Acute flaccid paralysis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Localisation begins before the laboratory. Brain disease usually creates upper motor-neurone signs, but acute bilateral cerebral or brainstem injury can be misleading. Spinal shock after cord injury, infarction or inflammation produces flaccidity and areflexia below the lesion before spasticity emerges. Root and peripheral-nerve disease gives areflexia with sensory symptoms; neuromuscular-junction disease gives fatigability without sensory loss; muscle disease produces proximal weakness with preserved sensation and reflexes until severe.

Tempo and associated findings narrow the cause. GBS progresses over days to a nadir within four weeks. Hyperacute onset with severe back pain can indicate cord infarction; compressive cauda equina adds saddle change and urinary dysfunction; diarrhoeal or respiratory infection supports GBS; descending cranial weakness with dilated pupils and constipation suggests botulism; episodic weakness after carbohydrate load with low potassium suggests periodic paralysis. Travel, vaccination, toxins, preserved foods, wounds and family history should be elicited without delaying stabilisation.

Respiratory failure can develop before the patient feels breathless. Diaphragm weakness causes orthopnoea, reduced voice volume and abdominal paradox, while bulbar weakness creates aspiration risk independent of vital capacity. Serial objective assessment and early intubation are safer than rescue after exhaustion. Cause-specific care follows: urgent decompression for compression, immunoglobulin or exchange for GBS, antitoxin for botulism, electrolyte correction for metabolic paralysis and antimicrobial treatment for neuroinvasive infection.

Key points

Acute flaccid paralysis describes rapid weakness with reduced tone and often reduced reflexes; it is not a final diagnosis and early spinal cord disease can also appear flaccid during spinal shock.
Guillain-Barre syndrome commonly produces progressive, broadly symmetric limb weakness and areflexia after infection, with sensory symptoms, pain, facial weakness and autonomic instability.
A sensory level, extensor plantar responses emerging later, early bladder dysfunction or a sharply asymmetric pattern favours spinal cord disease over uncomplicated Guillain-Barre syndrome.
Neuromuscular-junction disorders produce fatigable ocular, bulbar and respiratory weakness with preserved sensation; myasthenia often preserves reflexes, while botulism adds fixed pupils and descending paralysis.
Hypokalaemia, hypophosphataemia, severe magnesium disturbance, porphyria, toxins, tick paralysis and acute myopathy belong in the early reversible differential.
Assess forced vital capacity, cough, neck flexion, speech and swallow serially; normal saturation does not exclude neuromuscular hypoventilation.
Autonomic Guillain-Barre disease can cause extreme blood-pressure variation, arrhythmia, ileus and urinary retention, making unmonitored ward care unsafe in a progressing case.
Cerebrospinal fluid may show high protein with few cells after the first week, but early fluid can be normal and a marked pleocytosis should prompt infection or another cause.
Nerve-conduction and electromyography classify demyelinating, axonal, junctional or muscle processes, but initial studies can be non-diagnostic and must not delay respiratory support.
Intravenous immunoglobulin and plasma exchange are effective for non-ambulant or significantly progressing Guillain-Barre syndrome; corticosteroids do not improve GBS outcome.
In England, suspected acute flaccid paralysis or acute flaccid myelitis is urgently notifiable: telephone the local UKHSA health-protection team within 24 hours and report online within 3 days without waiting for virology or neurophysiology; use equivalent devolved-nation routes elsewhere.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Polyradiculoneuropathy

Guillain–Barré syndrome commonly causes rapidly progressive, broadly symmetrical weakness and areflexia after infection, with pain, sensory symptoms, cranial involvement and potentially severe autonomic dysfunction.

Spinal cord and cauda-equina disease

Cord infarction, inflammation or compression may initially appear flaccid during spinal shock; a sensory level, early sphincter dysfunction, asymmetry or later pyramidal signs supports this localisation.

Neuromuscular-junction and toxic disease

Myasthenia causes fatigable ocular, bulbar and respiratory weakness, while botulism produces descending paralysis with pupillary and autonomic features; both may preserve sensation.

Metabolic and muscle causes

Potassium, phosphate or magnesium disturbance, periodic paralysis, porphyria, toxic exposure and acute myopathy can interrupt muscle activation and should be sought early because several are reversible.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Motor pathway interruption
Disease affects anterior horn, root, peripheral nerve, neuromuscular transmission or muscle, reducing activation of the final common motor unit despite preserved intention to move.
2
Loss of tone and reflex activity
Reduced afferent–efferent reflex function produces hypotonia and depressed tendon reflexes; acute spinal shock can create the same appearance before upper motor-neurone signs emerge.
3
Bulbar and ventilatory spread
Progression to cranial, diaphragmatic and expiratory muscles weakens swallowing, cough and ventilation, often before breathlessness, oxygen desaturation or carbon-dioxide retention becomes obvious.
4
Autonomic involvement
When autonomic fibres are affected, vascular tone, cardiac rhythm, gut motility and bladder function become unstable, adding potentially fatal physiological risk to the motor deficit.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Ascending areflexic syndrome

Bilateral leg weakness progresses upward with absent reflexes, distal paraesthesia, back or radicular pain and relatively preserved sensation, supporting Guillain-Barre syndrome.

Cord or cauda warning

A defined sensory level, saddle anaesthesia, early urinary retention, severe spinal pain or asymmetric segmental deficit requires urgent spinal MRI.

Bulbar respiratory risk

Nasal speech, pooling saliva, weak cough, neck-flexion weakness and inability to count on one breath indicate declining ventilatory and airway reserve.

Botulism pattern

Blurred vision, fixed or sluggish pupils, ptosis, dry mouth and descending symmetric paralysis after food, wound or drug exposure suggests presynaptic toxin blockade.

Autonomic instabilityRed flag

Alternating hypertension and hypotension, bradycardia, tachyarrhythmia, ileus or urinary retention in GBS can deteriorate suddenly and needs monitored care.

Electrolyte paralysis

Generalised weakness with preserved sensation and a markedly low potassium or phosphate may reverse rapidly, but the cause and cardiac consequences require urgent treatment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serial forced vital capacity and cough assessmentFirst step
Why
Detect respiratory-muscle decline before gas exchange fails.
Interpretation and limitations
Trend with bulbar function and work of breathing; facial weakness can impair the mouth seal and one normal value does not guarantee safety.
02
ECG, cardiac monitoring and blood gas
Why
Identify autonomic arrhythmia, electrolyte effects and late hypoventilation.
Interpretation and limitations
Hypercapnia signals advanced weakness; continuous monitoring is needed when GBS progresses or potassium disturbance is severe.
03
Urgent MRI whole or targeted spine
Why
Exclude compression, infarction, myelitis and cauda-equina pathology.
Interpretation and limitations
Choose level and contrast from examination, but rapid or poorly localised syndromes may require extensive imaging before lumbar puncture.
04
Lumbar puncture
Why
Support GBS and investigate inflammatory or infectious polyradiculopathy.
Interpretation and limitations
Raised protein with few cells may be absent early; substantial white cells redirect assessment toward HIV, Lyme, CMV, malignancy or another mimic.
05
Nerve-conduction and electromyography
Why
Classify demyelinating or axonal GBS, junction disease, neuropathy and myopathy.
Interpretation and limitations
Early results can be equivocal; repeat studies and proximal or late responses may be needed, while treatment follows clinical severity.
06
Electrolyte and metabolic profile
Why
Find rapidly reversible potassium, phosphate, magnesium, glucose, thyroid, renal and liver abnormalities.
Interpretation and limitations
Interpret potassium with acid-base status, urine loss, medicines and ECG; cautious monitored replacement prevents rebound and arrhythmia.
07
Microbiology and toxin testing
Why
Identify botulism, poliovirus or another neuroinvasive infection requiring public-health action.
Interpretation and limitations
For suspected botulism, contact UKHSA immediately to arrange correct specimens and antitoxin; for possible poliovirus, follow the specialist stool and respiratory sampling pathway. These diagnostic discussions do not replace urgent statutory notification of suspected AFP or AFM.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Guillain–Barré syndrome

Symmetrical ascending or generalised weakness, areflexia and pain after infection support GBS; a marked cerebrospinal-fluid pleocytosis, sensory level or persistent asymmetry should redirect the diagnosis.

Acute spinal cord lesion

Back pain, a truncal sensory level, early bladder dysfunction or later extensor plantar responses favour infarction, inflammation or compression and justify urgent spinal imaging.

Myasthenia or botulism

Fluctuating ocular and bulbar weakness with normal sensation suggests junctional disease; fixed dilated pupils, constipation and descending weakness point more towards botulism.

Electrolyte paralysis or myopathy

Episodic weakness with an electrolyte disturbance or proximal weakness with muscle injury markers and preserved sensation supports metabolic paralysis or muscle disease rather than neuropathy.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First assessmentStabilise and localise simultaneouslyFirst stepWeakness evolves over hours to days with reduced tone or reflexes.

1Assess airway, cough, swallow, breathing pattern and circulation, obtain forced vital capacity and ECG and involve critical care early for any progressive bulbar or respiratory sign.
2Map cranial nerves, power, tone, reflexes, plantar responses, sensation and sphincter function, looking actively for a spinal level or descending pupillary syndrome.
3Correct dangerous glucose and electrolytes immediately while arranging urgent spinal imaging, infection work-up or neuromuscular testing from the localisation.

02Possible GBSMonitor before respiratory failureSymmetric progressive weakness and areflexia follow a compatible illness without a cord level.

1Admit under neurology, measure respiratory and bulbar function serially, use cardiac monitoring and avoid unmonitored transfer during autonomic instability.
2Obtain cerebrospinal fluid and neurophysiology when safe, checking HIV, Lyme, CMV or other mimics if cells, exposure or immune status are atypical.
3Start intravenous immunoglobulin or plasma exchange when non-ambulant or significantly progressing within the evidence window; do not prescribe corticosteroid as GBS treatment.

03Spinal pathwayDecompress or treat cord inflammation urgentlySensory level, sphincter change, severe back pain, asymmetry or later upper motor-neurone signs appear.

1Arrange urgent MRI of the relevant and adjacent spine with immediate spinal surgical or neurological discussion, maintaining immobilisation when trauma is possible.
2Treat compressive haematoma, abscess, tumour or disc through the emergency surgical pathway and obtain blood cultures before antibiotics if this causes no delay.
3For non-compressive myelitis, obtain specialist cerebrospinal-fluid, antibody and infection studies and start anti-inflammatory treatment only after key infection risks are addressed.

04RecoveryPrevent complications of prolonged weaknessThe cause is treated but axonal or muscular recovery remains incomplete.

1Provide thrombosis prevention, pressure care, nutrition, bowel and bladder management, pain control and gentle range preservation during immobility.
2Begin graded neuromuscular rehabilitation without pushing to exhaustion, supporting communication and psychological effects of awake paralysis.
3Reassess respiratory, autonomic, pain and walking recovery after discharge and counsel that fatigue may persist after headline strength returns.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Shortens disability in appropriately severe or progressing Guillain-Barre syndrome and is generally equivalent to plasma exchange.

Intravenous immunoglobulin for GBS

A standard specialist course totals 2 g/kg, commonly divided as 0.4 g/kg daily for 5 days, using NHS weight, infusion and renal protocols.

Assess thrombosis, renal impairment, haemolysis, fluid load and infusion reaction; do not routinely combine sequentially with plasma exchange. Current NHS England criteria state that a second GBS course is ineffective and may cause harm.

Neutralises circulating toxin before further nerve binding and should not wait for laboratory confirmation.

Botulinum antitoxin

UKHSA and the National Poisons Information Service arrange the current antitoxin product and adult administration as soon as clinical botulism is suspected.

It cannot reverse established paralysis and can cause hypersensitivity; airway, ventilation and wound or food-source management remain essential.

Reverses hypokalaemic paralysis and prevents arrhythmia while the renal, gastrointestinal, endocrine or channelopathy cause is treated.

Potassium replacement

Route, concentration and rate follow the current hospital hypokalaemia protocol, ECG, kidney function and severity; concentrated intravenous potassium requires monitored access.

Over-rapid replacement causes fatal hyperkalaemia; periodic-paralysis shifts may need smaller amounts than true depletion and require frequent repeat measurement.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Respiratory failure and aspiration

Diaphragmatic, bulbar and cough weakness cause hypoventilation, secretion retention and aspiration; physiological collapse can occur before oxygen saturation gives adequate warning.

Autonomic cardiovascular instability

Severe polyradiculoneuropathy may produce abrupt blood-pressure variation, tachyarrhythmia or bradyarrhythmia, ileus and urinary retention, requiring monitored specialist care.

Immobility-related injury

Paralysis promotes venous thrombosis, pressure damage, contracture, pain and deconditioning unless positioning, thromboprophylaxis and rehabilitation accompany disease-specific treatment.

Persistent neurological disability

Severe axonal loss or delayed treatment can leave long-term weakness, neuropathic pain, fatigue and dependence, even after the acute inflammatory or metabolic trigger resolves.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Measure forced vital capacity, cough, neck flexion, speech and swallow serially with frequency increased as weakness progresses.
Use continuous rhythm and blood-pressure monitoring during significant GBS autonomic disease and avoid triggers of profound vagal bradycardia where possible.
Repeat power, reflexes, sensory level, plantar responses and sphincter function because emerging upper motor-neurone signs can relocalise the syndrome.
Track sodium, potassium, phosphate, magnesium, renal function and acid-base state during metabolic correction and immunoglobulin treatment.
Assess aspiration, chest infection, venous thrombosis, pressure injury, ileus, urinary retention and neuropathic pain every day during immobility.
During recovery monitor fatigue, dysautonomia, pain, mood, mobility and work rather than ending follow-up when the patient first walks.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Spinal shock is flaccid

An acute cord lesion can initially remove reflex activity, so areflexia does not prove peripheral localisation when a level or sphincter syndrome exists.

Saturation is late

Respiratory muscle weakness first reduces ventilation and cough while oxygen transfer remains intact, making bedside mechanics more useful early.

CSF can start normal

Albuminocytological dissociation often evolves over the first week, so an early normal lumbar puncture cannot exclude GBS.

Cells challenge GBS

A substantial cerebrospinal-fluid pleocytosis requires renewed investigation for infections, inflammation or malignancy rather than forced criterion fitting.

Steroids do not treat GBS

Despite its immune mechanism, controlled evidence does not support corticosteroids; use immunoglobulin or exchange when criteria are met.

11Common pitfallsFrequent interpretation and management errors.

01
Treating acute flaccid paralysis as a diagnosis rather than a syndrome.
02
Missing cord compression because reflexes are absent during spinal shock.
03
Waiting for oxygen desaturation before measuring respiratory mechanics.
04
Excluding GBS after an early normal cerebrospinal-fluid protein.
05
Using corticosteroids as routine Guillain-Barre treatment.
06
Delaying botulism antitoxin until laboratory confirmation.
07
Correcting potassium rapidly without identifying redistribution.