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Differentials of acute flaccid paralysis

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I now have enough from authoritative sources to compile a thorough, well-organized answer. Here is the full differential:

Differentials of Acute Flaccid Paralysis (AFP)

AFP is defined as the sudden onset of weakness/flaccidity in one or more limbs, with reduced or absent deep tendon reflexes. The cause can be localized anatomically along the lower motor neuron (LMN) pathway.

1. Anterior Horn Cell (Spinal Cord - Gray Matter)

ConditionKey Features
PoliomyelitisAsymmetric, fever prodrome, no sensory loss, CSF pleocytosis; wild-type or vaccine-derived poliovirus
Non-polio EnterovirusesEV-D68 (major cause of biennial outbreaks in USA since 2014), EV-A71, CV-A7; children, preceded by respiratory illness
Acute Flaccid Myelitis (AFM)Predominantly children, fever + respiratory prodrome, onset of limb weakness within 10 days; MRI shows T2 lesions in gray matter
West Nile VirusAsymmetric, fever, encephalitis possible; arboviruses can cause AFP
Rabies (paralytic form)Ascending flaccid paralysis mimicking GBS; bulbar involvement; history of animal bite
  • Goldman-Cecil Medicine, block 51; Bradley and Daroff's Neurology, block 23

2. Nerve Roots / Peripheral Nerves (Polyneuropathy / Polyradiculopathy)

ConditionKey Features
Guillain-Barre Syndrome (GBS/AIDP)Most common cause of AFP globally; ascending paralysis, areflexia, preceding infection (Campylobacter, CMV, EBV); albumino-cytologic dissociation in CSF
Diphtheritic PolyneuropathyBulbar palsy first, follows Corynebacterium diphtheriae infection; palatal palsy, accommodation paresis
Traumatic NeuritisInjection injury to sciatic nerve (gluteal injection); asymmetric
Lead/Arsenic/Organophosphate poisoningToxic neuropathy; history of exposure
Transverse MyelitisCord inflammation; sensory level present + sphincter dysfunction differentiates from pure AFP
  • Park's Textbook of Preventive Medicine, block 3; Red Book 2021; Bradley and Daroff's, block 23

3. Neuromuscular Junction

ConditionKey Features
BotulismDescending paralysis (cranial nerves first - diplopia, dysarthria, dysphagia); NO fever, NO sensory loss; bilateral CN VI palsy is a hallmark; pupillary involvement distinguishes from GBS
Myasthenia Gravis (acute exacerbation)Fatigable weakness, ptosis, diplopia; worsened by exercise; anti-AChR antibodies
Lambert-Eaton Myasthenic SyndromeProximal weakness, autonomic features; improves briefly with repeated activity; associated with small cell lung cancer
Tick ParalysisAscending flaccid paralysis in children; caused by tick neurotoxin; resolves completely with tick removal; can mimic GBS
  • Harrison's 22E, block 18; Goldman-Cecil, block 44; Rosen's EM, block 24; Tintinalli's EM, block 15

4. Muscle (Myopathy)

ConditionKey Features
Hypokalemic Periodic ParalysisEpisodic weakness; triggered by carbohydrates, rest after exercise; low serum K+; thyrotoxic form common in Asian males
Hyperkalemic Periodic ParalysisAssociated with myotonia; triggered by fasting or cold
Acute Myositis (viral/inflammatory)CK elevation, myalgia, preceding viral illness
RhabdomyolysisSevere weakness, myoglobinuria, markedly elevated CK
  • Morgan and Mikhail's Anesthesiology, block 5

Quick Comparison Table: Key Distinguishing Features

FeaturePolioGBSBotulismTick ParalysisTrans. Myelitis
FeverYes (early)NoNoNoVariable
SymmetryAsymmetricSymmetricSymmetric (descend.)AscendingSymmetric
Sensory lossNoMild (paresthesias)NoNoYes (level)
ReflexesAbsentAbsentAbsent/reducedAbsentAbsent acutely
Cranial nervesBulbar onlyLateEarly (CN VI, VII)RareNo
CSFPleocytosisAlb-cyto dissociationNormalNormalCells + protein

WHO AFP Surveillance Note

The WHO and national programs (e.g., India) require all cases of AFP in children <15 years to be reported and stool samples sent for polio testing, because early polio is clinically indistinguishable from GBS, transverse myelitis, and traumatic neuritis. - Park's Textbook of Preventive Medicine, block 3

Bottom line: The most common causes worldwide are GBS and poliomyelitis (or non-polio enteroviruses where vaccination is complete). Always consider botulism when cranial nerve palsies accompany descending weakness, and tick paralysis in children with ascending weakness - because tick removal is curative.
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