further destabilise the area. Surgery may also be required to achieve an adequate biopsy and culture of the affected site in non responsive cases.

Simon LeMin, BVSc, MACVSc Animal Emergency Centre Underwood, QLD, Australia

Jason Mouatt, BVSc, FACVSc Veterinary Specialist Services Underwood, QLD, Australia

Peripheral Nerve Injury

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2005
Luisa De Risio, DMV, DECVN Animal Health Department, Faculty of Veterinary Medicine, University of Parma Italy
18284787

Traumatic peripheral nerve and nerve root injuries are common in companion animals and may be caused by motor vehicle accidents, fractures (humeral, pelvic, proximal femoral), fracture/luxations (sacroiliac, sacrocaudal), bite wounds, gunshot wounds, and iatrogenic lesions (misplaced intramuscular injections, surgical "misadventures"). The nerve injury may result from compression, crushing, stretching, laceration or complete transection.(3, 8, 16, 17) Clinical signs associated with peripheral nerve injury include: pain, proprioceptive deficits, lower motor neuron type motor dysfunction (paresis/plegia, muscle hypotonia, hypo/areflexia, neurogenic muscle atrophy), and hypo/anaesthesia. Peripheral nerve injuries have been classified based on the degree of functional and structural integrity of the nerve trunk:(4, 18, 19) 1. Neurapraxia--refers to a transient interruption in nerve function (impulse conduction) due to ischemia and/or mild paranodal demyelination. There is no structural damage to the axons and their supportive connective tissue. Neurapraxia is the mildest form of nerve injury and it is commonly caused by blunt trauma or compression. The degree of proprioceptive and motor dysfunction can be variable, nociception is usually preserved. Neurogenic muscle atrophy is unlikely to occur. Recovery is usually spontaneous, complete and occurs within one to two weeks once the compression and edema resolve. Local demyelination may take 4 to 6 weeks to resolve. 2. Axonotmesis--few to several axons and surrounding myelin are disrupted (structural damage), but the Schwann cells, their basal lamina and the endoneurium remain intact. Wallerian degeneration occurs. Distally to the point of injury the axons and their myelin sheaths degenerate and undergo phagocytosis. Degenerative changes also occur in the axons proximal to the injury site but usually involve only one to three nodes of Ranvier. Axonotmesis may result from severe stretching or crush injury of the nerve. The degree of proprioceptive, motor and nociceptive deficit is proportional to the number of axons that are damaged. In general, significant neurological dysfunction and neurogenic muscle atrophy are expected. Axonal regrowth occurs spontaneously (1 mm/day) along the connective tissue scaffold, but the time until return to function depends on the extent of injury and the distance from the denervated end-organs. 3. Neurotmesis--is the most severe type of injury and is characterised by complete severance of the nerve trunk (axons, Schwann cells, supportive connective tissue). It is associated with complete proprioceptive, motor and nociceptive dysfunction (i.e., no deep pain perception). Neurogenic muscle atrophy is severe. As in axonotmesis the distal segment undergoes Wallerian degeneration, but the proximal axons will not regrow to their end-organ since there is no guiding scaffold (Schwann cell basal lamina and the endoneurium have been disrupted). Scar tissue tends to interfere with sprouting axons and may result in neuroma formation. Consequently, surgical intervention is necessary to assist regenerating axons to reach and reinnervate their appropriate end-organs. The neurological examination, especially if repeated overtime, may help distinguishing between neurapraxia and axonotmesis or neurotmesis, however it might be difficult or even impossible to differentiate severe axonotmesis from neurotmesis on the basis of clinical assessment. Our ability to estimate clinically the severity of a nerve injury is mostly based on the relationship between the diameter of a nerve fibre and its susceptibility to compression. Large myelinated fibres, (supplying mainly proprioceptive function) are the most sensitive to injury. The slightly smaller myelinated fibres controlling motor function are the next most susceptible. Small non-myelinated fibres supplying

nociception are the most resistant to compression. Therefore, with increasing compression of a nerve, proprioceptive function will be impaired at first, followed by motor function and finally by nociception. The presence of deep pain sensation in the dermatome of a certain nerve implies a much better prognosis than its absence.(17) A thorough knowledge of the dermatomes and autonomous zones of the principal nerves of the limbs is essential to perform an accurate assessment of sensory function. (1, 7, 8, 13) It is important to remember that with brachial plexus nerve root avulsion there may be inconsistency in the pattern of sensory versus motor deficits as the ventral nerve roots appear more susceptible to damage than the dorsal nerve roots. Clinical signs associated with dysfunction of most commonly affected spinal peripheral nerves have been thoroughly described.(3, 7, 13, 17) The diagnostic investigation for patients with peripheral nerve injury will include: A minimum data base consisting of complete blood count, serum biochemistry profile and urinalysis to assess general health condition prior to anaesthesia for electrodiagnostics and/ or diagnostic imaging. In certain cases it might be indicated to perform also thoracic radiographs, abdominal ultrasound and a coagulation profile. Electrodiagnostic tests are useful in assessing nerve integrity, functionality, severity of damage, distribution of nerve injury and in monitoring reinnervation. Immediately after a brachial plexus or a peripheral nerve injury electromyography (EMG) can be used in the awaken animal to determine if some axons are still functional in the injured nerve and therefore if the muscle is still innervated by that nerve. By eliciting a withdrawal reflex (stimulating an area that the animal can definitely feel) and simultaneously recording EMG activity from a flexor muscle, motor unit action potentials will be recorded if any muscle function remains. For example, the presence of motor unit activity in the biceps brachii muscle of a dog or a cat with brachial plexus injury implies that some functional axons must have survived through the musculocutaneous nerve.(6, 17) However, the absence of compound muscle action potentials does not indicate the severity or permanency of the nerve damage because transient conduction block due to edema may also prevent conduction down a nerve.(6) Five to 10 days after peripheral motor nerve injury (that is the time required for the degeneration of the distal axonal segment), denervated muscle fibres exhibit spontaneous depolarizations that can be recorded by EMG (in the anaesthetized animal) in the form of fibrillation potentials and positive sharp waves.(14) If EMG studies are repeated over time they may help monitoring disease progression. The presence of giant motor unit potentials on EMG indicates reinnervation. Motor nerve conduction velocity (MNCV) and the recorded amplitudes of muscle evoked action potentials provide an accurate evaluation of the severity of the damage to the LMN. F-wave studies allow assessment of ventral nerve root function and may be useful in cases of proximal motor nerve injuries such as brachial plexus avulsion. Sensory function can be assessed by means of sensory nerve conduction velocity (SNCV) study and cord dorsum potential (CDP). For example, in a dog with sensory dysfunction following brachial plexus injury, the absence of the CDP with a normal SNCV indicates a complete nerve root injury above the dorsal root ganglion.(6) Intraoperative nerve action potential are used in human medicine in order to identify functional regeneration of an injured nerve and accurately trace the length of regenerating axons and the length of nonviable nerve.(9) These information are extremely helpful to decide whether and exactly where segmental nerve resection and reanastomosis should be performed. Survey radiographs are indicated when the nerve injury is likely to be associated with fractures (i.e., humeral, femoral, pelvic, sacrocaudal) or with intramedullary pinning. Ultrasound may be helpful in assessing nerve anatomy and further characterise traumatic nerve lesions in companion animals.(10) We have successfully used ultrasound to visualise sciatic nerve entrapment following penetrating wound in the caudal thigh of dogs previously attacked by a boar. A recent study in human medicine has shown that ultrasound can be a useful diagnostic aid in the determination of the precise localisation of the injured site along the involved peripheral nerve, the type of injury and the diagnosis of neuroma.(5) Computerized tomographic (CT)--myelography is indicated in the diagnosis of brachial plexus nerve root avulsion since it allows visualization of meningeal diverticula and abnormalities of

the spinalnerve roots. In a recentprospective study of 40 human patients suffering severebrachial plexus injuries, CT-myelography was found tobe 85% accurate in predicting the intraoperative findings.(11) MRI provides fine anatomic detail of soft tissue and can be used to visualise nerve structures. In veterinary medicine MRI has been successfully used in the diagnosis of peripheral nerve sheath tumors and will certainly have a role in the diagnosis of peripheral nerve injuries. In human medicine, it has been demonstrated that conventional MRI can detect signal changes in injured nerves and in denervated muscles.(11) In addition, in human medicine, the use of custom designed phase array coils has led to the development of MR neurography (MRN). MRN produces images with higher resolution improving the ability to visualize both normal and abnormal peripheral nerves in various regions of the body.(11) These advanced diagnostic imaging techniques may have an important role in the assessment of peripheral nerve and brachial plexus injuries in companion animals in the near future. Treatment of peripheral nerve injury depends on the cause, the severity and the site of the lesion. In general, anti-inflammatories and analgesics are indicated to relieve inflammation and pain. Physical therapy should be started in the early stages following nerve injury in order to maintain range of motion and minimise muscle atrophy. If the nerve injury produces monoparesis and knuckling such as with radial or sciatic nerve lesions, the paw should be protected by means of commercially available boots, splints or special bandages. When the primary cause of nerve injury can be identified (trauma by fractured/dislocated bone, excessively long femoral intramedullary pin, entrapment by inflammatory/fibrous tissue) it should be addressed surgically as soon as possible (fracture repair, intramedullary pin removal/shortening, neurolysis). If the nerve has been severed sharply (e.g., by a piece of glass or a knife), and the wound is not contaminated, immediate nerve repair is recommended. Special microsurgical instrumentation and magnification (ocular loupes or operating microscope) are required to perform a meticulous neurorrhaphy. The surgical repair must be accomplished with the least possible trauma to minimise inflammation and fibrosis. The sutures have to be positioned with no longitudinal and circumferential tension at the repair site. Excessive scar formation at the suture line will markedly decrease the progression of regenerating axons. An essential part of neurorrhaphy is accurate anatomical alignment of the nerve fascicles. Failure to match the fascicles in the two segments prevents regenerating axons from reaching their appropriate end-organs. The surgical techniques (epineural, perineural, nerve grafts) to perform nerve repair have been described.(15, 16) When the nerve lesion is caused by stretch and/or compressive forces associated with a closed traumatic injury, it is not possible to determine immediately whether the lesion is neurapraxic, axonometric or neurotmetic. Therefore medical management (analgesics, anti-inflammatories) and frequent re-evaluation (neurological examination, electrodiagnostics, and if indicated also diagnostic imaging) are advised. It is interesting to note that these guidelines are quite similar to the ones used in human medicine even though patient cooperation during clinical and electrodiagnostic assessment is much higher than in veterinary medicine and more sophisticated facilities are usually available. Hence, we can state that frequently the greatest diagnostic aid in patients with closed traumatic nerve injuries is the passage of time. Unfortunately, while awaiting for a possible improvement some complications may occur, these include: muscle atrophy and joint contracture (that can be prevented/ addressed with physiotherapy), abrasion of the dorsal surface of the paw (preventable with adequate foot protection), and paraesthesias with self mutilation. This latter complication results from abnormal sensation in an affected area due to pathological changes in the peripheral and/or central nervous system and may be difficult to control pharmacologically.(20) In those instances where limb dysfunction is profound and nerve damage is chronic (no improvement after 3 to 6 months post-injury), severe and irreversible, treatment options are quite limited. Muscle-tendon transfer alone or in association with carpal/tarsal arthrodesis may be indicated as a salvage procedure in selected cases.(2, 12) When these techniques have failed or are not indicated and delayed nerve repair is not an option, limb amputation may be the only possibility.

Future developments in the treatment of peripheral nerve injury include the use of neurotrophic and neurotropic factors to stimulate axonal survival and regeneration (trophic effect) and to direct growing axons to their proper target organ (tropic effect).

Luisa De Risio, DMV, DECVN

URL: http://www.vin.com/doc/?id=3854283

Approach to the Neurologic Camelid: Clinical Neurological Examination, Lesion Localization & Diagnostics ACVIM 2008 Claire E. Whitehead, BVM&S, MS, DACVIM, MRCVS London, UK
18286413

The presentation of neurological disease in camelids, as in other species, varies widely. There are many different causes of neurological signs (Table 1) and the clinician must be aware that metabolic and musculoskeletal disease can also present with neurologic signs. These conditions must be differentiated from those of true neurological origin by careful history-taking, physical examination and use of appropriate diagnostic tests. Table 1. Differential diagnoses of neurologic disease in South American camelids. Congenital Diseases Hydrocephalus Kyphosis Listeriosis Atlanto-occipital malalignment Traumatic Vertebral body subluxation/luxation* Vertebral body fracture* Viral, eg EHV-1, West Nile, EEE Trauma without subluxation/ luxation/ fracture* Clostridial myositis Rabies Degenerative Degenerative myelopathy Spondylosis Toxicities Tetanus Botulism Hip problems Rye grass staggers Cerebral hypoxia Peripheral nerve damage Musculoskeletal Bilaterally luxating patellae Nutritional problems Otitis media/interna* Brain abscess Vertebral body abscess Septicaemia/meningitis* Uraemic encephalopathy Hypomagnesaemia Infectious/Parasitic Diseases Meningeal worm (P tenuis infestation)--United States* Metabolic Diseases Pregnancy toxaemia* Hypo/hyperglycaemia Hepatic encephalopathy

Tick paralysis Ionophore toxicosis Other Hypo/hyperthermia* Mega-oesophagus Brain/spinal cord neoplasia Facial nerve paralysis

Gait abnormality

Determine Whether the Neurologic Signs are Due to a Lesion in the Nervous System Firstly, it is vital to obtain a thorough history of the problem, especially whether the clinical signs were acute or chronic in onset, the duration of clinical signs, deworming programme (parasitic myelopathy), diet and any dietary changes, and of course signalment. Determine whether or not a traumatic incident was observed, whether there have been any seizure episodes, and also how the problem began. For example, for a recumbent camelid, knowing whether the problem began with the forelimbs, hindlimbs or both can be useful historical information. In heat stress cases, patients often develop weakness in the forelimbs primarily, whereas patients with parasitic myelopathy develop ataxia and weakness typically in the hindlimbs first. When performing the basic clinical examination, look especially for evidence of cranial nerve deficits, postural or proprioceptive deficits, and ataxia, differentiating this from weakness. These may be difficult to assess in the recumbent animal, especially adults. However, with alpacas and youngsters, it is usually possible to assist the animal to stand, possibly with the use of a sling, so that placing reflexes can be tested. Sometimes, it may be hard to distinguish one condition from another clinically, and do not discount the possibility that two conditions may be present together, e.g., parasitic myelopathy with secondary heat stress in summer. Hematological and biochemical profiles may help identify metabolic causes. A spinal tap is easily performed in camelids from the lumbosacral space, and changes in the cerebrospinal fluid (CSF) will help establish whether a disease process involves the central nervous system (the technique is described later). Localisation of a Lesion Within the Nervous System This is a continuation of the clinical exam. Observe the resting animal, preferably while unstimulated, and assess mental status. Look for any head tilt, circling behavior, leaning to one side or head-pressing. A head tilt may be due to otitis, a vestibular lesion or possibly neck pain. If tremors are present and the head is involved, the lesion is likely to involve the cerebellum. Tremors may also occur with electrolyte imbalances (mainly hypocalcemia and hypomagnesemia), myelin disorders, with some toxins or with diffuse encephalitis. The presence of seizures indicates brain involvement, but this may be secondary to a metabolic abnormality

such as hypoglycemia or be due to a primary lesion. Depression, cortical blindness, and slow PLRs (not ophthalmic in origin) may indicate presence of a brain lesion. If the animal can walk, look for weakness versus ataxia, single or multiple limb involvement, whether the problem is unilateral or bilateral, or if one side of the animal or one half (front or back) is worse than the other. Assess the animal's gait and ability to turn in circles etc. Assessment of proprioception can be done, but may be difficult to assess in camelids with subtle problems since they often resent having their feet touched. Various reflexes can be assessed including withdrawal reflexes, anal tone, patellar reflex, gastrocnemius reflex etc. Withdrawal reflexes are best tested in camelids by squeezing the digits at the distal end of the digital pad using hemostats. Normal reflexes indicate that sensory and motor function are working normally. Absent or reduced reflexes indicate partial or complete loss of sensory or motor parts of the reflex (LMN). If unilateral, this is most likely to be due to a peripheral lesion whereas bilateral absence or reduction of reflexes is more likely to suggest the presence of a spinal cord lesion. Exaggerated reflexes indicate that there is an UMN defect. The panniculus reflex is difficult to assess in camelids, partly because of their thick skin but also because they may have be heavily fleeced for much of the year. I do not find this test particularly useful in camelids. Palpation of muscle masses is useful in evaluation of muscle atrophy (symmetrical versus nonsymmetrical) and general body condition. Examination of the cranial nerves should also be performed in the neurologic camelid. This should include evaluation of the palpebral reflex, facial sensation, menace response, pupillary light reflexes, and assessment of pupil size and symmetry. Look for nystagmus or strabismus. Observe facial symmetry and determine whether or not ptosis, enophthalmos, or rotation of the globe are present. Hearing may be difficult to test in camelids except by observing their reactions to their environment when unrestrained. Where specific hearing deficits are suspected, these may be evaluated using the Brainstem Auditory-Evoked Response test. The interpretation of data from the neurologic exam aids the clinician in determining the region affected and also whether the lesion is upper or lower motor neuron in origin (Tables 2 and 3). Lower motor neurons are the efferent nerves that connect the CNS to the muscles, while upper motor neurons initiate movements and control extensor muscle tone which is responsible for supporting the body at rest. Table 2. Characteristics of lower and upper motor neuron lesions. LMN lesions Paresis to paralysis Reduced/absent reflexes Loss of muscle tone UMN lesions Paresis to paralysis Normal or exaggerated reflexes Normal/Increased muscle tone

Muscle atrophy appears quickly Muscle atrophy is slow to appear Table 3. Localisation of spinal cord disease based on clinical neurologic features.

Spinal cord region C1-5 C6-T2 T3-L3 L4-S2 S1-3

Neurologic features UMN signs to all 4 limbs LMN signs to FL: UMN to HL Normal FL: UMN signs to HL Normal FL: LMN signs to HL Partial LMN signs to HL, incontinence

Determine the Cause of the Neurologic Lesion Once the clinician has established that he/she is dealing with a neurologic disease and then determined what neurological deficits are present, further diagnostics will be helpful in reaching a specific diagnosis. Some tests may be done easily in practice whereas others may be limited to specialist or referral facilities. CSF Sample Collection Normally CSF is taken from the lumbosacral space. Lumbosacral and atlanto-occipital CSF samples were compared in llamas that were experimentally infected with P tenuis.1 This study concluded that the site chosen would depend on the suspected location of the lesion. Welles et al (1994)2 stated that, based on work in horses, CSF from the lumbosacral space was more likely to have compositional abnormalities in neurological disease and that more useful information would therefore be obtained. In another report, samples from 3 llamas with suspected meningeal worm were collected simultaneously from the LS and AO spaces: the CSF collected from the LS space showed more significant elevations in protein and cell count.3 The lumbosacral tap is an easy procedure to perform in camelids and usually requires only a little local anaesthetic whereas the atlanto-occipital tap requires sedation or anaesthesia and is a risky procedure. A small area is clipped and prepared over the LS space after ensuring that the animal is squarely positioned and the hind legs are pulled forward in order to open up the LS space. The landmarks are the dorsal spinous process of L7 and the two wings of the ilia. These landmarks form a triangle within which an obvious depression can be palpated. Before the final scrub, inject 0.5-1ml local anaesthetic at the site using a 22G one inch needle. Using an 18G 3.5inch spinal needle in adults (20G in crias), insert the needle perpendicular to the skin on the midline about 35mm in front of an imaginary line drawn between the two ilia. It helps to anchor the wrist on the animal's pelvis as this is done because the skin is quite thick. In an adult, the needle needs to be advanced 2-4cm and "two pops" are usually felt as the needle goes through the dura into the subarachnoid space. If unsuccessful, ensure midline placement and try directing the needle a bit more cranially. Usually the patient will "jump" when the needle penetrates the dura. When the stylet is removed, CSF will be observed in the hub. Collect 2-3ml CSF and split the sample into a plain tube for CSF profile (protein/creatine kinase (CK)/electrolytes etc) and an EDTA tube for cytology (red and white cell counts and differential counts). Welles et al (1994)2 observed rapid deterioration of leukocytes in CSF after collection and advised careful handling and refrigeration

as soon as possible following collection. Their method did not indicate that any preservative was used: it is likely that collecting CSF into EDTA tubes will reduce the deterioration of cells. The most important variables to consider in the CSF are protein concentration and cytology but in certain disease situations other variables such as sodium and glucose may be useful. CK concentration may also be of value in indicating CNS disease although some studies have shown that it may increase due to the presence of epidural fat in the sample. Normal CSF protein concentration in camelids is less than 45-50 mg/dl, normal CK concentration is less than 10 IU/L and white cell count should be less than 3 cells/l. The normal white cell population may be predominantly lymphocytes or neutrophils depending on the amount of blood contamination (more neutrophils with increasing blood contamination). In the absence of blood contamination there should be no eosinophils. In camelids, the proportion of eosinophils increases in meningeal worm (parasitic myelopathy)1,2,3,4,5 and can be up to 99% of total white cells--eosinophilic pleocytosis with increased protein concentration in the CSF is present in most affected camelids. However, a normal eosinophil count does not necessarily rule out meningeal worm: in experimental infection of llamas with P tenuis, the time post-inoculation at which eosinophils increased in CSF varied. Also, prior treatment with anthelmintics may affect cell counts. Clinical observations suggest that the length of time following initial development of clinical signs until CSF is collected can result in lower percentages of eosinophils seen on cytology. P tenuis infestation is the only parasitic myelopathy so far reported in camelids. Increased protein indicates a disturbance of the blood-brain-barrier and this may occur in any inflammatory disease process including trauma, parasite migration, meningitis and otitis: if protein electrophoresis shows increased globulin only, this indicates intrathecal synthesis of globulins. Welles et al2 found in their study that in healthy llamas with red cell counts <1400 /l, the protein concentration was only minimally altered. Glucose concentration in llama CSF is approximately 40% of serum concentration.2 This compares with cattle in which CSF glucose is approximately equivalent and monogastric species in which it is 60-80% of serum concentrations: rapid changes in serum glucose, as in stress for example, will take 30mins to 3hours to equilibrate in CSF.2 Bacterial infections will decrease CSF glucose and also increase neutrophil count--for example, in bacterial meningitis in crias. Increased sodium concentration in the CSF could reflect severe metabolic derangements and may occur in salt toxicity due to unavailability of water, and in crias with hyperosmolar syndrome. This can cause intense CNS depression and needs to be carefully managed. Sodium concentrations should not be reduced too rapidly or cerebral oedema and herniation of the brainstem may occur. Radiographs Depending on the clinical signs, localisation of lesion, and CSF findings, spinal or skull radiographs may be useful. These may highlight obvious luxations, fractures or soft tissue injuries as well as demonstrate congenital malformations such as kyphosis. Two views are essential for cervical films as single view films may not pick up subluxations etc. For more subtle lesions, a myelogram may be indicated but is rarely found to be necessary in order to

reach a diagnosis. Camelids have 7 cervical, 12 thoracic, 7 lumbar, 5 sacral vertebrae and 10-15 coccygeal vertebrae. Ultrasonography May be useful in evaluation of soft tissue injuries and hydrocephalus. Computed Tomography (CT) CT may be required to visualise a suspect area, especially where the head is involved. We have found that, in the case of suspected otitis interna, CT gives a significantly better image of the tympanic bullae than plain radiographs and the extent of soft tissue involvement can be delineated using contrast CT. CT also guides the surgical approach in these cases. It is also useful if a brain mass/abscess or vertebral body abscess is suspected, although MRI is likely to be preferred if soft tissue or subtle lesions are suspected. General anaesthesia is required. Electromyography (EMG) Measures the electrical activity of muscle. It is useful to detect denervation and can allow localisation to specific spinal cord segments. It may be used to direct the clinician to a particular problem area. This is a good tool for investigating myopathies and neuropathies. Muscle Biopsy Muscle biopsies may be useful if a myopathy is suspected rather than a neuropathy. References 1. Rickard LG et al. J Zoo Wildlife Med 1994;25(3):390. 2. Welles EG, et al. Am J Vet Res 1994;55(8):1075. 3. Scarratt WK, et al. Prog Vet Neurology 1996;7(4):124. 4. Pugh DG, et al. Comp Cont Ed 1995;17(4):600. 5. Baumgrtner W, et al. JAVMA 1985;187(11):1243. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Claire Whitehead, BVM&S, MS, DACVIM, MRCVS The Royal Veterinary College Hatfield, Hertfordshire, United Kingdom

The Neurological Examination

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2001
Joane Parent Canada
18271203

It is likely in this world of technology, that a computer program will soon be available to guide the veterinarian toward lesion localisation. No matter how sophisticated the program, the neurological examination will remain pivotal. The veterinarian will need to be able to perform the tests and more importantly interpret the responses. The time allowed for this presentation does not permit covering the entire examination. Only the tests commonly performed poorly, misinterpreted or simply forgotten are reviewed. The neurological examination is composed of six parts: the evaluation of the mental status, gait and posture, cranial nerves reflexes, postural reactions, spinal reflexes and pain perception. Of these, it is the evaluation of the mental status and gait and posture that are the most important to localize the lesion. The mental status dictates if the lesion is intra or extra-cranial. The evaluation of the gait and posture is crucial in determining if the nature of the gait abnormalities is related to the nervous system or to a musculo-skeletal problem.

1. MENTAL STATUS
The mental status is the most important clue in differentiating intra- from extracranial disease in the animal with cranial nerve abnormalities. The abnormalities of the mental status relate to the brainstem or to the thalamocortex. The mental status cannot be evaluated in the examination room, even if the animal has had time to relax. In most cases, the evaluation is obtained from the history, not from observation of the animal. Dogs and cats are excited and/or fearful in the hospital environment. This adrenaline surge hides the mental changes, especially if subtle. The history is crucial and must be thoroughly performed.

a. Brainstem: State of consciousness

The bulk of the brainstem parenchyma is made of the reticular formation or the so-called Ascending Reticular Activating System (ARAS). This formation is responsible for the arousal of the cerebrum. When this system is affected, the animal becomes somnolent, lethargic, stuporous or comatose. However, he is aware of his surrounding because his intelligence (cerebrum and thalamus) is not affected. The owner must be asked specific questions regarding the mental status of the animal: Is the animal as playful? Does he sleep more than before? Is he quieter, lethargic? If the animal is historically somnolent and this is accompanied by cranial nerve deficits, the disease is intracranial and involves the brainstem.

b. Thalamocortex: Behaviour
The thalamocortex is the site of the intelligence, and goal-directed behaviours. The abnormalities can be obvious such as with patients circling compulsively or head pressing, but this is rare. In most cases, the changes are subtle especially with chronic illness, relying only on the history to bring them out. The animal is unable to relate normally with his environment. There is a decrease or an absence of the animals awareness. Beware of the animal that bumps into objects. Patients that are blind because of ocular diseases are cautious while walking and rarely do bump into objects. The blindness in the patient that collides with objects is central and relates to a brain disease. Another example is the older dog becoming deaf. This may be the fact. However, ensure that the animal is aware of his surroundings. Even a deaf dog can "feel" the garage door opening. If the animal no longer greets the owner at the door, there may be a more serious problem. The brain may not register what the eye sees or the ear hears.

2. TRIGEMINAL NERVE
The trigeminal nerve has three branches: (1) Ophthalmic (sensory) (2) Maxillary (sensory) and (3) Mandibular (sensory and motor). This large nerve innervates the masticatory muscles and provides sensation for most of the head. The masticatory muscles are palpated for symmetry and atrophy. The

sensory part of the nerve is assessed mainly through the palpebral reflexes. In these reflexes, the trigeminal nerve is the afferent limb (sensory), while the facial nerve (VII) is the efferent limb (motor). The evaluation of the ophthalmic branch is assessed by touching the medial canthus (medial corner of the eye where the lid margins meet) and observing for a blink reflex. Touching the lateral canthus and observing for a blink reflex assesses the maxillary branch. Touching the base of the ear and observing for a blink reflex assesses the mandibular branch. The indicated areas to touch are the only ones that consistently give a blink reflex in the normal animal. Touching the canthi and the ears assesses the reflex arc, i.e., the cranial nerves V and VII but DOES NOT assess if the information gets to the cerebral cortex. This is evaluated by stimulating the nasal septum. The animal may or may not blink but the head will be pulled away as a pain response. This test should be done gently using cotton swabs (Q-tips) to reveal subtle differences between sides. Start with a gentle stimulus and gradually increase the strength of the stimulus going from side to side, until a consistent response (normal or not) is obtained. The nasal septum is the only area that consistently elicits a pain response in the domestic species. This latter test provides an evaluation of the cortical response to pain.

3. GAIT AND POSTURE

The evaluation of the gait is important in lesion localization. For the small cat or dog, the examiner lets the animal walk freely on the floor of the examination room while taking the history. Most hospital rooms do not allow a good examination of the gait because of their small size. It is preferable that the medium to large size dog be leash-walked by the owner in the parking lot, back yard or sidewalk. Use a non-slippery floor such as concrete, grass, asphalt, etc. The dog is evaluated at different paces, towards and away from the examiner. The clinician observes the front limb gait as the animal is coming toward him/her and the hind limb gait as the animal is going away from him/her. Particular attention is given to the foot placement when the animal turns or changes speed. A series of questions are then answered. The questions should not be left unanswered. If unsure, look at the gait again and again.

1. Is the animal able to walk? 2. If the animal is walking, is the gait normal? 3. Which limb(s) is/are affected: one limb, both hind limbs, the hind and front limbs, or the ipsilateral limbs only? 4. Is there ataxia? 5. If there is ataxia, of which type: vestibular, cerebellar or proprioceptive?

4. PROPRIOCEPTIVE POSITIONING
Performed appropriately, proprioceptive positioning (knuckling) is an invaluable tool to evaluate proprioception. To evaluate proprioceptive positioning of the hind limbs, the clinician is positioned behind the animal. The animal's weight must be supported with a hand (and forearm in the large dog) between and behind the hind limbs. For the evaluation of the front limbs, the examiner's hand is placed between the limbs and behind or in front of the limbs. The paw is then slowly knuckled over. The flexion of the toes stimulates hundreds of proprioceptors located in the tendons and joints of the toes. The test must be done with care to enhance subtleties. A pet that knuckles does not necessarily have proprioceptive deficits. Orthopaedic problems, generalized weakness and patients personality may all have an effect on the test. The test results must be taken in the light of the entire examination.

5. PATELLAR REFLEXES
The patellar reflex (tendinous or monosynaptic reflex) is elicited by tapping the patellar tendon. There are two components to the reflex: the ascending sensory pathway and the descending pathway or lower motor neuron. Both must be intact for the reflex to be present. To elicit the reflex, the limb is positioned in a relaxed flexion to tighten the patellar tendon. This reflex is the most often erroneously found to be absent. It is important to pay attention to details when eliciting it to ensure its absence is real and not the result of poor technique. If the reflex is absent yet the animal can walk and/or stand, the lesion likely involves the sensory pathway and not the lower motor neuron.

6. WITHDRAWAL OR FLEXOR REFLEXES

The withdrawal (flexor) reflexes are difficult to examine objectively because in most of our patients, purposeful movements are still present (so pain perception is as well) and the animal inhibits the response, leading to a falsely decreased reflex. A normal animal should be able to bring his body to the examiner's hand while flexing the limb. The front limb reflexes can be used as a comparison for the hind limbs and vice versa. Musculo-skeletal disorders may affect the nature of the flexor and patellar reflexes. The patellar reflex may be absent or decreased in a dog with a cruciate rupture because the tension in the tendon cannot be raised. Hip dysplasia, polyarthritis and muscle diseases may lead to decreased flexor reflexes because the animal is too weak to withdraw his limb with force. The neurological examination should be done in a methodical and stringent manner every single time paying attention to details. A neurological form should always be filled. Although the examination when performed on a regular basis becomes a routine, the form serves as a "check list" ensuring that all parameters have been evaluated. More importantly, it is an invaluable document in the follow up and monitoring of progressive and protracted nervous system diseases.

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Joane Parent Canada

Lameness Examination in Working Dogs

AUSTRALIAN VETERINARY ASSOCIATION PROCEEDINGS 2010
Andrew Worth Centre for Service and Working Dog Health and Research, Massey University, Veterinary Teaching Hospital, Massey University, Palmerston North, New Zealand
24156548

STEP 1: GAIT ASSESSMENT

I like to modify the traditional approach of history taking, physical exam and then lameness examination by beginning with an assessment of the animal's gait, ideally outside in good light on a non-slippery surface. I like to be able to anticipate lameness evaluations and meet the client in the car park if possible. This is made easy by having the consultations booked with keywords such as 'lameness' or 'stiffness', to alert you there is a case coming up that will need a gait evaluation. I try to meet the owners at their car, or walk them back outside before going near the consult room. I like to blind myself so without taking any history I observe the gait to form an unbiased opinion. Then I ask the client to identify the leg they think is affected by pointing it out, just so that there is no confusion over the leg that is the cause of concern. Examine the patient from three directions: walking towards you, walking away from you and from the side. We are all familiar with the concept of a 'head bob' for forelimb lameness (the animal raises its head and neck when the lame leg is placed) and 'hip hike' for hind limb lameness (the hip appears to lift over the affected leg). When an animal is lame, the swing and stance phases are shortened, thereby reducing the amount of time spent on the affected limb. During the examination, observe the length of the stance phase, the position of the contact point, the position of the lift point, the plane of the stride and whether or not the limb is abducted or adducted during the cycle. Note alterations in joint angles; a reduction in flexion is common with joint disease. Observe the area of foot contact; normally the main pad is the first to touch the ground followed by the toes. The opposite may occur when there is reluctance to fully load the foot.

Recognising Hind Limb Lameness

With a hind limb lameness, weight is shifted forward by extending the neck and lowering the head. There may be a change from the normal side to side oscillation of the tail to a more vertical oscillation. The "up" motion of the tail occurs when the affected limb contacts the ground. The stride length is shortened and the pelvis is tilted in the axial plane so that the hemipelvis on the affected side is more

dorsal. When there is unilateral hip disease, the pelvis is tilted sideways, and an oscillating motion is seen towards the affected side. This manoeuvre minimises hip motion by using lateral bending of the spine to achieve forward movement. When viewed from the rear, the pelvis of an animal with bilateral hip disease swivels from side to side (Marilyn Munroe style).

Forelimb Lameness
With lameness in a forelimb, the animal lifts its head when the affected limb bears weight (and appears to dip its head when the sound limb contacts the ground). Note: When there is shortening of a forelimb stance phase, there is also a slight shortening of the opposite hind limb step as the animal hastens to remove weight from the forelimb. This phenomenon can often cause a misdiagnosis.

STEP 2: HISTORY TAKING AND PALPATION OF TOPOGRAPHICAL ANATOMY

After the gait assessment comes history taking, which I typically combine with a "pat-down" of the patient. While I am taking the history I have my hands on the patient stroking it and looking for asymmetry of muscle and bone. This gentle start gains the patient's confidence ahead of potentially painful manipulation later. You should look for any loss of muscle mass over the scapula and humeral areas and check the thigh circumference and the cranial tibialis muscles. The latter is an indicator of long nerve neuropathies (can be seen in Labradors presented with laryngeal paralysis). History questions: 1. Identify the problem - in the eyes of the owner 2. Onset, duration, progression, response to rest 3. Any association with trauma 4. Any juvenile bone disease 5. Response to medication or other therapy so far 6. Patient's environment and exercise regimen 7. Diet composition, quantity fed and mineral supplementation important in the younger patient

STEP 3: PHYSICAL EXAMINATION

Resist the temptation to skip the full physical examination and just move right to the ortho exam. Concurrent injuries or disease could affect both the prognosis and safety of sedation or anaesthesia required at a later time. It is important to palpate regional lymph nodes for lymphadenopathy. Body temperature may be elevated in some disease states (abscessation, cellulitis, marked tissue injury). Lack of an elevated temperature should not be used as an exclusion criteria for joint injection or IMPA, (in one study only 18% of dogs with confirmed polyarthritis were febrile).

STEP 4: BASIC SPINAL NEUROLOGICAL EXAMINATION

I next perform a very basic neurological examination at the same time checking for the relative amount to weight the animal is placing on each limb. With the patient standing on the floor or table, each paw is lifted (check the amount of weight transferred to the other leg as you do this) and placed on its dorsum (knuckling response). Check for the speed with which the animal replaces the paw. This tests conscious proprioception and loss of this response is a sensitive indication of spinal cord disease. However, it can also be caused by peripheral nerve lesions, thus the loss of CP gives us no insight as to upper versus lower motor neuron dysfunction. Remember too that this reflex is consciously mediated, hence an animal can "choose" not to respond normally, which is typically seen when the reflex is repeated many times over, or the animal has a painful lesion in the limb being tested (e.g., a fracture). In trauma cases it is necessary to ascertain the presence of any nerve injury when the CP is altered. Test the withdrawal reflex by pinching the skin of the digits. Ensure you test medial and lateral toes. A centrally mediated response (vocalisation, turning to bite, trying to move off) indicates the integrity of the nerve pathway (ruling out LMN disease) even if a withdrawal of the limb is not stimulated due to fracture or muscle trauma. Testing the myotactic reflexes follows in order to localise a spinal lesion (not performed if above all normal). The neurological examination is most important in the recumbent patient. For example, an animal with bilateral cranial cruciate ligament can present recumbent and unable to rise. This "won't" walk state must be differentiated from "can't" walk. Helping such an animal to its feet will allow an

assessment of proprioception / myotactic reflexes and withdrawal reactions. These would be expected to be normal unless there is major structural disability.

STEP 5: THE ORTHOPAEDIC EXAM

Commences with evaluation of the affected limb and begins distally. Avoid the temptation to immediately focus on the most likely cause of disease, rather, develop a systematic approach so that nothing is missed. Work your way up the limb until swelling or tenderness is noted. If by now I have a focal area of discomfort, I will complete the examination above and beyond that site then come back to the sore area last to maximise the patient's patience with manipulations. Localisation of solitary limb lameness is based around the demonstration of pain and pathology. Loss of joint range of motion, presence of crepitation or effusion and peri-articular thickening indicate presence of pathology and, in the latter, evidence of chronicity. The other limbs should not be neglected either, especially if a potentially genetic disease is present. A pup with mildly subluxated hips has a good prognosis, but if there is bilateral elbow pain it may not be a viable proposition. This brings me on to one of the real traps for both owners and vets - bilateral disease. Due to lesions in both fore or hind limbs some dogs will into appear asymmetrical in gait to the owners. A common example would be a large breed pup with elbow dysplasia. These dogs may walk with abducted elbows and a short striding gait, but not appear overtly lame. This session will concentrate on specific examination and manipulation as it applies to working dogs undergoing lameness assessment. Video and pictorial demonstration will be used to illustrate each step. Amongst other topics we will cover: Biceps disease: DDX bicipital tenosynovitis, biceps avulsions, biceps calcifying tenopathy Exam: Biceps retraction testing, biceps insertion traction, palpation of the inter-tubercular groove during above Findings: Pain on manipulation at stretch of biceps Medial glenerohumeral ligament injury: Shoulder joint laxity / instability Exam: Abduction test of Bardet, sedation or anaesthesia required Findings: Normal < 30 degs, abnormal > 50 degs, grey zone between Sesamoid disease: DDX fracture, fragmentation Exam: Forced flexion of the digits, palmar / plantar pressure to the MCPJt Findings: Repeatable pain in association with radiographic signs Traumatic joint instability: Requires manipulation +/- sedation and stress radiography

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Andrew Worth Centre for Service and Working Dog Health and Research Massey University Veterinary Teaching Hospital, Massey University Palmerston North, New Zealand

Common Non-Surgical Diseases of the Canine Spine

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2008
Jacques Penderis, BVSc, MVM, PhD, CVR, DECVN, MRCVS Institute of Comparative Medicine, Faculty of Veterinary Medicine, University of Glasgow Glasgow, UK
18293636

INTRODUCTION
The disease of the canine spine can be classified based on whether the primary presenting complaint is spinal pain or neurological deficits. Clinically important spinal cord diseases presenting with pain: Meningitis Discospondylitis Intervertebral disc disease* Lumbosacral syndrome* Bone tumour* Vertebral malformations (atlanto-axial subluxation)*
* May progress to develop neurological deficits

Clinically important spinal cord diseases presenting with neurological deficits: Intervertebral disc disease Fibrocartilaginous embolism Lumbosacral syndrome Trauma Neoplasia Vertebral malformations (atlanto-axial subluxation, hemivertebrae) Chronic degenerative radiculomyelopathy (CDRM or degenerative myelopathy) in the GSD

MENINGITIS
Causes of meningitis in dogs and cats include: Immune mediated form commonest: steroid responsive meningitis / arteritis (SRMA) (Bacterial: rapidly fatal) (Viral [distemper]) (Protozoal [Toxoplasma / Neospora]) Breeds affected by SRMA: Large pure breeds (Pyrenean mountain dog, Newfoundland, pointer, Weimaraner, Vizsla) Beagles

Clinical Signs of SRMA

Typically a waxing and waning course, associated with bouts when the dog appears unwell, demonstrates pyrexia, marked cervical pain and inappetence.

Diagnosis
CSF tap is definitive, with evidence of elevated white cell counts, primarily consisting of large numbers of non-degenerate neutrophils. Haematology / biochemistry may support inflammation but are nonspecific. Advanced imaging (besides MRI) is usually normal and myelography is contra-indicated.

Treatment
Prednisolone: tapering from an initial immunosuppressive dose for 2 to 4 weeks. Continue tapering the dose over 4 to 6 months. Some patients require longer treatment or different drugs. May be self limiting after 12-18 months.

DISCOSPONDYLITIS
Discospondylitis is a concurrent infection of the intervertebral disk and of the adjacent vertebral bodies (vertebral osteomyelitis). Discospondylitis is more common in middle-aged large/giant breed dogs. Males are more commonly affected than females (ratio of 2:1). The most common sites affected are mid-thoracic vertebrae; C6-C7 and L7-S1.

Aetiology
Discospondylitis is a septic condition, usually spread by haematogenous route. It can also be secondary to penetrating wounds, foreign bodies, etc. Commonly encountered infectious agents are coagulase-positive Staphylococci, Streptococcus species, Brucella canis and E. coli.

Clinical Presentation
Signs are often non-specific in the early stages. Spinal pain is usually present, while systemic signs (fever, weight loss) are reported in only 30% of cases. With progression, degeneration of the disc can lead to protrusion/extrusion.

Diagnosis
Leukocytosis is usually absent. CSF analysis is often normal. Blood and urine cultures are reported to be positive in 45-75% and 25-50% of cases, respectively. Brucella titres should be obtained in intact animals in endemic regions. Radiographic demonstration of discospondylitis is usually sufficient for diagnosis, but radiographic changes may not appear for up to 3 weeks. Magnetic resonance imaging is the diagnostic procedure of choice.

Treatment
Treatment of discospondylitis is prolonged (2 to 4 months) and relapses are not uncommon. Empirical treatment can be initiated after all samples (urine, blood, disc aspirate) have been taken for culture and sensitivity. Cage rest is important to minimize the risk of pathologic fracture. Analgesia should be provided.

INTERVERTEBRAL DISC DISEASE

Intervertebral disc disease is an important cause of canine neurological disease, accounting for over 2% of all diseases diagnosed in the dog. Affected patients typically present with signs of pain or varying degrees of spinal cord dysfunction. Disc disease in the dog was first classified by Hansen as: Type I, where herniation of the nucleus pulposus occurs through the annular fibres of the disc into the spinal canal; and Type II, where annular protrusion into the spinal canal is caused by shifting of the nucleus pulposus material. Both Hansen type I and type II disc disease are always preceded by disc degeneration. A third type of disc extrusion, traumatic disc extrusion, may also occur. This happens when trauma causes rupture of a disc that demonstrated no obvious preceding degenerative changes, resulting in spinal cord injury with no or minimal residual compression.

FIBROCARTILAGINOUS EMBOLISM (FCE)

Aetiology
FCE is characterised by ischaemia of the spinal cord secondary to the acute occurrence of emboli, consisting of disc-derived fibrocartilage, within the arterial and, occasionally, venous blood supply of the spinal cord. FCE often occurs in association with vigorous exercise or mild trauma (60% in one study).

Breed Predisposition
FCE occurs in either sex of usually adult dogs, but may occur from as early as a few months of age. FCE occurs virtually exclusively in non-chondrodystrophoid breeds and particularly in active medium/large breeds. However, there appears to be a breed predisposition for the development of FCE in miniature Schnauzers. In non-giant breeds, 80% of cases occur between 3 and 6 years of age.

Clinical Presentation
The onset of FCE is typically peracute and may be associated with a brief episode of pain, but thereafter the disease is non-progressive and pain-free. It may occur in any region of the spinal cord, but appears to be more frequent in the cervical and the thoracolumbar regions, particularly the cervical and lumbar enlargements. The neurological deficits are usually asymmetrical.

Diagnosis
Diagnosis is based on the correct history and signalment with no evidence of spinal cord compression. MRI is the most useful imaging modality for making an ante mortem diagnosis of FCE and the primary imaging feature is asymmetrical hyperintensity within the spinal cord on T2-weighted images.

Treatment and Prognosis

Treatment is by nursing care and early instigation of physiotherapy is very beneficial. As there is no residual spinal cord compression there is no need for decompressive surgery or for strict cage rest, and physiotherapy can therefore be started as soon as the diagnosis is confirmed.

LUMBOSACRAL SYNDROME
Lumbosacral syndrome comprises diseases affecting the caudal lumbar (L4-L7) and sacral segments of the spinal cord, as well as the nerve roots supplied by these spinal cord segments forming the cauda equine. The nerves affected by lumbosacral syndrome may include the femoral, sciatic, obturator, pudendal, pelvic and coccygeal nerves and result in variable involvement of the pelvic limbs, tail, bladder, anal sphincter and perineum.

Clinical Signs
The primary clinical signs of lumbosacral syndrome (the presence or absence of the individual clinical signs will depend on the underlying lesion) can roughly be subdivided into 3 categories: Neurological deficits pertaining to the pelvic limbs: Pelvic limb paresis or ataxia Decreased lumbosacral trunk reflexes in the pelvic limb Pelvic limb or hip region muscle atrophy Neurological deficits pertaining to the sacral and coccygeal nerve roots: Decrease or loss of the anal reflex and dilation of the anal sphincter Decreased or absent perineal reflexes Urinary incontinence Faecal incontinence Hypoaesthesia or analgesia of the perineal region, pelvic limb or tail Tail paralysis Pain-related clinical signs:

Pain over the lumbosacral region Reduced activity, in particular reluctance to jump and climb stairs Nerve root signature (referred pain due to nerve root entrapment)

Causes
The causes of lumbosacral syndrome are varied and include (based on the DAMNIT classification): Degenerative: lumbosacral stenosis, intervertebral disc disease, spinal synovial cysts Developmental: spina bifida, sacrocaudal dysgenesis, dermoid sinus, myelodysplasia, transitional lumbar or sacral vertebrae, osteochondritis dissecans Angiopathic: aortic ischaemic myelopathy, fibrocartilaginous embolism, haemorrhage, ascending and descending syndrome Neoplastic: primary and secondary spinal cord tumours, nerve root tumours Inflammatory and Infectious: abscessation, discospondylitis, (granulomatous meningoencephalomyelitis), (mycotic diseases), (parasitic migration) Trauma: spinal trauma Of these causes of lumbosacral syndrome, the most important is lumbosacral stenosis.

LUMBOSACRAL STENOSIS
Lumbosacral stenosis is due to stenosis of the vertebral canal at the level of the lumbosacral junction with consequent compression of the nerve roots. In some cases, the stenosis may be lateralised and only affect one intervertebral foramen. The most common cause of lumbosacral stenosis is a Hansen type-II intervertebral disc extrusion at the level of the lumbosacral junction, but other causes have been reported. The condition is most common in large breed dogs, often working dogs. The disease tends to occur in middle-aged dogs, with an increased incidence in male dogs (with a male to female ratio of 4:1). German shepherd dogs, boxers and Rottweilers are over-represented. Affected dogs demonstrate one or more of the features of lumbosacral syndrome, with pain over the lumbosacral region (particularly on palpation and lumbosacral hyperextension) being one of the most consistent clinical signs.

TRAUMA
Spinal trauma is a common cause of spinal dysfunction and includes endogenous and exogenous causes. Exogenous causes are most often secondary to road traffic accident or fall from a height. Vertebrae can be divided in three anatomical compartments: Ventral: ventral longitudinal ligament, ventral part of the annulus fibrosus and ventral vertebral body Middle: dorsal portion of the annulus fibrosus, dorsal longitudinal ligament and dorsal vertebral body Dorsal: pedicles, vertebral arches, articular facets, joint capsules, spinous process and interspinous ligament

Treatment
Assessment of instability: considered unstable if there is a lesion of two or more compartments. The aim of spinal trauma treatment is to: 1) prevent further mechanical damage to the spinal cord; and 2) treat/prevent secondary pathophysiological events. The choice of treatment (conservative or surgical) depends on severity of the lesion (especially number of vertebral compartments involved), owner's finance, surgeon expertise and preference.

NEOPLASIA
Neoplasia affecting the spinal cord is common in both dogs and cats and the exact clinical signs depend on the localisation of the lesion, with respect to the level of the spinal cord affected (e.g., cervical versus caudal lumbar). Neoplasia of the spine is classified both with respect to the physical

localisation in relation to the meninges and spinal cord (into extradural, intradural but extramedullary and intramedullary).

VERTEBRAL MALFORMATIONS (ATLANTO-AXIAL SUBLUXATION, HEMIVERTEBRAE)

Atlanto-Axial Subluxation
Toy and small breeds such as the Chihuahua and Yorkshire terrier are at highest risk as a result of failure of development of the dens (aplasia or hypoplasia). Onset of clinical signs in dogs with the congenital form usually occurs in young animals, although the problem can develop at any age, especially following minor trauma. Clinical signs are those associated with cervical spinal cord compression: pain, ataxia and/or upper motor neuron paresis/paralysis.

Malformations of the Vertebral Body and Disc

Most of these malformations are incidental findings and do not cause any significant neurological deficits, however in some cases, the spinal canal can be severely reduced, causing compression of the spinal cord.

Malformations of the Vertebral Arch and Spinal Cord Spina Bifida

Incomplete closure of the vertebral arch. It is most commonly reported in English bulldogs and can cause paraparesis and urinary and faecal incontinence.

Congenital Syringomyelia and Spinal Dysraphism (Myelodysplasia)

Malformations of the spinal cord have been described in Weimaraner and other breeds of dogs.

Sacro-coccygeal Dysgensis
Reported in the Manx cat as well as pugs and bulldogs. The clinical signs include paraparesis and urinary/faecal incontinence.

CHRONIC DEGENERATIVE RADICULOMYELOPATHY (CDRM OR DEGENERATIVE MYELOPATHY)

Chronic degenerative radiculomyelopathy (CDRM) is a degenerative neurological disorder resulting in progressive pelvic limb ataxia and paresis in older large breed dogs, particularly the German shepherd dog. The underlying pathogenesis is unclear, but is likely to have a genetic basis.

Clinical Signs
Affected dogs are generally over six years of age and the mean age of onset is around 9-years of age. Clinically, dogs present with a gradual progression of an initial insidious pelvic limb ataxia. The neurological abnormalities are bilateral and usually symmetrical (although mild asymmetry is not uncommon). The lesion is diffuse and there are therefore no focal localising signs, such as focal pain or cutaneous trunci reflex cut-off. Due to involvement of the dorsal roots, the patellar reflex is decreased or lost in about 25% of cases. The duration of clinical disease prior to euthanasia on humane grounds is around 6 to 18 months.

Diagnosis
There is currently no in vivo diagnostic test: definitive diagnosis requires neuropathological examination.

Treatment
A variety of treatment regimes have been proposed, but there is no reliable evidence to suggest that any of these treatments offer any benefit. Concurrent osteoarthritis will, however, exacerbate the abnormal pelvic limb gait, and treatment with NSAIDs may result in apparent temporary improvement.

Jacques Penderis, BVSc, MVM, PhD, CVR, DECVN, MRCVS Institute of Comparative Medicine, Faculty of Veterinary Medicine University of Glasgow Glasgow, United Kingdom

Paraparesis in the Ageing Large-Breed Dog: Other 'Non-degenerative' Causes, Diagnostic Approaches and Treatment British Small Animal Veterinary Congress 2011 Joan R. Coates, BS, DVM, MS, DACVIM (Neurology) Clydesdale Hall, Department of Veterinary Medicine, College of Veterinary Medicine, University of Missouri, Columbia, MO, USA
21494037

Introduction Orthopaedic, spinal cord, nerve, neuromuscular junction and muscle disease can all cause abnormal pelvic limb movement in older dogs. Due to the multiplicity of anatomical dysfunctions and the fact that these disorders can mimic and overlap each other; a diagnostic dilemma is posed to the clinician. Paraparesis is a non-specific term for bilateral motor dysfunction of the pelvic limbs. Weakness is an inability to carry out a desired movement with normal force because of a reduction in strength of the muscles necessary to carry out the movement. Changes in muscle tone that are elicited by passive movements include flaccidity, spasticity and rigidity. The terms lower motor neuron (LMN) and upper motor neuron (UMN) are applied to differentiate two basic types of neurological weakness. Clinical signs of UMN weakness manifest as general proprioceptive (GP) ataxia and spastic paraparesis/plegia with normal to increased spinal reflexes and muscular hypertonia. LMN weakness clinically manifests as paresis, paralysis, hyporeflexia to areflexia and muscle atrophy that is severe and rapid in onset. Neuroanatomical localisation to thoracolumbar spinal cord is specified to the spinal cord areas based upon signs of UMN or LMN limb weakness. These areas include the thoracolumbar spinal cord (T3L3), and the lumbar intumescence (L4S2). The sacral and coccygeal regions are localised according to LMN signs involving the perineal region, bladder function, urethral tone and tail tone. The term fatigability describes when one or more muscles become weaker with repetitive but normal use and may imply neuromuscular dysfunction. Signalment Signalment is important to consider as some breeds are predisposed to specific diseases. In older, large-breed dogs, disorders that often overlap with each other include: degenerative lumbosacral stenosis, osteoarthritis, degenerative myelopathy, Hansen type II intervertebral disc disease (IVDD) and hip dysplasia. The aged patient also can be affected by diseases of the muscle, nerve and neuromuscular junction that can confound the diagnosis of spinal cord disease. Aged patients often have concurrent orthopaedic and neurological disorders which further complicate the examination process. Clinical History Clinical history is important in defining the location and cause of the disorder. Onset (sudden or insidious), rate of progression (gradual or rapid) and temporal relation (intermittent/episodic, stable or chronic) can be established. Disorders that may mimic each other as acute paraparesis

include: fibrocartilaginous embolism (FCE), aortic thromboemboli, trauma, discospondylitis, IVDD, bilateral cranial cruciate rupture and early polyradiculoneuritis. Disorders that mimic each other as chronic progressive paraparesis include: hip dysplasia, bilateral cruciate rupture, degenerative lumbosacral syndrome, polyneuropathies, degenerative myelopathy and Hansen type II IVDD. Disorders causing episodic weakness include myopathy, neuromuscular junction disease (e.g., myasthenia gravis) and metabolic disorders (e.g., cardiac and pulmonary dysfunction, and endocrine and electrolyte disturbances). Clinical Examination Thorough physical, orthopaedic and neurological examinations of the patient are crucial to localising the weakness and avoiding unnecessary diagnostic testing and client expense. A patient with suspected orthopaedic disease should have a neurological examination and vice versa. Mental status, gait and posture are evaluated during observation of the patient. Often a non-specific clinical sign associated with paraparesis is reluctance to rise. The extent of muscle atrophy may further delineate presence of LMN disease. Gait is evaluated at a slow and fast pace. In neurological disease, more strenuous exercise will exacerbate the paraparesis, whereas clinical signs will improve with exercise in animals with orthopaedic disease. Exercise intolerance and episodic weakness often are not obvious until exercise. A stiff or stilted stride is characteristic for an animal with arthritic, muscle, nerve or neuromuscular junction disease. Animals with UMN disease will show GP ataxia reflective of a longer spastic stride. Paw replacement (proprioceptive positioning) is a non-weightbearing test that is useful for discrimination between orthopaedic and neurological lameness. Diagnostic Approach and Treatment Spinal Cord Diseases Clinical presentation of thoracolumbar spinal cord disorders commonly manifests as disturbances reflective of sensory, motor and autonomic dysfunction. Abnormal gait descriptions include GP ataxia (loss of proprioception), paresis (weakness) and paralysis (loss of voluntary motor function). Loss of bladder function usually occurs with paraplegia. The degree in severity of motor and sensory deficits from spinal cord disease is dependent upon the rapidity of disease onset, the extent of spinal cord involvement and the area within the vertebral column affected. Presence of asymmetry is common in vascular and compressive myelopathies (e.g., IVDD, spinal cord neoplasia). Presence of spinal hyperaesthesia assists with localisation when present and for determining a differential diagnosis. Spinal hyperaesthesia usually indicates a compressive and/or an inflammatory cause. Paraspinal structures innervated by nociceptive fibres include the vertebrae, meninges, nerve roots and intervertebral disc. Disorders that classically do not manifest spinal cord hyperaesthesia are the degenerative spinal cord diseases, intramedullary neoplasia and fibrocartilaginous embolic myelopathy. Degenerative myelopathy is a non-painful, slowly progressive disease of the long tracts and ganglia of the thoracolumbar spinal cord. The disease commonly occurs in the aged dog of various breeds. The initial neurological signs consist of GP

ataxia/UMN paraparesis. Diagnosis is based on ruling out compressive myelopathy with crosssectional imaging and LMN disorders with electrodiagnostic studies. Spinal cord disorders in older dogs exhibiting spinal hyperaesthesia that often result in a slowly, progressive paraparesis include Hansen type II IVDD and degenerative lumbosacral stenosis. Hansen type II IVDD usually manifests as an insidious UMN paraparesis. Hansen type II IVDD occurs in non-chondrodystrophic breeds, such as German Shepherd Dogs and Labrador Retrievers. Type II IVDD develops at a slower rate, and clinical signs occur when the animal is 512 years of age. Fibroid metaplasia can lead to gradual disc protrusion. True extrusion of nucleus pulposus into the epidural space usually does not occur but rather a protrusion or bulge of the annulus fibrosus occurs. Both the annulus fibrosus and nucleus pulposus may protrude but the nucleus pulposus is contained within an intact, but degenerate annulus. Acute onset of clinical signs with Hansen type II IVDD is less common, and compression from this protrusion results in a slowly progressive focal myelopathy. Diagnosis is based on myelography and/or cross-sectional imaging (magnetic resonance imaging (MRI) and computed tomography (CT)). Prognosis is guarded to fair depending on early surgical decompression. Degenerative lumbosacral stenosis (DLSS) refers to compression of the cauda equina at the lumbosacral articulation; it is relatively common and has been reported in older dogs of various breeds. The most usual clinical sign of DLSS is caudal lumbar pain. Dogs may experience difficulty rising, and at this stage the clinical signs are easily confused with hip dysplasia or other orthopaedic disorders. Recurring lameness of one or both pelvic limbs is common. Dogs may stand with the pelvic limbs tucked under the caudal abdomen presumably to flex the lumbar vertebral column and lessen nerve root compression. The owner frequently reports that the dog does not jump or has difficulty climbing stairs. Exercise often exacerbates the signs because vascular engorgement within the foramen further worsens the nerve compression (neurogenic intermittent claudication). The gait is usually short strided. Urinary dysfunction occurs with severe disease. Diagnosis is determined by survey radiography, cross-sectional imaging and electrodiagnostic studies. Abnormal findings on survey radiography include osteochondrosis of the sacral end-plate, transitional vertebrae, spondylosis, subluxation, sclerosis of the end-plates and bony proliferation of the articular processes. CT and MR imaging have the advantage of better bone and soft tissue resolution, respectively. Transverse, dorsal and sagittal planes provide determination of lesion extent. Both flexed and extended views are used to accentuate any abnormal compression and help establish the presence of a dynamic lesion which may affect surgical treatment. The management of DLSS is based on an evaluation of the severity and duration of the clinical signs. Indications for conservative management include the first episode of clinical signs or when the pain is intermittent. Confined rest for 48 weeks and pain management are recommended for dogs with an initial episode of only pain. The recovery rate with conservative management is between 24 and 50%. Indications for surgical management include failure of conservative management, severe pain and severe neurological deficits (in particular incontinence). Choices of surgical procedures include dorsal decompression, discectomy, foraminotomy, and fixationfusion. Prognosis is fair to good if clinical signs improve following early surgical intervention. Prognosis is guarded in dogs with severe neurological deficits and urinary and faecal incontinence for more than a few weeks.

Other neurological disorders that exhibit spinal hyperaesthesia and present as paraparesis are spinal neoplasia and inflammatory diseases. Spinal neoplasia may be primary (extraduralvertebral: osteosarcoma, chondrosarcoma, fibrosarcoma, myeloma; intradural-extramedullary: nerve sheath tumour, meningioma, nephroblastoma) or metastatic (mammary carcinoma, prostatic carcinoma, haemangiosarcoma). Inflammatory disorders include infectious/noninfectious myelitis/meningitis and discospondylitis. Neuromuscular Diseases Myopathy usually presents with generalised weakness and exercise intolerance that can be episodic or persistent. Commonly in myopathic and neuropathic disease, the pelvic limbs are affected first and more severely than the thoracic limbs. Gait is usually stiff and stilted or bunny hopping. Muscle palpation with myopathy may reveal severe atrophy or hypertrophy and tremors/fasciculation. Dysphagia, dyspnoea and dysphonia can be clinical signs. Depending upon the severity of atrophy, range of joint movement may be limited. Muscle pain may or may not be evident upon palpation. Creatine kinase activity, an enzyme specific for skeletal and myocardial muscle, may be increased. Because of the short half-life (6 hours), increased enzyme activity reflects active disease. Electromyography allows detection of abnormalities within the muscle. Many primary muscle diseases are characterised by spontaneous high-frequency discharges, i.e., myotonic and pseudomyotonic. Nerve conduction velocities are within normal limits. Muscle biopsy can characterise the myopathy. Neuropathy is characterised by a flaccid paresis, postural reaction deficits and neurogenic muscle atrophy. Paraesthesia may be evident depending upon sensory involvement. In neuropathies with both proximal and distal involvement, the patient may be unable to walk or may walk with a stilted stride to support its weight. If the weakness is distributed more distally (e.g., distal symmetrical polyneuropathy), the stride may show a 'pseudohypermetria' where the paw is flipped out to accommodate. Cranial neuropathy and muscle fasciculation may also be present. Myotatic and flexor reflexes are often decreased or absent. Electromyography shows spontaneous activity (e.g., positive sharp waves and fibrillation potentials). Nerve conduction studies may show polyphasia and abnormal waveforms and slow conduction velocities. Diagnosis is often made by nerve and muscle biopsy. The neuromuscular junction disorder in older dogs that is most often confused with other paraparetic disorders is generalised myasthenia gravis (MG). MG may manifest as an episodic weakness with only pelvic limb involvement. Affected animals can show a shortened stride that progresses to collapse. Strength returns with rest. Fatigability is noted upon repetitive reflex evaluations, i.e., patellar and blink reflexes. A provisional diagnosis can be made by administering intra venous edrophonium chloride (Tensilon test). Electrodiagnostic testing using repetitive nerve stimulation and single-fibre electromyography can further document fatigability. The gold standard test is considered a radioimmunoassay for acetylcholine receptor antibodies. Joan R. Coates , BS, DVM, MS, DACVIM(Neurology) Department of Veterinary Medicine, College of Veterinary Medicine University of Missouri Columbia, MO , USA

Imaging the Head: Seeing What's on the Inside British Small Animal Veterinary Congress 2011 Lorrie Gaschen, DVM, PhD, DrMedVet, DECVDI Veterinary Clinical Sciences, Baton Rouge, LA, USA
21493924

Introduction Small animal patients with disease localised to the brain or nasal cavity only have radiographs performed as a screening method when trauma has occurred or skull deformation is present. In all other instances cross-sectional imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) are the modalities of choice. MRI is the modality of choice for brain imaging as it allows the best resolution of brain structures for the most accurate localisation of lesions. MRI pulse sequences allow anatomical details and signal intensities of different tissue types in the brain to be identified. Grey and white matter can be distinguished, which is not possible in CT. The brain parenchyma and ventricular system can be differentiated from one another due to differences in soft tissue and fluid X-ray attenuation in CT. If a lesion does not create a mass effect, and does not enhance when intravenous iodinated contrast medium is given, it will usually go undetected on CT images. Furthermore, the anatomy of the caudal fossa region (cerebellum, brainstem) is extremely difficult to visualise in CT due to beam hardening artefacts in that region. Nasal disease is another important indication for imaging the skull. Survey radiography is a screening method when skull deformation is present or to identify other bony defects due to the presence of aggressive fungal or neoplastic disease of the nasal cavity. CT and MRI provide a much better assessment of nasal cavity disease than radiography and are the modalities of choice. With the widespread availability of CT and MRI, skull radiography for nasal disease is being performed less and less. Congenital Diseases Hydrocephalus, lissencephaly, agenesis of various structures, meningoceles and Rathke cleft cysts have all been reported, with hydrocephalus being by far the most common. Arachnoid cysts and quadrigeminal cysts are not uncommon. MRI is the method of choice for detecting most congenital defects. Ultrasonography can be used to detect hydrocephalus in puppies and kittens and is an inexpensive and non-invasive modality that does not require sedation or anaesthesia. The bregmatic fontanelle and foramen magnum windows can be used to examine the brain. Transverse and sagittal planes of the brain can be examined for the presence of a dilated ventricular system. The lateral ventricles can be seen in most patients and the third and fourth ventricles as well as the mesencephalic aqueduct in some. A curved array, 7.512 MHz probe is adequate. If lateral ventricular height of the dorsal horn at the interthalamic adhesion exceeds 0.35 cm or if the ratio between the height of the lateral ventricle and the width of the cerebral

hemisphere (ventricle/ hemisphere ratio) exceeds 0.19, the ventricles are considered enlarged. However, there is a poor correlation between clinical signs and ventricular size. Quadrigeminal cysts can also be detected at the foramen magnum with ultrasonography. CT and MRI provide a more thorough approach to identifying the causes of hydrocephalus. CT and MRI enable accurate assessment of ventricular size, extent of cortical atrophy and the presence of any focal lesions that may account for an obstructive cause of the hydrocephalus. Using MRI, ventricular enlargement secondary to loss of brain parenchyma (hydrocephalus ex vacuo) can be distinguished from obstructive hydrocephalus based on enlarged cortical sulci and subarachnoid space. Chiari-like malformations in dogs result in compression of the cerebellum and brainstem and cervical spinal cord malformation such as syringohydromyelia. Cavalier King Charles Spaniels are most commonly affected but it can occur in other small-breed dogs as well. The condition is characterised by crowding of the caudal fossa, resulting in attenuation of the subarachnoid space surrounding the cerebellum, compression and, in severe cases, herniation of the cerebellum into or through the foramen magnum. Because of the inherent disadvantages of CT for showing details in this region of the skull, MRI is the method of choice for diagnosing this disease. Cerebellar hypoplasia is another type of congenital defect in both cats and dogs that is best seen with MRI. The cerebellum appears small with increased amounts of CSF surrounding it. Acquired Brain Diseases Inflammatory brain diseases are very common in veterinary medicine and are mainly reported in dogs. Infectious causes such as canine distemper virus and feline infectious peritonitis are common. MRI is required to identify the signal intensity changes associated with infection, which appear as T2 hyperintensities of the cerebellum and brainstem. The cerebrum may also be affected. Contrast enhancement of the meninges may also occur and is a sign of meningitis. Bacterial infections can spread into the brain via a haematogenous route, through intracranial extension of extracranial disease (otogenic infections) and foreign body migration. Both CT and MRI can be used to identify these changes, with MRI being the modality of choice. One of the difficulties of cross-sectional imaging is the overlap in the appearance of abscesses, granulomas and tumours of the brain. Infectious lesions, such as cryptococcosis, can be solitary or multifocal. Toxoplasmosis and neosporosis are protozoal infections which are often multifocal. In cats, toxoplasmosis is multifocal and contrast-enhancing in MRI. MRI shows the distribution of the lesions best; all lesions have varying degrees of MRI and CT contrast enhancement. Non-infectious inflammation can also occur. CT can show zones of decreased attenuation (hypodense regions) in the brain, generally the cerebellum, that can cause mass effect. The oedema associated with the inflammation creates this appearance. The most common noninfectious inflammatory neurological disease is granulomatous meningoencephalitis (GME) and it commonly affects the brainstem in middle-aged small-breed dogs; it is best identified with

MRI. It demonstrates none to intense contrast enhancement and is hyperintense on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images and either isointense or hypointense on T1. Another type of inflammation, necrotising meningoencephalitis (NME), is also of unknown aetiology and affects similar dogs to GME. Its appearance is similar to that of GME but it affects the cerebrum more frequently. Specific forms have been described in Pugs and Yorkshire Terriers. Meningoencephalitis can be identified with MRI in some instances. Lesions tend to be localised to the meninges where contrast enhancement can be detected. Enhancement of the cerebrum and cerebellum is also possible. The intracranial vasculature can also be observed with CT and MRI. In CT, intravenous contrast is necessary. In MRI, the vasculature can be assessed with both contrast and non-contrastenhanced magnetic resonance angiography. Aneurysms require angiography to be identified. Cerebrovascular malformations are uncommon as are aneurysms. They can lead to haemorrhage that can be detected with both CT and MRI. However, the underlying malformation requires angiography to make a diagnosis. Infarcts can occur in dogs due to hypothyroidism, hypertension, chronic renal disease, neoplasia, sepsis, fibrocartilaginous infarcts and coagulopathies and protein-losing nephropathy or enteropathy. MRI is required to identify infarcts, and special sequences such as diffusionweighted imaging may be required and can show changes immediately. Haemorrhage appears differently over time on both CT and MRI. Acute haemorrhage is hyperdense on CT. On MRI, signal changes vary from hyperintense to hypo-intense on T1- and T2-weighted images during different stages of haemorrhage and resolution. Intracranial mass lesions are first categorised as to their intra-axial, extra-axial or ventricular locations, then whether they are focal, multifocal or diffuse. Not all masses are tumours. Haematomas and granulomas appear similar to neoplasms. Tumours can be classified according to their location. Meningiomas are extra-axial tumours, typically broad based with meningeal enhancement (dural tail sign) and have expansile growth into the cranium, causing a mass effect and perilesional oedema. They can be seen with both CT and MRI in most cases due to their contrast enhancement. Glial tumours are intra-axial masses that have a variable MRI appearance and variable contrast enhancement. Choroid plexus tumours are ventricular tumours, typically in the third or fourth ventricles and are contrast-enhancing. Lymphoma and histiocytic sarcoma appear as either intra-axial or extra-axial masses hypointense on T1- and hyperintense on T2-weighted MRI images and exhibit contrast enhancement. Because of their variable appearance, they may mimic other tumour types. Pituitary tumours can also be identified on cross-sectional imaging studies. Microadenomas are difficult to see on both CT and MRI studies. Macroadenomas can be identified on both CT and MRI and have a specific location at the sella turcica, expand dorsally and are intensely contrastenhancing. Their anatomical location makes the diagnosis in most cases.

Diseases of the cranial nerves can also be identified mainly on MRI studies. Trigeminal nerve sheath tumours are among the most common. Nasal Cavity Disease Nasal tumours, such as adenocarcinoma, fibrosarcoma, chondrosarcoma, squamous cell carcinoma and lymphoma, affect the nasal cavity and can destroy turbinate bones and invade the brain at the level of the cribriform plate. In endemic areas, fungal agents can lead to similar damage. Both CT and MRI are adequate for diagnosis of aggressive lesions of the nasal cavity. However, rhinitis and inflammation have minimal imaging changes. Biopsy of the nasal cavity is indicated in all cases for a definitive diagnosis.

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Lorrie Gaschen , DVM, PhD, DrMedVet, DECVDI Veterinary Clinical Sciences Baton Rouge, LA, USA

How I Treat...Back Pain in Chondrodystrophic Dogs

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2009
Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN College of Veterinary Medicine, University of Georgia
19506695

Hansen first classified intervertebral disc disease (IVDD) as type I and type II. Hansen type I IVDD is herniation of the nucleus pulposus through the annular fibers and extrusion of nuclear material into the spinal canal. Hansen type I IVDD is commonly associated with chondroid disc degeneration. The disc commonly extrudes through the dorsal annulus, causing dorsal, dorsolateral, or circumferential compression of the spinal cord. Chronic disc extrusion is characterised by extradural fibrous adhesions whilst acute disc extrusion is characterised by extradural haemorrhage and soft disc material. Hansen type I IVDD typically affects small, young, chondrodystrophic dogs and has an acute onset but it can occur in large nonchondrodystrophic dogs, often also having an acute onset. Neurologic dysfunction is a secondary consequence of IVDD. Extrusion of the nucleus causes primary cord injury and associated clinical neurologic signs by concussion and later by compression. Acute and severe disc extrusions cause pannecrosis of the gray and white matter. Sequential haemorrhage, oedema, and neuronal necrosis depend on the severity and type of injury. The treatment for this disc extrusion is often determined by multiple factors including; neurologic status of the dog, delay in presentation for veterinary attention, concurrent medical treatment, concurrent vertebral instability, previous episodes of spinal pain, method of diagnosis of the extrusion, lesion localisation and economics. This means that criteria for such treatment need to remain 'fluid' and therefore specific treatments may differ in similar patient circumstances. The method of diagnosis of IVDD is considered to be an important factor in decision-making. Although myelography is well described in the veterinary literature, common problems encountered such as poor distribution of contrast medium, the presence of spinal cord swelling and neurologic deterioration have led to the belief that it is not the technique of choice in the human field. Computed tomography (CT) can be an adjunctive procedure to myelography to further delineate the extent of a compressive lesion or as a sole technique for detecting IVDD. CT myelography may provide a diagnostic image when there is obstruction of contrast medium flow. CT or magnetic resonance imaging (MRI) are extremely useful for diagnosing foraminal or lateral disc extrusions, as well as the extent of associated extradural and subarachnoid haemorrhage. MR imaging is the best available method for early recognition of disc degeneration in dogs. MR imaging is especially useful as a sensitive, accurate, and non-invasive method for evaluating the caudal lumbar spine and lumbosacral space in dogs. Cerebrospinal fluid analysis should always be performed to rule-out concurrent inflammatory disease. This will be more important with protrusions where the clinical signs may be more chronic progressive in nature and difficult to differentiate from other diseases.

THORACOLUMBAR IVDD
Hansen type I most commonly occur within the thoracolumbar region of chondrodystrophoid breeds. The most common site for Hansen type I IVDD in large nonchondrodystrophic breeds is the interspace between L1 and L2. Functional grading schemes describing hyperesthesia and motor and sensory dysfunction have been used to provide a mechanism for determining treatment for thoracolumbar IVD extrusions. However, the degree of neurologic dysfunction is variable with similar degrees of extrusion and so usually can only be used to assess prognosis rather than treatment options. Advanced imaging studies are again essential. Myelography may provide up to 75% accuracy in the determination of affected space and lateralization of the disc, especially when combined with neurological examination and history. However, CT has been shown to be at least 90% accurate at site localisation and 96% accurate with prediction of lateralization. Similar studies are lacking at present with respect to the MRI in veterinary patients, but my own experience is that this modality offers similar results in terms of localisation accuracy. My indications for non-surgical treatment of this condition are limited to a first-time episode of spinal pain only or financial constraints of the owner. Conservative therapy consists of strict cage rest

for 4-6 weeks, pain relief and/or muscle relaxant use (diazepam). My indications for surgical management of thoracolumbar IVD extrusion are therefore cases with spinal pain only that are nonresponsive to conservative therapy, recurrent disease, cases with neurologic deficits with deep pain, and cases with loss of deep pain perception for less than 72 hours; although I have infrequently had positive experiences with cases that have lost deep pain perception for up-to 7 days duration. The method of choice for surgical decompression is often determined by the imaging study and lesion localisation. With T10-L4 extrusions, I will most often perform a hemilaminectomy at the site of extrusion and extend the defect in the bone cranially and caudally up to a maximum of five intervertebral spaces if necessary until normal epidural fat is identified. For extrusions caudal to L4, I will often perform a dorsal laminectomy and try to combine this with a hemilaminectomy after nerve root visualisation is possible. If there is no deep pain perception present I will perform a durotomy to visualise the spinal cord parenchyma and asses prognosis. I will routinely fenestrate disc spaces T11L3 after decompressive surgery in chondrodystrophoid dogs. Methylprednisolone sodium succinate (MPSS) remains the standard of care in humans. MPSS has been shown to be effective because of its free radical scavenging properties rather than its antiinflammatory effect. In order to obtain this effect, it must be used at high doses and treatment should be initiated within 8 hours of injury. Suggested protocols include initiation of treatment with MPSS within three hours of injury at a dose rate of 30mg/kg given intravenously and followed with either a constant rate infusion of 5.4mg/kg/hr for 24 hours, or second and third boluses of 15mg/kg at two and six hours after the first dose and then a constant rate infusion of 2.5mg/kg/hour for 24 hours. If treatment is initiated between 3 and 8 hours after injury, the recommendation is to continue treatment for 48 hours rather than 24 hours. Delaying initiation of treatment for more than 8 hours has a detrimental effect on outcome in people. As MPSS has both glucocorticoid and free radical scavenging effects, it is postulated that delaying treatment until after the majority of free radical induced damage has occurred is more likely to result in glucocorticoid side-effects. Indeed, although there continues to be wide spread use of glucocorticoids, such as dexamethasone, to treat acute spinal cord injuries in veterinary practice, there is no good evidence that such drugs are beneficial and the side effects have been well documented and at this time they cannot be recommended as efficacious treatments. Recently, substances that fuse membranes ("fusogens") have been proposed as a treatment for acute spinal cord injury. Polyethylene glycol (PEG) is a hydrophilic polymer that targets damaged membranes following intravenous administration and seals membranes preventing intracellular leak of ions and subsequent axonal disruption, restoring axonal conduction. In an experimental model of spinal cord injury in guinea pigs, there was rapid improvement of electrophysiological parameters and of the cutaneous trunci reflex following treatment with PEG. No adverse effects were reported in a phase I trial of PEG completed in dogs with paralysis and loss of pain sensation due to acute disc herniations; 60% of the dogs did recover function but this preliminary study was not blinded and included a historical control group.

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Simon R. Platt , BVM&S, MRCVS, DACVIM (Neurology), DECVN College of Veterinary Medicine University of Georgia

Rolling, Leaning and Falling--Canine Vestibular Dysfunction

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2009
Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN College of Veterinary Medicine, University of Georgia
19506735

INTRODUCTION
The onset of a head tilt is a cardinal sign of vestibular disease. It is the most consistent sign of unilateral vestibular dysfunction, which occurs as a result of the loss of anti-gravity muscle tone on one side of the neck. Bilateral vestibular disease may also cause a head tilt if the disease process is not symmetrical but usually does not cause such a sign. The vestibular system has two functional components; the peripheral component is located in the inner ear and the central component is located in the brain stem and cerebellum. Unfortunately, a head tilt is not specific for a brainstem or a peripheral vestibular system lesion localisation, nor does it indicate a specific aetiology. Generally, central vestibular disease is associated with different aetiologies and a worse prognosis than peripheral vestibular disease. Therefore, it is essential to approach these cases aiming to primarily further localise the neurological lesion. Clinical signs due to disease of the peripheral vestibular system: Head tilt, circling, falling or rolling toward the side of the lesion If nystagmus is present it is horizontal or rotatory with the fast phase away from the side of the lesion May have concurrent facial nerve paralysis (CN VII) and Horner's syndrome (ptosis, miosis and enophthalmos) with middle and inner ear lesions Clinical signs due to disease of the central vestibular system: Head tilt, circling, falling, or rolling toward or away from the side of the lesion Conscious proprioceptive deficits, hemiparesis or hemiplegia on the side of the lesion if unilateral or worse on one side if bilateral Nystagmus may be horizontal, rotatory or vertical if present May be depressed or stuporous May have facial paralysis (CN VII) but Horner's syndrome is rare

CAUSES OF PERIPHERAL VESTIBULAR DISEASE

Idiopathic vestibular syndrome is a common cause of peripheral vestibular disease in the dog. The onset of the vestibular disease may be so acute that is accompanied by vomiting, but this is not specific for this aetiology. Postural reactions are normal in this disease, and there is no facial paresis or Horner's syndrome. This can be only by diagnosed by ruling out the other causes; however, it is the only differential of peripheral disease that will start to improve in 72 hours with no specific treatment. If the patient is closely monitored over this time course, marked resolution of the nystagmus can be seen. This will be followed by improved gait over a 7-day period and improvement of the head tilt over a 2-month period. The head tilt may never completely resolve. If there is evidence of facial nerve involvement or Horner's syndrome further ancillary tests should be considered. Otitis media-interna. Up-to 50% of cases of peripheral vestibular disease are due to otitis mediainterna. Infection of the middle ear can cause vestibular disease due to the production and spread of bacterial toxins into the inner ear. The infection can directly damage the inner ear with spread to the labyrinth. The bacteria commonly responsible for this disease are Staphylococcus spp., Streptococcus spp., E. coli and Pseudomonas spp. If the culture results are negative but bacterial otitis interna is suspected, then oral enrofloxacin 5 mg/kg every 12 hours for dogs or a combination of oral trimethoprim sulfadiazine (TMP-SDZ) 15-30 mg/kg orally every 12 hours and oral cephalexin 22 mg/kg every 8 hours may be administered. Antibiotic therapy should be continued for 6-8 weeks. Tear production should be monitored to detect sicca associated with facial nerve (CN 7)

involvement or antibiotic therapy and artificial tears administered if necessary to prevent keratitis and corneal ulceration. Aminoglycosides are contraindicated in otitis interna/media. In cases of concurrent otitis externa and media with a ruptured tympanic membrane, the external and middle ears are gently flushed with saline or a 2.5% acetic acid solution and caustic ear cleaning substances are avoided if possible. Diluted ear cleaning solutions may be necessary in some cases for debris that cannot be cleared by other means, but thorough rinsing is essential so residual cleaning solution does not irritate the vestibular labyrinth. Topical treatment of the external ear canal with small amounts of low residue non-irritating antibiotic solutions for a few days may be given but the accumulation of greasy ointments in the middle ear should be avoided. The vestibular signs may resolve in 1-2 weeks but if antibiotics are prematurely discontinued, the clinical signs and infection recur and can be more difficult to treat. Corticosteroids are usually not required and are avoided if osteomyelitis is present. In acute cases oral prednisone 0.25 mg/kg once daily for 1-3 days is sometimes given to reduce inflammation and swelling of the vestibular labyrinth. In animals with recurring otitis, underlying dermatologic problems such as atopy or hypothyroidism should be investigated and treated. Ear hygiene should be monitored but care should be taken when cleaning the external ear canals. Surgical intervention: External ear canal ablation and bulla osteotomy in refractory cases. Nasopharyngeal polyps. Polyps are pedunculated masses, which arise from the lining of the tympanic cavity, eustachian tube, or nasopharynx. Non-septic otitis media/interna may occur secondary to occlusion of the eustachian tube due to a nasopharyngeal polyp and polyps may occur as a result of chronic middle ear infection or from ascending infection from the nasopharynx. Diagnosis may require advanced imaging if physical examination and skull radiographs are not helpful. Neoplasia. Neoplasia of the structures of the ear includes squamous cell carcinoma, ceruminous gland adenocarcinoma and lymphoma. Ototoxicity. There are many drugs listed as being ototoxic and can potentially cause both vestibular dysfunction and deafness. The deafness caused by such drugs is often permanent whereas the vestibular disease may resolve or at least the dog may compensate for the abnormality. The most common topical drug implicated in this scenario is chlorhexidine. Trauma. Head trauma may cause the onset of vestibular disease, which may be peripheral or central depending upon the severity of the trauma. Middle ear haemorrhage subsequent to a trauma may cause peripheral vestibular disease seen with or without facial paresis and Horner's syndrome. Congenital disease. Peripheral vestibular disease may be evident in young animals and attributed to a congenital malformation or degeneration of the inner ear structures. If the abnormality is bilateral, these animals may not have a head tilt or nystagmus; however, they will frequently have a symmetrical ataxia, a wide-based stance, and a side-to-side movement of the head in the horizontal plane. They may also be deaf. Numerous breeds have been associated with congenital vestibular disease (German shepherd, Doberman, English Cocker, Beagle, Siamese, Burmese, Tonkinese). Clinical signs usually begin around 3-4 weeks of age (when the animal begins to ambulate) and may consist of a head tilt, nystagmus, strabismus, ataxia, circling, falling, rolling, and abnormal head movements. Many learn to compensate by 2-4 months of age but some will remain permanently affected. Recurrence can occur. With bilateral disease, there is usually no abnormal nystagmus and normal nystagmus cannot be elicited.

CAUSES OF CENTRAL VESTIBULAR DISEASE

Inflammatory disease. The common infectious diseases responsible for inflammation of the brain and its structures are canine distemper, Toxoplasma, bacteria and Cryptococcus. Whilst all the above infections can cause vestibular disease, they often have a multifocal central nervous system distribution and may also cause profound systemic abnormalities. The prognosis for each patient not only depends on the infectious etiology but also on the severity of the presenting signs, neurological as well as systemic. There are several inflammatory diseases of unknown aetiology and presumed immune-mediated. These include granulomatous meningoencephalomyelitis (GME) and necrotizing meningoencephalitis and can both affect the central vestibular system as part of a multifocal disease.

Neoplasia. The most common tumours to cause central vestibular disease in cats are meningiomas and lymphomas located at the cerebello-medullary pontine angle. Tumors of the forebrain can also cause central vestibular disease due to caudal transtentorial herniation with secondary compression of the brain stem. Metronidazole toxicity. Dosages greater than 30mg/kg/day can result in vestibular disease. The onset is acute and usually occurs when animals receive high doses for a long duration (e.g., after being on high doses for 7 to 12 days). Dose reductions need to be made in patients with liver and kidney disease as the drug is metabolized and excreted by these organs, respectively. Clinical signs may include generalized ataxia, nystagmus, anorexia, and vomiting. In severe cases, altered mental status, seizures, and opisthotonus may be present. Removal of the drug and supportive care (IV fluid diuresis) usually results in quick recovery. Occasionally, deficits are permanent. Cerebrovascular disease. Cerebrovascular disease (CVD) may cause a peracute onset of central vestibular signs. Ischemia may be embolic or thrombotic and is the most common form of CVD; its causes may be due to sepsis, neoplasia, endocrine disease, hypertension or may commonly be idiopathic. In some areas of the country this can result from aberrant parasite migration through the nervous system. Non-traumatic hemorrhage, the other form of CVD, is bleeding into the parenchyma of the brain that may extend into the ventricles. Recovery from this disorder can be complete but can depend on the underlying disorder.

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Simon R. Platt , BVM&S, MRCVS, DACVIM (Neurology), DECVN College of Veterinary Medicine University of Georgia

Update on Spinal Surgery II--Thoracolumbar Spine

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2004
Simon J. Wheeler, BVSc, PhD, DECVN, Dipl Mgmt, FRCVS (Veterinary Neurology) Hertfordshire, UK
18281006

In this lecture, advances in the treatment of thoraco-lumbar and lumbar spinal conditions will be covered. Particular emphasis will be on the conditions seen most often in general practicethoracolumbar disc herniations and lumbo-sacral conditions. More information can be found in Small Animal Spinal Disorders, 2nd edition, by NJH Sharp & SJ Wheeler, Elsevier, London. Available from www.veterinary-neurology.com.

THORACOLUMBAR DISC DISEASE

Thoracolumbar disc disease is a common disorder in dogs that affects mainly chondrodystrophoid breeds. Peak incidence in these breeds is between three and six years of age. Over 50% of lesions occur at the T1/13 and T13/L1 discs and more than 85% occur between T11/12 and L2/3 inclusive. Non-chondrodystrophoid breeds are affected less frequently, usually after middle age. Back pain and neurological deficits in the pelvic limbs are features of thoracolumbar disc disease; urinary dysfunction may occur with more severe lesions. Neurological deficits range from mild ataxia and paraparesis to paraplegia, which may be accompanied by depressed or absent deep pain sensation caudal to the lesion. There is often an associated panniculus reflex cut-off. Approximately 10-15 per cent of dogs show LMN deficits because of lesions between L3/4 and L6/7 discs. Survey radiographs may indicate if disc disease is present but are only 60-70% accurate in identifying the exact location. CSF should be collected from all dogs prior to myelography. Either myelography or advanced imaging should be performed for definitive diagnosis. A lumbar injection is preferred for myelography because there is often considerable spinal cord swelling, which tends to cause cervical myelograms to stop cranial to the lesion. Lateral and ventrodorsal images should be taken. If it is unclear on which side the disc material is located, oblique views or a CT myelogram should be used. CT adds accuracy and speed to the evaluation of chondrodystrophoid breeds with disc herniations. CT is non-invasive as the mineralised disc material shows clearly without the need for contrast even when it is not visible on survey radiographs. It is also usually much easier to decide what side(s) the disc material is on from CT or MRI. The increased sensitivity of CT and MRI reveal some disc herniations that are only incidental findings and that are not responsible for causing clinical signs (Figure 1).

Figure 1.

A: CT scan performed prior to myelography, shows a centrally located, mineralised mass that occupies much of the vertebral canal (arrows). B: Sagittal T2-weighted MRI through the lumbar region of an 11-year-old paraparetic Labrador with disc herniations at T12/13 to L3/4; the L2/3 and L3/4 sites are shown here.

Many dogs will recover from moderate neurological deficits following either nonsurgical or surgical treatment. Patients with marked deficits seen within eight hours of spinal cord injury may benefit from concomitant methylprednisolone sodium succinate (MPSS) therapy. Strict cage rest is the overriding principle in non-surgical therapy although judicious use of analgesics or anti-inflammatory drugs may also be needed. These drugs should be withheld when feasible in order to encourage the animal to rest. The animal must rest quietly in a confined space (traveling cage size) for at least two weeks, during which time it should only be removed to urinate and defecate. A satisfactory response should be followed by a further two weeks rest and a gradual increase in activity between the fifth and eighth weeks. This is the minimum time needed for an avascular structure like the anulus fibrosus to repair. Activities like jumping should be avoided for four to six months. Animals that will not rest or are confined inadequately may fail to respond or get worse. The patient must be evaluated regularly for any deterioration, which indicates treatment failure, as does a lack of improvement within two weeks. Although a useful initial option for some dogs with grade 1 or 2 lesions, non-surgical therapy is rarely the treatment of choice for dogs with grade 3 lesions or worse, especially if there are no financial constraints. The major long-term problem is that over one-third of dogs will suffer recurrence. Another disadvantage is that the dog can deteriorate during treatment, possibly as far as grade 5, often due to poor owner compliance. A short course of corticosteroids without cage rest does not constitute effective nonsurgical treatment. A high proportion of dogs referred for emergency decompression have been treated in the preceding days or weeks using corticosteroids without cage confinement. Such treatment can relieve discomfort with a consequent increase in activity. Although decompression is the surgical treatment of choice for disc disease it does demand good quality imaging. Imaging usually identifies the affected interspace but determining which side to decompress can be more problematic. Good surgical technique is needed to retrieve as much disc material as possible once the spinal cord has been exposed. Any material on the contralateral side must be removed by probing over or under the spinal cord or bilateral decompression may be needed. Decompression by hemilaminectomy is the treatment of choice for dogs with spinal cord compression causing persistent or recurrent grade 1 signs and for most with neurological deficits. The rate of recovery is faster after decompression than after either non-surgical treatment or fenestration and there is less likelihood of residual neurological deficits. Corticosteroids provide no overall benefit when used with decompressive surgery, except possibly MPSS for dogs that present within the first eight hours of injury Concomitant fenestration should be performed at the time of the decompression. Minihemilaminectomy removes less bone than a standard hemilaminectomy but only gives good access to the ventral portion of the vertebral canal. Pediculectomy also preserves the facet joint and removes less bone than a standard hemilaminectomy. The prognosis is very good for dogs with grade one, two, and three deficits, especially following decompression. Decompression is clearly the treatment of choice for dogs with grade five lesions, with between 60-70% recovering in most studies. Most dogs that recover regain deep pain do so within two weeks.

LUMBOSACRAL DISEASE
The clinical signs seen with lumbosacral lesions differ from those seen at other locations of the spine, mainly because of the unique anatomical structure of the region. The vertebral canal in this region contains only cauda equina. The spinal cord ends within L6 vertebra in most dogs; in L7 in cats and some small dogs. Motion in the normal lumbar spine is greatest at the lumbosacral joint. In some dogs, abnormal motion probably leads to degenerative changes such as spondylosis deformans, osteophyte proliferation and soft tissue overgrowth of the joint capsules. These degenerative changes then appear to reduce the overall range of motion. Clinical problems can arise due to compression of neural structures in the vertebral canal and intervertebral foraminae.

A number of abnormalities may combine to cause compression of the cauda equina or L7 nerve roots. These include: Stenosis (multilevel) of the vertebral canal. Hansen Type II disc herniation at the L7/S1 intervertebral space. Subluxation, osteophytosis or thickening of the articular processes. Epidural fibrosis. Soft tissue proliferation, usually of the joint capsule or ligamentous structures. Vascular compromise of the spinal nerves. Osteochondrosis of the sacrum. Instability and malalignment between L7 and S1. The role of instability is unclear and it is difficult to quantify regardless of the imaging technique. This can pose a problem for surgical decision-making. Lumbosacral lesions can cause pelvic limb gait abnormalities, lameness, or LMN neurological deficits. Pain is common but the signs vary depending on the nature and severity of the neurological impairment. There may be pain with no deficits; mild paresis with conscious proprioceptive deficits; or paraparesis, tail paralysis, and incontinence. Lameness in performance animals may be exacerbated by work. Incontinence results from pelvic and pudendal nerve dysfunction. Urinary incontinence is usually LMN in nature with dribbling of urine and a bladder that is easily expressed by manual pressure. Dogs with chronic degenerative lumbosacral lesions may present with non-specific clinical signs, but low back pain is quite different from that seen in thoracolumbar lesions. Diagnosis of lumbosacral disease depends on recognising the historical features and clinical signs and on a careful physical examination, which should pinpoint the source of pain. It is advisable that the patient be anaesthetised or sedated heavily when radio-graphing the lumbosacral joint. Rotation of the spine and pelvis must be avoided. The main role of survey radiographs is to rule out neoplasia, trauma and discospondylitis. Many clinically normal dogs have radiographic abnormalities of the lumbosacral junction. Conversely, occasional dogs with lumbosacral disease will have normal survey radiographs. Neurological localisation of a patient will indicate a lesion of L4-S3 spinal cord segments. It may be possible to define the location more accurately, for example by the patellar reflex. Consideration of the diagnostic imaging of these patients frequently focuses on the LS joint alone. This policy runs the serious risk of missing lesions elsewhere in the vertebral column that are involving the L4-S3 cord segments or ascribing significance to incidental lesions of the LS joint. Myelography can therefore be useful to assess the low lumbar region and the rest of the spinal cord. Cervical injection is preferred, as it avoids the potential for epidural contrast leakage in the area of interest. Dorsal elevation or attenuation of the column may be seen. CT is particularly useful as it shows the vertebral canal, lateral recesses, intervertebral foramen and articular processes in cross-sectional images (Figure 2)

Figure 2.

Marked foraminal compression is evident on A: Transverse CT scan and B: 3D reconstruction. Same dog as in 10.6C.

MRI provides better soft tissue resolution than CT as well as an ability to acquire images in multiple planes without image degradation, earlier detection of disc degeneration and evaluation of the entire lumbar spine in a single sagittal examination. Transverse images provide the best visualisation of disc or foraminal anatomy. One potential disadvantage of MRI is over-diagnosis, even by expert neuroradiologists (Figure 3).
Click on the image to see a larger view.

Figure3.

T2-weighted MRI of the lumbosacral spine of a seven-year-old Labrador with lumbosacral pain. A: Image made with the spine in flexion. There is loss of signal in the lumbosacral disc but minimal compression of the cauda equina (arrowhead). B: Image from the same dog made with the spine in extension. There is severe compression at L7/S1 caused by both disc and ligamentum flavum (arrowhead).

Most dogs are treated initially with rest and anti-inflammatory medication. This may be successful if pain is the main clinical sign. Surgical treatment is indicated when nonsurgical treatment has failed, in working dogs and those with marked pain or neurological deficits. Further indications for surgery include CT or MR findings of increased soft tissue suggestive of epidural fibrosis, especially if it enhances with contrast. The choice of surgical procedure is then between dorsal laminectomy, distraction and fusion, or a combination of the two. Definitive criteria for these procedures are lacking. Decompression of the cauda equina and spinal nerves can be achieved by dorsal laminectomy, which can be combined with foraminal decompression or even facetectomy. The anulus fibrosus should be excised once the cauda equina is retracted laterally when there is marked bulging of the disc. Routine fenestration may also be warranted. Redundant joint capsule can also be removed. Laminectomy often provides rapid relief of pain with improvement of mild gait abnormalities and minor neurological deficits; it does not address instability if this is a contributing factor. Decompression by laminectomy can be combined with fixation and fusion. There are a number of similarities between lumbosacral disease and caudal cervical spondylomyelopathy. A rationale can therefore be made for lumbosacral distraction and stabilisation. The principle is the same, namely to open the vertebral canal and intervertebral foramen, relieve pressure on neural tissues, and prevent abnormal motion. Distraction of the dorsal aspect of L7 and S1 is achieved using screws placed through the articular processes of L7/S1 and into the body of the sacrum. Fusion is promoted by removing the articular cartilage from the facet joints and by a cancellous bone graft. This can be combined with dorsal laminectomy, especially for dogs with marked neurological deficits, severe pain, or a large disc herniation.
Simon J. Wheeler, BVSc, PhD, DECVN, Dipl Mgmt, FRCVS (Veterinary Neu Hertfordshire, U

Vestibular Diseases in the Dog and Cat: Old and New Diagnostic Methods British Small Animal Veterinary Congress 2006 C.H. Vite, DVM, PhD Ryan Veterinary Hospital, School of Veterinary Medicine, University of Pennsylvania USA
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The vestibular system is responsible for maintaining an animal's balance and normal orientation relative to the earth's gravitational field. This system maintains the position of the eyes, trunk and limbs in reference to the position of the head. Anatomy The vestibular apparatus is contained within the petrosal portion of the temporal bone (in what is also known as the inner ear). It comprises a membranous and bony labyrinth. The bony labyrinth consists of three communicating fluid-filled portions: the vestibule, the semicircular canals and the cochlea. These fluid-filled regions contain perilymph, a fluid with ionic composition similar to cerebrospinal fluid. Perilymph is secreted by arterioles of the periosteum surrounding the labyrinth and drains into the subarachnoid space through the perilymphatic duct. The Path of the Vestibular Neurons The vestibular neurons travel with the vestibulocochlear nerve. They enter the skull through the internal acoustic meatus. The vestibular neurons then enter the medulla between the caudal cerebellar peduncle and the spinal tract of the trigeminal nerve and terminate in the vestibular nuclei. A few neurons terminate in the fastigial nucleus and the flocculonodular lobes of the cerebellum. The Vestibular Nuclei There are four vestibular nuclei (rostral, medial, lateral and caudal) which are in the lateral wall of the fourth ventricle. The vestibular nuclei receive afferents from the vestibulocochlear nerve and from the fastigial nucleus of the cerebellum. Efferent Fibres Fibres from the lateral vestibular nucleus descend in the ipsilateral ventral funiculus and synapse on interneurons in the ventral grey column forming the vestibulospinal tract. These interneurons are facilitatory to ipsilateral extensor muscles. They are inhibitory to ipsilateral flexor muscles and to contralateral extensor muscles. Fibres from the medial vestibular nucleus descend in the dorsal portion of the ventral funiculus through the cervical and craniothoracic spinal cord segments, forming the medial longitudinal fasciculus (MLF). The MLF controls the position of the limbs and trunk with respect to the position of the head.

Fibres of the MLF also project rostrally to cranial nerves III, IV and VI. The MLF controls eye position with respect to the position of the head. Cerebellar Involvement The caudal cerebellar peduncle is the pathway for afferent vestibular neurons projecting to the cerebellum. Acute Vestibular or Cerebellar Signs Regardless of whether the lesion is located centrally or peripherally, the following signs characterise vestibular system dysfunction: Loss of balance Vestibular ataxia characterised by regularly falling toward the side of the lesion Abnormal posture characterised by leaning, turning of the head, neck and body, and/or rolling toward the side of the lesion Head tilted toward the side of the lesion. (A head tilt exists when an imagined horizontal line running through both ears is tilted from the horizontal plane) Ventral strabismus of the eye on the side of the lesion. The strabismus may not be noted until the head is elevated or returned to the horizontal plane Abnormal nystagmus with the slow phase directed toward the side of the lesion There are normal and pathological causes of nystagmus. Physiological nystagmus is nonpathological and is associated with movement of the head. It has a fast and a slow phase, with the fast phase being in the direction of head motion. The labyrinth initiates the slow phase, and the fast phase is elicited by the brain stem. Abnormal nystagmus is associated with pathology. It may be seen when the head is not moving (spontaneous or resting nystagmus) or it may be induced by moving the head into different positions (induced nystagmus). Abnormal nystagmus is associated with disease of the vestibular system. Post-rotatory nystagmus occurs after rotating the head. The fast phase of the nystagmus is in the opposite direction of the direction in which the head was moved. If peripheral vestibular disease is present, post-rotatory nystagmus is depressed when the patient has been rotated away from the side of the lesion. In cases where vestibular system involvement is present but signs are mild, ataxia may be accentuated by blindfolding the animal; ataxia and head tilt may be accentuated by lifting the animal off the ground; and nystagmus may be accentuated by placing the animal on its back.

A common mistake is to attribute compulsive circling to disease of the vestibular system. With compulsive circling there is no ataxia, no loss of balance and no abnormal nystagmus. Compulsive circling is associated with disease of the cerebral hemispheres and diencephalon. Localising Signs of Vestibular System Dysfunction to the Peripheral or Central Portions of the Vestibular System Vestibular system dysfunction may result from disease of the inner ear, medulla or cerebellum. The presence of neurological deficits in addition to the ones listed above helps to determine where the lesion is located. Inner Ear/Vestibular Nerve Disease of the inner ear or vestibular nerve results in only the signs listed above. Auditory dysfunction is rarely recognised. The direction of the nystagmus is usually horizontal or rotary and is unchanged when the position of the head is altered. If disease also affects the middle ear, signs of CN VII dysfunction (drooping lip and ear and absent palpebral blink) and a Horner's syndrome may result. Normal tear production is generally present over the eye affected with an abnormal palpebral blink response. Diseases of the inner ear/vestibular nerve include: Otitis interna/media. Imaging of the osseous bullae and/or deep otic examination may confirm middle ear disease. Computed tomography (CT) and magnetic resonance imaging (MRI) are more sensitive at diagnosing middle ear disease than are plain film radiographs Evidence of infection of the inner ear alone is rarely visible on either CT or MRI images. Treatment with cephalosporins, enrofloxacin or trimethoprim/sulfa +/-bulla osteotomy are recommended Idiopathic labyrinthitis. Older dogs and cats of any age may be affected. CN VII dysfunction and Horner's syndrome do not occur. No abnormalities are found on blood work, images of the bullae, deep otic examination or thyroid testing. Antibiotics are recommended but may not be necessary. Spontaneous recovery is common Other causes. Congenital vestibular syndromes have been described in Beagles, German Shepherd Dogs, Dobermans, Cocker Spaniels, Smooth Fox Terriers, Akitas and other dogs. Siamese, Burmese and Tonkinese cats have also been affected. Signs of vestibular dysfunction are generally present at birth. Polyneuropathy, tumours and trauma involving the inner ear or vestibular nerve may result in vestibular system dysfunction. Hypothyroidism may be associated with polyneuropathy and, occasionally, vestibular signs resolve only after the institution of thyroid hormone supplementation. In general, these animals are treated with antibiotics until a definitive diagnosis is made. Aminoglycosides at high doses may result in deafness and signs of peripheral vestibular dysfunction Medulla/Cerebellum

Disease of the medulla may result in changes in mental status due to involvement of the ascending reticular activating system. Due to involvement of the upper motor neurons and the proprioceptive system, hemiparesis and postural reaction deficits may occur. Due to involvement of other brain stem regions, dysfunction of cranial nerves V-XII may occur ipsilateral to the side of the lesion. The direction of the nystagmus may be horizontal, rotary or vertical and may change when the position of the head is altered. Dysmetria, menace deficits ipsilateral to the side of the lesion, and head and neck tremors may result from disease of the cerebellum. Inflammatory and neoplastic causes commonly result in vestibular dysfunction due to involvement of the medulla and/or cerebellum: Canine distemper virus infection, toxoplasmosis, neosporosis, cryptococcosis, granulomatous meningoencephalomyelitis, parasitic migration and other meningoencephalitides may result in vestibular system dysfunction Neoplasia may be suspected on the basis of cerebrospinal fluid abnormalities and images of the brain Metronidazole intoxication at doses greater than 30 mg/kg will frequently result in an acute onset of vestibular system dysfunction with vertical nystagmus and, occasionally, seizures. Supportive care, requiring a week or more of hospitalisation, results in recovery although months may be required before all signs resolve Thiamine deficiency may result in vestibular system dysfunction. Intramuscular thiamine hydrochloride (25-50 mg) can resolve the signs Infarction of the medulla or cerebellum may be suspected on the basis of cerebrospinal fluid abnormalities and images of the brain Other causes of chronic progressive signs of central vestibular dysfunction include: cerebellar hypoplasia, cerebellar abiotrophy, storage disease and demyelination Exceptions to the Rules of Localisation Bilateral involvement of the inner ear may result in a wide-based stance and swaying of the body, without evidence of nystagmus or strabismus. However, when the animal is lifted off the ground a severe loss of balance is evident. In general, depriving the animal of tactile or visual sensory information causes a worsening of the signs of vestibular disease. Disease of the cerebellum and medulla occasionally results in head tilt, strabismus and slow phase of the nystagmus directed away from the side of the lesion (paradoxical vestibular syndrome). In these instances, the postural reaction deficits remain ipsilateral to the side of the lesion.
References 1. De Lahunta, A. Vestibular system--special proprioception. In: Veterinary Neuroanatomy and Clinical Neurology (second edition). Philadelphia: WB Saunders, 1983; 238-254. 2. Troxel, M; Drobatz, K; Vite, CH. Analsysis of traditional and novel neurological examination techniques for the diagnosis of vestibular dysfunction in dogs. Journal of the American Veterinary Medical Association (in press). C.H. Vite, DVM PhD University of Pennsylvania PA, USA

Diagnostic Investigation of Feline Nasopharyngeal Disease

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2007
Vanessa Barrs
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Presentation for upper respiratory signs is common in feline practice. From the findings of a thorough history and physical examination including careful observation of the respiratory pattern, it is usually possible to localise upper respiratory disorders to the sinonasal cavity, larynx or caudal nasal cavity/nasopharynx (Table 1). The nasopharynx is dorsal to the soft palate and extends from the choanae to the larynx. Nasopharyngeal diseases arise from tissues within, bordering or contiguous with the nasopharynx, including the base of the skull, caudal nasal ethmoturbinates, auditory tubes, middle-ears, palate and pharyngeal mucosa.

Table 1. Localisation of feline upper respiratory disorders.

For each category, some or all of clinical signs listed may be present. Localising signs are asterisked. Sinonasal cavity disease: Nasal discharge Epistaxis Sneezing* Facial distortion Caudal nasal cavity/nasopharyngeal disease: Inspiratory dyspnoea Stertor (inspiratory)* Excessive swallowing Gagging Paroxysmal reverse sneezing* Coughing Sneezing Nasal discharge Epistaxis Halitosis Dysphonia Concurrent otitis externa/head shaking Concurrent media/interna (OMI) Laryngeal disease: Stridor (inspiratory)* Cough Dysphonia Gagging Retching Dysphagia

CLINICAL SIGNS OF CAUDAL NASAL CAVITY/NASOPHARYNGEAL DISEASE

An obstructive respiratory pattern characterised by a normal or mildly increased respiratory rate and inspiratory dyspnoea, together with stertor, localises disease to the caudal nasal cavity or nasopharynx. A stertor is a snoring or snorting sound that results from turbulent air-flow caused by

airway obstruction rostral to the larynx. This sonorous respiration is characteristic of caudal nasal cavity/nasopharyngeal disease. Other signs that may be present are listed in Table 1. Nasal discharge is present in some cats due to obstruction of nasopharyngeal drainage by a mass lesion or because of concurrent sinonasal cavity disease. Cats with nasopharyngeal disease may develop otitis media/interna (OMI) from occlusion of the pharyngeal openings of the auditory tube by a mass lesion (e.g., cryptococcal granuloma). A mucoid effusion develops in the tympanic bullae. This is often complicated by secondary ascending bacterial infection with oropharyngeal flora. OMI may also develop because of direct involvement of the tympanic bullae in the disease process (e.g., nasopharyngeal polyp).1,2 Rupture of the tympanic membrane from polyp growth or infection can cause otitis externa and clinical signs of head-shaking, or ear-scratching/grooming. In cats with nasopharyngeal disease and OMI, head-shaking, signs of peripheral vestibular disease, Horner's syndrome and/or facial nerve palsy may occur, ipsilateral to the affected bulla. Rarely, in cats with nasopharyngeal disease and OMI there may be intracranial extension of infection through the internal acoustic meatus, resulting in signs of central nervous system dysfunction.3

AETIOLOGIES
Once disease has been localised to the caudal nasal cavity/nasopharynx, the following differential diagnoses should be considered:

Table 2. Differential diagnoses of caudal nasal cavity/nasopharyngeal disease.

Neoplasia Lymphoma Carcinoma Other Inflammatory Nasopharyngeal polyp Nasopharyngeal stenosis Infectious Mycotic nasopharyngeal diseases Cryptococcosis Aspergillosis Atypical bacterial infections Mycobacteria Accumulation of excessive nasal secretions Infectious/inflammatory rhinosinusitis Sinonasal cavity disease Foreign body Congenital Choanal atresia Palatine defects The most frequent causes of nasopharyngeal disease in cats are neoplasia, non-infectious inflammatory disease, and in certain geographical regions such as Australia, mycotic granulomatous infections, especially cryptococcosis.2,4-5

Neoplasia
Of neoplastic diseases lymphoma is by far the most common, followed by carcinomas.

Inflammatory
Nasopharyngeal polyps are the most common inflammatory cause and are thought to occur in response to ascending oropharyngeal viral infection. These pedunculated growths arise from the mucosa of the tympanic bullae or auditory tube and protrude into the nasopharynx. Polyps may also extend through the tympanic membrane into the horizontal ear canal, or rarely, through the internal acoustic meatus of the tympanic bulla into the cranial vault.3 Acquired nasopharyngeal stenosis (NPS) is characterised by the presence of a web of fibrous scar tissue (cicatrix) that spans the nasopharynx caudal to the choanae and has a small central aperture. It occurs as an inflammatory response to mucosal ulceration of the nasopharynx. In cats this is thought to occur secondary to viral or bacterial upper respiratory infections.6-7 Acquired NPS has also been described in other species secondary to caustic burns, oropharyngeal surgery or reflux of gastric contents through the nares during general anaesthesia.

Infectious
Infectious agents that cause granulomatous disease are a differential diagnosis for feline nasopharyngeal disease, including fungi and bacteria. Cryptococcal infections that originate in the caudal nasal cavity can develop into mass lesions that obstruct one or both choanae.5 Nasopharyngeal involvement is common in sino-orbital aspergillosis infections of cats.8 This newly recognised clinical syndrome in cats is characterised by a retrobulbar mass (exophthalmos, prolapse of the nictitating membrane, ocular discharge and exposure keratitis), stertor and oral cavity lesions including palatine ulceration and/or mass lesions in the pterygopalatine fossa. This distinctive constellation of clinical signs reflects the propensity of sinonasal cavity aspergillosis in cats to invade contiguous tissues including the orbit, nasopharynx, palate and cribriform plate. Importantly, signs of rostral nasal cavity or sinus infection may be subtle or absent. Preliminary investigations by the author's group have shown that in contrast to canine sinonasal aspergillosis which is typically caused by Aspergillus fumigatus, infections in cats involve other species of Aspergillus including Neosartorya sp. Identification of nasopharyngeal involvement is important clinically, since biopsy of nasopharyngeal lesions is a reliable method of obtaining tissues for definitive diagnosis through fungal culture and histopathology.

Excessive Nasal Secretions

Any cause of sinonasal cavity disease, including infectious and inflammatory rhinosinusitis can cause accumulation of nasal secretions in the caudal nasal cavity/ nasopharynx, resulting in presentation for stertor. Infection with Feline Herpesvirus causes epithelial necrosis and osteolysis of nasal turbinates. In severe infections turbinate destruction may be permanent, resulting in chronic rhinosinusitis, often with secondary bacterial infection.

Foreign Bodies
Nasopharyngeal foreign bodies, such as plant or food material, may enter the nasopharynx during incomplete vomition, during attempts to swallow or during regurgitation in oesophageal motility disorders.

Congenital
Choanal atresia is a congenital anomaly characterised by developmental failure of the caudal nasal cavity to communicate with the nasopharynx. Unilateral, membranous choanal atresia has recently been described in a Himalayan cat, and should be considered as a differential diagnosis for chronic unilateral nasal discharge.9 In other species the choanal obstruction may be unilateral or bilateral, partial or complete, and membranous or bony.

DIAGNOSTIC INVESTIGATION
Diagnostic investigation of cats with nasopharyngeal disease is relatively straightforward and should be conducted in two stages. The first stage includes non-invasive investigations. Sedation may be required for some procedures. The second stage includes imaging and biopsy collection, performed with the patient under general anaesthesia.

Stage 1
1. Otoscopy: Thorough otoscopic examination should be performed to visualise the integrity of both tympanic membranes. In cats with nasopharyngeal polyps, there may be extension of growth through the tympanic membrane into the horizontal ear canal. Pink, fleshy masses and otitis externa may be observed. In cats with OMI the tympanic membrane may be discoloured or bulging. 2. Neurological Examination: A neurological examination should be performed in any cat with nasopharyngeal disease and suspected middle-ear involvement. Signs of peripheral vestibular disease in cats with OMI include vomiting, head tilt, circling, ataxia and spontaneous nystagmus in the absence of postural reaction deficits. Facial nerve palsy and components of Horner's syndrome (ptosis, miosis, enophthalmos, prolapse of the nictitating membrane) ipsilateral to the affected bulla may be seen concurrently. It is important to distinguish between peripheral vestibular disease and central vestibular disease in all patients since intracranial extension of infection from the middle-ear can occur. 3. Serology: A latex cryptococcal antigen agglutination test (LCAT) detects the presence of cryptococcal antigen in serum. A positive titre is indicative of active infection. 4. Aspiration Cytology & Microbial Culture: Where present, enlarged local lymph nodes (mandibular or retropharyngeal) or facial soft-tissue masses should be aspirated. Bacterial culture of superficial nasal swabs is usually unrewarding since normal flora is present and bacterial infections are usually secondary to underlying disease. Exceptions include infection with Bordetella bronchiseptica or Actinomyces sp, which may be primary pathogens. Cytology and fungal culture of nasal swabs is useful for the detection of Cryptococcus sp, and to perform in vitro susceptibility testing of the fungal pathogen. Since the nasal cavity of healthy cats can be colonised with Cryptococcus sp, diagnosis also requires cytological evidence of inflammation or the presence of abundant organisms. Step 3 (LCAT) should always be performed since fungal infection may not be detectable on swabs of the rostral nasal cavity. 5. Thoracic Radiography: Thoracic radiography is useful to screen for lower respiratory tract involvement in the primary disease process, e.g., metastatic pulmonary neoplasia, pulmonary cryptococcosis.

Stage 2
If definitive diagnosis is not obtained using these non-invasive procedures, the following diagnostic investigations should be performed, sequentially, under general anaesthesia: 1. Soft Palate Inspection: The soft-palate should be inspected during induction of general anaesthesia and intubation. A large nasopharyngeal mass will cause ventral deviation of the soft-palate and can be palpated dorsal to the soft-palate. After intubation, some large nasopharyngeal masses can be digitally massaged into the oropharynx for biopsy or removal. Nasopharyngeal polyps can be removed with firm traction, using curved extraction forceps by grasping the rostral stalk of the polyp. Haemorrhage is usually minimal. Recurrence is common and ventral bulla osteotomy is often required. 2. Diagnostic Imaging: The nasal cavity, nasopharynx, frontal sinuses and tympanic bullae should be assessed in patients with caudal nasal cavity/nasopharyngeal disease. The diagnostic imaging modality used will depend on availability. If radiography is used views should include lateral skull, ventrodorsal skull, dorsoventral occlusal view or open-mouth ventrodorsal view and rostrocaudal open-mouth or rostro 10 ventro-caudodorsal oblique view. Nasopharyngeal masses are most easily identified as soft-tissue opacities dorsal to the soft-palate on a lateral skull radiograph. The sensitivity of radiography for the detection of acute otitis media, as identified by loss of aeration of the bullae, is low. Chronic otitis media is more readily detected as mild bony reaction and thickening of the tympanic bulla wall. Computed tomography (CT) is more sensitive than radiography. Furthermore, middle-ear involvement in cats with caudal nasal cavity/nasopharyngeal disease is more common than previously thought. Recently, a third of cats with nasopharyngeal disease were found to have effusive bulla disease on CT. The most common neoplasm implicated was nasopharyngeal lymphoma.10 On CT, destruction of maxillary turbinates is commonly seen in cats with inflammatory or neoplastic sinonasal disease.11 However, severe destruction of both maxillary turbinates and ethmoturbinates, particularly where unilateral, and/or lysis of paranasal bones

is more predictive of sinonasal neoplasia than inflammatory disease. CT is also useful to document involvement of extrasinonasal structures including facial soft-tissues, the orbit and calvarium in cats with neoplasia or filamentous fungal infections. CT is generally superior to magnetic resonance imaging (MRI) for evaluation of destructive lesions in bony structures contiguous with the nasopharynx. In patients with suspected otogenic intracranial infection, MRI after intravascular contrast administration is superior for evaluation of intracranial softtissues.3 3. Visualisation of the Nasopharynx: The patient is placed in dorsal recumbency with an intraoral gag in place. Large nasopharyngeal mass lesions may be visualised by retraction of the soft palate with a spay hook. Visualisation of the choanae requires retroflexed nasopharyngeal endoscopy. Regional anaesthesia of the pharynx with 2% topical lignocaine gel and maxillary nerve blocks using 0.5% bupivacaine facilitate a decreased plane of general anaesthesia in some, but not all cats, during nasopharyngeal endoscopy. When the choanae are clearly visualised endoscopically, a size 5 or 6 Fr urinary catheter is inserted via each ventral nasal meatus into the nasopharynx, to check patency and dislodge foreign material or masses. Mass lesions in the choanae/nasopharynx can be biopsied using endoscopic biopsy forceps. In cats with suspected sinonasal cavity disease rhinoscopy should be performed after nasopharyngeal endoscopy. Haemorrhage, although mild, is common during rhinoscopy and can impair visualisation of the nasopharynx. Cup biopsy forceps are useful to obtain 'blind' tissue biopsies from the nasal cavity. Care should be taken not to advance biopsy forceps caudal to the medial canthus of the eye, to prevent inadvertent penetration of the cribriform plate. 4. Nasal Cavity Lavage: Flushing saline from the nasal cavities into the nasopharynx is useful to dislodge foreign bodies and diagnostic fragments of friable tumours or granulomas. A cuffed endo-tracheal tube, with adequate insufflation to seal the trachea and protect from aspiration of lavage solution, should be used. The pharynx is packed with sterile swabs to prevent aspiration and to trap flushed material. A 10 ml aliquot of sterile saline is flushed vigorously through one naris into the ventral nasal meatus, whilst occluding the other naris, and then repeated on the other side. Diagnostic tissue specimens dislodged during this procedure can be retrieved from the packing material in the pharynx for cytology, culture and histopathology. Harvesting of biopsy samples utilising this flushing technique obviates the need for endoscopic biopsy and often yields larger biopsy specimens than can be obtained using endoscopy alone. 5. Other Procedures: Where endoscopic visualisation of the nasopharynx is hampered by excessive secretions or haemorrhage, fine-needle aspirates of mass lesions through the softpalate can be obtained for cytological analysis. Alternatively, though rarely necessary for diagnostic purposes, the soft-palate can be incised longitudinally, leaving the caudal edge intact, to facilitate superior access to the rostral nasopharynx.2

Vanessa Barrs Valentine Charlton Cat Centre, Faculty of Veterinary Science, The University of Sydney NSW, Australia

Use, Misuse & Abuse of MRI ACVIM 2005 Laurent S. Garosi, DVM, DECVN, MCRVS Newmarket, Suffolk, UK
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INTRODUCTION The past ten years has seen a dramatic increase in the availability of sophisticated neurodiagnostic tests (electrodiagnosis, computed tomography, magnetic resonance imaging). The advantage of using such technology is undeniable in terms of diagnostic capability and progress in the understanding of complex neurological problems. Unfortunately, despite and sometimes because of, their relatively high sensitivity, these diagnostic tests often lack specificity in determining the exact nature of the disease process. The clinician must therefore still rely on clinical acumen to choose appropriate diagnostic tests and interpret results of these. A precise localisation of the problem within the nervous system (anatomic diagnosis) and understanding of the suspected disease process (differential diagnosis) are the keys to a successful management. MRI IN THE CONTEXT OF CLINICAL NEUROLOGY Until recently, most practitioners and veterinary students considered neurology as the "dark side" of veterinary medicine. The advances made in diagnostic imaging have made this discipline more "understandable" and accessible to every practitioner. With unlimited media availability provided by the internet, the general public has become more informed and sometimes more critical of what can or cannot be done for their beloved companion. Consequently, the demand from pet owners for diagnostic modalities such as MRI has increased. MRI is now more readily available to the veterinary community and considered as an "indispensable tool" in most referral practices. Unfortunately, advances in therapy seem to lag behind the progress made in the availability of this diagnostic imaging technique. MRI is the preferred imaging method for humans with central nervous system disease. Its main advantages rest on its highly accurate soft tissue resolution, multiplanar capability and absence of ionizing radiation risk when compared to other imaging techniques. Numerous MRI radiofrequency pulse sequences have been designed in order to improve soft tissue contrast resolution. The possibilities are nearly endless. The most common pulse sequences used to image the brain and spinal cord are those based upon the spin-echo. T1weighted images are useful for visualizing anatomy. Gadolinium-enhanced T1-weighted images allow for identification of regions within the CNS where the blood-brain barrier is not intact. T2weighted images are used for identifying regions of increased free water (regions of edema, cellular infiltration or inflammation). Other pulse sequences used for small animal MRI include fluid-attenuated inversion recovery (FLAIR) (used to suppress CSF signals in order to examine lesions of the brain parenchyma which are near to the ventricle or subarachnoid space), gradient echo (increased sensitivity of blood products and calcification), diffusion- and perfusionweighted (use for early detection of infarction) and fat-saturation techniques. Common MRI artifacts are important to recognize and include motion, susceptibility, signal void, partial volume and signal drop-off artifacts. Compared to man, MR imaging does require that the veterinary patient be anesthetized. Other than the risks associated with this general anesthesia (especially in patients with severely compromised brain function), there is no conclusive evidence for irreversible or hazardous bioeffects related to short-term exposures of human beings to static magnetic fields up to 2.0 Tesla. When compared with other imaging techniques, MRI also has the benefit of the absence of ionizing radiation risk.

MR imaging is likely to add information to that obtained by conventional imaging techniques when 1) the area of the suspected lesion cannot be evaluated using other means, 2) the information produced by conventional imaging techniques is limited, 3) a lesion is evident on other imaging techniques but more 3-D information is required for example for treatment planning. INVESTIGATION OF BRAIN DISEASES Because of its excellent soft tissue resolution, MRI imaging of the brain is indicated in the diagnostic work-up of animals with neurological signs of brain disease. Diseases that affect the brain are divided into a) extra-cranial disease (toxic or metabolic), b) intra-cranial structural brain disease (cerebrovascular, inflammatory or infectious, neoplastic, degenerative, anomalous or trauma) and (c) intra-cranial functional brain disease (mainly diseases caused by abnormal neurotransmission or ion channel disorders such as primary epilepsy, narcolepsy or diseases classified as "movement disorders"). Elimination of extra-cranial causes of brain disorder is a pre-requisite to MRI evaluation of brain disease. Signal intensity on MRI scans is a reflection of subtle biochemical and biophysical tissue properties. As a result, MRI has excellent soft tissue contrast resolution and high sensitivity to many disease processes affecting the brain. Previously considered uncommon, cerebrovascular accidents, and in particular brain infarcts, are increasingly recognized in dogs or cats with the advance of neuro-imaging. The improved resolution of imaging methods has made the identification of small pathological process such as lacunar infarcts possible. These infarcts are now clearly the most common category of infarcts in man and dogs. Initial hopes that MRI signal intensity would be diagnostic for specific pathologic processes have not been borne out. Radiologists and neurologists have long tried to correlate histopathological results and MR signal intensity using combination of sequences to distinguish non-neoplastic from neoplastic disease (and to further classify different types of neoplastic disease). The combined results of sequences might in some cases be strongly suggestive of a specific pathological process. However, pathological processes such as inflammatory mass and neoplasia share some MRI characteristics as well as similarities in origin, shape, or anatomic site. In many cases, the interpretation of the imaging findings relies on the clinical understanding of the suspected disease process (differential diagnosis), the use of other diagnostic tests (cerebrospinal fluid analysis, antibody titers, metastatic work-up, coagulation profile, etc.), a good understanding of disease process mechanism, and/or histological diagnosis after tissue biopsy (ultrasonographic guided, stereotactic or surgical). Magnetic resonance techniques may still hold the key to non-invasive specific histological diagnosis. Magnetic resonance spectroscopy (MRS) provides metabolic information about brain tumors beyond what is obtained from anatomic images. Magnetic resonance spectral patterns have been shown in man to be distinct for different tumor types and grades. Response to radiation therapy is also reflected by MRS patterns. MRS is also of use in the investigation of intrinsic metabolic disease where, while it is usually of insufficient sensitivity to measure the specific chemical responsible for the disorder, it can detect the secondary chemical pathological changes. In some situations, these secondary chemical changes may be specific for the disorder. The validity and utility of MRS in canine patients with brain tumors as well as patient with intrinsic metabolic disease is currently being analyzed at the Animal Health Trust.

The absence of abnormalities on MRI evaluation of the brain could indicate a) incorrect anatomical diagnosis (disease affecting parts of the nervous system other than the brain), b) toxicity or metabolic disease affecting the brain function without causing macroscopic parenchymal changes (hepatic encephalopathy, electrolyte imbalance or hypoglycemia), c) diseases causing very subtle parenchymal changes that might not be detected with a low field magnet (small infarct or hemorrhage and degenerative disease), or d) functional brain disease (primary epilepsy and movement disorders). INVESTIGATION OF SPINAL CORD DISEASES Diseases affecting the spinal cord are broadly divided into a) compressive diseases (disc herniation, vertebral fracture/luxation, spinal malformation, neoplasm) and b) non-compressive diseases (spinal cord malformation, inflammatory/infectious CNS disease, degenerative diseases and vascular accident). Suspected spinal cord disease is a common indication for MRI in small animals. Traditionally, plain radiography and myelography have been the techniques of choice for the investigation of spinal cord disease. However, myelography provides no information about the spinal cord parenchyma other than whether it is compressed, displaced or swollen. MRI offers the double advantage of showing spinal cord parenchymal changes (such as those associated with inflammation, edema, syringo-hydromyelia, infarct or neoplasia) and allowing transverse images (greatly assisting with the localization of the compressive tissue). MRI also has the benefit of being safer than conventional myelography as a subarachnoid injection is not required. Unfortunately, without an accurate anatomic diagnosis (suspected spinal cord segments affected), MRI evaluation of the spinal cord can be extremely time-consuming, especially in large dogs, and can lead to over-diagnosis of incidental changes such as mildly herniating discs. Other limitations are mainly technical (magnetic field strength, field of view allowed, accurate positioning of the animal and setting of different imaging planes). MRI evaluation of the spinal cord could be normal in the case of a) incorrect anatomical diagnosis (particularly with neuromuscular disease, brain disease or disease affecting other spinal cord segments than the ones imaged), b diseases for which the parenchymal changes can only been seen microscopically (especially degenerative disease such as degenerative myelopathy), or c) diseases causing very subtle parenchymal changes that might not be detected with a low strength magnet (vascular disease such as fibrocartilaginous embolism or inflammatory disease of the spinal cord). INVESTIGATION OF NERVE AND MUSCLE DISEASES The peripheral nervous system consists of 12 pairs of cranial nerves and 36 pairs of spinal nerves that extend from, or to, the spinal cord and brainstem. Diseases affecting the peripheral nervous system can affect one single peripheral nerve (mono-neuropathy) or multiple peripheral nerves (polyneuropathy). Common indications of MRI in investigation of peripheral nerve disease include the investigation of a) cauda equina syndrome (very often technically difficult using myelography and epidurography), b) brachial plexopathy, and c) cranial nerve neuropathy. The main limitations of MRI in these cases are mainly technical (choice of adequate imaging plane and sequences), operator-dependant (detailed knowledge of anatomy) and inherent poor specificity in differentiating neoplastic from non-neoplastic disease processes.

Electromyography is better than MRI for muscle disease evaluation, and a muscle biopsy is the only manner in which a definitive diagnosis can be made. However, MRI has proven useful adjunctive diagnostic procedure for cases of polymyositis where diagnosis is elusive, particularly if a specific anatomic localization cannot be reached by other means. The MRI signal intensity of normal muscle is intermediate between that of fat and cortical bone. MRI studies in man and in dogs have showed a good correlation between uniform hyperintensity on T1-W and T2-W images showing enhancement after contrast medium administration and muscle inflammation identified histopathologically. INVESTIGATION OF VASCULAR RELATED NEUROLOGICAL DISORDER In addition to stroke, vascular-related neurological disorders include aortic thrombo-embolism (ischemic neuromyopathy), congenital portosystemic shunt (hepatic encephalopathy) and other vascular malformations (such as caudal vena cava malformation) as possible cause of exerciseinduced weakness and collapse. In addition to its use for tissue evaluation, MR imaging (i.e., magnetic resonance angiography or MRA) can non-invasively assess the vascular system. Two techniques can be used 1) time of flight (TOF) MRA and 2) contrast MRA. The TOF MRA can be implemented on every MR system, is easy to use and do not need contrast medium injection. TOF may be used in either a 2-D (sensitive to slow-flowing blood) or a 3-D sequence (high spatial resolution and sensitive to fast-flowing blood). Contrast MRA is based on the use of paramagnetic contrast agents in combination with gradient-echo sequences. Paramagnetic contrast media strongly enhance the MR signal due to T1 shortening. Image data can be collected during the whole measurement cycle, demonstrating arterial and venous contrast pass. In all MRA techniques, image contrast is the result of blood motion. Although less invasive, one of the main limitations of MRA is its lower resolution compared with conventional angiography which becomes progressively worse as the vessel luminal size decreases. Laurent S. Garosi, DVM, DECVN, MCRVS The Animal Health Trust Kentford - Newmarket, UK

The Wobbler Dog: A Surgical Dilemma WSAVA/FECAVA/BSAVA World Congress 2012 Bjrn P. Meij, DVM, PhD, DECVS Yalelaan, Utrecht, The Netherlands
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Caudal cervical spondylomyelopathy (CCSM) causing wobbler syndrome is a condition of young dogs (1 year, Great Dane, Basset Hound) or middle-aged to older animals (68 years, Dobermann, Rottweiler). Anatomical abnormalities include stenosis of the cranial apertura of the cervical vertebral canal, vertebral body deformation and asymmetry of the articular facets. Degenerative lesions include intervertebral disc degeneration (IVDD) and Hansen type II fibrinoid disc herniation (protrusion), ligamentous hypertrophy of the dorsal longitudinal ligament (ventral to the spinal cord) and the ligamentum flavum (dorsal to the spinal cord) and joint capsule proliferation. Wobbler syndrome (syndrome = the clinical description of a complex of signs) is characterised by posterior paresis and ataxia, proprioceptive deficits, forelimb lameness and mild cervical pain. The neurological deficits can eventually progress to the thoracic limbs and evolve into tetraparesis and tetraparalysis. The clinical signs in the wobbler dog can typically be a mix of upper motor neuron disease (spinal cord) and lower motor neuron disease (compression of nerve roots that contribute to the plexus brachialis). CCSM is usually a progressive disease that has a slow onset but neurological deficits may also progress acutely bringing the dog down. Cervical radiography under sedation or anaesthesia of the C4T1 region may show spondylosis, vertebral body malformation, tapered cranial cervical apertura, end-plate sclerosis and collapsed intervertebral disc space. Also cervical instability may already be evident on the neutral views but may be evoked by stress views (flexion, extension and linear distraction and compression). The cervical instability shows the dynamic component of the disease: compression on the spinal cord worsens in extension and lessens in flexion. Myelography with stress views (Figure 1) demonstrates the effect of the dynamic compression: unstable vertebrae, ligament hypertrophy and disc protrusion contribute to a ventral and/or dorsal component in the spinal cord compression. Stress views are essential to provide the localisation, and the static or dynamic nature of the spinal cord compression. With the availability of magnetic resonance imaging (MRI) many clinicians have replaced myelography with MRI, but specifically with CCSM the dynamic component of the disease may be missed when MRI is only performed in a neutral position. Myelography followed by computed tomography (CT) (myelo-CT) and scanning in different positions may also be very informative. In the Dobermann usually one junction is involved (C5C6, C6C7, C7T1) and in the Great Dane more vertebrae can be affected (C4 T1). Since the wobbler dog is a clinical diagnosis the clinician should always be aware of the differential diagnoses. Discospondylitis (infection of the intervertebral disc usually caused by Staphylococcus) or neoplasia (e.g., lymphoma of the vertebral body) in a Dobermann may give exactly the same appearance of wobbler dog as CCSM.

Figure 1. Myelography in an 8-year-old Dobermann with caudal cervical spondylomyelopathy at C6C7.

Neutral (A), extension (B), flexion (C) views.

The Surgical Dilemma In mild cases of wobbler syndrome medical treatment is the first strategy. Conservative treatment consists of a chest harness for life, bodyweight reduction when applicable, exercise regulation (omit exercises that worsen the ataxia from the daily pattern), physiotherapy (hydrotherapy or exercises for proprioception) and administration of non-steroidal anti-inflammatory drugs or corticosteroids. This will usually lead to some clinical improvement and may slow down the progression. However, since the disease is progressive there may come a decision point to proceed for surgical treatment. The dilemma in surgery has several aspects. When a dynamic component has been diagnosed a surgical technique such as ventral decompression that only deals with static compression may not be sufficient. In the case of a dynamic component, in addition to decompression, the cervical region needs also to be stabilised but here we have a paradox: the cervical region is a highly flexible region and surgical techniques to stabilise the unstable cervical junction are prone to surgical failure. When spinal segments have been fixated and fused another problem arises in the so-called adjacent segment disease ('domino effect'): stabilisation of one junction may relocate the stress to the next weak link in the chain. Another dilemma is the time point in the disease process to advise surgery: in many textbooks it says that the aim of surgery is to slow down or stabilise the neurological deficits but in that view it may be the best approach to stabilise early in the disease onset. The goals of surgical treatment are decompression, stability or both. The myelographic examination, myelo-CT or MRI findings usually determine which surgical technique is chosen as the best treatment option. Ventral decompression ('ventral slot') is indicated in static ventral compressive spinal cord lesions but these are rare in the true wobbler dog. Ventral distraction and stabilisation is indicated in one or multiple dynamic ventral compressive spinal cord lesion(s), e.g., cervical instability, type II disc degeneration and dorsal longitudinal ligamentous hypertrophy. Linear distraction of cervical vertebral bodies results in decompression at the site of the dynamic lesion and (temporary) fixation of the vertebral bodies allows fusion to take place which is promoted by cancellous or corticocancellous bone grafts harvested from the proximal humerus. Surgical techniques that have been performed in the past include: distraction with a cylindrical cortical allograft kept in place with a plastic Lubra plate, distraction with Steinmann pins or screws and fixation with a polymethyl methacrylate (PMMA) bridge, Harrington rod distraction device, screw and washer technique (Figure 2) and the modified distraction-stabilisation technique using an interbody PMMA plug. Arthrodesis of the cervical vertebrae is promoted by packing cancellous bone around the affected cervical junction. Fusion of cervical vertebrae by the surgical techniques listed is usually by ventral spondylosis, as interbody fusion is obstructed by metal implants or PMMA plugs. The ideal spinal fusion would be direct continuous bone bridging at the level of the vertebral bodies and techniques to stimulate this are now reported or under development. Cervical locking plates and interbody titanium cages or smart devices will probably offer a better way to treat cervical instability and promote fusion than the techniques reported in earlier days. However, the paradox between a highly flexible cervical spine and rigid implants remains.

Figure 2. Myelography in an 8-year-old Dobermann with caudal cervical spondylomyelopathy at C5C6.

Before (A) and after screw and washer fixation (B). Dorsal decompression (e.g., by continuous dorsal laminectomy) is indicated in static or dynamic dorsal compressive spinal cord lesions, e.g., osteophytes around articular facets or interarcuate (flaval) ligamentous hypertrophy. At Utrecht University 23 dogs (21 Dobermanns and two Great Danes) were surgically treated for CCSM. The surgical procedures included Lubra plate and cortical graft (two dogs), Steinmann pins and PMMA bridge (three dogs), Harrington rod distraction device (four dogs), ventral decompression ('ventral slot', three dogs), dorsal (hemi)laminectomy (one dog) and screw and washer (10 dogs). The Lubra plate and Harrington rod techniques had a high rate of surgical implant failure and the procedures were abandoned. The ventral decompression technique resulted in neurological worsening in two of three dogs. Clinical and neurological stabilisation or improvement was seen with the Steinmann pin and PMMA technique (two of three dogs), the screw and washer technique (eight out of 10 dogs) and following dorsal laminectomy in a Great Dane. Complete surgical arthrodesis by spondylosis of the cervical vertebrae was observed with

the screw and washer technique. However, with long-term follow up it was seen that the vertebral bodies collapsed on the washer and the screw tip touched the opposite cortex close to the spinal canal.

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Bjrn P. Meij, DVM, PhD, DECVS Utrecht, The Netherlands

Sarcomas of Soft Tissues

WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2006
Jolle Kirpensteijn, DECVS, DACVS Professor, Head Soft Tissue Surgery, Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Utrecht
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INTRODUCTION
Sarcomas of soft tissues (STS) are common in companion animals and pose a therapeutic and diagnostic challenge for the practising veterinarian. STS is defined as a malignant tumour of the extraskeletal connective tissues. These tissues, all of mesoderm origin, surround, support or connect other anatomic structures and are present in any part of the body. Because soft tissues are estimated at 40% proportional body weight, it is not surprising that numerous soft tissue tumours arise with regularity. STS form an assembly of tumours of different histogenetic origin, with ubiquitous localisation possibilities, and variation in biological behaviour. Still, STS are often grouped together because of their shared mesodermal origin, similarities in clinical presentation, and communality in diagnostic and therapeutic approach. In general, STS are fleshy (the Greek word 'Sapkoua' or 'sarkoma' is often translated as flesh-like mass), infiltrative and locally aggressive tumours that have a variable metastatic potential. This chapter will describe the common STS in dogs and cats. Visceral and other organ-specific STS (e.g., splenic hemangiosarcoma) will be discussed in the representative chapters.

INCIDENCE
STS are common tumours and comprise from 15% (skin and subcutaneous tissues) to 35% (spleen) of all canine tumours, dependent on original tumour location. Cats are afflicted less frequently (7% reported for skin and subcutaneous tissues). The annual incidence of STS in the United States is estimated to be 35/100.000 for dogs and 17/10000 for cats at risk. These data are not available for the European countries.

EPIDEMIOLOGY
Little is known about the pathogenetic cause of STS in dogs and cats. Changes in genetic make-up, chronic trauma, foreign bodies, vaccinations, parasites and radiation have been associated with STS in both species. P53 mutations and MDM2 gene amplification were observed in a subgroup of canine soft tissue sarcoma; however, familial predispositions have not been reported. No sex or breed predilections have been found, although certain breeds seem to be afflicted with tumours more commonly than others. For example, retrievers seem predisposed to development of soft tissue sarcomas of the head (oral cavity/mandibular/maxillary region) with often a low grade histologic appearance but high aggressiveness. Whether STS predisposition is caused by a breed-specific genetic abnormality or by a high inbreeding coefficient due to the popularity of the breeds, is at present unknown. In general, most studies report medium to large breeds to be affected more commonly, with an overrepresentation of the older animal. Trauma was associated with the incidence of STS. It is unclear if trauma causes an owner to be more aware of problems in that area or if trauma is an initiating cause in STS. The presence of foreign bodies or material (such as vaccinations) may induce chronic stimulation of the tissues and promote neoplastic transformation. An example of this is the parasitic infestation of Spirocerca lupi and the incidence of oesophageal cancer. Radiation has also been associated with sarcoma formation, although sarcoma formation after extracorporal therapeutic radiation seems to be rare.

CLASSIFICATION
All soft tissues are exposed to the risk of benign or malignant tumour formation. Extensive classification schedules are available from human literature and are simplified to fit into the companion animal situation. Any classification schedule, however, is complicated by overlapping patterns of dedifferentiation or by the inability to recognize the appearance of the cell of origin. A classification by localisation, grade and tumour stage seems more logical and may prove more useful at present.

Advances in histochemical, electron microscopic and biogenetic markers will improve the ease of classification in the future. Muscle actin, desmin, vimentin, factor VIII actigen and lysozyme are suggested to be useful for the differential diagnoses of STS, and cytokeratins for synovial cell sarcomas specifically.

DIAGNOSIS
The diagnostic plan for STS is not essentially different from any other tumour type. The physical appearance is noticed depending on the location of the tumour and, in general, peripherally-located tumours are more easily detected and often smaller than more centrally-located STS. Clinically, STS often are solid masses that seem well-circumscribed and encapsulated. However, this is based upon the presence of a pseudocapsule of atrophic remains of surrounding tissue and wedged tumour cells, while infiltration through this pseudocapsule and through fascia leads to attachment to deeper structures. Pain is associated with location, pressure of the tumour or tumour invasion. Some peripheral nerve sheath tumours have been reported to be sensitive to the touch. A clinical differentiation between benign and malignant is not possible, so additional diagnostics are necessary. Moreover, rate of growth of the tumour often does not predict the biologic behaviour correctly. Additional biopsy specimens should be obtained in all cases. The easiest method of biopsy is fine needle aspiration (FNAB), and this method should be used as the first step in the diagnosis. Although many STS are not well-diagnosed by FNAB because of their limited exfoliative character, many other tumour types can be excluded as well as some inflammatory processes; in particular if infection can be demonstrated while overlying skin is intact. Chronic traumatic inflammation as cytologic diagnosis of FNAB should fit with history and site. In case of any doubt and in particular also if cytology indicates mesenchymal proliferation in absence of an inflammatory response, this provides a solid indication for further diagnostic work-up. Incisional, excisional or thick needle core biopsy (TNCB) specimens should be obtained. TNCB is the easiest and fastest method and requires minimal sedation. Multiple core biopsies should be performed and submitted to the pathologist. Sufficient tissue, however, is often better acquired by incisional or excisional biopsies. Excisional biopsies are only advantageous when adequate margins can be obtained. In all other cases an incisional biopsy is preferred. Normal tissue should be incorporated in the biopsy specimen to evaluate peripheral infiltration of the tumour. Incisional biopsies should always be performed in such a manner that removal of the scar is possible in future radical excisions or adjunctive radiation therapy protocols. Adjunctive diagnostic evaluations should include routine blood work, radiographs of the local tumour site for possible underlying bone infiltration, ultrasound of the tumour, radiographs of the chest for possible metastatic spread, FNAB of the regional lymph node and CT or MRI imaging techniques. In evaluating soft tissues, MRI has many advantages over CT imaging, however, is often not available or cost-effective. A pulmonary CT scan is preferred above plain radiographs. Although haematogenous spread of STS is more common, undifferentiated STS may spread to regional lymph nodes, warranting evaluation of these lymph nodes. For example, synovial cell sarcomas are often reported to spread through the lymphatics. Proper imaging should be performed of more centrallylocated lymph nodes along the lymphatic tract, in cases of suspected or proven metastasis to the regional lymph node. For example, metastasis to regional lymph nodes in the limb or inguinal area, should be followed by ultrasound examination of the internal iliac area. In addition, there are indications that splenic metastases are not uncommon in cases with synovial cell sarcomas. The most important factors in STS evaluation are the determination of tumour grade and tumour stage. Tumour grade is determined through histological evaluation and varies among grade I (low grade or well differentiated) to grade III (high grade or poorly differentiated). Tumour grade is determined by degree of differentiation, cellular pleiomorphism, cellularity and matrix formation, as well as mitotic index and amount of tumour necrosis. Experienced pathologists may apply a different weight to the respective factors in different types of STS to assess tumour grade. In human sarcomas, the tumour grade has a major impact on tumour staging. Tumour staging is based on four parameters: histological grade (G), tumour size (T), regional lymph nodes (N), and distant metastasis (M). Factors reported to be of prognostic importance in canine STS are size, site, grade and presence of local or distant metastases. The prognostic effect of localisation of the tumour is most likely dependent on the difficulty of complete excision. The higher the stage of the disease, the poorer the prognosis

GENERAL CONSIDERATIONS
STS pose a problem to the veterinarian mainly because they tend to be locally aggressive. Complete surgical excision is often impossible because of localisation or size of the tumour. Recurrence is common after incomplete resection and is the primary reason to refer STS to the Utrecht University Surgical Oncology Service. Most recurrences will occur within 2 years after primary tumour removal. Recurrence is caused because STS tend to spread into deeper or surrounding tissues by invasion or extension next to natural anatomic structures. These finger-like outgrowths of the tumour are often compared to the tentacles of an octopus. Cutting of the tumour mass (cf. body of the octopus) leaves these tumour extensions (cf. tentacles) in the patient. Through this, the tumour homeostasis is disrupted and fast growing tumour cells thrive causing fast tumour regrowth. Early detection and diagnosis of the original STS will facilitate complete removal and prevent recurrence. Shelling out STS is the most common cause for recurrence. Education and communication should be directed in the future to achieve these goals of early detection and complete removal. Overall metastatic rate is estimated to be 20%. Among STS subtypes there exists considerable variation. In part, this appears based on a link between subtype and frequency distribution of histologic grade. Low to moderate rate of metastasis is seen in (mostly low grade) hemangiopericytoma and the closely related malignant peripheral nerve sheath tumour. Similarly, a low to moderate rate of metastasis is seen in most fibrosarcomas (the subgroup of oral cavity/mandibular/maxillary fibrosarcomas is the exception to the rule). Synovial cell sarcoma and undifferentiated sarcomas are more frequently of high grade and have a relatively high rate of metastasis, i.e., 40-60%. Rhabdo or leiomyosarcomas are relatively less common, and liposarcomas are rare; these last subtypes have a moderate rate of metastasis, except for embryonal rhabdomyosarcoma (high rate). Metastases spread by haematogenous routes and lymph node involvement is reported to be rare. High grade tumours, such as synovial cell sarcoma and rhabdomyosarcoma have an higher incidence of lymphatic spread especially in late stages of the disease.

HISTOLOGICAL SUBTYPES
Fibrosarcoma
Fibrosarcoma (FSA) was the most commonly diagnosed STS. The recent more complete pathological differentiation in subtypes, however, will decrease the total number of 'pure' FSA in dogs and cats. For instance, neuroFSA, a diverse group of tumour types derived from fibroblast associated with nerves, are currently grouped under the nomenclature malignant peripheral nerve sheath tumours (PNST) instead of under FSA. Per definition, FSA are tumours derived from the fibrocytes. FSA are relatively more common in the cat than in the dog and have a locally-aggressive behaviour. They can occur anywhere in the body, but are most commonly seen in the skin and subcutaneous tissues and the oral cavity. The canine, histologically-low-grade-and-biologically-high-grade, FSA, located in the oral cavity, and mandibular and maxillary region, is a tumour that should be mentioned specifically. This tumour, most commonly associated with young dogs, has an aggressive biological behaviour, whilst diagnostic surgical biopsies depict a low histological grade. Feline FSA occur often on the limbs in older animals without a sex or breed predilection.

Malignant Peripheral Nerve Sheath Tumours (PNST)

Malignant PNST contain a group of tumours with varying nomenclature. Included in this group are neurofibrosarcoma and malignant schwannoma. PNST are locally aggressive and metastasise rarely (in less than 20% of the dogs). Metastasis rate is dependent on tumour grade, however. It is unclear at this moment what the cell of origin is in these tumours (i.e., fibrocytes or Schwann cells). PNST can occur anywhere in the peripheral nerve system. The most common location is the subcutaneous tissues of the distal extremities in de dog. PNST located in the closer proximity to the vertebrae (including those in the region of the plexus brachialis) often will cause nerve compression and signs of pain and neurological deficit. Invasion of these tumours into the spinal cord is not uncommon and may be seen in over half of cases of high histological grade. Before surgery, a CT-scan (or MRI) of the region is advised.

Haemangiopericytoma (HPC)
Haemangiopericytomas (HPC) were believed for long to stem from pericytes (cells with contractile properties surrounding small blood vessels), though proof is lacking for this histogenetic origin. HPCs form a whorl-like growth pattern at histological examination without visible connection with nerves. Biological behaviour of HPCs is similar to that of PNST, and many will stain positive for the immunohistochemical marker S100, indicating peripheral nerve origin. Therefore, some authors group HPC under PNST. HPC often have a slow rate of growth, yet are locally aggressive (infiltrative), but have a low (<15%) rate of metastasis. Older dogs (with boxers predisposed) are affected, and HPC consists of 5% of all skin and subcutaneous tumours. Most HPC's are located on the extremities.

Myxosarcoma
Myxosarcoma are FSA containing connective tissue cells that produce intracellular mucin. These tumours are often soft to the touch, but behave similarly to other FSA, in which tumour grade is the most important predictor of behaviour.

Haemangiosarcoma (HAS)
HSA are common tumours that arise from endothelial cells of blood vessels. HSA commonly are located in body cavities and are of extreme aggressiveness (see related chapter). Somewhat less common, they originate of capillaries in dermis, subcutis or deep-seated tissues, including muscle or even bone. Dermal/subcutaneous HSA have been reported in certain breeds (Whippet, Saluki, Blood Hound, pointers) and may be associated with exposure to ultraviolet light. Predilection sites include abdomen, prepuce and hind legs. Rupture of bad-quality, tumourous blood vessels is not rare, and may lead animals to be presented with haematoma, with or without knowledge by the owner of a pre-existing lump in the same area. Behaviour of extracavitary HSA depends on location and size. Strictly dermal HSA without invasion have a fair prognosis, with assessments of less than a 25% rate of metastasis. High rates of metastasis are seen with invasive lesions and with those of deeper anatomical location. Multifocal manifestation of HSA is not only seen with visceral forms, but also sometimes at dermal/subcutaneous sites, posing a major problem in the therapy. Dermal (stage I) HSA are small tumours, often located in the ventral-abdominal or preputial region, and associated with longer survival times (median survival 780 days) than the hypodermal (stage II) and deep muscular (stage III) located tumours. The deep muscular HSA have a larger size, do not have an anatomical predilection, and generally have a shorter survival (median survival 172 and 307 days, respectively). The majority of the cutaneous HSA, however, are superficial tumours. There appears to be some influence of hair length and skin colour. Dogs with short hair coats and lightly pigmented skin have more dermal type of HSA, less subcutaneous types, and more HSA of ventral smooth and hairless skin.

Liposarcoma
Liposarcomas are rare, malignant tumours derived from fat cells. Liposarcomas are observed in older animals and may be associated with foreign bodies or obesity. Liposarcomas are often firmer than 'normal' lipomas, are poorly defined and often occur in the ventral region of the body. Biological behaviour is characterised by local infiltration and early metastasis. Infiltrative lipoma is a form that is described in the dog and is comparable with the human well-differentiated liposarcoma. They have an infiltrative behaviour and are difficult to remove locally because of their infiltrative nature. Infiltrative lipomas are often observed in the muscles of the front and hind legs. Infiltrative lipomas can only be distinguished from benign lipomas if muscle invasion is present histologically. Clinically, they appear more attached to the deeper structures and less encapsulated.

Lymphangiosarcoma
Lymphangiosarcoma are rare tumours of the lymph vessels. Although often described in young animals, they can affect dogs and cats of all ages. The ventral thorax and abdomen is a predilection site of the cat. The tumours have a soft and cystic like appearance and may coincide with peripheral oedema. Lymph fluid may 'sweat' through the skin of affected sites. Lymphangiosarcomas are invasive and have a high metastatic potential

Leiomyosarcoma
Malignant transformation of smooth muscle cells are the origin of leiomyosarcoma. They can occur in any part of the body, but are described as firm, lobulated masses most commonly associated with the digestive tract from oesophagus to rectum or the urogenital tract. Clinical signs may relate to obstruction or bleeding due to ulceration. Transformation of benign leiomyomas to leiomyosarcomas has been suggested but not scientifically proven. Leiomyosarcomas are infiltrative tumours that metastasise late in the disease process. Multiple leiomyosarcomas are possible and warrant thorough examination of the abdomen before or during the surgery. Paraneoplastic hypoglycaemia has been associated with leiomyosarcoma.

Rhabdomyosarcoma
Rhabdomyosarcoma, a tumour from the striated muscle cells, is relatively rare in the dog. Two forms have been described: the first occurring in the urogenital tract of young dogs (mainly bladder) and is referred to as juvenile-type or botryoid rhabdomyosarcoma. The second form occurs in the older animal and is described affecting the tongue, pharynx, myocard and rarely other skeletal muscle locations Rhabdomyosarcomas are locally aggressive and metastasise early.

Synovial Cell Sarcoma

Synovial cell sarcoma (SCS) are tumours that arise from tenosynovial tissue and are often associated with lameness. Predilection sites are the stifle and elbow joint but other locations near joints, tendons or bursae have been described. Also, in this tumour type, the origin of the tumour cell is not clear (synovial cell versus periarticular connective tissue cell). Histologic typing may divide those with onecell population (monophasic) from those with two-cell populations (biphasic), with either one being epithelial-like, the other mesenchymal. Immunohistochemistry often demonstrates a positive signal for both cytokeratins as well as for desmin, reflecting the mixed differentiation. Local invasion of underlying bone is common in later stages of the disease and is easily recognisable on routine radiographs by punched-out bone lesions. The tumour invades the bone at the attachment of the joint capsule or tendons to the bone. SCS are locally aggressive and metastasise late in the disease process. Metastasis rates of up to 50% have been reported, again depending on tumour grade. SCS metastasise to lymph nodes, lungs, spleen and liver.

TREATMENT
Surgery is the primary therapy of STS, with or without adjunctive therapy. The surgical goal is to completely remove the STS and, as a result, a large margin of normal tissue is sacrificed. An example of this type of surgery is the amputation of a limb. Limb-sparing surgeries are an alternative, but can only be performed in combination with adjunctive therapy modalities such as radiotherapy, chemotherapy and immunotherapy.

Surgery
Surgery is only successful if large margins of normal tissue are obtained, with margins of 2-3 cm normal tissue advocated. The objective local failure rate for marginal excisions (peel-out or shellingout STS) in humans is 86%; however, these rates, based on large numbers, are unknown in dogs and cats. Failure rates after wide local excisions and more radical excisions (such as amputations) were 49% and 14% in humans, respectively. Extrapolation from human data is tempting, but should be interpreted with caution. Recurrence rates of 60-70% are reported in marginally-excised, canine haemangiopericytomas and STS. Although most STS tend to recur within a year after surgery, adequate follow-up of 2 to 3 years is necessary. Wide surgical excision is often complicated by the anatomic localisation of the tumour to important structures. In these cases a more conservative surgery is planned (e.g., limb spare). The owner should be made aware of the increased chance of recurrence compared to radical excision. In general, a repeat surgery is more complicated if the STS has recurred and failure is more likely. The first surgery has the largest chance for complete removal. Recurrence, as of yet, is not associated with an increased risk of metastases, however. It is the authors' opinion that the incidence of metastases depend more on tumour grade than on the type of surgery performed. The recurrence rate decreases when the surgery is performed by more experienced oncologic surgeon. Experience often correlates to a more radical surgery, knowledge of innovative reconstruction techniques and better understanding of the pathophysiological properties of the tumour.

Radiation Therapy
Conventional techniques of radiation are rarely successful, while fractionated radiotherapy as a sole therapy using megavoltage irradiation yields a one-year control of about 50-60%. Radiation therapy is associated with acute-onset and with chronic side effects. Radiation is more effective with minimal (microscopic) disease than with more bulky disease. Radiation in combination with surgery results in increased disease free intervals. The radiation therapy is used to treat the microscopic disease left behind after marginal excision of the tumour bulk, achieving identical results compared to radical excision (80-90% at 2 years). Forrest, et al. (J Vet Med Intern 2000) showed a median time to recurrence after incomplete excision of STS and radiotherapy of 798 days. Of STS-subtypes, HPC seems relatively sensitive. Surgical excision and radiotherapy did not increase median tumour-free and survival times compared to complete excisions in feline FSA. Most cats of the first group had incomplete (dirty) surgical excisions, however. Radiation has also been used in combination with local or whole-body hyperthermia. The addition of whole body hyperthermia was not associated with a better local tumour control, and most dogs experienced local failure or metastatic disease. Two-year recurrence free rates of approximately 30% were described. Intraoperative radiotherapy has been described to cause STS formation in approximately 20% of dogs treated.

Chemotherapy
Chemotherapy can be used to treat local and systemic disease. Chemotherapy is used for palliation in macroscopic and may be of limited benefit in eliminating microscopic local or metastatic disease in STS. Multidrug chemotherapy protocols, including anthracyclines (doxorubicin, mitoxantrone), have been advocated as the most successful. Combination therapy of an anthracycline with vincristine and cyclophosphamide appear more effective in a limited series of STS. The scientific data supporting the efficacy of these protocols in dogs and cats are currently missing, however. More randomised studies using large populations evaluating the effect of chemotherapy are necessary.

Immunotherapy
The treatment of STS with immunotherapy is under review at Utrecht University. Interleukin-2, a cytokine and immunostimulant, was combined with marginal surgery in a pilot study of 17 dogs with MPNST and is currently tested in a double-blind prospective study. The initial results from the pilot study are encouraging. A pilot study in 17 dogs showed a recurrence free percentage at two years of approximately 70%.

Photodynamic Therapy
Photodynamic therapy was used after surgery in dogs with HPC and appeared to have no advantage over other forms of therapy in regards to preventing recurrence. Complications, including delayed wound healing and infection, and limited efficacy decrease the applicability of this therapy type in dogs with STS. References
1. Kirpensteijn J, Rutteman GR, BSAVA Manual 2003

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Jolle Kirpensteijn, DECVS & ACVS Faculty of Veterinary Medicine Utrecht University Utrecht, The Netherlands

Pelvic Fractures in Cats: When and How to Repair British Small Animal Veterinary Congress 2010 Katja Voss, DrMedVet, DECVS University Veterinary Teaching Hospital Sydney, Camperdown, NSW, Australia
19884963

Introduction Pelvic fractures account for 20-30% of feline fractures. Many patients have concurrent injuries to the thorax and abdomen, and other fractures. Besides a thorough physical and orthopaedic examination, a neurological examination is performed with emphasis on the sciatic, the pudendal and the coccygeal nerves. Sciatic nerve or pelvic plexus injuries occur in more than 10% of cats with pelvic fractures and are most commonly associated with sacroiliac luxations and ilial fractures. Injury to the pudendal and coccygeal nerves (flaccid tail) is also common and is usually caused by concurrent sacrococcygeal fractures or luxations. Cats with pelvic fractures should routinely undergo abdominal and thoracic radiographs and blood analysis. Haematuria is common in cats with pelvic fractures. It can be caused by injury to any part of the urinary system, and although it is often self-limiting the patients must be monitored closely for signs that indicate urinary tract trauma that requires medical or surgical intervention. It can also be severe enough to cause anaemia. Orthogonal radiographs of the pelvis are performed to identify and classify the pelvic fractures, and are also crucial to diagnose or rule out concurrent spinal (e.g., sacrococcygeal) or hip joint injury. Pelvic fractures are classified into sacroiliac luxations, ilial body fractures, acetabular fractures, pelvic floor fractures and fractures of the pelvic margin. Because the pelvis is ringshaped, at least two fractures/luxations are present in most cases. The following combinations of injuries are common: Ilial body and pelvic floor fracture Ilial body fracture and contralateral sacroiliac luxation, with/without pelvic floor fracture Unilateral sacroiliac luxation and pelvic floor fracture Bilateral sacroiliac luxation, with/without pelvic floor fracture Pelvic Fractures--When to Repair The decision for conservative or surgical treatment depends on the localisation of the fractures, the degree of pelvic canal narrowing and the presence or absence of neurological deficits. Surgical stabilisation is generally indicated in fractures that involve the weight-bearing elements of the pelvis, that is the acetabulum, the ilial body and the sacroiliac joint. Cats with neurological deficits and/or extreme pain should also undergo surgery to explore for possible nerve entrapment within the fracture fragments. In cases with bilateral injury of the weight-bearing parts of the pelvis, the question arises whether to perform uni- or bilateral stabilisation. Unilateral surgery is often sufficient in cats with an intact pelvic floor because reduction and

stabilisation of one hemipelvis automatically results in adequate reduction of the lesion of the other hemipelvis. Cats with bilateral injuries and concurrent fractures of the pelvic floor have instability of both hemipelvises and often require bilateral fracture/luxation repair. Fractures of the non-weight-bearing parts of the pelvis (pelvic floor, the ilial wing, ischium) are generally treated conservatively with cage rest and pain management. Unilateral fractures of the ilium and sacroiliac luxations can also be treated conservatively if they are not or only minimally displaced. The animals should then be re-radiographed to monitor for progression of healing and for signs of pelvic canal narrowing. Pelvic canal narrowing of more than 40% is likely to result in chronic obstipation or constipation. Pelvic Fractures--How to Repair A selection of 1.5 mm to 2.7 mm screws and plates with adequate instrumentation is needed for surgical stabilisation of pelvic fractures. It is advantageous to have an oscillating drill mode available to reduce the risk of iatrogenic damage to nerves during drilling. Sacroiliac Luxations Sacroiliac luxations are most commonly repaired by insertion of a lag screw across the joint, using a dorsolateral approach. The size of the area for safe screw insertion is very small in cats, but guidelines have recently been published that facilitate adequate screw placement. The sacroiliac lag screw should penetrate at least 50-60% of the width of the sacrum to prevent screw loosening. Anatomical reduction also helps to enhance fixation stability. Stabilisation of sacroiliac luxation has also been described using positional screws inserted through a ventroabdominal approach. The ventroabdominal approach has the advantage of the surgeon being able to stabilise bilateral sacroiliac luxations via a single approach. The approach can also be extended cranially or caudally to repair intra-abdominal injuries or concurrent fractures of the pelvic floor. Ilial Fractures Plate osteosynthesis is used to stabilise most ilial fractures. The plates are typically positioned on to the lateral surface of the ilium. They are bent slightly more concave than necessary to facilitate restoration of pelvic canal width. The caudal screws are usually inserted first so the caudal fragment can be used to help lever the fracture into reduction before inserting the cranial plate screws. Lateral plating is associated with a relatively high incidence of screw loosening that can result in medial displacement of the caudal fragment and subsequent pelvic canal narrowing. Screw holding power is especially a problem in the ilial wing where the bone is very thin. Inserting the cranial plate screws across the sacroiliac joint or placing two plates parallel to each other are options to improve bone purchase. Plates can also be placed along the dorsal rim of the ilium, which has been shown to reduce the incidence of screw loosening and the degree of pelvic canal collapse as compared to lateral plating. Insertion of the screws is more difficult than with lateral plating (using a C-guide helps),

but the longer screws purchase more bone. Screws placed at the level of the acetabulum are aimed medially to exit the medial cortex of the pelvis. Long oblique fractures of the ilium are common in cats. These can be stabilised with two or three interfragmentary lag screws or 'skewer pins' that are placed perpendicular to the fracture and create interfragmentary compression. This counteracts the tendency of the caudal fragment to rotate distally. A 'skewer pin' consists of a K-wire driven across the fracture, and a figure-ofeight wire that is placed around the free ends of the pin and is tightened laterally. Dorsal plating is also a very good technique for long oblique fractures. Acetabular Fractures Acetabular fractures must be reduced and stabilised surgically to avoid development of severe coxarthritis and chronic pain. An approach to the hip joint using a trochanteric osteotomy gives the best exposure of the acetabulum. Plate osteosynthesis is the most widely applied stabilisation method. Perfect plate contouring is necessary to obtain anatomical reduction. Short plates with a minimum of two screws cranial and caudal to the fracture can be used in simple transverse fractures, whereas longer plates are required for oblique and multifragmentary fractures. Acetabular physeal fractures are occasionally seen in kittens. These can be repaired using a screw and tension band technique that involves placing one screw cranial and caudal to the fracture, and using a figure-of-eight wire to create interfragmentary compression. In kittens younger than 12 weeks of age, there is a possibility of premature fusion of the acetabular bones resulting in abnormal hip development. The prognosis is good for kittens older than 16 weeks. Although cats can have an acceptable limb function after femoral head and neck excision, this technique is a salvage procedure and should only be used for non-reconstructable fractures. The decision to perform a femoral head and neck excision is sometimes only made intraoperatively. Postoperative Treatment and Prognosis Postoperative treatment consists of adequate pain management and cage confinement for 2-4 weeks that is followed by restriction of activity for another 3-6 weeks. Gentle manual expression of the bladder or placement of an indwelling urinary catheter and/or application of enemas may be required to avoid urinary and faecal retention in patients that are not ambulatory in the immediate postoperative period. Complications after pelvic fracture surgery include implant loosening, pelvic canal narrowing with subsequent obstipation, and iatrogenic nerve injury. Avascular necrosis of the skin around the back and tail sometimes develops due to skin avulsion at the original trauma. The prognosis is good to excellent in cats with ilial fractures, but residual lameness is observed in up to 30% of cats with sacroiliac luxation repaired with a lateral lag screw. Prognosis after acetabular fractures depends on fracture type and ability to restore the hip joint during surgery.
Katja Voss, DrMedVet, DECVS University Veterinary Teaching Hospital Sydney Camperdown, NSW, Australia

Neurological Conditions: Case Studies WSAVA/FECAVA/BSAVA World Congress 2012 Gillian Calvo, RVN, A1 DipHE, CVN, DAVN (Small Animal), Cert Canine Hydrotherapy University Veterinary Hospital, University College Dublin, Belfield, Dublin, Republic of Ireland
23011648

Intervertebral Disc Disease Intervertebral disc disease (IVDD) in the dog is the most common neurological disorder requiring nursing care. The localisation rather than the disease process is most responsible for the presenting clinical signs. Patients with IVDD can present with pain, ataxia, paresis or paralysis, loss of deep pain sensation, urinary and occasionally faecal incontinence. It occurs most frequently in the chondrodystrophoid dogs (e.g., Dachshund, Pekingese, French Bulldog, Beagle, Basset Hound, Cocker Spaniel) but also affects the nonchondrodystrophoid breeds. The clinical presentation of an animal with IVDD varies with the site of the lesion, the onset of the problem and associated with this the dynamic force of the compression (acute speedy disc herniations usually cause more clinical signs compared to a gradual slow compression), the mechanical displacement of the spinal cord (i.e., the more compression the worse the clinical signs), the changes the compression produces within the spinal cord (intramedullary changes secondary to hypoxia), the mechanical displacement of the spinal cord and the duration of clinical signs. Compression of the spinal cord in disc disease is caused by either a disc extrusion or a disc protrusion (Figures 13). A normal intervertebral disc (IVD) consists of a nucleus pulposus in the middle surrounded by the annulus fibrosus. The nucleus pulposus has a gel-like consistency and its function is to absorb shock and dissipate forces evenly over the IVD structure. Dogs with a Hansen type I herniation/extrusion show premature ageing of the nucleus pulposus, leading to degeneration and mineralisation of the nucleus pulposus. The nucleus has a decreased ability to absorb shock and once the annulus fibrosus of the intervertebral disc ruptures, the nucleus pulposus extrudes ('explodes') into the spinal canal causing compression of the spinal cord. This type of disc herniation is more commonly reported in chondrodystrophic dogs. Dogs with a Hansen type II herniation/protrusion are affected by a slow degenerative process of the annulus fibrosus. The annulus fibrosus hypertrophies and bulges into the vertebral canal and, over time, leads to spinal cord compression. This type of disc herniation is more commonly reported in nonchondrodystrophic dogs.

Figure 1. Normal disc.

Figure 2. Disc extrusion (Hansen type I).

Figure 3. Disc protrusion (Hansen type II).

Cervical Disc Disease Cervical disc disease is a common condition in chondrodystrophic breeds with Hansen type I disc extrusion and nonchondrodystrophic breeds with Hansen type II disc protrusions. Patients with cervical disc disease can present with varying degrees of neurological deficits and functional abilities. Clinical presentation: Neck pain, more severe in acute versus chronic presentation Low head carriage, reduced movement of the head Pain on palpation of the spine and neck muscles Reluctance to eat due to pain when lowering head to the bowl Potentially kyphosis (hunched back)

Neurological deficits: All four limbs are affected. Exception: monoparesis or lameness of only one thoracic limb due to compression of the nerve root (nerve root signature) Ataxia, ambulatory or nonambulatory tetraparesis (voluntary movement present), or tetraplegia (no voluntary movement) Symmetrical or asymmetrical +/- Proprioceptive deficits in all limbs Upper motor neuron (UMN) bladder Potential respiratory deficits in tetraplegic patients N.B. It is uncommon to have reduced / absent deep pain sensation in cervical disc disease. Surgical decompression of cervical disc disease is commonly achieved with a ventral slot technique (Figure 4: disc herniation causes ventral compression of the spinal cord at C67; Figure 5: ventral slot at C56). Figure 4. C67 cervical disc extrusion.

Figure 5. C56 ventral slot.

Thoracolumbar Disc Disease Thoracolumbar disc disease is a common condition in chondrodystrophic breeds but also occurs in nonchondrodystrophic breeds. Type I disc extrusions are most frequently seen. The area of the spinal cord commonly affected by thoracolumbar disc disease is T11 to L2 vertebrae. Surgical decompression of thoracolumbar disc disease is usually achieved with a hemilaminectomy technique (Figure 6: L12 disc extrusion; Figure 7: L12 left-sided hemilaminectomy).

Figure 6. L12 disc extrusion.

Figure 7. L12 left-sided hemilaminectomy.

Clinical presentation of patient: Pain on palpation of the thoracolumbar spine Kyphosis Reluctance to exercise / run or jump Reluctance to be lifted and occasional associated pain

Neurological deficits: Ataxia/paraparesis of pelvic limbs or paraplegia of pelvic limbs (in most severe cases) Symmetrical or asymmetrical (one pelvic limb is more affected) Proprioceptive deficits in the pelvic limbs Upper motor neuron (UMN) bladder: as a general rule, voluntary urination is lost when the patient loses the ability to ambulate Loss of deep pain perception in the pelvic limbs and tail with severe spinal cord lesions N.B. The thoracic limbs are not affected by thoracolumbar disc disease and therefore should remain neurologically intact. Lumbosacral Disc Disease Lumbosacral disc disease is most commonly seen in mature large breed dogs caused by a Hansen type II disc protrusion. Surgical decompression of lumbosacral disc disease is usually achieved with a dorsal laminectomy technique (the dorsal spinous process and the dorsal roof of the spine is removed). Clinical presentation of patient: Pain on palpation of the lumbosacral spine Crouched gait Low tail carriage Reluctance to exercise/run or jump, especially difficulty jumping into the car +/- Urinary and faecal incontinence Neurological deficits: Weakness of pelvic limbs (paraparesis) and tail with a crouched gait, patients are usually ambulatory Tail paralysis in most severe cases Symmetrical +/- Proprioceptive deficits in the pelvic limbs

Lower motor neuron (LMN) bladder N.B. The thoracic limbs are not affected by lumbosacral disc disease and therefore should remain neurologically intact. Nursing Care for Post-Surgical Disc Disease Patients Surgical treatment may alter those deficits and functional abilities and a repeat of the original neurological examination is performed postoperatively once the patient has recovered from the anaesthetic and has received suitable analgesia. Conservative treatment requires close monitoring to recognise changes in the neurological signs. Subtle changes are often picked up by the veterinary nurse during nursing and are part of the overall assessment of the patient. Assess/monitor the patient for: Pain: pain score at least once daily Urine abnormalities: colour, odour Decubital ulcer formation Progress in physiotherapy (deterioration in limb/ bladder function?) Respiratory compromise (especially in patients with cervical disease). Increased respiratory noise is an indication of lung disease especially in recumbent patients. Loss of superficial sensation (e.g., chewing limbs or penis) and/or deterioration in deep pain perception or complete loss. Nursing the Patient Mattress and padded, absorbable bedding that draws urine away from the patient, i.e., acrylic bedding (Vetbed) in recumbent/partially recumbent patients. Bladder management (patientdependent choice of bladder management): Monitoring and expression of bladder every 46 hours (UMN bladder!) Intermittent catheterisation of bladder every 46 hours Indwelling urinary catheter drainage every 4 hours and clean with Hibitane twice daily if in situ If a UTI (urinary tract infection) develops, antibiosis should be based on urine culture results via cystocentesis.

Nebulisation and coupage every 4 hours with sodium chloride 0.9% solution if pneumonia is suspected or diagnosed. Tetraparetic recumbent patient: turn every 4 hours if unable to turn completely unaided. If recommended by the veterinary surgeon, take the dog out 34 times a day; use protective boots to avoid scuffing of nails and toes. Paraparetic patients: if assistance with walking is required use a pelvic harness or sling as required. Tetraparetic patients: use of harness or leads looped between the front legs instead of leads around the neck (surgery in the ventral neck area!). If assistance with walking is required use a hoist, or a harness for the thoracic and pelvic limbs or a sling. Rehabilitation and Physiotherapy Rehabilitation is the process of restoring the maximum function, independence and quality of life following illness or injury. The first step in the physiotherapy process is to identify whether physiotherapy is indicated in the presented patient. Initial assessment includes a history and a thorough examination of the musculoskeletal system to identify any problems the patient may have. Based on these findings treatment goals (short-term and long-term) are determined taking into account the abilities of the patient and the expectations of the owners, and a treatment plan is established. Where possible, objective outcome measures are used to monitor progress. Physiotherapy Treatments A wide variety of techniques and modalities are available. The selection of the appropriate treatment method for the individual patient is based on the diagnosis and the initial assessment. Often a combination of multiple techniques is applied. Physiotherapy begins as soon as possible after surgery. Suitable analgesia is required for effective physiotherapy to take place. The benefit of physiotherapy is to reduce pain especially with regard to muscle spasms, increase circulation, encourage lymphatic drainage and increase nerve conductivity. After 2448 hours or when the veterinary surgeon feels the patient is stable enough, proprioceptive reeducation (body's awareness of movement and where the various parts of the body (e.g., the paw) are located in relation to each other (spatial orientation)) and coordination and balance exercises can commence, including muscle strengthening and active assisted exercises. Cold Therapy (Cryotherapy) Acute stages of inflammation e.g., post-surgery or trauma

Apply cold packs on the incision or trauma site for 1520 minutes every 46 hours (up to every 2 hours in severe injuries) the first 2448 (or 72 hours) hours after surgery Cover ice packs with a damp towel and never apply ice directly to skin to avoid intolerance and ice burns. Cold therapy is most effective during the acute phase of inflammation and provides analgesia, reduces inflammation and oedema formation, reduces blood flow (vasoconstriction) and controls bleeding and reduces muscle spasms. Heat Therapy (Thermotherapy) Used once the acute phase is over (> 72 hours) Hot packs are applied for 1520 minutes every 34 hours Can be easily made by filling disposable gloves with hot water. Always check the temperature on yourself before applying to the patient. Commercial heat packs are available which regulate and maintain temperature for the duration of treatment improving effectiveness. This technique is beneficial prior to massage on muscles in spasm as it encourages relaxation and ultimately pain relief, vasodilation, increases cellular metabolism and aids in connective tissue mobility prior to exercise. This technique is advisable and particularly beneficial over the dorsal neck and shoulder musculature following cervical decompressive surgery. Massage Massage has multiple beneficial effects for the patient: Pain relief (removal of noxious chemicals and release of endogenous endorphins) Increase in circulation (aids healing due to increasing oxygen supply to tissue, increase in venous and lymphatic return) Mobilisation of adhesions and tissues (using friction and effleurage) Improving proprioceptive awareness due to manual stimulation of the body Preparation of muscle for exercise and reduction of muscle fatigue following exercise Reduction of tension and anxiety Improves the bond between the patient and the therapist (or the owner)

It also allows you to assess for any muscle pain and atrophy, detect tissue sores or decubital ulcers Massage should not be performed over areas of acute inflammation, infection, open wounds or areas of malignancy. Range of Motion Movement of a joint through the maximum motion possible Passive, i.e., the therapist provides the force to move the joints Active, whereby the patient provides the force to move the joint themselves Passive range of motion (ROM) includes moving the joint into flexion to the first point of resistance, then similarly into extension and this is repeated in a rhythmic manner 1520 times holding each stretch for 10 seconds to enable surrounding soft tissues to adapt/stretch in response Using a cycling motion in the limbs simulates normal gait pattern Moving a joint through its full ROM involves the nerves, muscles, tendons, ligaments, joint capsule plus fluid, articular cartilage and blood vessels ROM exercises are beneficial to maintain joint flexibility and joint homeostasis Therapeutic Exercise Exercises represent the final element in achieving maximum recovery. Therapeutic exercise is the systematic performance or execution of planned physical movements, postures or activities intended to prevent long-term physical impairment, enhance function, reduce the risk of injury, optimise overall health and enhance fitness and wellbeing. In all dogs with neurological dysfunction or proprioceptive deficits resulting in joint injury or surgery, recovery of balance and proprioception is most important in the rehabilitation. Balance is the ability to adjust the equilibrium either when standing or during movement. Proprioception is the sense that indicates whether the body is moving and also where the various parts of the body are located in space and in relation to each other (spatial orientation). Proprioception is very well developed in sporting and working dogs due to the increased demand. The sense of proprioception decreases with age and is often impaired especially after injury to the nervous system. General exercise include exercises that require response to changes in the surface such as wobble boards, balance pads, trampolines, changes of direction when running, ball-playing, dancing and standing on the physioball. Sufficient strength needs to be built up for the neurological patient to perform exercises focusing on balance and proprioception. However, strength exercise to increase the muscle mass only accompanies the rehabilitation plan rather than being a main focus in the recovery. Dogs with

weakness require support using harnesses or physioballs to stand or walk. Swimming is also used to build up muscle strength with the buoyancy support of the water. Building up flexibility and endurance (stamina) is usually not part of the initial or medium-term rehabilitation plan for neurological patients but is in orthopaedic patients. Depending on the ability of the patient, the patient moves through different stages of the therapeutic exercise as coordination and strength improves. These stages range from 'assisted' exercise to 'active-assisted' exercise to 'free-active' exercise and finally 'resistance' exercise. Assisted Exercise The patient is unable to perform any movement and thus requires an external force to perform passive movement. This includes ROM exercises. Active-Assisted Exercise Active-assisted exercises are used with patients who have some control over their body and limb function but require reeducation in proprioception and gait. Assisted walking using a pelvic harness (Figure 8) for patients after a hemilaminectomy, or a hoist after a ventral slot can provide sufficient assistance for the patient to go for walks. Care must be taken in hemilaminectomy patients that the pelvic sling does not cause skin trauma or put pressure on male genitalia especially the testes. Abdominal support slings (Figure 9) can be used in patients who require minimum help on the hindlimbs. It is not advisable to use this method with patients who are unable to bear their own weight as inadequate support of the spine occurs due to abdominal pressure causing flexion of the lumbar spine. Patients with cervical disease (e.g., post ventral slot) requiring support on all four limbs can be walked with the aid of a hoist for maximum support (Figure 10) or an 'A' frame for less support (Figure 11). Figure 8. Pelvic harness.

Figure 9. Abdominal support sling.

Figure 10. Mechanical hoist.

Figure 11. 'A' frame.

Free-Active Exercise Once patients are weightbearing and have sufficient coordination, strengthening and proprioception exercises against gravity and bodyweight can be initiated:

Sit to stand exercise Downward pelvic pressure Alternate limb lifting Corner tapping/hip swaying Trotting poles (Figure 12) / Cavaletti poles (Figure 13) A wobble board (Figures 14 and 15) can be used for proprioception training, coordination and balance. This exercise should be done once the animal is reasonably strong and just needs 'fine tuning'.

Figure 12. Trotting poles.

Figure 13. Cavaletti poles.

Figure 14. Wobble board.

Figure 15. Wobble board.

Resistance Exercise This exercise goes a step further than the free-active exercise as additional resistance, e.g., using additional weights in the free exercise is implemented. This can be achieved by using a rucksack with weights, distal limb weights or sledge pulling. Hydrotherapy Hydrotherapy can be used to improve general cardiovascular fitness, limb strength and coordination. Hydrotherapy has been shown to help relieve muscular pain and especially muscle spasm due to its moderately warm water temperature (28C) however a thermal spa would be more beneficial in achieving muscular relaxation (35C). The buoyancy of the water helps to support the patient's bodyweight and relieves pressure on the joints. Underwater Treadmill Active walking can be encouraged to improve limb strength, balance and coordination. Interval training is generally performed with short timed sessions on the treadmill with or without water. The resistance of water means 'treading' water for the patient is more difficult than if treadmill therapy is used dry (Figure 16). The use of water also helps to support the patient during the treatment. Figure 16. Underwater treadmill.

Gillian Calvo, RVN, A1, DHE, CVN, DAVN(Small Animal), Cert Canine Hydrotherapy University Veterinary Hospital University College Dublin Belfield, Dublin, Republic of Ireland

Ocular Examination
WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS, 2004
Ellen Bjerk s, DVM, PhD, DECVO Norwegian School of Veterinary Science, Department of Companion Animal Clinical Sciences Oslo, Norway
18281027

Examination of the eye includes History General examination Inspection Control of vision Examination of outer structures Schirmer tear test

Fluorescein staining Tonometry Examination of deeper structures Electrophysiology Imaging Vision should be assessed before pupil dilation through menace response, pupillary light reflexes, falling cotton ball, and obstacle course under different light conditions. This lecture is restricted to examination of intraocular structures.

THE ANTERIOR CHAMBER AND IRIS

The anterior chamber should only contain clear fluid, and the iris should be clearly visible. Uveitis with increased cell content of the aqueous humour may cause opacity of the fluid. In mild cases the aqueous look dusty (Tyndall effect). Larger exudates of leucocytes and fibrin may form sterile aggregates (hypopyon) with or without red blood cells present. Especially in the cat, immune complexes may sometimes be seen ventrally on the inside of the cornea as small brownish spots. Haemorrhage in the anterior chamber may be seen in connection with tumours and inflammations, in bleeding disorders, and also in connection with the inherited disease Collie Eye Anomaly. Pigmentation of the iris varies, often dependent on coat color. Iris in the two eyes may be of different colors, heterochromia. The iris contains small irregular folds. The pupil is round in dogs and large felines, biconvex in the cat. The most common congenital malformation is persistent pupillary membranes, more rarely iris colobomas. Especially in older dogs of small breeds, the iris may be more or less atrophied. This is seen as holes in the iris, or major parts of the iris may be lacking. The pupil will stay apparently dilated, which may cause some discomfort in bright weather. Normally the iris rests on the anterior lens capsule. Subluxation or luxation of the lens causes a deepening of the anterior chamber and also a characteristic shivering of the lens when the eye moves (iridodonesis). Iris cysts may be present in the anterior chamber. The cysts can be differentiated from tumours by their round and often transparent appearance.

GONIOSCOPY
Many dog breeds are predisposed to glaucoma. Inspection of the iridocorneal angle may be indicated as part of a breeding program in certain breeds. In cats the angle is easily visible, in dogs vision is obscured by the sclera. An extra curved lens, a gonioscopy lens, can be placed on the cornea after topical anaesthesia. The most commonly used gonioscopy lenses are the Barkan lo-vac and the Koeppe lens. The whole iridocorneal angle should be examined, and the width of the angle as well as the appearance of the pectinate ligament is noted. Gonioscopy findings of the two eyes are similar in almost all normotensive dogs. Gonioscopy is also indicated when an intraocular tumor is present and as a means of differentiation between primary and secondary glaucoma in breeds predisposed to primary glaucomas.

EXAMINATION OF THE POSTERIOR SEGMENTS Pupil dilatation

The most common medication for diagnostic use is Tropicamide. One drop is applied in the eye and in a normal eye maximum dilation is achieved after approximately 20 minutes. Repeated application may be indicated in some dogs. If uveitis is present, the effect of Tropicamide may be poor in the affected eye.

Lens
Initial examination is performed by directing light into the eye to allow the reflex from the fundus (retroillumination). Opacities may be seen as darker areas through the pupil. Directing the light from an angle allows localization of the opacities. The optimal instrument for examination of the lens, however, is a slit-lamp biomicroscope. This instrument consists of two parts; the microscope providing

10-20 x enlargements enables visualisation of small structures, and the light source, which can be directed into the eye at different angles and with a slit-formed light beam. Binocular vision also facilitates localisation of opacities within the lens. Normal easily distinguished variations include the suture lines of the lens, nuclear rings and small remnants of the hyaloid artery. On the posterior lens capsule occasional small dots representing remnants of the tunica vasculosa lentis may be seen, and on the anterior lens capsule small, pigmented dots representing remnants of the pupillary membrane are not infrequently observed.

Ophthalmoscopy
There are two principles for ophthalmoscopy, direct and indirect. In direct ophthalmoscopy the effective field of vision is determined by the illuminating system. Most direct ophthalmoscopes project a beam of light about one disc diameter. The visual field is restricted, and using a direct ophthalmoscope may be compared to peeping through a keyhole: You get a detailed view within a small field of vision. Thus, the direct ophthalmoscope is a good tool for close examination of details, for instance in examining the optic disc, but orientation is more difficult than with the indirect one, and it is difficult to examine the peripheral retina. The panoptic direct ophthalmoscope may represent a better tool than the traditional one. In indirect ophthalmoscopy the field of view is determined by the ratio of lens diameter and focal length. Given lenses of equal power, a larger lens provides a wider field of view. Given equal lens diameters, a stronger lens provides a wider field of view. To prevent image distortion, most indirect ophthalmoscopy lenses are aspheric with two different curved surfaces; the surface with the steeper curvature should face the examiner. Options for indirect ophthalmoscopy include the binocular indirect ophthalmoscope, where the light source sits on a headband, monocular indirect ophthalmoscope as a hand-held indirect ophthalmoscope, or a modified indirect ophthalmoscope with the use of as focal light source and a lens. Examination of the retina includes description of the optic disc, retinal vessels, tapetum and nontapetum. There are substantial normal variations in fundus color, size of tapetum, distribution of blood vessels and myelination of the optic disc. The optic disc is situated at the horizontal midline in the lower part of the tapetum. The degree of myelination around the nerve fibres decides the size and shape of the optic disc. A central cupping of the disc is often present, but must be distinguished from pathologic changes (colobomas). Cat discs are poorly myelinated and appear smaller than in the dog. Normally, 3-5 retinal veins from the periphery of the retina merge to form a vessel ring on the optic disc. About 20 small arterioles extend radially from around the disc. The tapetum is a triangular reflective layer situated in the dorsal half of the fundus. In puppies less than 8-12 weeks old the differentiation of the retinal layers are not yet complete, and the whole fundus appears blue with no visible tapetum. The color of the tapetum in dogs older than 12 weeks varies from yellow to bluish-green. In miniature breeds the tapetum can be limited to a minor area above the optic disc, or may even be totally absent. Only small reflective islets of tapetal tissue may be seen in some dogs. Except from some white animals, the tapetum is present in the cat. Non-tapetal fundus is mostly darkly pigmented, the degree of pigmentation varying according to coat and iris color. If the retina is poorly pigmented, brighter vessels from the underlying choroid can be seen extending radially towards the periphery. This is termed tigroid fundus. Albinotic fundus is tigroid fundus also lacking choroidal pigmentation. This is often seen in eyes with a blue iris ("wall eye" or "china eye").

Retinoscopy
Retinoscopy is performed to evaluate the animal's refractive status, that is, if the animal is nearsighted or far-sighted. Familiar myopia has been described in some dog breeds, and retinoscopy may be indicated in some behavioural problems. A streak retinoscope represents a practical, although not very sophisticated tool for veterinary ophthalmology. The retinoscope is held with one hand at a fixed distance from the animal's eye, and the examiner tries to neutralise the movements of light across the animal's fundus by adding lenses of varying strength in front of the animal's eye.

Electroretinography
Electroretinography (ERG) registers the response from the retina to light stimuli. After pupil dilation a contact electrode is placed on the retina and a reference electrode as well as a ground electrode on the head. The animal should be anesthetised for the procedure. The retina is stimulated with light of different wavelengths before, during and after dark-adaptation, and after light adaptation. There are many types of ERG equipment available. The important factor is to standardise examination methods, both regarding anesthesia, dark adaptation and recording. ERG can be used to establish an early diagnosis of photoreceptor disease, to distinguish blindness caused by photoreceptor disease from blindness from other causes and also to evaluate the function of the retina where it cannot be visualised, as in cataracts.

Ultrasound and other imaging techniques

Ultrasound is indicated to record space-occupying lesions and retinal detachment, aw well as other intraocular conditions, especially in cases where the fundus cannot be visualized. Radiography, MRI (magnetic resonance imaging) and CT (computer tomography) are also routinely used, but may be more indicated in central neuro-ophthalmic disease affecting vision, or in changes in periocular structures. For recording or diagnosis of retinal disease, fundus photography as well as fluorescein angiography represent useful tools. Fluorescein angiography is a dynamic method to explore the fundus vasculature and tissues. Serial photographs are taken the first 20 seconds after intravenous injection of a 10% fluorescein sodium solution, then less frequently during the following 3-5 minutes. The following stages are recorded: The choroidal phase, the arterial phase, the arteriovenous phase, the capillary phase and the venous phase. Changes can present as either hypofluorescence, representing either a filling defect or a masking effect, or hyperfluorescence representing leakage of dye from vessels, neovascularisation or a "window effect" where the choroidal vasculature is seen through the retinal pigment epithelium.

Histology
For histology the eye should be taken out as soon as possible after death. It should be carefully dissected, removing as much extraocular tissue as possible before fixation. Preference for fixation fluid may vary, one should discuss with the pathologist who performs the examination of the eye what to use. One common mistake is to use too small amount of fixation fluid; the amount should be about 10 x the size of the eye.

Ellen Bjerk s, DVM, PhD, DECVO Norwegian School of Veterinary Science Department of Companion Animal Clinical Sciences Oslo, Norway

Management of the Neurosurgical Patient WSAVA/FECAVA/BSAVA World Congress 2012 Bjrn P. Meij, DVM, PhD, DECVS Yalelaan, Utrecht, The Netherlands
23011846

Introduction Canine and feline neurosurgical patients are challenging, both for the nurse technician and for the veterinary neurosurgeon. This Nurse Masterclass Series will cover the management of the neurosurgical patient. Items that will be covered are assessment of neurological deficits, basic aspects on advanced imaging techniques for the neurosurgical patient, preparation of the dog and

cat for neurosurgery, neurosurgical instrumentation, special considerations during neurosurgery and the short-term postoperative neuro-care which will be the primary responsibility of the nurse technician. But the nurse technician may also be involved in the long-term postoperative care, rehabilitation and physiotherapy of the patient. The nurse technician plays an essential role in the management of the neurosurgical patient, both pre- and postoperatively. The Masterclass will cover a variety of neurological disorders that require neurosurgical intervention such as: intervertebral disc (IVD) degeneration and herniation, degenerative lumbosacral stenosis ('cauda equina syndrome'), caudal cervical spondylomyelopathy ('wobbler syndrome'), spinal tumours, spinal trauma, surgical brain tumours including pituitary adenomas and surgery of the peripheral nerves. The Masterclass is aimed at the experienced nurse technician with advanced skills and a learning ambition that goes beyond the standard surgeries. By following this Masterclass the nurse technician will gain new knowledge in the field of the management of the neurosurgical patient which will allow him/her to contribute significantly in the surgical success of these patients. Neurological Examination The neurological examination (and not imaging!) is the only examination that can give functional information on the spinal cord in a paretic or paralysed dog. The veterinarian will usually do a neurological grading of the neurosurgical patient. This is especially the case for dogs with intervertebral disc disease (IVDD) that are presented with paresis (reduced voluntary movements) or paralysis of the pelvic limbs (respectively paraparesis and paraparalysis). In case of neurological deficits of all four limbs this is called tetraparesis or tetraparalysis/tetraplegia. Grading of neurological deficits is based on postural reactions (proprioception = positional stance in space), voluntary motor function (standing and walking from A to B) and conscious nociception (= pain recognition by the brain).

Neurological grading: Grade 0 = normal Grade 1 = spinal pain, no neurological deficits Grade 2 = paresis, decreased proprioception, ambulatory (able to walk from A to B) Grade 3 = severe paresis, no proprioception, non-ambulatory (able to stand but not able to walk from A to B)

Grade 4 = paralysis, no proprioception, non-ambulatory (not able to stand and not able to walk from A to B), decreased bladder function, conscious nociception present Grade 5 = paralysis, no proprioception, non-ambulatory (not able to stand and not able to walk from A to B), no bladder function, conscious nociception absent With some practice, nurse technicians should be able to learn to grade patients using this grading system which will help the veterinary surgeon in the diagnostic work-up and decision tree when to wait, when to treat or when to refer. Also the grading will help to follow the success of treatment over time. Grading should be documented and dated in the medical records. In general, grades 1 and 2 can be treated conservatively (with medication) whereas grades 3, and especially grades 4 and 5 necessitate diagnostic work-up and immediate treatment to prevent further damage to the spinal cord. Grading can also be used for the prognosis: in general the prognosis will worsen with increasing grade, although many other factors, such as breed, aetiology, onset of disease, duration of deficits, bodyweight and the owner's motivation will influence the final prognosis. In case of grade 5, the prognosis is extremely poor for functional recovery when conscious nociception is absent for a period longer than 4872 hours. The Spinal Trauma Patient The spinal trauma patient may have other organ failures besides an unstable spine and should be approached with the greatest care and special considerations. Dogs with spinal fractures are usually extremely painful (when not completely paralysed) and are usually brought in on stretchers. The pitfalls are omitting to examine these patients for other ailments and failing to do a proper neurological examination the first time the animal enters the clinic. There are usually other trauma than the traumatised spine and these patients may have thoracic trauma (pneumothorax, diaphragmatic herniation, contusion of the heart), abdominal trauma (haemoabdomen, bladder rupture), shock, hypovolaemia or other limb fractures. The grading may be hampered by the inability to examine the animal due to pain. The first line of treatment is directed at the life-threatening diseases and not at the spinal fracture. The pain should be dealt with immediately with intravenous analgesics and the patient should be immobilised as well as possible (e.g., with a vacuum support cushion or a stretcher with braces). Extreme caution should be taken when giving these patients muscle relaxants since the muscle tone around the spine may be the last stabilising factor in fractures of multiple vertebral compartments. When the patient has been stabilised and the organs have been taken care of, imaging should be performed as soon as possible. However, this presents another dilemma: imaging of the awake patient is usually not possible due to the pain, will lead to low-quality radiographs and may pose a greater risk of dislocation of vertebrae. On the other hand, sedation or anaesthesia will take away muscle tone and therefore may contribute to spinal instability, which may worsen and even transect the spinal cord, when animals are handled without care. In the end, anaesthesia is mandatory when imaging spinal fractures, as it provides analgesia and allows the production of high-quality radiographs. However, it is essential to support the spine, preferably in a vacuum cushion, and the staff should transfer the cushion (with dog) from table to

table and not the dog itself. Also, all staff should be informed that the patient has a spinal fracture so accidental traction on the spine in different directions will not occur. Imaging of the Neurosurgical Patient Radiography and contrast radiography are still considered valuable diagnostic techniques to diagnose conditions that require neurosurgery. Contrast radiography includes myelography and epidurography. Radiography of the spine is best performed under sedation to produce highquality radiographs. Oblique views when aiming for optimal ventrodorsal or lateral views make precise radiographic interpretation of the spine very difficult due to overlapping bony structures. Myelography is performed under anaesthesia and the contrast agent is injected in the subarachnoid space around the spinal cord between the skull and C1, or between L4 and L5 or L5 andL6. Especially with cervical myelography, the contrast agent may leak into the brain and cause convulsions when the dog wakes up from anaesthesia. This may be prevented by elevating the head after contrast injection. Myelography may show extradural compression by a spaceoccupying lesion (like a herniated disc). Myelography is able to image the dynamic nature of a disc herniation, e.g., in case of caudal cervical spondylomyelopathy (CCSM, wobbler disease). Flexion/extension, traction and axial compression views of the cervical region are indicated for confirmation of the diagnosis CCSM. The developments in veterinary neurosurgery have been advanced by imaging techniques such as computed tomography (CT) and/or magnetic resonance imaging (MRI). These imaging techniques are a neurosurgeon's delight! CT is a radiographic technique producing transverse slices of the spine or skull. Indications for CT are spinal fractures, skull fractures, IVDD, degenerative lumbosacral stenosis, discospondylitis, spinal cord tumour and pituitary and brain tumours. Pituitary tumours are enhanced by a contrast agent because the pituitary gland is outside the blood-brain barrier. Brain tumours are enhanced by a contrast agent because of damage to or loss of the blood-brain barrier by the tumour. MRI is a technique that depends on the magnetic dipole of the hydrogen proton. MRI involves: A hardware component (magnetic field, radio-transmitter that excites the protons, and a radioreceiver that receives radio-signals. The contrast agent (magnetisation or spin density of tissue, relaxation times. e.g., T1, T2, and a contrast agent e.g., gadolinium). The software component that generates pulse sequences (timing diagram) through mathematical calculations (Fourier transformation) on the radio-signals. Indications for MRI are IVDD, degenerative lumbosacral stenosis (cauda equina disease), caudal cervical spondylomyelopathy (wobbler disease), discospondylitis, spinal cord tumour and pituitary and brain tumours. In contrast to CT, MRI is able to visualise oedema of spinal cord parenchyma and is diagnostic for spinal cord infarction or fibrocartilaginous thromboembolic myelopathy (FCE). Also, the result of an acute type 1 extrusion of nucleus pulposus in chondrodystrophic dogs (e.g., French Bulldog) that severely damages the spinal cord and starts a

negative spiral of oedema, ischaemia and spinal cord necrosis (called myelomalacia), is visible on T2-weighted MRI as a hyperintense signal in the spinal cord parenchyma. During neurosurgery, the veterinary surgeon usually requires on hand all the available imaging data (radiographs, myelogram, CT and MRI) for localisation of the correct surgical approach and intraoperative feedback of surgical findings in relation to the imaging findings. Also preoperative planning and three-dimensional (3D) measurements on sizes of space-occupying lesions and tumours are an enormous help for the surgeon. The Brain Patient The patient that undergoes brain or pituitary surgery requires special care. Apart from the routine monitoring devices, it is imperative in brain surgery to have some type of monitoring of blood pressure and possibly also intracranial pressure. Infusion with mannitol is used to lower the intracranial pressure. The temperature of the surgical unit should be kept below room temperature. A 'cold' brain requires less oxygen. Brain and pituitary surgery requires some type of magnification (operating loupes) or an operating microscope, also for the assisting nurse technician. Postoperative neurosurgical care is done in the intensive care unit and patients are kept sedated for some hours after brain surgery before waking them up. As soon as they are awake the first neurological examination is done to assess brain function. In case of pituitary surgery in dogs for tumours that cause Cushing's disease (the pituitary tumour produces excess adrenocorticotropic hormone (ACTH)) the postoperative monitoring includes electrolytes (sodium, potassium). In the ICU, the dogs are stimulated to drink immediately after surgery to regulate their water balance. The hormonal substitution therapy in dogs after hypophysectomy includes thyroxine, cortisone and desmopressin (a synthetic vasopressin analogue). In cats with acromegaly (the pituitary tumour produces excess growth hormone (GH)) that are undergoing pituitary surgery the same considerations are taken into account as for dogs with Cushing's disease but, in addition, these cats usually have insulin-dependent diabetes mellitus which will resolve quickly after surgery. Therefore continuous monitoring of glucose levels is imperative in the postoperative phase and short-acting insulin medications should be administered to prevent hypoglycaemic events. Neurosurgical Indications and Procedures The following diseases are the most common indications for neurosurgery: Intervertebral disc disease (IVDD) with cervical disc disease (C23, C34, C45) and thoracolumbar (T1112, T1213, T13L1, L12, L23) disc disease in chondrodystrophic dogs (e.g., French Bulldog, Dachshund). Disc herniations are usually type 1 (extrusion) herniations of the nucleus pulposus. In the cervical region a ventral approach is used called a ventral fenestration (incision of the annulus fibrosus) and decompression (ventral slot of the vertebral bodies). In the thoracolumbar area a left or right-sided approach is used called hemilaminectomy and lateral fenestration. Degenerative lumbosacral stenosis in nonchondrodystrophic dogs (e.g., German Shepherd Dog). Disc herniations are usually type 2 (protrusion) herniations of the annulus fibrosus and

nucleus pulposus. In the lumbosacral area the most common approach is dorsal laminectomy, followed by dorsal fenestration of the disc and nucleotomy (removal of the nucleus pulposus). Caudal cervical spondylomyelopathy (wobbler disease) in non-chondrodystrophic dogs (e.g., Dobermann). In this disease, the type 2 disc herniation is usually more dynamic in nature and requires decompression but also stabilisation using a variety of techniques such as screw and washer, pins and polymethylmethacrylate (PMMA), or cervical locking plates. Atlanto-axial instability in miniature dogs (e.g., Chihuahua). The most common approach is the ventral approach with lag screw fixation. The nurse technician should be aware of postoperative respiratory depression and apnoea in this condition since the respiratory centre is close to the surgical field and may be temporarily affected. Some of these patients need to be ventilated postoperatively for some time. Spinal cord tumours. The approach is dependent on the localisation but usually the approach is not a standard technique. In the cervical area and thoracolumbar, lumbar and lumbosacral area spinal tumours are best approached by dorsal laminectomy. In the thoracolumbar area, dorsal laminectomy leads to an unstable spine which requires some type of fixation afterwards e.g., Lubra plates, vertebral plates or pin-PMMA fixation technique. Brain tumours. Tumours of the neurocranium can be approached through craniotomy. The term craniectomy is used when the bone flap that is created during craniotomy is not replaced. The location of the tumour dictates the approach. The most common approaches to the calvarium are: rostrotentorial transparietal or transtemporal craniotomy with or without osteotomy of the zygomatic arch; unilateral or bilateral transfrontal sinus craniotomy; caudotentorial craniotomy; or suboccipital craniotomy. Craniotomy approaches can be combined or modified to improve exposure to various aspects of the cerebral hemispheres and cerebellum. Most craniotomies are performed with the cat in sternal recumbency. A head stand, a vacuum cushion and/or surgical tape is used to stabilise the head during the surgical procedure. Pituitary tumours. The pituitary tumour is usually approached by the oral route to the brain via a transoral, transnasal microsurgical trans-sphenoidal hypophysectomy. The dogs and cats are in sternal recumbency and the maxilla is supported on a metal bar attached to the operating table. The mandible is reflected downwards and the approach to the base of the skull is through the soft palate, through the nasopharynx and through the sphenoid bone. The surgery is considered a contaminated surgery because the approach is through the mouth and nose. Special Considerations During Neurosurgery Neurosurgical instrumentation for the approach and detachment of muscles include periosteal elevators and Gelpi retractors. Laminectomies are performed with an electrical or air-powered burr unit. The advantage of an electrical burr is that the speed of rotations can be fine-tuned. Foot pedal-controlled burring is preferred over hand console-controlled burring since this adds to stability of the burr in the surgeon's hand. Also, irrigation can be automatically integrated in the hand burr but continuous lavage with saline from a syringe by the nurse technician is just as efficient and more reliable than equipment! Copious lavage is a prerequisite in neurosurgery to

provide cooling during burring, to remove the bone shavings and to keep the surgical field free of blood. Once the surgeon has entered the spinal canal or the bony calvarium, the spinal cord, nerves and brain are explored with fine ball-tipped neurosurgical probes. Long instruments are preferred which keeps the hands out of the surgical field. During neurosurgery haemostasis is primarily controlled by bipolar electrocautery. Approaches to the spine require detaching of muscular attachments and this causes profuse bleeding. This can be kept to a minimum by precauterising muscular attachments with bipolar electrocautery before cutting the attachments. Typically a nurse technician can assist and speed up this phase of the surgery. Bipolar electrocautery has the advantage over monopolar electrocautery that the current will pass between the tips of the bipolar forceps and will not affect the adjacent muscle tissue or nerves (or spinal cord). In monopolar electrocautery the current goes from the tip of the monopolar to the contact plate which may cause unwanted twitching and movements of the surgical field. During most neurosurgical procedures some type of magnification is required to assess the condition of nerves, spinal cord or brain and to assess the sharp margins between normal and affected tissue. Especially in spinal cord and brain tumour surgery, the surgeon is moving on the cutting edge between normal and affected (tumour) tissue. In neurosurgery it may not be possible to take safe margins with tumour excision so the aim is tumour management by debulking (cytoreduction) rather than complete tumour excision. This requires a different mindset than in standard tumour surgery. Rehabilitation of the Neurosurgical Patient Neurosurgery is only the first step in recovery of the patient off its legs. Canine rehabilitation should start on the first day after surgery whenever possible and practical. The paralysed patient requires intensive care and its owner requires guidance. Bedding of the patient should be kept dry, clean and soft at all times. The animal should be turned at regular intervals. Paralysed patients frequently have no voluntary urination. 'Bladder' management requires catheterisation or frequent attempts to empty the bladder by manual abdominal pressure. Animals that soil the perineal region with urine and faeces in the postoperative period run a great risk of development of decubitus ulcers or dermatitis in the perineal region. Urine weakens the skin barrier and enables bacteria to enter through the skin and cause redness and infection. As long as the animal is not urinating spontaneously and has to be catheterised, there is an indication to treat with systemic antibiotics. This may even take up to 2 weeks after surgery. Pain medication postoperatively may include non-steroidal anti-inflammatory drugs (e.g., carprofen) and/or morphine-like substances (e.g., oral tramadol or fentanyl patches). The use of postoperative steroids after laminectomies is highly controversial. Rehabilitation of the paralysed patient may include frequent bathing, muscle massage, exercising standing with support bags, wheelchair walking, hydrotherapy with an underwater treadmill, swimming and exercises for proprioception, etc. The veterinary surgeon may refer the animal to an animal physiotherapist within the practice or outside. A referral letter is made to inform the physiotherapist on the medical history and to provide a channel for feedback on follow-up. Postoperative recovery of conscious nociception is fast (2448 hours), recovery of motor

function may take 6 weeks and recovery of postural reactions (proprioception) may take up to 6 months!

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Bjrn P. Meij, DVM, PhD, DECVS Utrecht, The Netherlands

Root Canal Therapy in the Dog

AUSTRALIAN VETERINARY ASSOCIATION PROCEEDINGS 2009
Rod Salter, BVSC, MACVSC (Veterinary Dentistry) Melbourne Veterinary Dentistry and Oral Surgery Service, Sandringham
20183764

Anatomically the tooth is divided into the crown, (the portion visible above the gum line) the neck (the junction) and the root (the portion under the gingiva enclosed in the socket). The apex of the tooth is the tip of the root. Lateral canals provide passage between the central pulp cavity and periodontal tissues in locations other than at the apex. Lateral or accessory canals are uncommon in dogs and cats. The pulp, located within the tooth, emerges from the tooth and connects with the periodontal ligament at the apex. The pulp is composed of soft connective vascular and nerve

tissue. It contains odontoblasts, fibroblasts, fibrocytes, collagen fibbers, elastic fibbers, blood vessels, and nerves. It is this tissue that responds most dramatically to any insult or injury to the dentition. Innumerable dentinal tubules perforate the dentin at right angles to the pulp and contain cytoplasmic extensions from the odontoblasts called Tomes fibbers. The odontoblasts function to produce dentin throughout the vital life of the tooth, resulting in thicker dentinal walls and narrower pulp cavities as the teeth mature. In young animals, in which the apex is not yet fully developed, the pulp connects with the surrounding periapical tissue through a wide opening. After the root lengthens, the opening at the apex narrows. With increasing age and exposure to physiologic functioning, a layer of cementum gradually covers the dentin and the pulp chamber and root canal narrow. Pulp tissue consists of four layers. The odontoblastic layer covers the periphery of the pulp chamber, with processes extending into the dentinal tubules. Weil's basal layer (cell-poor layer), lies next to the odontoblastic layer in mature teeth. A cell-rich layer is located between the cell-poor layer and the fourth layer which is the central pulp. The dental pulp is a blood-rich organ. Vessels that pass through the apical foramina are distributed throughout the pulp. Most vessels are thin walled with large lumens. Pulp also contains lymph vessels. Physiologically the pulps functions are formative, nutritive, sensory, and defensive. Pulpal tissues produce dentin. As maturation occurs, additional layers of dentin are added, with each odontoblast enclosed and remaining vital in its dentinal tubule that extends to the dentinoenamel / dentinocemental junction. The dentinal tubules and the odontoblastic process narrow toward the periphery of the tooth, tapering to an almost closed structure at the enamel junction cemental wall. The cellular content of the dentinal tubules is significant in endodontic treatment inasmuch as open dentinal tubules can lead to pulpal disease. Pulpal disease decreases dentinal deposition, which ceases entirely after pulpal death. The pulp provides nutrients to the surrounding tissues during and after development. The sensory function of the pulp is a response to pain via nerves that enter the apical foramen. As regards pathophysiology the pulps response to injury is via inflammation. Continued severe irritation results in pulpal death because hyper vascularity and swelling in a closed space effect necrosis once arterial inflow ceases, a consequence of excessive pressure within the pulp space. Pulpal insult can result from extension of the inflammatory process through the dentinal tubules, by direct dentinal insult from topical irritants, through localisation of blood-borne bacteria in hyperaemic pulp, or as a result of periodontal disease in combination periodontic-endodontic lesions. Pulpal damage also occurs as a result of trauma (pulpal exposure resulting from coronal fracture or intradental haemorrhage without pulp exposure), penetration by bacteria from such factors as caries or external resorption, or iatrogenic factors, or it can be idiopathic in origin. Pulpal disease passes from reversible hyperaemia to an irreversible pulpitis and ends in suppurative pulpitis and necrosis. Periapical inflammation and abscess formation are extensions of the pulpal inflammatory response. Microorganisms present in dentin and canals constitute the main sources of dentin microbial irritants of the dental pulp and periapical tissues, respectively. As a consequence of pulp exposure to the oral cavity, the pulp system harbours bacteria and their by-products. The pulp does not have the capability to rid itself of these damaging bacteria as they are located within both the pulp and the dentinal tubules. At best, the defences will temporarily halt or slow their spread or tissue destruction. Sooner or later the bacterial infection will be extensive and will spread throughout the canal. Then bacteria and/or bacterial by-products and other irritants from necrotic tissue will diffuse from the root canal into the periapical tissues with resultant development of a periapical inflammatory lesion. Severity of trauma and the degree of apical closure are important factors in the recovery of the pulpal tissue from physical trauma. Teeth sustaining minimal trauma and teeth with immature apexes have more chance of pulpal survival than do teeth that have been subjected to severe trauma or teeth with closed apexes.

Secondary dentin is formed by the odontoblasts after root formation has been completed. The continuous deposition of dentin results in a progressive reduction in the size of the pulp chamber and root canal. The formation of secondary dentin is the tooth's response to the stimuli of the normal aging process. The formation of tertiary dentin results from irritation of odontoblastic processes within the dentinal tubules. Tertiary dentin is produced by the odontoblasts that are directly affected by the irritation. In cases of dental attrition and abrasion, the formation of tertiary dentin will usually seal off the pulp cavity. With progressive wear, the tertiary dentin may become clinically evident as a brown spot in the centre of the occlusal surface. This can be differentiated from an exposed pulp chamber by probing with a dental explorer. The brown colour is explained by the irregular nature of the tertiary dentine which causes it to stain easily. With severe dental abrasion, pulp exposure may occur if tertiary dentin formation cannot keep pace with the rapid wear. Dentin exposed by uncomplicated dental fractures is initially painful because of the presence of intradentinal nerve fibers and fluid movement through the tubules. Pain is manifested by sensitivity to heat, cold and pressure. The pain eventually disappears as sclerosis and calcification of the dentinal tubules occur. Complicated dental fractures cause pulp exposure. Haemorrhage occurs and an acute pulpitis ensues which is very painful. Soon thereafter, bacterial invasion and obliteration of the blood vessels cause pulp necrosis. Blood vessel obliteration occurs because the narrow root canal does not allow for the swelling associated with an inflammatory reaction. At this stage the condition is no longer painful and it can go unnoticed for a considerable period of time. Sooner or later, however, the infection spreads through the apical delta and causes a periapical periodontitis, which in turn progresses to a periapical granuloma or a periapical abscess. At this stage the condition is painful and facial soft tissue swelling may be evident. A periapical granuloma is visible on radiograph as a round radiolucent area. The pulp tissue in essence reacts to numerous various irritants like other connective elsewhere in the body. The dentinal tubules which continuously "harbour" bacteria and necrotic material ensure the contamination is continuous and persistent. Pulp pathology can range from a transient inflammation (reversible pulpitis) to irreversible pulpitis, which will proceed to total necrosis. Clinically significant is the usual absence of noticeable symptoms to the patient, regardless of the severity or progress of inflammation. Thus, the destruction of the pulp often proceeds without the knowledge of the patient the owner or the vet! Injury to pulp tissue results in cellular damage and release of nonspecific mediators of inflammation, such as histamine, bradykinin, and arachidonic acid metabolites. In addition to nonspecific inflammatory preparations, reactions, immunologic responses can also initiate and perpetuate pulpal diseases. Potential pulpal antigens include bacteria and their by-products, which directly or through dentinal tubules can initiate different types of immunologic reactions. The presence of potential antigens and the identification of immunocompetent cells such as PMN leukocytes, macrophages, lymphocytes, plasma cells and mast cells as well as various classes of immunoglobulins indicate that mediators of immunologic reactions also participate in pathologic changes during pulpal pathosis. As a consequence of these releases, there is increased vascular permeability, vascular stasis, and emigration of leucocytes at the site of injury. Increased capillary permeability due to inflammation causes movement of fluid from the vessels into the tissue. If removal of fluid by venules does not keep up with filtration of fluid from capillaries, an exudate forms in the pulp. The pulp is encased in rigid walls therefore, a small increase in tissue pressure as a result of increased capillary permeability causes passive compression and even complete collapse of the venules at the site of pulpal injury. Affected teeth may first present with a pink or blue tingeing of the tooth. If the pulpitis is reversible, the colour may eventually diminish and the tooth will return to its normal appearance. If irreversible destruction has occurred, the colour changes to a purple-gray as the pulp dies and the blood cell components are degenerated. If exudate produced during irreversible pulpitis is absorbed or drains through caries or an exposure into the oral cavity, pulpal necrosis is delayed and the radicular pulp may remain intact for long periods. In contrast, closure or sealing off of inflamed pulps induces rapid and total pulp necrosis and periapical pathosis. In addition to liquefaction necrosis, ischemic necrosis of dental pulp can occur as a result of traumatic injury and disruption of blood supply. Depending on the severity of irritation, its

duration, and host response, periapical pathology of pulpal origin can range from slight inflammation to extensive tissue destruction. Injury to periapical tissues usually results in cellular damage and release of nonspecific as well as specific immunologic mediators of inflammatory reactions Once the pulpal tissue becomes infected, organisms will continue to invade, seeking new nutrients. As the apical periodontal ligament is the only directly associated soft tissue in this situation, bacterial involvement will eventually extend to these tissues. The periapical tissues have good collateral circulation, which allows the building of a defensive barrier in an attempt to confine the pathogens and their toxins within the root canal system and periapical tissues. In more chronic cases, this barrier generally takes the form of granulation tissue, although it may take purulent or cystic forms at the apex. However, in acute periapical disease abscess formation is more common. Chronic proliferative changes at the apex stimulate dissolution or resorption of periapical bone. This results in the classic periapical lucency on radiographs. Whether an acute or chronic process develops depends on the severity of trauma, pathogenicity of the organism, degree of organism challenge, and host resistance.

PULPECTOMY / ROOT CANAL THERAPY

Although the objective of endodontic therapy is the management and treatment of the injured pulp, attention must be given to the tissues surrounding the pulp, and periapical tissues. Root canal therapy has many advantages over extraction. The best reason is that the tooth is saved rather than resorting to "toothenasia". Standard root canal therapy is less traumatic for the patient and more aesthetically pleasing to the owner than surgical extraction, and the cost of root canal therapy is similar to that of surgical extraction. The objectives of endodontic therapy are to relieve pain, remove infection, prevent further infection, restore and maintain function, and avoid complications associated with extraction.. "In the treatment of any disease, a cure can only be affected if the cause is removed. Since endodontic diseases originate from an infected or affected pulp, it is axiomatic that the root canal must be thoroughly and carefully debrided and obturated." Dr. I Wolch, 1975. There are three major goals of veterinary endodontic therapy that should be attained for reasonable assurance of success: 1) Initially the entire contents of the pulp chamber and canal should be removed with endodontic files and irrigation, 2) Using endodontic files, the canals should be cleaned and enlarged so as to give the canal a slight funnel shape, and 3) The apex (or apices) of the treated tooth should be sealed and the canal packed with an endodontic filling material, and the coronal end sealed against further invasion of organisms. This then constitutes "The Endodontic Triad." The preparation phase means proper coronal access. Before the endodontic system can be dressed, any unsupported or fractured tooth structure should be removed to provide a clear view of the remaining sound tooth structure. This phase is concerned with the debridement of the root canal system and shaping of the root canal in preparation to receive a specific type of filling. Sterilization involves irrigation of the root canal to disinfect the canal and remove pulp tissue remnants and dentin debris, and the installation of intracanal medication for staged treatment. Obturation is the development of a fluid-tight three dimensional seal at the apical foramen and total obliteration of the root canal. This is to eliminate the avenues of leakage from the oral cavity or periradicular tissues into the root canal system. Preparation: Coronal access: This should be well planned to gain straight line access to the root canal. Preoperative radiographs should always be taken to assess the shape and location of the canals, root pathology, and periapical pathology. Coronal access is made with a variety or burs including #l or #2 round bur, or a #330 pear bur. Initial penetration through the enamel should be perpendicular to the enamel, and then angled toward the apex once into the dentin. Access sites: Canine teeth: Fracture location can play a role, but usually 2-4mm coronal to the gingival margin. Check depth and angle with a radiograph. Incisor teeth: Through the fracture site, on the facial surface, or on the lingual or palatal surface.

Mandibular teeth: Mesial root: Through the mesio-occlusal pit on the lingual side, and the distal root on the occlusal surface. Maxillary 4th premolar teeth: Mesial roots: Transcoronal approach, about way from the gingival margin to the cusp on the buccal aspect of the crown, the distal root, about 1 mm distal to the buccal groove on the buccal aspect of the crown. The palatal root can be accessed separately if necessary, or is accessible via the transcoronal approach. Be careful to avoid furcation perforation. A furcation is the site where 2 roots separate from the crown. Prevention of perforation of this area demands that you follow the principles of access preparation, have a thorough knowledge of tooth anatomy and the use of radiographs. Continue preparation by locating the canals with a pathfinder or small size endodontic file. The goal is to leave as much tooth structure as possible while removing enough to allow easy instrumentation. Cleaning and shaping the canal involves the use of a variety of instruments including barbed broaches, Hedstrom files, K-type files, K-type reamers, Gates-Glidden drills, and Peeso reamers. Barbed broaches are used for pulp extirpation. Fully rotate with the canal to engage the pulp tissue. Never force or allow broach to bind against the walls, and don't use in small canals. Hedstrom files have an excellent cutting effect, and cuts only in one direction--retraction. The file resembles a wood screw. If used with rotation, the flutes are locked in the dentin, and are easily fractured if turned or twisted. A K-reamer has half as many twists as a K-file. Both of these cut by being tightly inserted into the canal, twisted clockwise turn, and withdrawn. The cut is made during retraction of the reamer, and penetration and retraction with the file. General file principles: Use 1 to 3 times and then replace. Larger files can be used longer. Inspect the files for unraveling, twists, and bends. Discard if defective! Gates Glidden Drills and Peeso Reamers are engine driven instruments used on a slow speed contra angle handpiece. They are used to prepare the coronal portion of the root canal. Gates Glidden drills tend to separate near the shank. Many instrument aids are available. Talk to the supplier and find what works best for you. Chelating agents lubricate the file, soften the dentin and remove the smear layer. The smear layer is a combination of organic and inorganic debris crushed into a fine paste along the walls of the pulp cavity. The smear layer is created by instrumentation. The disadvantages of removing the smear layer are that it may help occlude the apex and lateral canals, and may help seal the dentinal tubules. The advantages of removing the smear layer are improved removal of bacteria, and may improve the canal sealer interlock. Root canal irrigants should be used frequently during the process of instrumentation. Sodium hypochlorite (bleach) is an antimicrobial that helps dissolve organic debris. Be sure to protect the oral tissue when irrigating with this product. Hydrogen peroxide can be used in conjunction with bleach. It has a good effervescent action, and some antimicrobial properties. Throughout the debriding or filing process, the root canal must be recapitulated. A smaller diameter file is intermittently inserted to the measured apical length and the small bits of debris that are packed into the apex are removed to insure total canal debridement. This confirms the patency of the canal, dislodges dentin chips and debris. Instrumentation and recapitulation continues until clean shavings emerge on the file and the desired canal shape is achieved. The goal is a continuously tapered preparation of the root canal. There are two basic approaches. I. Step-back technique: Preparation is begun at the apex working back up the canal coronally with larger and larger instruments. 2. Step (crown)-down technique: Preparation begins coronally and is advanced apically using smaller and smaller instruments. 3. Hybrid approaches. With the Step-back technique, establish the working length with a small file and endostop. Confirm the working length radiographically. Prepare the apical portion of the canal first with recapitulation using progressively larger files. The step back is done in 1 mm. increments. The Gates Glidden drills are used for coronal and midroot preparations. With the Step-down technique (crown-down technique)--Prepare proper access and locate the canal. The working length is not established first. The coronal 2/3 of the canal is enlarged first using files and

Gates Glidden burs. The apical portion if prepared last. This minimizes binding of files in the coronal 1/3 of the canal. The goals of either technique is an apex that is clean with "natures" shape basically unchanged, a body shape that is smooth, continuous flowing, and tapered, and the canal is free of pulp remnants and debris. When satisfied with the shape of the canal, irrigate again with bleach and water, then dry with paper points. These are available in 25 and 55 mm lengths, with the 25mm at the same sizes as files, and 55mm, in extra fine, fine, medium and coarse. If persistent haemorrhage is encountered when drying the canals, there is vital pulp tissue remaining, haemorrhage from the periapical tissues, or root resorption present. If this happens, consider 2-stage therapy. Dry the canal, place calcium hydroxide intracanal medication (paste filler, Kfile or injection) as a temporary filling, and complete the procedure 3-4 weeks later. The goal of obturation is a 3 dimensional fill and a tight seal. The ability to achieve this is highly dependent on the quality of the canal preparation. Failure to fully obdurate and seal the canal will lead to endodontic failure. You are ready for obturation when the canal is clean and shaped to an optimal size and is dry. Two basic obturation techniques are vertical and lateral compaction. Root canal sealers fill the space gutta percha is unable to fill. The ideal characteristics are: tacky when mixed to provide good adhesion to the canal wall, radio opaque, will not shrink upon setting, not stain, bacteriostatic, sets slowly, tissue tolerant, and soluble in common solvents. Most root canal sealers are eugenol based (zinc oxide-eugenol); non-eugenol based such as epoxy resins and glass ionomers, and therapeutic sealers such as calcium hydroxide. Most of these come as a powder and liquid spatulated together to thicken consistency and are then introduced into the prepared root canal. The canal may be filled by utilizing a Lentulo spiral filler on a reduction gear contra angle, or by using endodontic files or gutta percha points to place the cement into the canal. Gutta percha is the most commonly used material to obturate root canals. They come in various lengths, with the standard sized corresponding to file sizes, or conventional, that are more tapered and pointed. Spreaders and pluggers are used to compact gutta percha into the prepared root canal. Spreaders have pointed tips, and pluggers have flat tips. Many types and sizes of spreaders and pluggers are available. A minimum of 4 films are taken during a procedure: 1) Preoperative, 2) Working length, 3) Master cone placement, and 4) Final obturation. The master cone is selected based on the final apical file used. The cone is grasped with cotton pliers at a position that approximates the working length. It should fit to working length or shorter (.5mm), contact the walls in the apical portion and demonstrate slight resistance to removal. The fit is confirmed radiographically. Prepare the sealer and place into the canal. Seat the master cone. Excess sealer will extrude out the access point. Proceed with either lateral or vertical compaction. With lateral compaction, the spreader is inserted, allowed to remain 1 minute as gutta percha is compacted laterally and somewhat apically. The spreader is removed using rotation and coronal gutta percha is removed. The depth of penetration is measured using an endostop on the spreader. Auxiliary points that seat to penetration depth are chosen. That point is dipped in sealer and inserted into the canal. The spreader is returned to the canal to laterally compact again. Secondary vertical compaction also occurs. The process is continued until the canal is fully obturated and a radiograph is taken to confirm the fill. With vertical compaction, the master cone is seated in the canal. Use heated pluggers to soften and prefit cold pluggers to condense the gutta percha. Heated instruments are penetrated into the gutta percha, left 2-3 seconds to allow heat transfer, and removed. Large pluggers are used to compact the gutta percha. Heated instruments are again inserted to selectively remove coronal gutta percha. Midsize pluggers are used to compact the gutta percha. The process is repeated with a smaller plugger until the apical gutta percha mass is compacted.

There is no statistical difference in filling efficiency between lateral vs. vertical compaction. Vertical compaction does fill accessory canals with a significantly greater incidence. Remove the gutta percha from the access preparation, clean excess sealer from the walls. Place an intermediate layer to prevent contact of the composite with any remaining sealer. Acid etch the dentin and enamel, place bonding agent, place composite and light cure, and smooth the composite. Place a final layer of unfilled resin or composite sealant and cure. Coronal leakage through improperly placed restorations can result in endodontic failure. Final radiographs should be taken after the restorative is placed. Follow-up radiographs should be taken at 1 and 3 years if there was no periapical lucency present, and initially at 6 to 9 months if periapical lucency was present. Additional film intervals are based on the results of the first follow-up films.

SPEAKER INFORMATION
(click the speaker's name to view other papers and abstracts submitted by this speaker) Rod Salter, BVSc, MACVSc (Veterinary Dentistry) Melbourne Veterinary Dentistry and Oral Surgery Service Sandringham