Synopsis
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.
- 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 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.
Key red flags
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.
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.
Investigation priorities
Identify reversible metabolic disturbance or ingestion in acute ataxia or weakness.
Management branches
A child develops acute ataxia, inability to walk or flaccid weakness.
- Use ABCDE and assess cough, swallow, breathing pattern, vital capacity and autonomic observations.
- Map cerebellar, sensory, upper or lower motor-neurone features and examine bladder function.
- Admit rapidly progressive, bulbar, respiratory, focal or encephalopathic presentations urgently.