Indian J Pediatr (October 2012) 79(10):13511357 DOI 10.

1007/s12098-012-0831-8

SYMPOSIUM ON PGIMER PROTOCOLS IN NEUROLOGICAL EMERGENCIES

Approach to a Child with Acute Flaccid Paralysis

Sunit C. Singhi & Naveen Sankhyan & Ravi Shah & Pratibha Singhi

Received: 26 January 2012 / Accepted: 8 June 2012 / Published online: 12 July 2012 # Dr. K C Chaudhuri Foundation 2012

Abstract Acute flaccid paralysis (AFP) is a clinical syndrome characterized by rapid onset weakness, that many times includes respiratory and bulbar weakness. AFP is a broad clinical entity with an array of diagnostic possibilities. An accurate and early diagnosis of the cause has important bearing on the management and prognosis. The immediate priorities in a child who presents with acute progressive weakness are; to detect and manage respiratory muscle weakness, to detect and manage bulbar weakness, evaluate for cardiovascular instability, detect and manage dyselectrolytemia or toxemia, and to detect and manage a spinal compression (traumatic, intraspinal collections). Urgent imaging of the spine is needed in settings where a spinal cord involvement is suspected. Compressive or traumatic spinal lesions may need early neurosurgical intervention. Anterior horn cell injury is usually due to direct viral infection. More distal pathologies are generally immune mediated and respond to immunomodulation. Irrespective of the cause, generalized weakness frequently affects respiratory and bulbar function. Such children need careful monitoring and respiratory support. Keywords Polio . Acute weakness . Paraparesis . Transverse myelitis . Guillain Barre syndrome

Introduction Acute flaccid paralysis (AFP) is a clinical syndrome characterized by rapid onset weakness, that frequently includes respiratory and bulbar weakness. The weakness usually progresses to maximum within days to weeks. The term flaccid indicates the absence of spasticity or other signs of disordered central nervous system motor tracts such as hyperreflexia, clonus or extensor plantars [1]. AFP is broad clinical entity with an array of diagnostic possibilities. An accurate and early diagnosis of the cause has important bearing on the management and prognosis. If not managed appropriately, paralysis can progress to respiratory failure and death. Another issue of public health importance is the immediate reporting of all cases of AFP to the polio surveillance team(Box 1). Any case meeting the AFP definition undergoes a thorough investigation to determine if the paralysis is caused by polio. Each case of AFP is to be reported and 2 stool samples (24 h apart, each 810 g) are collected within 14 d of paralysis onset and sent to WHO accredited laboratory.

S. C. Singhi (*) : N. Sankhyan : R. Shah : P. Singhi Department of Pediatrics, Advanced Pediatrics Centre, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh 160012, India e-mail: sunit.singhi@gmail.com

1352 Box 1 Acute flaccid paralysis (Epidemiological definition-WHO 2005)

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This protocol focuses on the clinical evaluation of a child presenting with AFP and provides a practical clinical approach to diagnosis in the Emergency department. For a detailed discussion on AFP the reader is referred to other reviews on the subject [1]. The objectives of this article are: to provide a practical approach to diagnosis in an individual patient; to provide an approach to rational use of diagnostic tests and discuss the common causes of AFP in children.

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Diagnostic Approach Initial Assessment and Stabilization Every child with AFP is a medical emergency requiring systematic evaluation and management. Initial assessment of any such acutely ill child should concentrate on rapid cardiopulmonary assessment and resuscitation. Following are the key areas on initial assessment; & Detect and manage respiratory muscle weakness: Any child with acute weakness should be evaluated for respiratory muscle weakness. Younger children with respiratory muscle weakness may present with non-specific irritability, sweating, poor feeding and shallow or paradoxical respiratory efforts. Older children may complain of respiratory difficulty, may have excessive sweating, agitation, air hunger, reduced single breath count/chest expansion or shallow/paradoxical respiratory efforts. Careful serial examinations may be critical in such children to pick up the weakness early. Early elective intubation and respiratory support are critical to save these affected children. Detect and manage bulbar weakness: Symptoms of voice change, poor cry, pooling of secretions, gurgling sounds in throat, poor ability to swallow and choking on feeds may be markers of bulbar dysfunction. Care should be taken to avoid oral feeding, providing regular suction and ensuring entral nutrition via nasogastric feeding. &

Evaluate for cardiovascular instability: Conditions leading to AFP (Spine trauma, myelitis, Guillain Barre syndrome) can also result in cardiac rhythm abnormalities and cardiovascular insufficiency. These issues will require a priority management. Hence, attaching a quadriparetic child to an ECG/cardiac monitor is an early step in the management. Rule out dyselectrolytemia or toxemia: Hypokalemia and snake envenomation are important causes of flaccid paralysis. These causes should be excluded in all children with AFP by history and examination, early in management course. A rapid assessment of electrolytes and ECG should be sought in all such children. To rule out a spinal compression (traumatic, intraspinal collections). : At the outset, patients with possible spinal injury due to trauma or other lesions requiring urgent neurosurgical intervention should be identified on history and examination. Immediate spinal stabilization and administration of corticosteroids in those with trauma would be a priority, while neurosurgical relief of spinal compression may be warranted to prevent long term disability.

History The first step is to determine if an unwell child actually has muscle weakness. Many children with weakness present with nonspecific symptoms of irritability, lethargy and clumsy walk or refusal to walk. Children with abnormal gait, limp or refusing to walk may present initially to orthopedic or trauma clinics. Pseudoparalysis due to limb pain may result from trauma, arthritis/arthralgia, myostis, joint or periosteal bleeds or joint or periarticular infections or inflammations. It is useful to remember the possible causes of AFP in children using a neuro-anatomical approach (Table 1). Information is derived from the history and focused neurological examination looking at pattern of tone, tendon reflexes, sensory examination, signs and symptoms of bladder and/or bowel involvement. (Table 2).

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Investigations The choice of the initial investigations would depend on the information gained from history and examination. Moreover, the urgency to arrive at the diagnosis would also dictate the sequence and choice of investigations. A step wise and judicious use of investigations would help reach the diagnosis with the minimum use of resources (Fig. 1). 1. MRI Spine: It is indicated when there is a suspicion of spinal cord compression or transverse myelitis. More specifically, any child with history of neck or back trauma, rapid onset flaccid profound quadreparesis, early or persistent bladder or bowel involvement, sensory loss or sensory level on examination, spinal tenderness, neurocutaneous markers, or appearance of UMN signs on examination (e.g., up going plantars) should get an MRI of the spine. 2. CSF examination: This is helpful to narrow the diagnostic possibilities. A raised CSF cell count would be seen in patients with transverse myelitis, infective myelitis viz. polio or enteroviral myelitis, varicellas or herpes myelitis, rabies, etc. A raised CSF protein with normal cell count (albuminocytological dissociation) suggests Guillain Barre syndrome, post diphtheritic

Table 2 Selected clues in history and examination while evaluating a child with acute flaccid paralysis Points in history and/or examination Fever at onset Remarks

Trauma: head/neck

Exposure

Polio or enteroviral myelitis, Transverse myelitis, myositis, epidural abscess, and Koch spine (prolonged history) Trivial trauma may lead to spinal compression in patients with cervical vertebral instability (Patients with Downs syndrome, congenital cervicovertebral anomalies or juvenile idiopathic arthritis) Toxins: lead, arsenic Snake envenomation Dog bite: Rabies Guillain Barre syndrome or transverse myelitis Sore throat, neck swelling, diphtheretic polyneuropathy (non/partly immunized) Diarrhea: Hypokalemia, enteroviral myelitis Exertion or post parandial: Hypokalemic periodic paralysis Intramuscular injection: Polio, traumatic sciatic neuritis Compressive myelopathy, transverse myelitis Compressive myelopathy, transverse myelitis Botulism (H/o honey exposure) Guillain Barre syndrome, Rabies, acute myelopathy Guillain Barre syndrome, Rabies, Varicella zoster virus, ascending myelitis Diphtheria, Botulism Myasthenia Gravis, Botulism Guillain Barre syndrome, Myasthenia Gravis, Botulism Myasthenia Gravis Myositis, inflammatory myopathy, (myalgias may be severe in Guillain Barre syndrome) Absent: Guillain Barre syndrome, Polio, Diphtheria, spinal shock, at level of spinal cord damage Preserved : Myasthenia Gravis, periodic paralysis, Botulism Exaggerated: Below level of spinal lesion, Upper motor neuron lesion Spinal trauma, epidural abscess or other extradural compression Polio, enteroviral myelitis, Guillain Barre syndrome, transverse myelitis

Preceding infectious prodrome/vaccination

Precipitating factors

Sensory loss/level Early bowel/bladder involvement Constipation in <1 y Prominent autonomic signs/symptoms Ascending weakness Descending weakness Prominent and early ptosis Facial weakness Fluctuating symptoms, fatigability Muscle tenderness

Table 1 A neuroanatomical differential diagnosis of acute flaccid paralysis in children Site Spinal cord Pathophysiology Compressive Inflammatory Viral Disease Traumatic spinal injury, epidural abscess, hematoma, discitis Transverse myelitis Poliomyelitis, vaccine associated poliomyelitis, Enteroviral myelitis, Japanese encephalitis

Anterior horn cell

Roots/nerves

Vascular Anterior spinal artery infarction Immune mediated Guillain Barre syndrome, Toxin Post diphtheritic, porphyria, arsenic Viral Rabies Trauma Injection related sciatic neuritis

Muscle stretch reflexes

Neuromuscular Immune mediated Myasthenia Gravis junction Drugs, toxins Organophosphates, snake venom, drugs (aminoglycosides), Botulism Dyselectrolytemia Hypermagnesemia Muscle Infection Viral myositis Inflammation Inflammatory myopathy (polymyositis) Channelopathy Hypokalemic periodic paralysis Dyselectrolytemia Hypokalemia

Spinal tenderness, painful spine movement Neck stiffness

1354 Fig. 1 Approach to child with acute paraplegia or paraparesis

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Acute paraparesis/plegia

Features of spinal cord compression* / Sensory level on examination

Yes CEMRI spine as early as possible

No DTRs /+

Compressive myelopathy

Noncompressive myelopathy +

Ocular/bulbar involvement?

Symmetric? +

Neurosurgery

DTR Deep tendon reflexes; CPK Creatine phosphokinase; TM Transverse myelitis; GBS Gullain Barre Syndrome, NCV Nerve conduction velocity; CSF Cerebrospinal fluid. *Bony tenderness/deformity, root pains, girdle sensation /early bladder or bowel involvement #other possibilities according to clinical features as described in text

consult+ steroids

AcuteTM:Treat with high dose steroids and consult

Myasthenia, Botulism

CPK,K + , Urine myoglobin

GBS#

Polio, GBS, Traumatic neuritis. Get NCV Viral myositis, periodic paralysis, Rhabdomyolysis IVIG,Neuro consult,NCV, CSF

polyneuropathy or rarely may be seen in transverse myelitis. The CSF can be normal early in the course of these illnesses. 3. Nerve Conduction studies and Electro Myography (EMG): These studies confirm the involvement of nerves and help in diagnosis of anterior horn cell diseases. These are particularly helpful to confirm Guillain Barre syndrome. The repetitive nerve stimulation test helps to diagnose myasthenia gravis and botulism. Rarely, these may aid the diagnosis of an inflammatory myopathy. 4. Creatine Kinase: Raised levels of muscle enzyme creatine kinase reflects acute muscle fiber injury and may point towards a muscle disease. In the setting of AFP this may be seen in children with viral myositis or inflammatory myopathy.

Differential Diagnosis of AFP (Table 3) Some of the commonly encountered causes of AFP are discussed below; Guillain Barre Syndrome (GBS) With the control of polio, GBS is the most common cause of AFP in children. Worldwide its incidence is 0.64 cases per 100,000 per year [2]. It most commonly occurs after an

infection triggered immune mediated attack on the nerve axons or myelin. Antecedant respiratory or gastrointestinal illnesses are commonly found in the history [3]. The most common underlying subtype of the syndrome is the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) but the other common subtype of acute motor axonal neuropathy (AMAN) may be equally common in Indian children [4]. In the typical cases, the first symptoms are usually pain, paraesthesia, or weakness in the limbs which spreads proximally. Weakness may progress rapidly, and approximately 50 % of the children will reach nadir by 2 wk, 80 % by 3 wk, and the rest by 4 wk. Risk factors for children requiring ventilation are cranial nerve involvement, increased CSF protein during first week of illness and short period between antecedent illness and the onset of symptoms [5]. Investigations required for confirming the diagnosis are; nerve conduction studies and lumbar puncture (to document CSF albumin-cytological dissociation). A raised CSF protein concentration is present in about 80 % of patients, but CSF protein content is more likely to be normal during the first days of the illness [3]. When a child presents in the acute phase, the differentiation from polio or enetroviral myelitis can be done based on CSF. Viral myeltis would show CSF pleocytosis, which would be conspicuously absent in GBS. CSF should be analyzed before treatment with intravenous immunoglobulin (IVIG) as IVIG can cause aseptic meningitis. Management of a child with GBS would involve a meticulous observation for respiratory, bulbar muscle weakness. Early elective intubation and ventilatory support are important in the acute phase. During hospitalization, monitoring for

Indian J Pediatr (October 2012) 79(10):13511357 Table 3 Characteristics to aid differential diagnosis of acute flaccid paralysis Feature Transverse myelitis Poliomyelitis Guillain-Barre syndrome Traumatic neuritis (following injection)

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Development of paralysis Fever at onset of weakness Paralysis Progression of paralysis Muscle tone Deep-tendon reflexes Sensation

From hours to four days 24 to 48 h from onset From hours to 4 wk to full paralysis May be present High, always present at Uncommon onset of flaccid paralysis Symmetric Asymmetric, Descending Reduced Decreased or absent Symmetric, mostly ascending Ascending Reduced Absent

From hours to four days Present, if underlying infection being treated with IM injections Affects only one limb

Cranial nerve involvement Respiratory insufficiency Autonomic signs and symptoms Cerebrospinal fluid Bladder dysfunction Nerve conduction velocity: third wk

Reduced during acute phase Absent in lower limbs(early); hyperreflexia(late) Anesthesia of lower limbs with sensory level Absent Sometimes Present

Reduced Decreased or absent

Severe myalgia, backache, no sensory changes Only when bulbar involvement is present Only when bulbar involvement is present Rare

Cramps, tingling, hypoanesthesia of palms and soles Often present, affecting nerves VII, IX, X, XI, XII Occurs in severe cases

Pain in gluteus

Absent Absent

Normal or Pleocytosis Present- early and persistent Normal

Mild elevation of lymphocytes 10 to 200/mL Rare Abnormal: anterior horn cell disease (normal during first 2 wk) Stool viral detection

Frequent in severe cases (blood pressure Hypothermia in alterations, sweating, blushing, and affected limb body temperature fluctuations) Albumin-cytologic dissociation (usually Normal <10 cells/ml, never >50cells/ml) Occasionally (Transient, at the peak of weakness, 13 d (30 %)) Abnormal: slowed conduction, decreased motor amplitudes Nerve conduction studies Never Abnormal: s/o motor-sensory axonal damage Nerve conduction studies, Electromyography

Diagnostic test

MRIspine

Adapted and modified from Global Program for Vaccines and Immunization: Field Guide for Supplementary Activities Aimed at Achieving Polio Eradication. Geneva, World Health Organization, 1996

autonomic instability and prevention of nosocomial complications are essential to optimize outcomes. IVIG is the treatment of choice in the authors setting for GBS, given the availability, ease of administration and the safety compared with plasmapheresis. It is given in the dose of 2 g/kg spread over 25 d. Anterior Horn Cell Viral Myelitis Poliomyelitis Both the wild polio virus and the vaccine associated polio virus cause anterior horn cell affliction to result in flaccid paralysis. Children under 5 y are the most frequently affected. However, older individuals and adults can also develop

poliomyelitis. The initial symptoms of polio are non-specific and include fever, headache, vomiting, constipation, neck stiffness and pain in limbs. The paralysis follows or accompanies these symptoms. The maximal weakness evolves quickly over 12 d. A history of intramuscular injections precedes paralytic poliomyelitis in about 5060 % of patients, patients may present initially with fever and paralysis (provocation paralysis). Clinical characteristics of poliomyelitis include; 1. Fever at onset 2. Rapid progression of paralysis within 2448 h 3. Asymmetric, proximal more than distal limb paralysis 4. Preservation of sensory function often with severe myalgias 5. Residual paralysis at 60 d [6]. Most of the children with paralytic polio die from complications of bulbar paralysis and respiratory failure. Management is mainly focused on meticulous supportive care.

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Indian J Pediatr (October 2012) 79(10):13511357 Table 4 Summary of approach to diagnosis in a child with acute flaccid paralysis 1. ABCs Ensure protection of airway and adequate ventilation (especially if there is respiratory muscle weakness, shallow respiration, dysphagia, weak gag) Check and support: BP and Heart Rate Immobilize neck if history of neck/head trauma Send electrolytes and get an ECG- to look for hypokalemia 2. Examination and classification into pattern for example, Flaccid Paraparesis with sensory level (early bladder dysfunction)Transverse myelitis, compressive myelopathy Flaccid afebrile symmetric para/quadriparesis (+/ bulbar and respiratory involvement) with areflexia and minimal sensory loss (but often sensory symptoms) : Acute neuropathy or polyradiculopathy (esp., Guillain Barre Syndrome) Flaccid, febrile, pure motor, asymmetric, paralysis (no bladder involvement) often with meningismus: Enteroviral, polio, or vaccine associated poliomyelitis Flaccid motor-sensory lower limb monoparesis after IM injection: Injection neuritis Ophthalmoplegia, ptosis, bulbar weaknes with motor weakness: Miller-Fischer variant of Guillain Barre Syndrome, Botulism, Myasthenia Gravis Proximal muscle weakness, muscle tenderness without sensory symptoms or signs and with preserved reflexes: Viral myositis, Inflammatory myopathy (e.g., dermatomyositis) 3. Investigations (according to the suspected site of lesion and cause of paralysis) Neuroimaging (spinal cord) MRI indicated in all cases of myelopathy, suspected transverse myelitis X- ray spine: suspected atlantoaxial dislocation, vertebral tuberculosis Electrophysiologic testing (NCV & electromyography): Guillain Barre syndrome Lumbar puncture (CSF): Guillain Barre syndrome, suspicion of viral myelitis Biochemistry: Creatine Kinase, Potassium, Magnesium, Phosphate ECG: Hypokalemia Urine for porpho-bilinogens in porphyria, toxins: arsenic 4. Management (depends on the underlying etiology identified) All children: meticulous supportive care, anticipate and identify respiratory, bulbar weakness (except in injection neuritis), shock due to reduced vascular tone (spinal cord disease), Autonomic instability, complications of immobilization and prevention of nosocomial infections. Specific therapy: Guillain Barre syndrome: IVIG, 2 g/kg over 25 d Transverse myelitis: IV methy-prednisolone 1030 mg/kg, daily (max-1 g) for 35 d Compressive myelopathy: spinal immobilization, surgical intervention, steroids (acute traumatic myelopathy) Dermatomyositis, Myasthenia Gravis: Immunomodulation Hypokalemia: Intravenous potassium correction

Non Polio Enteroviral Myelitis Non polio enteroviruses can cause a polio like paralytic disease. Among all known nonpolio enteroviruses, enterovirus-71 has been most strongly implicated in outbreaks of central nervous system disease and AFP. The clinical syndrome frequently is associated with aseptic meningitis, hand, foot and mouth disease and hemorrhagic conjunctivitis [7]. Weakness associated with enterovirus disease can be severe and permanent. Other Viruses Causing AFP Rabies The common presentation of human rabies is with fever, behavioral and autonomic instability and hydro/aero phobia. However, a minority of the patients can present primarily with paralytic disease. This type of presentation follows a prodrome of paraesthesias in the bitten area, ascending paralysis or paralysis progressing from the bitten limb. Sphincter disturbances and autonomic instability is common. Disease progression is slower in paralytic rabies [8]. The disease can be easily missed if a history of animal bite is not actively sought. Frequently the bite may not be recent and the parents may not give the history, unless specifically asked for. Herpes group of viruses can lead to AFP by triggering GBS or transverse myelitis, causing polyradiculoneuropathies in immunocompromized hosts [9]. Japanese encephalitis virus can also preferentially affect the anterior horn cell and cause paralysis associated with encephalitis [10]. Transverse Myelitis It is an acute demyelinating disorder of the spinal cord. It may occur alone or in combination with demyelination in other portions of the nervous system. It is believed commonly that previous infection or immunization triggers transverse myelitis, but no evidence supports such a notion [11]. The common presentation includes an acute phase of spinal shock with flaccid paraparesis or quadreparesis, urinary retention or incontinence, absent reflexes and mute plantars, sensory loss/level is frequently present. After a few weeks, the signs of UMN dysfunction appear, in the form of spasticity, and hypereflexia. This disorder should be suspected in any child with rapid onset flaccid profound quadreparesis, early or persistent bladder or bowel involvement, sensory loss or sensory level on examination, with suggestion of UMN signs on examination (e.g., up going plantars). In such a situation an urgent spinal MRI is needed to establish the diagnosis. Other causes of acute myelopathy like trauma, paraspinal/epidural spinal abscess, hematoma or anterior spinal artery syndrome need exclusion in this setting. The management of transverse

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myelitis consists of immunosuppression and supportive care. Attention is needed to maintain airway, breathing and circulation, bladder catheterization and exclusion of compressive myelopathy by imaging. High dose pulse corticosteroids are the recommended form therapy [11]. Methylprednisolone is given in a dose of 1030 mg/kg/d (max:1 g/d) for 5 d followed by oral prednisolone 12 mg/kg/d for 2 wk and then tapered over subsequent 24 wk. Traumatic Neuritis (Following Injection)

(snake bite). Evaluation of spine by imaging may be needed urgently in patients with suggestive clinical features. Once these causes are excluded, most distal pathologies are generally immune mediated and respond to immunomodulation. Irrespective of the cause, generalized weakness frequently affects respiratory and bulbar function. Such children need to be carefully monitored and treated.

Conflict of Interest None.

Traumatic neuritis is suspected in cases in which there is one limb involvement and definite history of injection in that limb (usually less than 24 h) before the onset of paralysis. It is associated with pain and hypothermia of affected limbs. It is sometimes difficult to distinguish it from polio. However, sensory deficits and lack of CSF pleocytosis favor the diagnosis of traumatic neuritis. It is probable that some cases of polio are misdiagnosed as traumatic neuritis. Residual sensory deficits strongly favor the diagnosis of injection neuritis. Management is entirely supportive. Hypokalemic Paralysis This is an important differential in any child particularly in a younger child with AFP. An early recognition can prevent potentially fatal cardiac complications. In the developing countries, it most commonly results from diarrheal diseases. However, rarer familial chanellopathies, underlying disorders, such as renal tubular acidosis, primary/secondary hyperaldosteronism also need to be considered. Correction of potassium levels rapidly reverses the paralysis in these children.

Role of Funding Source

None.

References
1. Marx A, Glass JD, Sutter RW. Differential diagnosis of acute flaccid paralysis and its role in poliomyelitis surveillance. Epidemiol Rev. 2000;22:298316. 2. Hughes RAC, Rees JH. Clinical and epidemiological features of Guillain-Barr syndrome. J Infect Dis. 1997;176:S928. 3. Paradiso G, Tripoli J, Galicchio S, Fejerman N. Epidemiological, clinical, and electrodiagnostic findings in childhood Guillain-Barr syndrome: a reappraisal. Ann Neurol. 1999;46:7017. 4. Kalra V, Sankhyan N, Sharma S, Gulati S, Choudhry R, Dhawan B. Outcome in childhood Guillain-Barr syndrome. Indian J Pediatr. 2009;76:7959. 5. Rantala H, Uhari M, Cherry J, Shields WB. Risk factors of respiratory failure in children with Guillain Barre syndrome. Pediatr Neurol. 1995;13:28992. 6. Melnick J. Enteroviruses: polioviruses, coxsackieviruses, echoviruses, and newer enteroviruses. In: Fields BN, Knipe DM, Chanock RM, eds. Fields virology. Philadelphia: LippincottRaven Publishers; 1996. pp. 655712. 7. Wadia NH, Wadia PN, Katrak SM, Misra VP. A study of the neurologic disorder associated with acute hemorrhagic conjunctivitis due to enterovirus 70. J Neurol Neurosurg Psychiatry. 1983;46:599610. 8. Gadre G, Satishchandra P, Mahadevan A, et al. Rabies viral encephalitis: clinical determinants in diagnosis with special reference to paralytic form. J Neurol Neurosurg Psychiatry. 2010;81:81220. 9. Tyler KL. Herpes simplex virus infections of the central nervous system: encephalitis and meningitis, including Mollarets. Herpes. 2004;11:57A64A. 10. Misra UK, Kalita J. Anterior horn cells are also involved in Japanese encephalitis. Acta Neurol Scand. 1997;96:1147. 11. Frohman EM, Wingerchuk DM. Clinical practice. Transverse myelitis. N Engl J Med. 2010;363:56472.

Conclusions AFP is a broad clinical entity with an array of diagnostic possibilities. Every case of AFP is a medical emergency. A systematic anatomic/pathophysiological approach to diagnosis helps to narrow down the diagnostic possibilities in a given child (Table 4). Accurate and early diagnosis of the cause has important bearing on the management and prognosis. The immediate priorities are to detect and manage respiratory, bulbar muscle weakness, rapidly exclude causes which are reversible like dyselectrolytemia or toxemia