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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Ataxia and acute flaccid paralysis

Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
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Rapid weakness or brainstem dysfunction

Ascending weakness, weak cough, bulbar symptoms, autonomic instability, altered consciousness, acute focal ataxia, severe headache or bladder and sensory-level change requires emergency neurological assessment.

Action: Use ABCDE, measure serial respiratory function, obtain ECG and blood-pressure monitoring, protect swallowing and arrange urgent brain or spinal imaging and paediatric neurology or intensive-care input according to localisation.

Overview

Localise acute gait and limb dysfunction, distinguish cerebellar disease from sensory or vestibular ataxia, detect Guillain-Barré respiratory failure and complete urgent UK public-health action for acute flaccid paralysis.

Define the main problem before ordering tests. Ataxia produces inaccurate movement or unstable posture despite adequate strength. Weakness produces difficulty generating force. Ask onset and speed, preceding infection or vaccination, headache, vomiting, diplopia, vertigo, pain, sensory symptoms, bladder function, breathing, swallowing, medication and toxin access, travel and immunisation.

Observe sitting, standing and walking only when safe. Examine consciousness, pupils, eye movements and nystagmus, speech, cranial nerves, tone, power, reflexes, plantar responses, coordination, sensation and Romberg. Proximal versus distal, symmetrical versus asymmetric and upper versus lower motor signs determine brain, cord, root, nerve, junction or muscle localisation.

Postinfectious acute cerebellar ataxia commonly follows viral illness in younger children and begins abruptly with broad-based gait and dysmetria. Diagnosis requires a well child with no pressure, focal, encephalopathic or toxic feature and a trajectory toward recovery. Neuroimaging is needed when the pattern is atypical, progressive, asymmetric or persistent.

Aetiology

01

Postinfectious cerebellar ataxia

Transient immune cerebellar dysfunction can follow a viral illness, producing acute symmetrical gait and coordination difficulty in an otherwise recovering child.

02

Guillain Barré syndrome

Postinfectious immune attack on peripheral nerve roots and nerves causes rapidly progressive weakness, areflexia, pain and autonomic or bulbar involvement.

03

Central structural disease

Posterior fossa tumour, haemorrhage, stroke, demyelination, hydrocephalus or spinal cord disease produces focal or pressure-associated neurological signs.

04

Toxin or metabolic disturbance

Medicines, alcohol, carbon monoxide, hypoglycaemia, electrolyte disorders and inborn metabolic disease can cause acute ataxia or weakness.

Pathophysiology

  1. 1
    Cerebellar circuit dysfunction

    Vermis or hemisphere impairment disrupts timing and error correction, causing truncal instability, dysmetria, intention tremor and scanning speech.

  2. 2
    Sensory pathway failure

    Loss of proprioceptive input causes a stamping unstable gait that worsens with eye closure and may accompany peripheral neuropathy.

  3. 3
    Peripheral demyelination

    Guillain-Barré immune injury slows or blocks nerve conduction, producing weakness and reduced reflexes before secondary axonal loss in severe disease.

  4. 4
    Ventilatory pump failure

    Progressive diaphragmatic, intercostal and bulbar weakness reduces vital capacity, cough and airway protection before resting saturation necessarily falls.

Clinical features and red flags

Cerebellar ataxia

Broad-based gait, truncal sway, dysmetria, intention tremor, dysdiadochokinesia, nystagmus and scanning speech indicate cerebellar dysfunction.

Sensory ataxia

Impaired joint position, stamping gait and marked worsening with eye closure suggests proprioceptive pathway or peripheral nerve disease.

Guillain Barré pattern

Progressive symmetrical limb weakness, pain and reduced reflexes with preserved sensation or distal paraesthesia suggests acute polyradiculoneuropathy.

Spinal cord pattern

A sensory level, sphincter change, brisk reflexes or extensor plantars localises beyond an uncomplicated peripheral neuropathy.

Bulbar respiratory decline

Weak voice, poor cough, choking, paradoxical breathing, orthopnoea and falling vital capacity signal impending ventilatory failure.

Red flags requiring action

  • Rapidly ascending weakness, inability to walk, weak cough, drooling, nasal speech or orthopnoea suggests Guillain-Barré respiratory and bulbar progression.
  • Fluctuating tachycardia, bradycardia, hypertension or hypotension in acute flaccid weakness indicates dangerous autonomic involvement.
  • Acute ataxia with severe headache, vomiting, papilloedema, focal deficit or reduced consciousness requires urgent posterior fossa, stroke or raised-pressure imaging.

Investigations

  1. 01
    First-line glucose electrolytes and toxicology assessmentFirst stepFirst line
    Why
    Identify reversible metabolic disturbance or ingestion in acute ataxia or weakness.
    Interpretation and limitations
    Choose toxicology from access and phenotype; a normal routine screen cannot exclude every agent.
  2. 02
    Urgent MRI brain or spine
    Why
    Detect posterior fossa lesion, stroke, demyelination, cord compression or acute flaccid myelitis.
    Interpretation and limitations
    Image the anatomical localisation urgently; normal brain imaging does not answer a spinal syndrome.
  3. 03
    Serial forced vital capacity and ECG monitoring
    Why
    Detect respiratory muscle failure and autonomic instability during possible Guillain-Barré syndrome.
    Interpretation and limitations
    Trend is crucial; rapid decline, bulbar weakness or values around 20 mL/kg warrant critical-care assessment.
  4. 04
    Lumbar puncture
    Why
    Assess infection, inflammation and albuminocytological dissociation after pressure and safety review.
    Interpretation and limitations
    Normal protein early does not exclude GBS, while significant cerebrospinal fluid pleocytosis prompts an alternative diagnosis.
  5. 05

Differential diagnosis

01

Acute cerebellar ataxia

Symmetrical gait and limb incoordination after viral illness with preserved consciousness and no focal pressure sign supports a diagnosis of exclusion.

02

Posterior fossa lesion

Progression, morning vomiting, cranial nerve abnormality, papilloedema or asymmetric cerebellar signs requires urgent brain imaging and neurosurgical assessment.

03

Guillain Barré syndrome

Ascending symmetrical weakness, pain and areflexia after infection requires admission and serial respiratory and autonomic monitoring.

04

Transverse myelitis

Bilateral weakness with a sensory level, brisk or evolving reflexes and bladder dysfunction localises to spinal cord.

05

Acute flaccid myelitis or poliomyelitis

Acute often asymmetric flaccid weakness with grey-matter spinal involvement requires urgent neurological, virological and public-health evaluation.

Management

01TriageProtect breathing and localiseFirst stepA child develops acute ataxia, inability to walk or flaccid weakness.+
  1. 1Use ABCDE and assess cough, swallow, breathing pattern, vital capacity and autonomic observations.
  2. 2Map cerebellar, sensory, upper or lower motor-neurone features and examine bladder function.
  3. 3Admit rapidly progressive, bulbar, respiratory, focal or encephalopathic presentations urgently.
02ImageExclude central emergenciesHeadache, vomiting, focality, pressure signs, sensory level or bladder change is present.+
  1. 1Arrange urgent MRI brain or spine according to localisation, using CT only for a time-critical question.
  2. 2Defer lumbar puncture when mass effect or pressure makes it unsafe.
  3. 3Involve neurosurgery, stroke, infection or spinal teams immediately when imaging identifies treatable disease.

Complications

01

Respiratory failure

Guillain-Barré or brainstem disease can cause silent ventilatory decline, ineffective cough, aspiration and an eventual need for emergency intubation.

02

Autonomic collapse

Arrhythmia and extreme blood-pressure fluctuation can cause sudden cardiovascular instability and cardiac arrest during severe peripheral neuropathy.

03

Permanent neurological deficit

Axonal GBS, spinal cord infarction, acute flaccid myelitis or delayed structural treatment can leave lasting weakness and disability.

04

Missed poliovirus transmission

Failure to notify and sample acute flaccid paralysis can delay detection and control of imported or vaccine-derived poliovirus.

05

Falls and aspiration

Poor coordination, weakness and bulbar dysfunction cause injury, dehydration and pneumonia without mobility and swallow precautions.

Monitoring and follow-up

  • Measure vital capacity, cough, bulbar function and respiratory rate serially during progressive weakness.
  • Use continuous or frequent ECG and blood pressure observation when GBS autonomic dysfunction is possible.
  • Repeat power, reflexes, cranial nerves, gait and sensory-level assessment to detect changing localisation.
  • Monitor pain, bladder and bowel function, pressure areas, thrombosis risk and nutrition during immobility.
  • For postinfectious cerebellar ataxia, document objective recovery and re-image or reconsider if deterioration or persistence occurs.
  • Confirm UKHSA notification, timing of both stool samples and completion of any contact action.
  • Plan physiotherapy, orthoses, school reintegration and psychological support for prolonged recovery.

Special situations

Ataxia may be weakness

A child with GBS may sway and refuse to walk because proprioception and power are failing, not because the cerebellum is diseased.

Oxygen is a late marker

Neuromuscular ventilation can deteriorate with normal saturation until fatigue or atelectasis is advanced.

Early tests can be normal

Both cerebrospinal fluid protein and nerve conduction may remain normal early in clinically convincing GBS.

Romberg localises

Instability that worsens dramatically with eye closure points toward sensory rather than primary cerebellar ataxia.

Notification is syndromic

Public-health sampling starts from acute flaccid paralysis itself, not from laboratory confirmation of poliovirus.

Common pitfalls

  1. 01

    Calling every unsteady child cerebellar.

  2. 02

    Using normal saturation to dismiss respiratory weakness.

  3. 03

    Excluding GBS from a normal early lumbar puncture.

  4. 04

    Missing bladder and sensory-level signs of spinal disease.

  5. 05

    Diagnosing postviral ataxia before excluding toxin and tumour.

  6. 06

    Giving corticosteroids as effective GBS treatment.

  7. 07

    Waiting for virology confirmation before notifying acute flaccid paralysis.

Practice

Two practice questions

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Paediatrics and child healthOriginal SBA

Evolving Guillain Barré

A child develops ascending weakness and absent ankle reflexes one week after diarrhoea. Oxygen saturation is normal, but cough is weaker. What is the best next step?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE NG127 Neurological RecognitionUrgent referral for acute ataxia, weakness, swallowing and respiratory features.
  • NHS Guillain Barré SyndromeSymptoms, diagnosis, immunotherapy and recovery.
  • UKHSA Acute Flaccid Paralysis ReportingNotification and virological sampling for poliovirus surveillance.
  • UKHSA Polio National GuidelinesInvestigation, infection control and contact management for suspected polio.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

Guillain-Barré can advance over hours or days. Children may first report leg or back pain, refuse to walk or appear ataxic because of weakness and proprioceptive loss. Reflexes can be preserved early. Serial respiratory and bulbar assessment matters more than a single examination; forced vital capacity near or below 20 mL/kg, rapid decline or weak cough prompts intensive-care planning.

MRI brain or spine addresses structural localisation. Blood tests target glucose, electrolytes, inflammation, creatine kinase, toxicology and infection. CSF in GBS may show albuminocytological dissociation, but protein can be normal in week one and a substantial pleocytosis suggests another diagnosis. Neurophysiology may also be initially nondiagnostic and should be repeated if the clinical picture remains strong.

Acute flaccid paralysis surveillance protects population health. Discuss immediately with UKHSA and the regional virology service rather than waiting for polio confirmation. Collect the correct stool and respiratory or other specimens at the specified intervals, document travel and vaccination, and use infection-control advice. This public-health action runs alongside neurological diagnosis and respiratory care.

Key points

  • Ataxia is impaired coordination, not simply refusal to walk; observe truncal stability, gait base, eye movements, speech, finger-nose and heel-shin performance.
  • Separate cerebellar ataxia from sensory ataxia, vestibular imbalance and weakness by examining nystagmus, proprioception, Romberg, power and reflexes.
  • Acute ataxia in a child needs same-day assessment when sudden, persistent or accompanied by headache, vomiting, focal signs, reduced consciousness or toxin risk.
  • Guillain-Barré typically causes progressive symmetrical weakness with reduced or absent reflexes, often after infection; pain and autonomic symptoms are common in children.
  • Normal oxygen saturation and a normal early cerebrospinal fluid protein do not exclude evolving GBS; serial forced vital capacity, cough, bulbar function and autonomic observations are essential.
  • MRI brain is first-line for focal cerebellar or raised-pressure features; MRI spine is urgent for a sensory level, bladder dysfunction, back pain or upper motor-neurone signs.
  • Nerve-conduction studies support peripheral demyelination or axonal injury, while CSF classically shows raised protein with few cells after the first week.
  • IV immunoglobulin and plasma exchange are effective for non-ambulant or significantly progressive GBS; corticosteroids
  • Back pain, a sensory level, brisk reflexes, sphincter dysfunction or asymmetric limb findings suggests spinal cord compression, myelitis or infarction.
  • Acute flaccid paralysis is a public-health syndrome: notify the appropriate UKHSA health protection team urgently and collect virology samples through the current polio-surveillance pathway.
  • Possible sedative, anticonvulsant, antihistamine, alcohol or recreational-drug access should trigger toxicology-focused assessment without premature functional diagnosis.
    • Nerve-conduction studies and electromyography
    Why
    Confirm demyelinating or axonal peripheral neuropathy and distinguish nerve, junction and muscle disease.
    Interpretation and limitations
    Early studies may be normal or equivocal, so repeat testing when clinical progression strongly supports GBS.
  • 06
    UKHSA acute flaccid paralysis virology
    Why
    Detect poliovirus or another enterovirus and protect public health.
    Interpretation and limitations
    Notify urgently and collect protocolled stool specimens promptly rather than waiting for routine neurological results.
    • 03GBSMonitor and treat progressionSymmetrical progressive weakness and reduced reflexes suggest Guillain-Barré syndrome.+
    1. 1Use serial vital capacity, cough, swallow, ECG and blood-pressure monitoring in hospital.
    2. 2Give IV immunoglobulin or plasma exchange for non-ambulant or significantly progressive disease through neurology.
    3. 3Provide pain, thrombosis, pressure, bladder, rehabilitation and psychological care while recovery evolves.
    04Public healthReport acute flaccid paralysisAcute flaccid limb weakness meets the surveillance syndrome regardless of suspected cause.+
    1. 1Contact the UKHSA health protection team and regional virology service immediately.
    2. 2Collect two stool specimens 24–48 hours apart within 14 days and other advised samples.
    3. 3Document immunisation and travel and apply infection-control and contact advice without delaying neurological care.
    Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
    Shortens recovery in clinically important Guillain-Barré syndrome and is generally chosen over plasma exchange for practical paediatric delivery.

    Intravenous immunoglobulin

    For significantly progressive or non-ambulant paediatric Guillain-Barré syndrome, give a total 2 g/kg through the specialist protocol, usually 0.4 g/kg daily for 5 days or 1 g/kg daily for 2 days using the service's dosing weight.

    Screen for renal risk and thrombosis, monitor infusion reactions, haemolysis, aseptic meningitis and fluid load, and do not repeat automatically without neuromuscular specialist review.

    do not
    improve GBS recovery.
  • Any acute flaccid paralysis should prompt urgent UKHSA discussion and virological sampling, including two stool specimens 24–48 hours apart within 14 days of onset where the surveillance protocol advises.
  • Postinfectious acute cerebellar ataxia is a diagnosis of exclusion and should improve; deterioration or failure to recover triggers imaging and diagnostic review.