Synopsis
Distinguish cerebellar ataxia from sensory and vestibular imbalance, identify time-critical acute causes, and investigate subacute or chronic syndromes using a structured, cause-directed neurological pathway.
- Ataxia is impaired coordination not explained by weakness alone; localise it as cerebellar, sensory, vestibular or mixed before constructing the differential diagnosis.
- Sudden ataxia, severe gait inability, new headache, diplopia, dysarthria or focal signs is posterior circulation stroke until urgently assessed with brain and vascular imaging.
- Cerebellar disease produces broad-based gait, truncal instability, dysmetria, intention tremor, dysdiadochokinesia, gaze-evoked nystagmus and scanning or slurred speech.
Key red flags
Abrupt onset, new severe headache, focal weakness, dysarthria, diplopia or inability to stand requires immediate posterior circulation stroke assessment.
Investigation priorities
Exclude haemorrhage and identify vertebrobasilar occlusion or dissection during sudden-onset ataxia.
Management branches
Coordination or gait impairment began suddenly or over a few hours.
- Activate emergency neurological assessment, establish last-known-well, check glucose and observations, and identify headache, neck pain, focal signs and anticoagulant exposure.
- Arrange urgent non-contrast CT and head-and-neck vascular imaging, with MRI when required, while assessing thrombolysis or thrombectomy eligibility.
Key medicines
Parenteral thiamineWhen Wernicke encephalopathy is possible, give high-dose intravenous thiamine immediately using the current local alcohol-treatment protocol before or alongside carbohydrate when feasible; never delay emergency glucose for hypoglycaemia.
Cause-specific vitamin replacementReplace confirmed vitamin B12, folate or vitamin E deficiency using the relevant NICE, BNF and specialist regimen, with route and duration determined by cause and neurological severity.