Anda di halaman 1dari 7

Indian J Pediatr (October 2012) 79(10):1351–1357

DOI 10.1007/s12098-012-0831-8


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 Introduction

characterized by rapid onset weakness, that many times includes
respiratory and bulbar weakness. AFP is a broad clinical entity Acute flaccid paralysis (AFP) is a clinical syndrome
with an array of diagnostic possibilities. An accurate and early characterized by rapid onset weakness, that frequently
diagnosis of the cause has important bearing on the management includes respiratory and bulbar weakness. The weakness
and prognosis. The immediate priorities in a child who presents usually progresses to maximum within days to weeks.
with acute progressive weakness are; to detect and manage The term “flaccid” indicates the absence of spasticity or
respiratory muscle weakness, to detect and manage bulbar other signs of disordered central nervous system motor
weakness, evaluate for cardiovascular instability, detect and tracts such as hyperreflexia, clonus or extensor plantars
manage dyselectrolytemia or toxemia, and to detect and manage [1]. AFP is broad clinical entity with an array of diag-
a spinal compression (traumatic, intraspinal collections). Ur- nostic possibilities. An accurate and early diagnosis of
gent imaging of the spine is needed in settings where a spinal the cause has important bearing on the management and
cord involvement is suspected. Compressive or traumatic spinal prognosis. If not managed appropriately, paralysis can
lesions may need early neurosurgical intervention. Anterior horn progress to respiratory failure and death. Another issue
cell injury is usually due to direct viral infection. More distal of public health importance is the immediate reporting
pathologies are generally immune mediated and respond to of all cases of AFP to the polio surveillance team(Box
immunomodulation. Irrespective of the cause, generalized 1). Any case meeting the AFP definition undergoes a
weakness frequently affects respiratory and bulbar function. thorough investigation to determine if the paralysis is
Such children need careful monitoring and respiratory support. caused by polio. Each case of AFP is to be reported
and 2 stool samples (≥24 h apart, each 8–10 g) are
Keywords Polio . Acute weakness . Paraparesis . collected within 14 d of paralysis onset and sent to
Transverse myelitis . Guillain Barre syndrome 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
1352 Indian J Pediatr (October 2012) 79(10):1351–1357

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

This protocol focuses on the clinical evaluation of a & Evaluate for cardiovascular instability: Conditions
child presenting with AFP and provides a practical leading to AFP (Spine trauma, myelitis, Guillain
clinical approach to diagnosis in the Emergency depart- Barre syndrome) can also result in cardiac rhythm
ment. For a detailed discussion on AFP the reader is abnormalities and cardiovascular insufficiency. These
referred to other reviews on the subject [1]. The objec- issues will require a priority management. Hence,
tives of this article are: to provide a practical approach attaching a quadriparetic child to an ECG/cardiac
to diagnosis in an individual patient; to provide an monitor is an early step in the management.
approach to rational use of diagnostic tests and discuss & Rule out dyselectrolytemia or toxemia: Hypokalemia
the common causes of AFP in children. and snake envenomation are important causes of flaccid
paralysis. These causes should be excluded in all chil-
dren with AFP by history and examination, early in
management course. A rapid assessment of electrolytes
Diagnostic Approach
and ECG should be sought in all such children.
& To rule out a spinal compression (traumatic, intraspinal
Initial Assessment and Stabilization
collections). : At the outset, patients with possible
spinal injury due to trauma or other lesions requiring
Every child with AFP is a medical emergency requiring
urgent neurosurgical intervention should be identified
systematic evaluation and management. Initial assess-
on history and examination. Immediate spinal stabili-
ment of any such acutely ill child should concentrate
zation and administration of corticosteroids in those
on rapid cardiopulmonary assessment and resuscitation.
with trauma would be a priority, while neurosurgical
Following are the key areas on initial assessment;
relief of spinal compression may be warranted to
& Detect and manage respiratory muscle weakness: Any prevent long term disability.
child with acute weakness should be evaluated for res-
piratory muscle weakness. Younger children with respi-
ratory muscle weakness may present with non-specific History
irritability, sweating, poor feeding and shallow or para-
doxical respiratory efforts. Older children may complain The first step is to determine if an unwell child actually has
of respiratory difficulty, may have excessive sweating, muscle weakness. Many children with weakness present
agitation, air hunger, reduced single breath count/chest with nonspecific symptoms of irritability, lethargy and
expansion or shallow/paradoxical respiratory efforts. clumsy walk or refusal to walk. Children with abnormal
Careful serial examinations may be critical in such chil- gait, limp or refusing to walk may present initially to ortho-
dren to pick up the weakness early. Early elective intu- pedic or trauma clinics. Pseudoparalysis due to limb pain
bation and respiratory support are critical to save these may result from trauma, arthritis/arthralgia, myostis, joint or
affected children. periosteal bleeds or joint or periarticular infections or
& Detect and manage bulbar weakness: Symptoms of inflammations.
voice change, poor cry, pooling of secretions, gur- It is useful to remember the possible causes of AFP
gling sounds in throat, poor ability to swallow and in children using a neuro-anatomical approach (Table 1).
choking on feeds may be markers of bulbar dysfunc- Information is derived from the history and focused
tion. Care should be taken to avoid oral feeding, neurological examination looking at pattern of tone,
providing regular suction and ensuring entral nutri- tendon reflexes, sensory examination, signs and symp-
tion via nasogastric feeding. toms of bladder and/or bowel involvement. (Table 2).
Indian J Pediatr (October 2012) 79(10):1351–1357 1353

Investigations Table 2 Selected clues in history and examination while evaluating a

child with acute flaccid paralysis
The choice of the initial investigations would depend on
the information gained from history and examination. Points in history Remarks
and/or examination
Moreover, the urgency to arrive at the diagnosis would
also dictate the sequence and choice of investigations. A Fever at onset Polio or enteroviral myelitis, Transverse
step wise and judicious use of investigations would help myelitis, myositis, epidural abscess, and
reach the diagnosis with the minimum use of resources Koch spine (prolonged history)
(Fig. 1). Trauma: head/neck Trivial trauma may lead to spinal
compression in patients with cervical
1. MRI Spine: It is indicated when there is a suspicion of vertebral instability (Patients with
spinal cord compression or transverse myelitis. More Downs syndrome, congenital
cervicovertebral anomalies or juvenile
specifically, any child with history of neck or back trau- idiopathic arthritis)
ma, rapid onset flaccid profound quadreparesis, early or Exposure Toxins: lead, arsenic
persistent bladder or bowel involvement, sensory loss or Snake envenomation
sensory level on examination, spinal tenderness, neuro- Dog bite: Rabies
cutaneous markers, or appearance of UMN signs on ex-
Preceding infectious Guillain Barre syndrome or transverse
amination (e.g., up going plantars) should get an MRI of prodrome/vaccination myelitis
the spine. Sore throat, neck swelling, diphtheretic
2. CSF examination: This is helpful to narrow the diag- polyneuropathy (non/partly immunized)
nostic possibilities. A raised CSF cell count would be Precipitating factors Diarrhea: Hypokalemia, enteroviral
seen in patients with transverse myelitis, infective my- myelitis
elitis viz. polio or enteroviral myelitis, varicellas or Exertion or post parandial: Hypokalemic
herpes myelitis, rabies, etc. A raised CSF protein with periodic paralysis
normal cell count (albuminocytological dissociation) Intramuscular injection: Polio, traumatic
sciatic neuritis
suggests Guillain Barre syndrome, post diphtheritic
Sensory loss/level Compressive myelopathy, transverse
Early bowel/bladder Compressive myelopathy, transverse
Table 1 A neuroanatomical differential diagnosis of acute flaccid involvement myelitis
paralysis in children Constipation in <1 y Botulism (H/o honey exposure)
Site Pathophysiology Disease Prominent autonomic Guillain Barre syndrome, Rabies, acute
signs/symptoms myelopathy
Spinal cord Compressive Traumatic spinal injury, epidural Ascending weakness Guillain Barre syndrome, Rabies,
abscess, hematoma, discitis Varicella zoster virus, ascending myelitis
Inflammatory Transverse myelitis Descending weakness Diphtheria, Botulism
Anterior horn Viral Poliomyelitis, vaccine associated Prominent and early Myasthenia Gravis, Botulism
cell poliomyelitis, Enteroviral ptosis
myelitis, Japanese encephalitis Facial weakness Guillain Barre syndrome, Myasthenia
Vascular Anterior spinal artery infarction Gravis, Botulism
Roots/nerves Immune mediated Guillain Barre syndrome, Fluctuating symptoms, Myasthenia Gravis
Toxin Post diphtheritic, porphyria, Muscle tenderness Myositis, inflammatory myopathy,
arsenic (myalgias may be severe in Guillain
Viral Rabies Barre syndrome)
Trauma Injection related sciatic neuritis Muscle stretch reflexes Absent: Guillain Barre syndrome, Polio,
Neuromuscular Immune mediated Myasthenia Gravis Diphtheria, spinal shock, at level of
junction spinal cord damage
Drugs, toxins Organophosphates, snake venom,
drugs (aminoglycosides), Preserved : Myasthenia Gravis, periodic
Botulism paralysis, Botulism
Dyselectrolytemia Hypermagnesemia Exaggerated: Below level of spinal lesion,
Upper motor neuron lesion
Muscle Infection Viral myositis
Spinal tenderness, Spinal trauma, epidural abscess or other
Inflammation Inflammatory myopathy
painful spine extradural compression
Channelopathy Hypokalemic periodic paralysis Neck stiffness Polio, enteroviral myelitis, Guillain Barre
Dyselectrolytemia Hypokalemia syndrome, transverse myelitis
1354 Indian J Pediatr (October 2012) 79(10):1351–1357

Fig. 1 Approach to child with Acute paraparesis/plegia

acute paraplegia or paraparesis

Features of spinal cord compression* / Sensory level on examination

Yes No

CEMRI spine as early as possible DTRs


Compressive Noncompressive
Ocular/bulbar Symmetric?
myelopathy myelopathy
+ involvement?

Neurosurgery AcuteTM:Treat with high

Myasthenia, GBS#
consult+ steroids dose steroids and consult
Botulism CPK,K +,
DTR Deep tendon reflexes; CPK Urine myoglobin
Creatine phosphokinase; TM
Transverse myelitis; GBS Gul-
lain Barre Syndrome, NCV Polio, GBS,
Nerve conduction velocity; CSF Traumatic
Cerebrospinal fluid. *Bony ten- neuritis. Get
derness/deformity, root pains, NCV
girdle sensation /early bladder
Viral myositis,
or bowel involvement #other IVIG,Neuro
periodic paralysis,
possibilities according to clinical Rhabdomyolysis consult,NCV,
features as described in text

polyneuropathy or rarely may be seen in transverse infection triggered immune mediated attack on the nerve axons
myelitis. The CSF can be normal early in the course of or myelin. Antecedant respiratory or gastrointestinal illnesses
these illnesses. are commonly found in the history [3]. The most common
3. Nerve Conduction studies and Electro Myography underlying subtype of the syndrome is the acute inflammatory
(EMG): These studies confirm the involvement of demyelinating polyradiculoneuropathy (AIDP) but the other
nerves and help in diagnosis of anterior horn cell dis- common subtype of acute motor axonal neuropathy (AMAN)
eases. These are particularly helpful to confirm Guillain may be equally common in Indian children [4]. In the typical
Barre syndrome. The repetitive nerve stimulation test cases, the first symptoms are usually pain, paraesthesia, or
helps to diagnose myasthenia gravis and botulism. weakness in the limbs which spreads proximally. Weakness
Rarely, these may aid the diagnosis of an inflammatory may progress rapidly, and approximately 50 % of the children
myopathy. will reach nadir by 2 wk, 80 % by 3 wk, and the rest by 4 wk.
4. Creatine Kinase: Raised levels of muscle enzyme crea- Risk factors for children requiring ventilation are cranial nerve
tine kinase reflects acute muscle fiber injury and may involvement, increased CSF protein during first week of illness
point towards a muscle disease. In the setting of AFP and short period between antecedent illness and the onset of
this may be seen in children with viral myositis or symptoms [5]. Investigations required for confirming the diag-
inflammatory myopathy. nosis 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
Differential Diagnosis of AFP (Table 3) first days of the illness [3]. When a child presents in the acute
phase, the differentiation from polio or enetroviral myelitis can
Some of the commonly encountered causes of AFP are be done based on CSF. Viral myeltis would show CSF pleocy-
discussed below; tosis, which would be conspicuously absent in GBS. CSF
should be analyzed before treatment with intravenous immu-
Guillain Barre Syndrome (GBS) noglobulin (IVIG) as IVIG can cause aseptic meningitis. Man-
agement of a child with GBS would involve a meticulous
With the control of polio, GBS is the most common cause of observation for respiratory, bulbar muscle weakness. Early
AFP in children. Worldwide its incidence is 0.6–4 cases per elective intubation and ventilatory support are important in
100,000 per year [2]. It most commonly occurs after an the acute phase. During hospitalization, monitoring for
Indian J Pediatr (October 2012) 79(10):1351–1357 1355

Table 3 Characteristics to aid differential diagnosis of acute flaccid paralysis

Feature Transverse Poliomyelitis Guillain-Barre Traumatic neuritis

myelitis syndrome (following injection)

Development From hours to four days 24 to 48 h from onset From hours to 4 wk From hours to four days
of paralysis to full paralysis
Fever at onset May be present High, always present at Uncommon Present, if underlying
of weakness onset of flaccid paralysis infection being treated
with IM injections
Paralysis Symmetric Asymmetric, Symmetric, mostly ascending Affects only one limb
Progression Descending• Ascending
of paralysis
Muscle tone Reduced during Reduced Reduced Reduced
acute phase
Deep-tendon Absent in lower Decreased or absent Absent Decreased or absent
reflexes limbs(early);
Sensation Anesthesia of lower Severe myalgia, backache, Cramps, tingling, hypoanesthesia Pain in gluteus
limbs with sensory no sensory changes of palms and soles
Cranial nerve Absent Only when bulbar Often present, affecting nerves VII, Absent
involvement involvement is present IX, X, XI, XII
Respiratory Sometimes Only when bulbar Occurs in severe cases Absent
insufficiency involvement is present
Autonomic signs Present Rare Frequent in severe cases (blood pressure Hypothermia in
and symptoms alterations, sweating, blushing, and affected limb
body temperature fluctuations)
Cerebrospinal Normal or Mild elevation of Albumin-cytologic dissociation (usually Normal
fluid Pleocytosis lymphocytes 10 <10 cells/ml, never >50cells/ml)
to 200/mL
Bladder dysfunction Present- early Rare Occasionally (Transient, at the Never
and persistent peak of weakness, 1–3 d (30 %))
Nerve conduction Normal Abnormal: anterior Abnormal: slowed conduction, Abnormal: s/o
velocity: third wk horn cell disease decreased motor-sensory
(normal during motor amplitudes axonal damage
first 2 wk)
Diagnostic test MRI–spine Stool viral detection Nerve conduction studies Nerve conduction studies,

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 complica- poliomyelitis. The initial symptoms of polio are non-specific
tions are essential to optimize outcomes. IVIG is the and include fever, headache, vomiting, constipation, neck
treatment of choice in the authors’ setting for GBS, stiffness and pain in limbs. The paralysis follows or accom-
given the availability, ease of administration and the panies these symptoms. The maximal weakness evolves
safety compared with plasmapheresis. It is given in the quickly over 1–2 d. A history of intramuscular injections
dose of 2 g/kg spread over 2–5 d. precedes paralytic poliomyelitis in about 50–60 % of patients,
patients may present initially with fever and paralysis (prov-
Anterior Horn Cell Viral Myelitis ocation paralysis). Clinical characteristics of poliomyelitis
include; 1. Fever at onset 2. Rapid progression of paralysis
Poliomyelitis within 24–48 h 3. Asymmetric, proximal more than distal
limb paralysis 4. Preservation of sensory function often with
Both the wild polio virus and the vaccine associated polio severe myalgias 5. Residual paralysis at 60 d [6]. Most of the
virus cause anterior horn cell affliction to result in flaccid children with paralytic polio die from complications of bulbar
paralysis. Children under 5 y are the most frequently affected. paralysis and respiratory failure. Management is mainly fo-
However, older individuals and adults can also develop cused on meticulous supportive care.
1356 Indian J Pediatr (October 2012) 79(10):1351–1357

Non Polio Enteroviral Myelitis Table 4 Summary of approach to diagnosis in a child with acute
flaccid paralysis

Non polio enteroviruses can cause a polio like paralytic 1. ABCs

disease. Among all known nonpolio enteroviruses, ● Ensure protection of airway and adequate ventilation
enterovirus-71 has been most strongly implicated in out- (especially if there is respiratory muscle weakness,
breaks of central nervous system disease and AFP. The shallow respiration, dysphagia, weak gag)
clinical syndrome frequently is associated with aseptic men- ● Check and support: BP and Heart Rate
ingitis, hand, foot and mouth disease and hemorrhagic con- ● Immobilize neck if history of neck/head trauma
junctivitis [7]. Weakness associated with enterovirus disease ● Send electrolytes and get an ECG- to look for hypokalemia
can be severe and permanent. 2. Examination and classification into pattern for example,
● Flaccid Paraparesis with sensory level (early bladder dysfunction)-
Transverse myelitis, compressive myelopathy
Other Viruses Causing AFP
● Flaccid afebrile symmetric para/quadriparesis (+/− bulbar and
respiratory involvement) with areflexia
Rabies The common presentation of human rabies is with and minimal sensory loss (but often sensory symptoms) : Acute
fever, behavioral and autonomic instability and hydro/aero neuropathy or polyradiculopathy (esp., Guillain Barre Syndrome)
phobia. However, a minority of the patients can present ● Flaccid, febrile, pure motor, asymmetric, paralysis (no bladder
primarily with paralytic disease. This type of presentation involvement) often with meningismus: Enteroviral, polio, or vaccine
follows a prodrome of paraesthesias in the bitten area, associated poliomyelitis
ascending paralysis or paralysis progressing from the bitten ● Flaccid motor-sensory lower limb monoparesis after IM injection:
Injection neuritis
limb. Sphincter disturbances and autonomic instability is
● Ophthalmoplegia, ptosis, bulbar weaknes with motor weakness:
common. Disease progression is slower in paralytic rabies Miller-Fischer variant of Guillain Barre
[8]. The disease can be easily missed if a history of animal Syndrome, Botulism, Myasthenia Gravis
bite is not actively sought. Frequently the bite may not be ● Proximal muscle weakness, muscle tenderness without sensory
recent and the parents may not give the history, unless symptoms or signs and with preserved
specifically asked for. reflexes: Viral myositis, Inflammatory myopathy (e.g.,
Herpes group of viruses can lead to AFP by triggering GBS
3. Investigations (according to the suspected site of lesion and cause
or transverse myelitis, causing polyradiculoneuropathies in of paralysis)
immunocompromized hosts [9]. Japanese encephalitis virus ● Neuroimaging (spinal cord)
can also preferentially affect the anterior horn cell and cause ○ MRI indicated in all cases of myelopathy, suspected transverse
paralysis associated with encephalitis [10]. myelitis
○ X- ray spine: suspected atlantoaxial dislocation, vertebral
Transverse Myelitis tuberculosis
● Electrophysiologic testing (NCV & electromyography):
It is an acute demyelinating disorder of the spinal cord. It Guillain Barre syndrome
may occur alone or in combination with demyelination in ● Lumbar puncture (CSF): Guillain Barre syndrome, suspicion
of viral myelitis
other portions of the nervous system. It is believed com-
monly that previous infection or immunization triggers ● Biochemistry: Creatine Kinase, Potassium, Magnesium, Phosphate
transverse myelitis, but no evidence supports such a notion ● ECG: Hypokalemia
[11]. ● Urine for porpho-bilinogens in porphyria, toxins: arsenic
The common presentation includes an acute phase of spinal 4. Management (depends on the underlying etiology identified)
shock with flaccid paraparesis or quadreparesis, urinary reten- ● All children: meticulous supportive care, anticipate and identify
respiratory, bulbar weakness (except in
tion or incontinence, absent reflexes and mute plantars, sen- injection neuritis), shock due to reduced vascular tone (spinal cord
sory loss/level is frequently present. After a few weeks, the disease), Autonomic instability, complications of immobilization
signs of UMN dysfunction appear, in the form of spasticity, and prevention of nosocomial infections.
and hypereflexia. This disorder should be suspected in any ● Specific therapy:
child with rapid onset flaccid profound quadreparesis, early or ○ Guillain Barre syndrome: IVIG, 2 g/kg over 2–5 d
persistent bladder or bowel involvement, sensory loss or sen- ○ Transverse myelitis: IV methy-prednisolone 10–30 mg/kg, daily
sory level on examination, with suggestion of UMN signs on (max-1 g) for 3–5 d
examination (e.g., up going plantars). In such a situation an ○ Compressive myelopathy: spinal immobilization, surgical
intervention, steroids (acute traumatic myelopathy)
urgent spinal MRI is needed to establish the diagnosis. Other
○ Dermatomyositis, Myasthenia Gravis: Immunomodulation
causes of acute myelopathy like trauma, paraspinal/epidural
spinal abscess, hematoma or anterior spinal artery syndrome ○ Hypokalemia: Intravenous potassium correction
need exclusion in this setting. The management of transverse
Indian J Pediatr (October 2012) 79(10):1351–1357 1357

myelitis consists of immunosuppression and supportive care. (snake bite). Evaluation of spine by imaging may be
Attention is needed to maintain airway, breathing and circu- needed urgently in patients with suggestive clinical fea-
lation, bladder catheterization and exclusion of compressive tures. Once these causes are excluded, most distal pa-
myelopathy by imaging. High dose pulse corticosteroids are thologies are generally immune mediated and respond to
the recommended form therapy [11]. Methylprednisolone is immunomodulation. Irrespective of the cause, general-
given in a dose of 10–30 mg/kg/d (max:1 g/d) for 5 d followed ized weakness frequently affects respiratory and bulbar
by oral prednisolone 1–2 mg/kg/d for 2 wk and then tapered function. Such children need to be carefully monitored
over subsequent 2–4 wk. and treated.

Traumatic Neuritis (Following Injection)

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 Role of Funding Source None.
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 diag- References
nosis of traumatic neuritis. It is probable that some cases of
polio are misdiagnosed as traumatic neuritis. Residual sen- 1. Marx A, Glass JD, Sutter RW. Differential diagnosis of acute
sory deficits strongly favor the diagnosis of injection neuri- flaccid paralysis and its role in poliomyelitis surveillance. Epide-
tis. Management is entirely supportive. miol Rev. 2000;22:298–316.
2. Hughes RAC, Rees JH. Clinical and epidemiological features of
Guillain-Barré syndrome. J Infect Dis. 1997;176:S92–8.
Hypokalemic Paralysis
3. Paradiso G, Tripoli J, Galicchio S, Fejerman N. Epidemiological,
clinical, and electrodiagnostic findings in childhood Guillain-Barré
This is an important differential in any child particularly in a syndrome: a reappraisal. Ann Neurol. 1999;46:701–7.
younger child with AFP. An early recognition can prevent 4. Kalra V, Sankhyan N, Sharma S, Gulati S, Choudhry R, Dhawan
B. Outcome in childhood Guillain-Barré syndrome. Indian J
potentially fatal cardiac complications. In the developing
Pediatr. 2009;76:795–9.
countries, it most commonly results from diarrheal diseases. 5. Rantala H, Uhari M, Cherry J, Shields WB. Risk factors of respi-
However, rarer familial chanellopathies, underlying disorders, ratory failure in children with Guillain Barre syndrome. Pediatr
such as renal tubular acidosis, primary/secondary hyperaldos- Neurol. 1995;13:289–92.
6. Melnick J. Enteroviruses: polioviruses, coxsackieviruses, echovi-
teronism also need to be considered. Correction of potassium
ruses, and newer enteroviruses. In: Field’s BN, Knipe DM,
levels rapidly reverses the paralysis in these children. Chanock RM, eds. Field’s virology. Philadelphia: Lippincott-
Raven Publishers; 1996. pp. 655–712.
7. Wadia NH, Wadia PN, Katrak SM, Misra VP. A study of the
neurologic disorder associated with acute hemorrhagic conjuncti-
vitis due to enterovirus 70. J Neurol Neurosurg Psychiatry.
AFP is a broad clinical entity with an array of diagnostic 8. Gadre G, Satishchandra P, Mahadevan A, et al. Rabies viral
possibilities. Every case of AFP is a medical emergency. A encephalitis: clinical determinants in diagnosis with special
reference to paralytic form. J Neurol Neurosurg Psychiatry.
systematic anatomic/pathophysiological approach to diag-
nosis helps to narrow down the diagnostic possibilities in a 9. Tyler KL. Herpes simplex virus infections of the central nervous
given child (Table 4). Accurate and early diagnosis of the system: encephalitis and meningitis, including Mollaret’s. Herpes.
cause has important bearing on the management and prog- 2004;11:57A–64A.
10. Misra UK, Kalita J. Anterior horn cells are also involved in
nosis. The immediate priorities are to detect and manage
Japanese encephalitis. Acta Neurol Scand. 1997;96:114–7.
respiratory, bulbar muscle weakness, rapidly exclude causes 11. Frohman EM, Wingerchuk DM. Clinical practice. Transverse my-
which are reversible like dyselectrolytemia or toxemia elitis. N Engl J Med. 2010;363:564–72.