Synopsis
Build a reproducible anatomical localisation from tempo, distribution and positive and negative neurological findings before choosing an aetiology, investigation or emergency pathway.
- Localise before naming a disease: decide whether the dominant lesion lies in cerebral cortex, subcortical white matter, brainstem, cerebellum, spinal cord, anterior horn cell, root, plexus, peripheral nerve, neuromuscular junction or muscle.
- Time course narrows mechanism. Maximal-at-onset deficit favours vascular or seizure-related disease; minutes to hours can be vascular, toxic or migrainous; days suggests inflammatory, infectious or metabolic disease; months to years suggests degenerative, compressive or hereditary disease.
- A unilateral upper motor neurone pattern below a facial lesion may arise in the contralateral hemisphere or ipsilateral cord; facial involvement, cortical signs and the exact pattern of sensory change separate these levels.
Key red flags
Contralateral face and limb deficit accompanied by aphasia, neglect, gaze deviation, homonymous field loss, apraxia, seizure or cortical sensory impairment points above the brainstem. Dominant-hemisphere language dysfunction and non-dominant visuospatial neglect are especially localising.
Investigation priorities
Identify reversible mimics, physiological instability and evolution while preserving a timed baseline.
Management branches
A new lateralised motor, sensory, visual, language, balance or brainstem deficit with abrupt or uncertain onset.
- Establish last known well, perform ABCDE, check capillary glucose, record an NIHSS-informed examination where trained and identify anticoagulants, bleeding risk, seizure and head trauma without delaying transfer.
- Contact the local stroke pathway immediately for urgent brain and vascular imaging; posterior-circulation symptoms and disabling deficits deserve escalation even when a simple screening tool is negative.