SPINAL CORD ANATOMY, LOCALIZATION, AND OVERVIEW OF SPINAL CORD SYNDROMES

Gregory Gruener, Jose Biller ABSTRACT

Spinal cord syndromes are unique clinical presentations that localize lesions to the spinal cord by their pattern of anatomic dysfunction while implying their underlying etiology. Recognizing these patterns and their significance is best accomplished by relearning and appreciating the relevant anatomy and relationships, which are the major focus of this review. This clinical-anatomic background will provide the framework for the clinical topics that follow in this issue.

KEY POINT:

A notch in the inferior aspect of the pedicle will contribute to the boundary of the intervertebral foramen when adjacent vertebrae are articulated and through which the spinal nerve and intervertebral vessels will pass.

ANATOMY OF THE SPINAL CORD Relationship to the Vertebral Levels and Spine The typical vertebra consists of a columnar body with a larger transverse than anterior-posterior diameter and serving as the primary support for the spine. The vertebral arch extends from the body, forming a protective enclosure, and consists of a pedicle on either side that unites posteriorly through the two laminae. Three processes arise from the vertebral arch, laterally the transverse and posteriorly the spinous, serving as the attachment site for muscles (Figure 1-1). Four separate articular processes, a superior pair extending cranially and an inferior pair extending caudally, serve to direct or limit movement to specific directions by articulating with the vertebra above and below (Figure 1-2).

A notch in the inferior aspect of the pedicle will contribute to the boundary of the intervertebral foramen when adjacent vertebrae are articulated and through which the spinal nerve and intervertebral vessels will pass. An intervertebral disc is interposed between each vertebral body and consists of alternating, crisscrossing bands of fibrous connective tissue, the annulus fibrosus, which surround a gelatinouslike core, nucleus pulposus. The vertebral discs will contribute 25% of the height of the vertebral column. Several ligaments and fibrous attachments of muscles help to bind together and enclose the vertebral column. The most prominent are the anterior longitudinal (along the anterior aspect of the bodies), the posterior longitudinal (along their posterior aspect), the ligamentum flavum (posterior wall of spinal canal), and the interspinous ligament. The fused periosteum of the cra-

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Relationship Disclosure: Dr Gruener has received personal compensation for speaking engagements with Medical Education Resources, Inc. Dr Biller has nothing to disclose. Unlabeled Use of Products/Investigational Use Disclosure: Drs Gruener and Biller have nothing to disclose.

Copyright 2008, American Academy of Neurology. All rights reserved.

 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

FIGURE 1-1

Functions of the constituent parts of a vertebra.

Reprinted with permission from Grant JCB. An atlas of anatomy. 6th ed. Baltimore: Williams & Wilkins, 1972.

nium and meningeal layer of the dura matter will separate caudal to the foramen magnum, forming an anatomic

space, epidural space, which extends the length of the spinal column (Figure 1-3). Within this space reside fatty

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FIGURE 1-2

Lateral view of a lumbar (second) vertebra.

Sup superior; Inf inferior. Modified with permission from Grant JCB. An atlas of anatomy. 6th ed. Baltimore: Williams & Wilkins, 1972.

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tissue and the vertebral venous plexus. The separation of these fused layers of connective tissue allows the vertebral column to move separately relative to the dural sac that surrounds the spinal cord and roots. The dorsal and ventral roots will enter a dural sleeve at the level of their intervertebral foramina, lateral to the dorsal spinal ganglia, fusing to form the spinal nerves. A layer of pia mater surrounds the surface of the spinal cord, and between it and the inner layer of the arachnoid tissue is the subarachnoid space. Between successive nerve roots, a bandlike extension of the pia mater will arise from the surface of the spinal cord, denticulate ligament, attaching to the dura and serving to anchor the spinal cord (Figure 1-4). The ventral nerve roots lie anterior and the dorsal nerve roots posterior to this ligament. The spinal cord is cylindrical in shape, but flattened dorsoventrally. It is widest at the cervical enlargement, and a second enlargement occurs in the lumbosacral level of the cord, both reflecting the innervation levels of the limbs. At birth the spinal cord typically extends to the lower border of L3. By adulthood its tip is usually at the L1-2 vertebral disk level but can end at T12 or descend to the lower border of the L2 vertebrae. Each segment of the spinal cord usually has a set of dorsal (sensory) and ventral (motor) rootlets that emerge and join together to form their corresponding root; dorsal roots have their corresponding ganglia (dorsal root ganglia). The dorsal and ventral roots will fuse to form the spinal nerve as it exits from the spinal canal. The spinal nerves then divide into individual branches. There are usually 31 pairs of spinal nerves: eight cervical, 12 thoracic, five lumbar, five sacral, and usually one coccygeal (Figure 1-5). The first pair of spinal nerves will exit between the skull and the atlas (C1), the next six above their respec-

tively numbered vertebrae (C2 through C7), but C8 above the T1 vertebrae. The remaining spinal nerves will exit below the vertebrae of the corresponding number. The spinal nerves will have a dorsal root ganglion usually located within the intervertebral foramen. C1 lacks a cutaneous sensory dermatome. Below the L1 vertebra, lumbar and sacral spinal nerve roots need to descend in order to reach their point of exit; this collection of spinal roots is called the cauda equina. The cord will terminate in a thin-walled sac covered by pia mater, the filum terminale, which fuses with the periosteum of the dorsal surface of the coccyx. The gray matter of the spinal cord can be divided into a posterior column

KEY POINT:

At birth the spinal cord typically extends to the lower border of L3. By adulthood its tip is usually at the L1-2 vertebral disk level but can end at T12 or descend to the lower border of the L2 vertebrae.

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FIGURE 1-3

Spaces associated with the spinal meninges.

Modified with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:49. Copyright 2007, Elsevier.

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINT:

The first pair of spinal nerve roots will exit between the skull and the atlas (C1), the next six above their respectively numbered vertebrae (C2 through C7), but C8 above the T1 vertebrae. The remaining spinal nerves will exit below the vertebrae of the corresponding number.

FIGURE 1-4

Relationships of the sixth cervical spinal nerve.

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:171. Copyright 2007, Elsevier.

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(or horn), a lateral column, and an anterior column (or horn) that respectively divide the adjacent white matter into a posterior, lateral, and anterior funiculus. At the junction between white and gray matter are short ascending and descending axons that arise from small neurons within the spinal cord gray matter and comprise the intrinsic or intersegmental reflex pathways, proprius bundles (or system) or fasciculi proprii and are named by their location. While the posterior funiculi primarily consist of ascending sensory fibers, they also contain their descending collateral fibers, which serve to further integrate intrinsic spinal reflexes and form their own distinct, but small, fasciculi. Within the gray matter of the spinal cord cell groups can be identified (right portion of Figure 1-6), with those in the posterior horn participating in sensory pathways and those in the intermediate and anterior horns serving motor functions. In addition, layers of synaptic inputs within the spinal cord have also been identified. These are called Rexed laminae and are labeled I to X (left side of Figure 1-6). Those within the posterior horn,
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laminae I through V, more clearly demonstrate a laminated appearance. Major Ascending Tracts The diagrammatic representation of both ascending and descending tracts within the spinal cord reflects a level of certainty that, while useful for comprehension, oversimplifies a more complex anatomic distribution and anatomic variations that likely exist (Nathan et al, 1990; Nathan et al, 1996; Nathan et al, 2001). Indeed, the concept of a tract as a homogenous group of fibers is also an oversimplification. Despite their shortcomings, however, such generalizations have proven to be clinically useful. The sensory pathways and tracts we will first review are responsible for transmitting sensory information that is perceived (conscious) as well as nonconscious sensation. The dorsal root ganglia contribute nerve fibers that at the dorsal root entry zone will further segregate into a medial group of large-diameter fibers, which will enter the posterior funiculi of the spinal cord, and a lateral group of small-diameter myelinated and unmyelinated fibers. This segregation is modality

specific and will give rise to the major ascending tracts within the spinal cord (Figure 1-7). This lateral group of fibers will divide into short ascending and descending branches within the tract of Lissauer and predominantly synapse on neurons within laminae I and II of the posterior horn. The posterior columnmedial lemniscal pathway receives its input from the largest group of sensory receptors (neuromuscular spindles and Golgi tendon organs) entering through the medial portion of the dorsal root entry zone. These fibers form a lamination within the posterior column, and most medial are those originating from the lower extremity and trunk, fasciculus gracilis, carrying sensory information from the lower extremity; and laterally is the fasciculus cuneatus, carrying similar sensory information from the upper trunk and limb (Figure 1-8). As these fibers enter the posterior column they bifurcate and one branch ascends to the medulla where it will synapse onto its second-order neuron within the nucleus gracilis or cuneatus. Those neurons will then project across the midline in the sensory decussation, continuing their ascent to the thalamus as the medial lemniscus. The thirdorder neurons of this pathway will then arise from the thalamus and project to the somatic sensory cortex. The other branch of that initial bifurcation of entering fibers will synapse within the posterior gray horn laminae II, III, and IV at various levels (the ascending branch also gives off collaterals to the dorsal gray horn). The traditional functions of this system are believed to be relaying conscious proprioception as well as discriminative touch. Yet, its role in supporting the motor cortex as it carries out its intricate and precise digital movements may better or more accurately characterize its function and importance (Davidoff, 1989). The other major conscious sensory

FIGURE 1-5

Vertebral column, spinal cord, and nerve relationships.

Modified with permission from Moore KL, Dalley AF. Clinically oriented anatomy. Philadelphia: Lippincott William & Wilkins, 1999:478.

pathway is the anterolateral spinothalamic tract (Figure 1-9). This tract arises from neurons in laminae I, II, IV, and V that receive excitatory as well as inhibitory input from neurons within the substantia gelatinosa (lamina II). The axons that arise from those neurons cross in the anterior commissure of the spinal cord and arrange themselves in the anterolateral location within those spinal cord funiculi. There are two divisions, and the most anterior is the anterior spinothalamic tract, which has a somatotopic organization and mediates the sensory moContinuum: Lifelong Learning Neurol 2008;14(3)

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modality arranged with cervical representation most medial and sacral most lateral; pain, tickle, and itch sensory modalities are more peripheral while temperature is more medially represented within this tract. These tracts ascend, merge within the brainstem as the spinal lemniscus, are joined later by the trigeminal lemniscus (afferents from the head), and together terminate within the thalamus. Their third-order neurons will also project to the somatic sensory cortex. The spinoreticular tract arises from neurons within laminae V to VII and accompanies the spinothalamic pathway, both as a crossed and uncrossed tract, terminating within the brainstem. It serves as an arousal system for the cerebral cortex (through the reticular activating system), and it helps to interpret the nature of a stimulus (pleasurable or not). The spinocerebellar tracts provide nonconscious proprioception (Figure 1-8). Fasciculus gracilis collaterals provide information from lower limb primary afferents (especially muscle spindle), synapse upon the posterior thoracic nucleus in lamina VII (extends from T1 through L1 spinal cord levels, previously called the dorsal nucleus or Clarke column), and give rise to the posterior spinocerebellar tract. The tract ascends and reaches the cerebellum through the inferior cerebellar peduncle. A similar group of afferents from the fasciculus cuneatus provides information from the upper limb and synapses on the accessory cuneate nucleus, which gives rise to the cuneocerebellar tract. It also reaches the cerebellum through the inferior cerebellar peduncle. The following two spinocerebellar tracts will provide information about the state of internuncial function in regard to spinal cord reflexes and arise from the intermediate gray matter of the spinal cord. (1) The anterior spinocerebellar tract arises from the lower spinal cord

FIGURE 1-6

Spinal cord laminae and cell groups (midthoracic level).

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:182. Copyright 2007, Elsevier.

dality of touch and pressure. The lateral spinothalamic tract is lateral and posterior, somatotopically as well as

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FIGURE 1-7

Primary afferent neuron targets in the posterior horn.

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:183. Copyright 2007, Elsevier.

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and will initially cross, ascend to the superior cerebellar peduncle, cross again to its side of origin, and terminate within the cerebellum. (2) From the upper half of the spinal cord the rostral spinocerebellar tract will ascend and, through the inferior cerebellar peduncle, enter the cerebellum. The remaining tracts to be considered include the spinotectal tract, which ends in the superior colliculus, runs with the spinothalamic tract, and brings somatic sensory information to the superior colliculus. The spinoolivary tract projects to the inferior olivary nucleus and through its effects on the contralateral cerebellar cortex will modify motor activity. Major Descending Tracts The motor cell types within the anterior gray horns are of two types: (1) Alpha motor neurons (physiologically defined as tonic or phasic in regard to the physiologic/functional type of muscle fibers they innervate) supply the extrafusal skeletal muscle fibers, and (2) gamma motor neurons supply the intrafusal muscle fibers of neuromuscular spindles. The motor unit comprises an individual alpha motor neuron, its axon, and all the muscle fibers (varying from a few to hundreds, dependent on the precision of the movement) it will subsequently innervate. Recurrent axons of alpha motor neurons excite inhibitory internuncial neurons, Renshaw cells, which serve to inhibit their own firing (recurrent inhibition). At each segmental level of the spinal cord, however, alpha motor neurons also receive numerous inhibitory (usually on their soma) as well as excitatory (through synapses on their dendritic trees) inputs. These inputs arrive from both supraspinal pathways as well as through the propriospinal neurons (local) and their pathways. Most of these fibers and inputs will exert an inhibitory effect on alpha motor neurons. If

FIGURE 1-8

Ascending pathways (upper cervical level).

GF gracile fasciculus; CF cuneate fasciculus; PLT posterolateral tract; PSCT posterior spinocerebellar tract; RSCT rostral spinocerebellar tract; LSTT lateral spinothalamic tract; ASCT anterior spinothalamic tract; SOT spinoolivary tract; ASTT anterior spinothalamic tract; ST spinotectal tract; SRT spinoreticular tract.
Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:187. Copyright 2007, Elsevier.

those effects are abolished by a cord lesion, the disproportionately strong influence of the spinal intrinsic circuits will lead to the clinical phenomenon of spasticity. Figure 1-10 demonstrates the columnar organization of motor neurons into groups that then innervate muscles with similar function. Those most medial innervate the axial musculature, and moving traversely through those groups of neurons, they also move from the innervation of proximal to distal limb muscles and finally to the intrinsic muscles of the hand or foot. Another result of this neuronal organiContinuum: Lifelong Learning Neurol 2008;14(3)

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINTS:

The dorsal root ganglia contribute nerve fibers that will further segregate at the dorsal root entry zone into a medial group of large-diameter fibers that will enter the posterior funiculi of the spinal cord and a lateral group of small-diameter myelinated and unmyelinated fibers. The traditional functions of the posterior columnmedial lemniscal system are believed to relay conscious proprioception and to mediate discriminative touch. Yet, its role in supporting the motor cortex as it carries out its intricate and precise digital movements may better or more accurately characterize its function and importance.

FIGURE 1-9

Spinothalamic pathways (sensory modalities, upper cervical level).

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:187. Copyright 2007, Elsevier.

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zation is alpha neurons innervating extensor muscles lying ventral or anterior to those that innervate flexor muscles. Dysfunction of these neurons results in the clinical features of weakness, atrophy, and fasciculations, as well as areflexia when their loss is marked. The long descending tracts (corticospinal, reticulospinal, tectospinal, vestibulospinal, raphespinal) and aminergic and autonomic pathways will terminate on interneurons, which influence alpha and gamma motor neuron function. The rubrospinal tract is small and lies anterior to the lateral corticospinal; in humans its role is unclear. Similar to sensory pathways, the discrete locations indicated within the accompanying diagrams are used as simplifications and conceal a more complex and variable distribution of these pathways that explains the discrepancy at times encountered between clinical findings and visualized anatomic lesions.
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The majority of fibers that give rise to the corticospinal tract have their origin in primary motor cortex (perhaps 50%), but supplementary motor cortex and premotor cortex, as well as somatic sensory cortex, also contribute. Some of these projections will end on brainstem nuclei (corticobulbar or corticonuclear), while those from sensory cortex project onto sensory nuclei in the brainstem and spinal cord that modulate their transmission of sensory information. Those fibers that reach the medulla form the pyramids, visible on its ventral surface. Seventy percent to 90% of these fibers cross the ventral midline in the pyramidal decussation, giving rise to the lateral corticospinal tract within the spinal cord. A somatotopic organization results with fibers destined for the sacral area most lateral and those to the cervical, medial (Figure 1-11). The remaining fibers descend uncrossed either within the lateral corticospinal tract (uncrossed

lateral corticospinal tract) or the majority adjacent to the anterior median fissure as the anterior corticospinal tract to innervate paraspinal and axial muscles. At the appropriate level fibers will cross through the anterior white commissure to provide their contralateral innervation. All corticospinal neurons appear excitatory with glutamate as their neurotransmitter. The corticospinal tract innervates not only alpha and gamma motor neurons, but also Renshaw cells, excitatory and inhibitory internuncials, and, through presynaptic inhibition, suppresses some sensory transmission within the spinothalamic tract in voluntary movement. The proximity of the lateral corticospinal tract to the motor neurons that innervate distal limb muscles supports its role in facilitating the performance of skilled movements and the belief that an isolated pyramidal lesion only results in flaccid paralysis and loss of skilled motor function of the distal limb muscles.

The reticulospinal tracts, through shared internuncials with the corticospinal tract, act upon motor neurons of axial as well as proximal limb muscles. They are considered part of the extrapyramidal system of motor control (with the lateral vestibulospinal and tectospinal tracts) and are involved in locomotion as well as posture. The medullary reticulospinal tract is believed to act on flexor motor neurons and the pontine reticulospinal tract on extensor motor neurons. The tectospinal tract arises from brainstem tectum and orients the head to visual or auditory stimulation. The lateral vestibulospinal tract originates in the lateral vestibular nucleus (of Deiters) and helps in maintaining the center of gravity for the body. The raphespinal tract originates from its nucleus in the medulla and modulates sensory transmission from its position within the Lissauer tract. The aminergic pathways arise from their cell groups within the pons and medulla

KEY POINT:

The lateral spinothalamic tract is somatotopically, as well as modality, arranged with cervical representation most anterior and sacral most posterior. Pain, tickle, and itch sensory modalities are more peripheral while temperature is more medially represented within this tract.

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FIGURE 1-10 Anterior gray horn cell column and somatotopic organization.
Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:192. Copyright 2007, Elsevier.

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINT:

The long descending tracts (corticospinal, reticulospinal, tectospinal, vestibulospinal, raphespinal), and aminergic and autonomic pathways will terminate on interneurons, which then influence alpha and gamma motor neuron function.

and have inhibitory effects on sensory neurons and facilitatory effects on motor neurons through a widespread distribution in the spinal cord gray matter. The central autonomic pathways arise from the hypothalamus as well as associated brainstem nuclei, terminating on neurons within the intermediolateral cell columns. Vascular Supply of the Spinal Cord The arterial blood supply to the spinal cord comprises three longitudinally oriented vessels as well as contributions from numerous radicular vessels (Bowen and Pattany, 1999). A rich vascular plexus (arterial or pia vasocorona or plexus) arises from anastomoses between these vessels along the surface of the spinal cord and from which medullary vessels penetrate into both the white and gray matter. These penetrating vessels are end arteries and do not anastomose further.

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FIGURE 1-11 Descending pathways (upper cervical level).

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:198. Copyright 2007, Elsevier.

The anterior spinal artery arises from the union of the anterior spinal branches of the vertebral artery and descends within the anterior median fissure of the spinal cord down to the conus medullaris. Its largest caliber is at the lumbosacral area, and smallest at the thoracic area, which is also considered its watershed area. The two posterior spinal arteries also originate from the vertebral arteries but descend along the line of attachment of the dorsal nerve roots, posterolateral sulcus, on either side. At the conus medullaris, the anterior and posterior spinal arteries communicate though anastomotic branches (Figure 1-12). Thirty-one pairs of small radicular arteries enter every intervertebral foramen supplying their corresponding nerve roots. Some of these are larger and also supply the spinal cord, radiculomedullary branches. There may be six to 10 such arteries, and through their anterior radicular branch they contribute to the anterior spinal artery. The cervical and first two thoracic segments receive these arteries from branches of the vertebral and thyrocervical trunk, T3 to T7 spinal cord usually from an intercostal artery, and the remainder of the spinal cord receives the largest and most constant artery of Adamkiewicz (arises from a left-sided intercostal or lumbar artery, usually at the T9 through L2 spine level), which supplies the lumbar enlargement and conus medullaris. The posterior spinal arteries receive contributions from 12 to 16 posterior radicular arteries, including a radicular branch from the artery of Adamkiewicz. The intrinsic arterial supply of the spinal cord consists of a centripetal (posterior spinal arteries and the anterolateral plexuses) and a centrifugal (anterior sulcal arteries) system (Figure 1-13). The centripetal system is formed from radial arteries directed inward and supplying the posterior white columns, and through shorter

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KEY POINTS:

The majority of fibers that give rise to the corticospinal tract have their origin in primary motor cortex, but supplementary motor cortex and premotor cortex, as well as somatic sensory cortex, also contribute. Within the pyramidal decussation, 70% to 90% of fibers will decussate and give rise to the lateral corticospinal tract. A somatotopic organization develops with fibers to the sacral area most lateral and those to the cervical, medial. Thirty-one pairs of small radicular arteries enter every intervertebral foramen supplying their corresponding nerve roots. Some of these are larger and also supply the spinal cord, (radiculomedullary branches). There may be six to 10 such arteries, and through their anterior radicular branch they contribute to the anterior spinal artery.

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FIGURE 1-12 Arterial supply of the spinal cord.

Reprinted with permission from Moore KL, Dalley AF. Clinically oriented anatomy. Philadelphia: Lippincott William & Wilkins, 1999:487.

radial penetrating vessels the peripheral rim of perhaps one-third to onehalf of the spinal cord. The centrifugal system arises from sulcal arteries of the anterior spinal artery that pass back into the anterior medial sulcus and then turn right or left to supply the adjacent gray and white matter. Smaller branches from the anterior spinal artery

also contribute to the arterial vasocorona that envelops the spinal cord and through their short penetrating arteries supply the anterior rim of the spinal cord. In general, the centrifugal system (anterior spinal artery) supplies the anterior two-thirds of the spinal cord. Analogous to the arterial blood supply, venous drainage of the spinal
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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

FIGURE 1-13 Arterial supply of a spinal cord segment.

Reprinted with permission from Haerer AF. DeJongs: the neurologic examination. 5th ed. Philadelphia: Lippincott Company, 1992:582.

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FIGURE 1-14 Venous drainage of a spinal cord segment. Krauss WE. Vascular anatomy of the spinal cord. Neurosurg Clin N Am 1999;10(1):915.
Reprinted with permission from Mayo Foundation for Medical Education and Research. All rights reserved.

cord also involves a longitudinal system of veins, the larger posterior spinal vein and the anterior. Through a circumferentially arranged venous anastomosis, coronal venous plexus, within the pia mater on the spinal cords surface, they are connected (Figure 1-14). The anterior spinal vein will communicate superiorly with the venous system of the brainstem and inferiorly end at the dural sac in the sacrum. The posterior spinal vein communicates with radicular veins at the cervical level and extends down to the conus medullaris. At each spinal cord segment small radicular veins drain the nerve roots, but at some levels larger veins, medullary veins, will arise from the anterior median spinal

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vein. There are approximately 10 to 20 anterior veins and a similar number of posterior medullary veins, asymmetric in location and not concomitant with the medullary arteries. The largest are in the lumbar region: the great anterior medullary vein (usually accompanying the nerve roots between T11 and L3) and the great posterior medullary vein usually at L1 or 2. The posterior half of the spinal cord will drain into the posterior and the anterior half into the anterior medullary veins. These medullary veins follow and penetrate the dura with the nerve root and in the intervertebral foramen will unite with the radicular veins, internal and external vertebral plexus to form the intervertebral vein that drains blood from the spine and spinal cord. Prior to their exit from the dura matter, these veins are valveless (Gillilan, 1970; Krauss, 1999). The cervical intervertebral veins will drain into the deep cervical and vertebral veins and will empty into the superior vena cava through the brachiocephalic and subclavian vein. At the thoracic cord they will connect

FIGURE 1-15 Vertebral venous plexus.

Modified with permission from Moore KL, Dalley AF. Clinically oriented anatomy. Philadelphia: Lippincott William & Wilkins, 1999:466.

with the intercostal veins and then via the azygos and hemiazygous veins will enter the superior vena cava. The remainder of the venous drainage from the spinal cord can follow a similar pathway or, through the azygous and hemiazygous veins, enter the common iliac veins and then the inferior vena cava. Within the spinal canals epidural space is also a longitudinally and cir-

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FIGURE 1-16 Cord transection (modalities involved).

Reprinted with permission from Souayah N, Khella S. Neurology examination & board review. New York: McGraw Hill, 2005:44.

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cumferentially arranged anastomosis of valveless veins, the internal venous plexus (anterior and posterior) (Figure 1-15). It communicates with the spinal cord through the medullary and radicular veins, and vertebral body through a basivertebral vein, but it also drains to a separate plexus that surrounds the vertebra, the external vertebral plexus (anterior and posterior divisions). Through the previously mentioned routes, it will eventually empty into the superior or inferior vena cava. SPINAL CORD SYNDROMES A syndrome (symptom complex) represents a complex of signs and symptoms that appear in combination and present as a clinical picture. It may have a specific cause, disease, or inherited abnormality, but this is not a requirement and at times has resulted in some confusion in the use and diagnostic significance of the term. Some of the reported etiologies for the respective syndromes are listed in Table 1-1.

TABLE 1-1
Etiology

Spinal Cord Syndromes and Their Etiologies (Representative Examples) Complete Cord Transection BrownSe quard Syndrome Anterior Spinal Artery Syndrome

Vascular

*Aortic dissection, *vasculitis, *atherosclerosis of the aorta *Postinfectious, *multiple sclerosis, *postvaccinal Traumatic spine injury, herniated disc Epidural hematoma (anticoagulants) *Traumatic spine injury Postoperative spine, aorta or thoracic surgery, postoperative spinal arteriovenous malformation surgery, decompression injury

Inflammatory or infectious Traumatic Iatrogenic or toxin

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Metabolic

Endocrine Neoplastic Degenerative or Hereditary Tumor, paraneoplastic Intramedullary tumors Cervical spondylosis

HTLV-I human T-cell leukemia virus I; HAM human T-cell lymphotropic virusassociated myelopathy. *Classic or most common associated etiologies.

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Complete Cord Transection A complete cord transection disrupts the sensory tracts ascending from below the level of the lesion and the descending tracts from above (Figure 1-16). However, as many such lesions are incomplete, the clinical deficit will reflect the extent of the injury. On physical examination a sensory level will be detected, using pinprick loss, and is the most valuable finding that identifies the spinal cord as the site of the lesion. While sensory loss is expected to involve all modalities below

the level of the lesion, the actual spinal cord level involved may be higher and the presence of radicular pain or segmental paresthesias may serve as a more accurate localizer. Radiation of pain may also occur, and with cervical spinal cord lesions pain can radiate into the arms, thoracic into the chest or abdomen, and lumbar or sacral spinal cord into the legs. Careful examination for overlying vertebral spine tenderness may suggest an underlying destructive process such as a neoplasm or infection as the etiology, and pain that lessens

KEY POINT:

In cord transection, the most valuable finding that identifies the spinal cord as the site of the lesion is pinprick sensation. The actual spinal cord level involved may be higher; the presence of radicular pain or segmental paresthesias may serve as a more accurate localizer.

Posterolateral Column Syndrome

Central Lesion

Posterior Column Syndrome

Anterior Horn Cell Syndrome

Combined Anterior Horn Cell Pyramidal Syndrome

HTLV-1

HIV HTLV-1 (HTLV associated myelopathy, HAM, or tropical spastic paraplegia) Late sequelae of spinal cord injury Nitrous oxide myeloneuropathy

*Neurosyphilis

Poliomyelitis, West Nile virus

Epidural spinal cord compression Postradiation

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*Vitamin B12 deficiency *Copper deficiency myeloneuropathy Hexosaminidase deficiency

Intramedullary spinal cord tumors Cervical spondylosis *Syringomyelia *Spinal muscular atrophies (hereditary motor neuropathies) *Amyotrophic lateral sclerosis

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as anhidrosis, trophic skin changes, impaired temperature control, and vasomotor instability below the level of lesion can also be demonstrated (Cases 1-1 and 1-2). Brown-Se quard Syndrome A hemisection of the spinal cord results in this characteristic syndrome (Tattersall and Turner, 2000) (Figure 1-17). Loss of pain and temperature sensation occurs contralateral to the side of injury due to interruption of the crossed spinothalamic tract, but usually a clinical sensory level is one or two segments below the level of the lesion, reflecting the ascending nature of this crossing tract (Nathan et al, 2001). Below the site of the lesion there is ipsilateral loss of proprioceptive function due to interruption of the ascending fibers of the posterior columns, but such modalities of sensation may also arise from within the spinocerebellar tracts as well (Davidoff, 1989). Ipsilateral weakness below the lesion reflects the interruption of the descending corticospinal tract. In a slowly progressing lesion hyperreflexia and an extensor toe sign will be elicitable, while in an acute lesion those findings may initially be absent. Damage to the ventral roots or anterior horn cells results in segmental lower motor neuron findings at the level of the lesion, but these are clinically difficult to identify in thoracic spinal cord lesions. Finally, if spinal root irritation occurs, radicular pain, again at the site and side of the lesion, may be experienced and more clearly define the spinal cord level. Anterior Spinal Artery Syndrome The vascular nature of this syndrome is manifested in its abrupt onset with the deficit occurring within minutes or hours from its initiation (Novy et al, 2006). Clinically the syndrome presents with back or neck pain and at

quard FIGURE 1-17 Hemisection of the cord (Brown-Se syndrome).

Reprinted with permission from Souayah N, Khella S. Neurology examination & board review. New York: McGraw Hill, 2005:46.

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with sitting or standing is suggestive of a malignancy. While further historical details may be helpful, laboratory and radiologic studies are necessary to more definitively identify an etiology. Weakness, either paraplegia or tetraplegia, occurs below the level of the lesion, owing to the interruption of the descending corticospinal tracts. Initially, the paralysis may be flaccid and areflexive because of spinal shock, but eventually, hypertonic, hyperreflexive paraplegia or tetraplegia occurs with bilateral extensor toe signs, loss of superficial abdominal and cremasteric reflexes, and extensor and flexor spasms (Adams and Hicks, 2005). At the level of the lesion lower motor neuron signs (paresis, atrophy, fasciculations, and areflexia) in a segmental distribution and reflecting damage to the local anterior horn cells or their ventral roots may be demonstrated. These lower motor neuron signs may be quite subtle in thoracic lesions but can localize a lesion to a specific spinal cord level. Urinary and rectal sphincter dysfunction with incontinence, sexual dysfunction, and signs of autonomic dysfunction such
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times in a radicular pattern, usually followed by a flaccid paraplegia and less commonly tetraplegia. Urinary and bowel incontinence are usually present. A sensory level to temperature and pinprick is found that reflects the involvement of the spinothalamic tracts bilaterally, but posterior column modalities of sensation remain relatively intact (Figure 1-18). Although the thoracic spinal cord may be an anatomic watershed zone with respect to regional blood supply (Figure 1-19), the lumbosacral cord neurons appear to be more susceptible to ischemia (Duggal and Lach, 2002). The initial motor presentation progresses from a flaccid paraplegia to one of spasticity with hyperreflexia and Babinski signs (Case 1-3). Central Lesions In this and in the syndromes discussed below, the underlying pathologic process is usually an insidious one, and the features of the disease develop over an extended period of time. When fully developed, the specific syndrome is more clearly recognized, but early during the process features may be incomplete, leading to difficulty and a delay in recognizing the syndrome. This syndrome results from a pathologic process in and around the central canal, initially involving those tracts that cross through the gray matter (anterior and lateral spinothalamic tracts) (Figure 1-22). The resulting sensory impairment is termed a dissociated sensory loss (loss of pain and temperature sensation with preservation of position, vibration, and touch). The typical site of involvement in the cervical spinal cord and the particular sensory modalities initially involved result in a clinical presentation in which sensory loss occurs in a vest- or shawl-like pattern over the upper extremities and shoulders. As the size of the lesion increases, other fiber tracts will be involved, dependent on the direction and extent of the pathologic process. With extension anteriorly, a flaccid

FIGURE 1-18 Arterial spinal artery syndrome.

Reprinted with permission from Souayah N, Khella S. Neurology examination & board review. New York: McGraw Hill, 2005:46.

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FIGURE 1-19 Arterial supply of the spinal cord and watershed areas.
Reprinted with permission from Bradley WG, Daroff RB, Fenichel GM, Marsden CD, editors. Neurology in clinical practice. Volume II. 3rd ed. Boston: Butterworth Heinemann, 1999:1226.

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES Case 1-1

A 64-year-old right-handed man was brought to the emergency department after having fallen down a flight of steps. He was not able to move his limbs. His medical history included coronary artery disease, status post coronary artery bypass graft, diabetes mellitus, and schizophrenia, but no clear motor difficulties prior to this incident. He remembers that during the fall he hit his shoulders as he slid down the steps, but he experienced no loss of consciousness. Afterward he was aware of pain all over, but most of his discomfort was in both upper extremities and electrical in quality. Before being brought to the emergency department he noted that passive movements of his head intensified his upper extremity pain, but no associated worsening of his sensory symptoms occurred. On examination his vital signs were normal and he was in a rigid cervical collar. He had abrasions over both upper extremities. He was awake, alert, and followed all commands. His cranial nerve examination showed no clear abnormalities. He was able to shrug his shoulders but unable to lift his arms from the bed; proximal strength in the upper extremities was 2-3/5 and distal was 0/5. Lower extremity motor examination demonstrated weakness of hip flexion at 4-/5, and the other motor groups were 4/5. His tone appeared to be normal. Reflexes were depressed, but there appeared to be a right and perhaps a left extensor toe sign. Sensory examination demonstrated a decrease in pinprick up to the C4 level on the right and a patchy decrease in pinprick over the distal part of his left lower extremity; sacral sensation to pin was intact. Position sense appeared to be intact in his extremities. Rectal tone was normal; a urinary drainage catheter was in place. FIGURE 1-20 Cervical spine MRI (sagittal view, T2 Routine cervical spine x-rays weighted). demonstrated no clear fractures or prevertebral soft tissue swelling. Extensive degenerative changes were noted at multiple levels. An MRI of the cervical spine demonstrated spinal stenosis, worse at C3-4, and neuroforaminal stenosis from C3 to C5. There was an increase in spinal cord T2 signal intensity from C3 to C5 without enhancement, which was interpreted as edema (Figure 1-20). Over the next 12 hours his lower extremity strength improved and his sensory deficits appeared to retract, but upper extremity strength remained significantly impaired. No improvement with steroids was noted. His persistent deficit and underlying cervical spine stenosis led to the recommendation for cervical spine surgery. Comment. Spinal cord trauma presents with different anatomic syndromes that include transection, cervicomedullary syndromes with high cervical spine lesions, anterior or posterior cord syndromes, Brown-Se quard syndrome, conus/cauda equina syndrome, or, as in this case, a central cord syndrome. Recovery and manifestations are related to the site and extent of the trauma and underlying mechanisms, eg, presence of preexisting spinal stenosis. These influence eventual outcome and dictate immediate management.
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Case 1-2
A 43-year-old woman with no prior medical history began to develop episodic vertigo and jumpiness in her eyes when she was in her late 30s. Attributed to vertigo, the symptom persisted but did not result in a disability. It was not until several years later that she began to notice numbness over both of her hands, unaccompanied by neck or radicular pain. She attributed this to carpal tunnel syndrome precipitated by her administrative and secretarial work. It was the gradual involvement of ambulatory difficulties and an acute worsening over the last several months that led her to seek further evaluation. Her general physical examination and vital signs were normal. Cervical spine examination and hairline were normal; there was no spinal scoliosis. Her cranial nerve examination demonstrated a left Horner syndrome, and rotary nystagmus was evident on horizontal as well as downward gaze. She had weakness predominantly in the distal lower extremities, more so on the left side and to a 4/5 degree, but her tone appeared to be increased in all extremities. Sensory examination showed a decrease in pinprick over the right extremity that extended onto the upper thorax; similar, but lessmarked, findings were found on the left, suggesting a shawl-like pattern. Her reflexes were generally increased, and she demonstrated bilateral Babinski signs. An MRI scan of her brain and cervical spinal cord demonstrated a Chiari type-one malformation associated with syringomyelia. She underwent foramen magnum decompressive surgery, upper cervical spine laminectomy, and fusion and shunt placement (fourth ventricle to upper cervical spine). The FIGURE 1-21 Cervical spine MRI (sagittal view, T1 postoperative cervical spine MRI scan weighted). is shown in Figure 1-21. Since surgery her neurologic deficit has remained relatively stable, but recently she has begun to experience lower extremity radicular pain secondary to lumbar degenerative disc and neural foraminal stenosis. Comment. The insidious nature of this patients deficit initially delayed her seeking further clinical evaluation. However, the presence and pattern of her nystagmus, bilateral upper extremity sensory impairment, and cortical spinal tract involvement suggest an intramedullary spinal cord lesion that may extend into the brainstem. The onset of syringomyelia is often insidious, and symptom onset occurs between the ages of 25 and 40. A presentation with isolated findings may delay identification while the combination of brainstem dysfunction (eg, vertigo, oscillopsia, dysphonia, and facial sensory loss), dissociated sensory loss in the extremities, and later involvement of upper and lower motor neurons usually suggest the diagnosis. Radiologic confirmation is necessary for definitive diagnosis. Surgical interventions and extent are dependent on the assumed etiology and preexisting neurologic deficit. Decompression surgery or shunting procedures may be required in selected cases.
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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINTS:

The sensory impairment in central cord lesions is termed a dissociated sensory loss (loss of pain and temperature sensation with preservation of position, vibration, and touch). The lamination of the lateral spinothalamic tract results in fibers conveying sensation from the sacrum to be more laterally/ superficially placed within the spinal cord. These are often preserved for an extended period of time with central spinal cord lesions (sacral sensory sparing).

Case 1-3
A 67-year-old right-handed woman was brought to the emergency department by her husband. Without any clear precipitants, she had awakened with severe low back pain, accompanied by radicular pain down both lower extremities, and abdominal discomfort. She had gone to her toilet but was unable to raise herself. While being transported to the emergency department she developed urinary incontinence and later bowel incontinence. On evaluation, her vital signs and cardiac and vascular examinations were normal. Her examination was significant for lower extremity paraplegia and hyporeflexia. Plantar stimulation elicited no response; a Beevor sign was present. She demonstrated a sensory level to pinprick up to T10, decreased temperature to L1, and normal position sense. Sacral sensation to pinprick was absent; rectal tone was absent, and a urinary drainage catheter was in place (initially 1000 cc of urine had been drained). There was no tenderness to percussion over the spine, and straight-leg raise was negative. Her pain resolved over 2 days. Steroids were initially administered because of the possibility of spinal cord compression, and an emergent MRI of the entire spine was performed as well as imaging of the aorta. Both were normal. Over the ensuing weeks her lower extremity strength improved, and hyperreflexia, as well as bilateral Babinski signs, appeared. However, her ambulation remained impaired. Her sensory deficits lessened, and although her bowel incontinence improved she required periodic urinary catheterization. Comment. While this initial clinical presentation suggested a spinal cord infarction and an anterior spinal artery syndrome, a compressive spinal cord or conus/cauda equina lesion required exclusion. Aortic dissection can also cause spinal cord ischemia/infarction, and such an evaluation is required as soon as possible. Usually (67%) of the time MRI demonstrates a T2-weighted abnormality, but a normal study does not exclude a spinal cord infarction, which then becomes a diagnosis of exclusion. Back or neck pain and radicular pain can occur at symptom onset (59%), resolving in several days, but later neurogenic pain can develop. In the majority of spontaneous cases (70%) an etiology is not discovered, but the possibility of mechanical stress-induced vascular compromise has been suggested in some cases. Prognosis is related to the extent of the injury, but ambulation usually remains impaired (Novy et al, 2006).

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paralysis with fasciculations and atrophy occurs as the anterior horns and their motor neurons are affected. Lateral extension involves the corticospinal tracts, resulting in spastic paralysis of muscles below the lesion, while posterior extension involves the posterior columns with disruption of their sensory modalities. The lamination of the lateral spinothalamic tract results in fibers conveying sensation from the sacrum to be more laterally/superficially placed within the spinal cord and are often preserved for an extended period of time
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with central spinal cord lesions, representing a form of sacral sensory sparing. At times an acute cervical spinal cord injury, especially after hyperextension injuries of the neck, results in a unique neurologic presentation that signifies an injury to the central portion of the spinal cord (distinguished from the man-in-the-barrel syndrome reported after ischemic cerebral lesions within the border zone between anterior and middle cerebral arteries and cruciate paralysis, a syndrome of

brachial diplegia after medullary lesions). Such individuals at first may be quadriplegic, but recovery of lower extremity strength often occurs early, and the prognosis may be better because of a predominantly white matter injury (Collignon et al, 2002). However, a unique pattern of weakness that is more pronounced in the arms, worse distally than proximally, characterizes the syndrome and the unique site of injury. Urinary dysfunction, as well as patchy sensory loss below the level of the injury or upper and lower levels of sensory loss (suspended sensory level), can be demonstrated (Cases 1-1 and 1-2).

FIGURE 1-22 Syringomyelia (modalities involved).

Reprinted with permission from Souayah N, Khella S. Neurology examination & board review. New York: McGraw Hill, 2005:45.

Posterolateral Column Syndrome Involvement of the posterior and lateral columns of the spinal cord will lead to a pattern of sensory loss that predominantly involves the modalities of position and vibratory sense and a motor syndrome of spastic paralysis that reflects involvement of the corticospinal tract (Figure 1-23). This pattern of dysfunction leads to a sensory ataxia with a positive Romberg sign, while pain and temperature sensation remain intact because of preservation of the spinothalamic tracts. A spastic-ataxic gait reflects this constellation of fiber tract dysfunction. This pattern of involvement usually develops insidiously, reflecting the underlying pathologic processes. In the syndrome known as subacute combined degeneration, related to a deficiency of vitamin B12 or copper, the initial neurologic manifestations may be those of limb paresthesia, predominantly involving the feet, followed later by the development of the more distinctive posterior column and corticospinal tract deficits. The complete features of this syndrome usually develop over an extended period of time.

Posterior Column Syndrome A process involving the posterior columns is characterized by loss of position sense, vibration sense, and two-point discrimination. These deficits occur distal to the lesion. The lack of proprioceptive information and feedback to the motor system affects those muscle groups required for discriminative movements, resulting in a sensory ataxia. While vision can partially compensate for this loss of proprioceptive information when the eyes are open, ataxia worsens when they are closed, resulting in the presence of a Romberg sign. The gait is described as ataxic (or stomp-

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FIGURE 1-23 Posterolateral column syndrome.

Reprinted with permission from Souayah N, Khella S. Neurology examination & board review. New York: McGraw Hill, 2005:44.

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINTS:

Dysfunction in the posterior column syndrome is characterized by a sensory ataxia with a positive Romberg sign while pain and temperature sensation remain intact because of preservation of the spinothalamic tracts. With dysfunction of the posterior columns in the cervical region, neck flexion may elicit an electriclike sensation that radiates down the back or into the arms (Lhermitte sign).

FIGURE 1-24 Combined anterior horn cellpyramidal syndrome.

Reprinted with permission from Souayah N, Khella S. Neurology examination & board review. New York: McGraw Hill, 2005:44.

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ing) in character, and the deficit can be more prominent in darkness or with eye closure as visual cues no longer can assist in maintaining balance. The affected limbs may become hypotonic but usually are not weak. At times other spinal cord lesions can produce a truncal ataxia but without the associated proprioceptive difficulties. In such cases, spinocerebellar tract dysfunction, as a manifestation of spinal cord compression, appears to be responsible for this clinical syndrome. With dysfunction of the posterior columns in the cervical region, neck flexion may elicit an electric-like sensation that radiates down the back or into the arms (Lhermitte sign). It is thought to represent increased mechanosensitivity of the dorsal columns with neck flexion further activating those sensory pathways. The symptom is most frequently associated with spinal cord involvement in multiple sclerosis. Anterior Horn Cell Syndrome Damage to the motor anterior horn cells leads to an ipsilateral flaccid paralysis accompanied by atrophy and fasciculations. Because larger muscles are supplied by motor neurons from more than one segment, damage to a single spinal cord segment may lead only to muscular weakness rather than complete paralysis of the affected motor group (Figure 1-10). When the lateral horns are involved, a decrease in sweating and vasomotor functions may also be demonstrated, as the
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cell bodies of the sympathetic neurons are involved. Combined Anterior Horn Cell Pyramidal Syndrome This syndrome is perhaps best exemplified by ALS. These lesions produce a combination of flaccid and spastic paralysis. Damage to the anterior horns or lower motor neurons will result in a flaccid paralysis with atrophy and fasciculations, while a lesion of the lateral corticospinal tract or upper motor neurons results in a spastic paralysis with associated hyperreflexia and Babinski sign (Figure 1-24). The degree of injury to either site can be highly variable and reflected in the clinical presentation. If one site is more or predominantly affected, an additional lesion in the other at the same level may not produce noticeable effects. INTRAMEDULLARY VERSUS EXTRAMEDULLARY CORD LESIONS Neoplasms arising within the spinal canal tend to produce their symptoms and signs in a slow and progressive manner, although an acute presentation can occasionally be encountered. When arising from lesions within the spinal cord (intramedullary), symptoms often begin within the vicinity of the central canal. Sensory symptoms are initially less localizing and dissociation of sensory loss can occur. Early

KEY POINT:

TABLE 1-2

Clinical Features of Intramedullary Versus Extramedullary Spinal Cord Lesions Extramedullary

Radicular in type and distribution; an early and important symptom Contralateral loss of pain and temperature; ipsilateral loss of proprioception More marked than at level of lesion

Symptoms and Signs

Spontaneous pain

Intramedullary
Burning in type and poorly localized

A more symmetric pattern of sensory loss and motor dysfunction is more consistent with a conus than a cauda equina lesion.

Sensory deficit

Dissociation of sensation; patchy distribution Less marked than at level of lesion

Changes in pain and temperature sensations over perineum (saddle area) Lower motor neuron involvement Upper motor neuron involvement Muscle stretch reflexes Corticospinal tract signs Trophic changes

Segmental

Widespread with atrophy and fasciculations Late, minimal Late, minimal changes Late Marked

Prominent, early Increased early, markedly Early Usually not marked

Data from Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2007:111. Data from Haerer AF. DeJongs the neurologic examination. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 1992:588.

evidence of lower motor neuron findings, later accompanied by corticospinal tract findings, characterizes these lesions, and their clinical presentation can mimic a syrinx. Extramedullary lesions can arise from the dura and adjacent structures (extramedullary intradural) or can have an extradural site of origin such as the vertebral bodies or extradural space (extramedullary extradural). Spontaneous pain, especially in a radicular pattern, can be a presenting feature and suggests the level of involvement. Subsequent motor and sensory changes are usually slow to develop, and because of the asymmetric nature of such lesions a

Brown-Se quard pattern may appear. The features of either type of clinical syndrome are described and contrasted in Table 1-2. CONUS MEDULLARIS VERSUS CAUDA EQUINA LESIONS The close anatomic localization of the conus medullaris and overlying cauda equina makes distinction of either syndrome difficult, and at times involvement of both structures occurs. A symmetric pattern of sensory loss and motor dysfunction is more consistent with a conus than a cauda equina lesion. The clinical features of both conditions are further described and contrasted in Table 1-3.
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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

TABLE 1-3

Clinical Features of Conus Medullaris and Cauda Equina Lesions Conus Medullaris
Not common or severe; bilateral and symmetric; over perineum and thighs

Symptoms and Signs

Spontaneous pain

Cauda Equina
May be most prominent symptom; severe and radicular in type; unilateral or asymmetric; over perineum, thighs, legs, and back Saddle distribution; may be unilateral and asymmetric; all modalities affected; no dissociation of sensation Asymmetric; more marked; atrophy may occur; usually no fasciculations Patellar and Achilles reflexes may be absent Late and less marked Decubitus less marked Less marked impairment Gradual and unilateral

Sensory deficit

Saddle distribution; bilateral, usually symmetric; dissociation of sensation

Motor loss

Symmetric; not marked; fasciculations may be present Only Achilles reflex absent Early and marked Decubitus common Erection and ejaculation impaired Sudden and bilateral

Reflex loss Bladder and rectal symptoms Trophic changes Sexual function Onset

Data from Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2007. Data from Haerer AF. DeJongs the neurologic examination. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 1992:591.

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REFERENCES AND SELECT READINGS Note: There are many general textbooks of neuroscience, neuroanatomy as well as clinical neurology that you may have found useful. The following recommendations represent our bias and are driven by familiarity with and the usefulness we have found in the following general resources for teaching and review.
Adams MM, Hicks AL. Spasticity after spinal cord injury. Spinal Cord 2005;43(10):577586. Bowen BC, Pattany PM. Vascular anatomy and disorders of the lumbar spine and spinal cord. Magn Reson Imaging Clin N Am 1999;7(3):555571. Bradley WG, Daroff RB, Fenichel GM, Marsden CD, editors. Neurology in clinical practice. Volume II. 3rd ed. Boston: Butterworth Heinemann, 1999:1226. Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2007. Collignon F, Martin D, Le nelle J, Stevenaert A. Acute traumatic central cord syndrome: magnetic resonance imaging and clinical observations. J Neurosurg 2002;96(1 suppl):29 33. Davidoff RA. The dorsal columns. Neurology 1989;39(10):13771385. Duggal N, Lach B. Selective vulnerability of the lumbosacral spinal cord after cardiac arrest and hypotension. Stoke 2002;33(1):116 121. Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007. Gillilan LA. Veins of the spinal cord. Anatomical details; suggested clinical applications. Neurology 1970;20(9):860 868. Grant JCB. An atlas of anatomy. 6th ed. Baltimore: Williams & Wilkins, 1972. Haerer AF. DeJongs the neurologic examination. 5th ed. Philadelphia: Lippincott, Williams & Wilkins, 1992. Krauss WE. Vascular anatomy of the spinal cord. Neurosurg Clin N Am 1999;10(1):9 15. Moore KL, Dalley AF. Clinically oriented anatomy. Philadelphia: Lippincott Williams & Wilkins, 1999. Nathan PW, Smith M, Deacon P. Vestibulospinal, reticulospinal and descending propriospinal nerve fibres in man. Brain 1996;119(pt 6):1809 1833. Nathan PW, Smith M, Deacon P. The crossing of the spinothalamic tract. Brain 2001;124(pt 4):793 803. Nathan PW, Smith MC, Deacon P. The corticospinal tracts in man. Course and location of fibres at different segmental levels. Brain 1990;113(pt 2):303324. Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol 2006;63(8): 11131120. Souayah N, Khella S. Neurology: examination & board review. New York: McGraw Hill, 2005. Tattersall R, Turner B. Brown-Se quard and his syndrome [erratum published in Lancet 2000;356(9226):344]. Lancet 2000;356(9223):61 63.

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