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 syndromecharacterized by rapid onset weakness, that many times includesrespiratory and bulbar weakness. AFP is a broad clinical entitywith an array of diagnostic possibilities. An accurate and earlydiagnosis of the cause has important bearing on themanagementand prognosis. The immediate priorities in a child who presentswith acute progressive weakness are; to detect and managerespiratory muscle weakness, to detect and manage bulbarweakness, evaluate for cardiovascular instability, detect andmanage dyselectrolytemia or toxemia, and to detect andmanagea spinal compression (traumatic, intraspinal collections). Ur-gent imaging of the spine is needed in settings where a spinalcord involvement is suspected. Compressive or traumatic spinallesionsmay need early neurosurgical intervention. Anterior horncell injury is usually due to direct viral infection. More distalpathologies are generally immune mediated and respond toimmunomodulation. Irrespective of the cause, generalizedweakness 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 syndromecharacterized by rapid onset weakness, that frequentlyincludes respiratory and bulbar weakness. The weaknessusually progresses to maximum within days to weeks.The term “flaccid” indicates the absence of spasticity orother signs of disordered central nervous system motortracts such as hyperreflexia, clonus or extensor plantars[1]. AFP is broad clinical entity with an array of diag-nostic possibilities. An accurate and early diagnosis ofthe cause has important bearing on the management andprognosis. If not managed appropriately, paralysis canprogress to respiratory failure and death. Another issueof public health importance is the immediate reportingof all cases of AFP to the polio surveillance team(Box1). Any case meeting the AFP definition undergoes athorough investigation to determine if the paralysis iscaused by polio. Each case of AFP is to be reportedand 2 stool samples (≥24 h apart, each 8–10 g) arecollected within 14 d of paralysis onset and sent toWHO accredited laboratory.

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

Indian J Pediatr (October 2012) 79(10):1351–1357DOI 10.1007/s12098-012-0831-8

This protocol focuses on the clinical evaluation of achild presenting with AFP and provides a practicalclinical approach to diagnosis in the Emergency depart-ment. For a detailed discussion on AFP the reader isreferred to other reviews on the subject [1]. The objec-tives of this article are: to provide a practical approachto diagnosis in an individual patient; to provide anapproach to rational use of diagnostic tests and discussthe common causes of AFP in children.

Diagnostic Approach

Initial Assessment and Stabilization

Every child with AFP is a medical emergency requiringsystematic evaluation and management. Initial assess-ment of any such acutely ill child should concentrateon rapid cardiopulmonary assessment and resuscitation.Following are the key areas on initial assessment;

& Detect and manage respiratory muscle weakness: Anychild with acute weakness should be evaluated for res-piratory muscle weakness. Younger children with respi-ratory muscle weakness may present with non-specificirritability, sweating, poor feeding and shallow or para-doxical respiratory efforts. Older children may complainof respiratory difficulty, may have excessive sweating,agitation, air hunger, reduced single breath count/chestexpansion or shallow/paradoxical respiratory efforts.Careful serial examinations may be critical in such chil-dren to pick up the weakness early. Early elective intu-bation and respiratory support are critical to save theseaffected children.

& Detect and manage bulbar weakness: Symptoms ofvoice change, poor cry, pooling of secretions, gur-gling sounds in throat, poor ability to swallow andchoking on feeds may be markers of bulbar dysfunc-tion. Care should be taken to avoid oral feeding,providing regular suction and ensuring entral nutri-tion via nasogastric feeding.

& Evaluate for cardiovascular instability: Conditionsleading to AFP (Spine trauma, myelitis, GuillainBarre syndrome) can also result in cardiac rhythmabnormalities and cardiovascular insufficiency. Theseissues will require a priority management. Hence,attaching a quadriparetic child to an ECG/cardiacmonitor is an early step in the management.

& Rule out dyselectrolytemia or toxemia: Hypokalemiaand snake envenomation are important causes of flaccidparalysis. These causes should be excluded in all chil-dren with AFP by history and examination, early inmanagement course. A rapid assessment of electrolytesand ECG should be sought in all such children.

& To rule out a spinal compression (traumatic, intraspinalcollections). : At the outset, patients with possiblespinal injury due to trauma or other lesions requiringurgent neurosurgical intervention should be identifiedon history and examination. Immediate spinal stabili-zation and administration of corticosteroids in thosewith trauma would be a priority, while neurosurgicalrelief of spinal compression may be warranted toprevent long term disability.

History

The first step is to determine if an unwell child actually hasmuscle weakness. Many children with weakness presentwith nonspecific symptoms of irritability, lethargy andclumsy walk or refusal to walk. Children with abnormalgait, limp or refusing to walk may present initially to ortho-pedic or trauma clinics. Pseudoparalysis due to limb painmay result from trauma, arthritis/arthralgia, myostis, joint orperiosteal bleeds or joint or periarticular infections orinflammations.

It is useful to remember the possible causes of AFPin children using a neuro-anatomical approach (Table 1).Information is derived from the history and focusedneurological examination looking at pattern of tone,tendon reflexes, sensory examination, signs and symp-toms of bladder and/or bowel involvement. (Table 2).

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

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Investigations

The choice of the initial investigations would depend onthe information gained from history and examination.Moreover, the urgency to arrive at the diagnosis wouldalso dictate the sequence and choice of investigations. Astep wise and judicious use of investigations would helpreach the diagnosis with the minimum use of resources(Fig. 1).

1. MRI Spine: It is indicated when there is a suspicion ofspinal cord compression or transverse myelitis. Morespecifically, any child with history of neck or back trau-ma, rapid onset flaccid profound quadreparesis, early orpersistent bladder or bowel involvement, sensory loss orsensory level on examination, spinal tenderness, neuro-cutaneous markers, or appearance of UMN signs on ex-amination (e.g., up going plantars) should get an MRI ofthe spine.

2. CSF examination: This is helpful to narrow the diag-nostic possibilities. A raised CSF cell count would beseen in patients with transverse myelitis, infective my-elitis viz. polio or enteroviral myelitis, varicellas orherpes myelitis, rabies, etc. A raised CSF protein withnormal cell count (albuminocytological dissociation)suggests Guillain Barre syndrome, post diphtheritic

Table 1 A neuroanatomical differential diagnosis of acute flaccidparalysis in children

Site Pathophysiology Disease

Spinal cord Compressive Traumatic spinal injury, epiduralabscess, hematoma, discitis

Inflammatory Transverse myelitis

Anterior horncell

Viral Poliomyelitis, vaccine associatedpoliomyelitis, Enteroviralmyelitis, Japanese encephalitis

Vascular Anterior spinal artery infarction

Roots/nerves Immune mediated Guillain Barre syndrome,

Toxin Post diphtheritic, porphyria,arsenic

Viral Rabies

Trauma Injection related sciatic neuritis

Neuromuscularjunction

Immune mediated Myasthenia Gravis

Drugs, toxins Organophosphates, snake venom,drugs (aminoglycosides),Botulism

Dyselectrolytemia Hypermagnesemia

Muscle Infection Viral myositis

Inflammation Inflammatory myopathy(polymyositis)

Channelopathy Hypokalemic periodic paralysis

Dyselectrolytemia Hypokalemia

Table 2 Selected clues in history and examination while evaluating achild with acute flaccid paralysis

Points in historyand/or examination

Remarks

Fever at onset Polio or enteroviral myelitis, Transversemyelitis, myositis, epidural abscess, andKoch spine (prolonged history)

Trauma: head/neck Trivial trauma may lead to spinalcompression in patients with cervicalvertebral instability (Patients withDowns syndrome, congenitalcervicovertebral anomalies or juvenileidiopathic arthritis)

Exposure Toxins: lead, arsenic

Snake envenomation

Dog bite: Rabies

Preceding infectiousprodrome/vaccination

Guillain Barre syndrome or transversemyelitis

Sore throat, neck swelling, diphthereticpolyneuropathy (non/partly immunized)

Precipitating factors Diarrhea: Hypokalemia, enteroviralmyelitis

Exertion or post parandial: Hypokalemicperiodic paralysis

Intramuscular injection: Polio, traumaticsciatic neuritis

Sensory loss/level Compressive myelopathy, transversemyelitis

Early bowel/bladderinvolvement

Compressive myelopathy, transversemyelitis

Constipation in <1 y Botulism (H/o honey exposure)

Prominent autonomicsigns/symptoms

Guillain Barre syndrome, Rabies, acutemyelopathy

Ascending weakness Guillain Barre syndrome, Rabies,Varicella zoster virus, ascending myelitis

Descending weakness Diphtheria, Botulism

Prominent and earlyptosis

Myasthenia Gravis, Botulism

Facial weakness Guillain Barre syndrome, MyastheniaGravis, Botulism

Fluctuating symptoms,fatigability

Myasthenia Gravis

Muscle tenderness Myositis, inflammatory myopathy,(myalgias may be severe in GuillainBarre syndrome)

Muscle stretch reflexes Absent: Guillain Barre syndrome, Polio,Diphtheria, spinal shock, at level ofspinal cord damage

Preserved : Myasthenia Gravis, periodicparalysis, Botulism

Exaggerated: Below level of spinal lesion,Upper motor neuron lesion

Spinal tenderness,painful spinemovement

Spinal trauma, epidural abscess or otherextradural compression

Neck stiffness Polio, enteroviral myelitis, Guillain Barresyndrome, transverse myelitis

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polyneuropathy or rarely may be seen in transversemyelitis. The CSF can be normal early in the course ofthese illnesses.

3. Nerve Conduction studies and Electro Myography(EMG): These studies confirm the involvement ofnerves and help in diagnosis of anterior horn cell dis-eases. These are particularly helpful to confirm GuillainBarre syndrome. The repetitive nerve stimulation testhelps to diagnose myasthenia gravis and botulism.Rarely, these may aid the diagnosis of an inflammatorymyopathy.

4. Creatine Kinase: Raised levels of muscle enzyme crea-tine kinase reflects acute muscle fiber injury and maypoint towards a muscle disease. In the setting of AFPthis may be seen in children with viral myositis orinflammatory myopathy.

Differential Diagnosis of AFP (Table 3)

Some of the commonly encountered causes of AFP arediscussed below;

Guillain Barre Syndrome (GBS)

With the control of polio, GBS is the most common cause ofAFP in children. Worldwide its incidence is 0.6–4 cases per100,000 per year [2]. It most commonly occurs after an

infection triggered immune mediated attack on the nerve axonsor myelin. Antecedant respiratory or gastrointestinal illnessesare commonly found in the history [3]. The most commonunderlying subtype of the syndrome is the acute inflammatorydemyelinating polyradiculoneuropathy (AIDP) but the othercommon subtype of acute motor axonal neuropathy (AMAN)may be equally common in Indian children [4]. In the typicalcases, the first symptoms are usually pain, paraesthesia, orweakness in the limbs which spreads proximally. Weaknessmay progress rapidly, and approximately 50 % of the childrenwill reach nadir by 2 wk, 80 % by 3 wk, and the rest by 4 wk.Risk factors for children requiring ventilation are cranial nerveinvolvement, increased CSF protein during first week of illnessand short period between antecedent illness and the onset ofsymptoms [5]. Investigations required for confirming the diag-nosis are; nerve conduction studies and lumbar puncture (todocument CSF albumin-cytological dissociation). A raisedCSF protein concentration is present in about 80 % of patients,but CSF protein content is more likely to be normal during thefirst days of the illness [3]. When a child presents in the acutephase, the differentiation from polio or enetroviral myelitis canbe done based on CSF. Viral myeltis would show CSF pleocy-tosis, which would be conspicuously absent in GBS. CSFshould be analyzed before treatment with intravenous immu-noglobulin (IVIG) as IVIG can cause aseptic meningitis. Man-agement of a child with GBS would involve a meticulousobservation for respiratory, bulbar muscle weakness. Earlyelective intubation and ventilatory support are important inthe acute phase. During hospitalization, monitoring for

Acute paraparesis/plegia

Features of spinal cord compression* / Sensory level on examination

Yes No

CEMRI spine as early as possible

Compressivemyelopathy

Noncompressivemyelopathy

Neurosurgery

consult+steroids

AcuteTM:Treat with highdosesteroids andconsult

DTRs

Symmetric?

/+

GBS#

+

Ocular/bulbar

involvement?

Myasthenia,

Botulism CPK,K+,Urine myoglobin

+

IVIG,Neuroconsult,NCV,CSF

Viral myositis,periodic paralysis,Rhabdomyolysis

Polio, GBS,

Traumatic

neuritis. Get

NCV

Fig. 1 Approach to child withacute paraplegia or paraparesis

DTR Deep tendon reflexes; CPKCreatine phosphokinase; TMTransverse myelitis; GBS Gul-lain Barre Syndrome, NCVNerve conduction velocity; CSFCerebrospinal fluid. *Bony ten-derness/deformity, root pains,girdle sensation /early bladderor bowel involvement #otherpossibilities according to clinicalfeatures as described in text

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autonomic instability and prevention of nosocomial complica-tions are essential to optimize outcomes. IVIG is thetreatment of choice in the authors’ setting for GBS,given the availability, ease of administration and thesafety compared with plasmapheresis. It is given in thedose of 2 g/kg spread over 2–5 d.

Anterior Horn Cell Viral Myelitis

Poliomyelitis

Both the wild polio virus and the vaccine associated poliovirus cause anterior horn cell affliction to result in flaccidparalysis. 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-specificand include fever, headache, vomiting, constipation, neckstiffness and pain in limbs. The paralysis follows or accom-panies these symptoms. The maximal weakness evolvesquickly over 1–2 d. A history of intramuscular injectionsprecedes paralytic poliomyelitis in about 50–60 % of patients,patients may present initially with fever and paralysis (prov-ocation paralysis). Clinical characteristics of poliomyelitisinclude; 1. Fever at onset 2. Rapid progression of paralysiswithin 24–48 h 3. Asymmetric, proximal more than distallimb paralysis 4. Preservation of sensory function often withsevere myalgias 5. Residual paralysis at 60 d [6]. Most of thechildren with paralytic polio die from complications of bulbarparalysis and respiratory failure. Management is mainly fo-cused on meticulous supportive care.

Table 3 Characteristics to aid differential diagnosis of acute flaccid paralysis

Feature Transversemyelitis

Poliomyelitis Guillain-Barresyndrome

Traumatic neuritis(following injection)

Developmentof paralysis

From hours to four days 24 to 48 h from onsetto full paralysis

From hours to 4 wk From hours to four days

Fever at onsetof weakness

May be present High, always present atonset of flaccid paralysis

Uncommon Present, if underlyinginfection being treatedwith IM injections

Paralysis Symmetric Asymmetric, Symmetric, mostly ascending Affects only one limb

Progressionof paralysis

Descending• Ascending

Muscle tone Reduced duringacute phase

Reduced Reduced Reduced

Deep-tendonreflexes

Absent in lowerlimbs(early);hyperreflexia(late)

Decreased or absent Absent Decreased or absent

Sensation Anesthesia of lowerlimbs with sensorylevel

Severe myalgia, backache,no sensory changes

Cramps, tingling, hypoanesthesiaof palms and soles

Pain in gluteus

Cranial nerveinvolvement

Absent Only when bulbarinvolvement is present

Often present, affecting nerves VII,IX, X, XI, XII

Absent

Respiratoryinsufficiency

Sometimes Only when bulbarinvolvement is present

Occurs in severe cases Absent

Autonomic signsand symptoms

Present Rare Frequent in severe cases (blood pressurealterations, sweating, blushing, andbody temperature fluctuations)

Hypothermia inaffected limb

Cerebrospinalfluid

Normal orPleocytosis

Mild elevation oflymphocytes 10to 200/mL

Albumin-cytologic dissociation (usually<10 cells/ml, never >50cells/ml)

Normal

Bladder dysfunction Present- earlyand persistent

Rare Occasionally (Transient, at thepeak of weakness, 1–3 d (30 %))

Never

Nerve conductionvelocity: third wk

Normal Abnormal: anteriorhorn cell disease(normal duringfirst 2 wk)

Abnormal: slowed conduction,decreasedmotor amplitudes

Abnormal: s/omotor-sensoryaxonal damage

Diagnostic test MRI–spine Stool viral detection Nerve conduction studies Nerve conduction studies,Electromyography

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

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Non Polio Enteroviral Myelitis

Non polio enteroviruses can cause a polio like paralyticdisease. Among all known nonpolio enteroviruses,enterovirus-71 has been most strongly implicated in out-breaks of central nervous system disease and AFP. Theclinical syndrome frequently is associated with aseptic men-ingitis, hand, foot and mouth disease and hemorrhagic con-junctivitis [7]. Weakness associated with enterovirus diseasecan be severe and permanent.

Other Viruses Causing AFP

Rabies The common presentation of human rabies is withfever, behavioral and autonomic instability and hydro/aerophobia. However, a minority of the patients can presentprimarily with paralytic disease. This type of presentationfollows a prodrome of paraesthesias in the bitten area,ascending paralysis or paralysis progressing from the bittenlimb. Sphincter disturbances and autonomic instability iscommon. Disease progression is slower in paralytic rabies[8]. The disease can be easily missed if a history of animalbite is not actively sought. Frequently the bite may not berecent and the parents may not give the history, unlessspecifically asked for.

Herpes group of viruses can lead to AFP by triggering GBSor transverse myelitis, causing polyradiculoneuropathies inimmunocompromized hosts [9]. Japanese encephalitis viruscan also preferentially affect the anterior horn cell and causeparalysis associated with encephalitis [10].

Transverse Myelitis

It is an acute demyelinating disorder of the spinal cord. Itmay occur alone or in combination with demyelination inother portions of the nervous system. It is believed com-monly that previous infection or immunization triggerstransverse myelitis, but no evidence supports such a notion[11].

The common presentation includes an acute phase of spinalshock with flaccid paraparesis or quadreparesis, urinary reten-tion or incontinence, absent reflexes and mute plantars, sen-sory loss/level is frequently present. After a few weeks, thesigns of UMN dysfunction appear, in the form of spasticity,and hypereflexia. This disorder should be suspected in anychild with rapid onset flaccid profound quadreparesis, early orpersistent bladder or bowel involvement, sensory loss or sen-sory level on examination, with suggestion of UMN signs onexamination (e.g., up going plantars). In such a situation anurgent spinal MRI is needed to establish the diagnosis. Othercauses of acute myelopathy like trauma, paraspinal/epiduralspinal abscess, hematoma or anterior spinal artery syndromeneed exclusion in this setting. The management of transverse

Table 4 Summary of approach to diagnosis in a child with acuteflaccid 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 andrespiratory involvement) with areflexiaand minimal sensory loss (but often sensory symptoms) : Acuteneuropathy or polyradiculopathy (esp., Guillain Barre Syndrome)

● Flaccid, febrile, pure motor, asymmetric, paralysis (no bladderinvolvement) often with meningismus: Enteroviral, polio, or vaccineassociated poliomyelitis

● Flaccid motor-sensory lower limb monoparesis after IM injection:Injection neuritis

● Ophthalmoplegia, ptosis, bulbar weaknes with motor weakness:Miller-Fischer variant of Guillain BarreSyndrome, Botulism, Myasthenia Gravis

● Proximal muscle weakness, muscle tenderness without sensorysymptoms or signs and with preservedreflexes: Viral myositis, Inflammatory myopathy (e.g.,dermatomyositis)

3. Investigations (according to the suspected site of lesion and causeof paralysis)

● Neuroimaging (spinal cord)

○ MRI indicated in all cases of myelopathy, suspected transversemyelitis

○ X- ray spine: suspected atlantoaxial dislocation, vertebraltuberculosis

● Electrophysiologic testing (NCV & electromyography):Guillain Barre syndrome

● Lumbar puncture (CSF): Guillain Barre syndrome, suspicionof 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 identifyrespiratory, bulbar weakness (except ininjection neuritis), shock due to reduced vascular tone (spinal corddisease), Autonomic instability, complications of immobilizationand prevention of nosocomial infections.

● Specific therapy:

○ Guillain Barre syndrome: IVIG, 2 g/kg over 2–5 d

○ Transverse myelitis: IV methy-prednisolone 10–30 mg/kg, daily(max-1 g) for 3–5 d

○ Compressive myelopathy: spinal immobilization, surgicalintervention, steroids (acute traumatic myelopathy)

○ Dermatomyositis, Myasthenia Gravis: Immunomodulation

○ Hypokalemia: Intravenous potassium correction

1356 Indian J Pediatr (October 2012) 79(10):1351–1357

myelitis consists of immunosuppression and supportive care.Attention is needed to maintain airway, breathing and circu-lation, bladder catheterization and exclusion of compressivemyelopathy by imaging. High dose pulse corticosteroids arethe recommended form therapy [11]. Methylprednisolone isgiven in a dose of 10–30mg/kg/d (max:1 g/d) for 5 d followedby oral prednisolone 1–2 mg/kg/d for 2 wk and then taperedover subsequent 2–4 wk.

Traumatic Neuritis (Following Injection)

Traumatic neuritis is suspected in cases in which there is onelimb involvement and definite history of injection in thatlimb (usually less than 24 h) before the onset of paralysis. Itis associated with pain and hypothermia of affected limbs. Itis sometimes difficult to distinguish it from polio. However,sensory deficits and lack of CSF pleocytosis favor the diag-nosis of traumatic neuritis. It is probable that some cases ofpolio are misdiagnosed as traumatic neuritis. Residual sen-sory deficits strongly favor the diagnosis of injection neuri-tis. Management is entirely supportive.

Hypokalemic Paralysis

This is an important differential in any child particularly in ayounger child with AFP. An early recognition can preventpotentially fatal cardiac complications. In the developingcountries, it most commonly results from diarrheal diseases.However, rarer familial chanellopathies, underlying disorders,such as renal tubular acidosis, primary/secondary hyperaldos-teronism also need to be considered. Correction of potassiumlevels rapidly reverses the paralysis in these children.

Conclusions

AFP is a broad clinical entity with an array of diagnosticpossibilities. Every case of AFP is a medical emergency. Asystematic anatomic/pathophysiological approach to diag-nosis helps to narrow down the diagnostic possibilities in agiven child (Table 4). Accurate and early diagnosis of thecause has important bearing on the management and prog-nosis. The immediate priorities are to detect and managerespiratory, bulbar muscle weakness, rapidly exclude causeswhich are reversible like dyselectrolytemia or toxemia

(snake bite). Evaluation of spine by imaging may beneeded urgently in patients with suggestive clinical fea-tures. Once these causes are excluded, most distal pa-thologies are generally immune mediated and respond toimmunomodulation. Irrespective of the cause, general-ized weakness frequently affects respiratory and bulbarfunction. Such children need to be carefully monitoredand treated.

Conflict of Interest None.

Role of Funding Source None.

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