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Glossary
Glossary·Condition

Stroke

Also known as: cerebrovascular accident, CVA, ischaemic stroke, haemorrhagic stroke, cerebral infarction

A sudden interruption of blood supply to part of the brain, causing focal tissue death (ischaemic stroke) or bleeding (haemorrhagic stroke), with both local and brain-wide consequences.

A stroke occurs when blood flow to a region of the brain is suddenly cut off — either because an artery is blocked (ischaemic stroke, ~85% of cases) or because a vessel ruptures and bleeds into brain tissue (haemorrhagic stroke, ~15%). Within minutes of losing blood supply, neurons in the affected region begin to die irreversibly.

Focal consequences

The immediate, local damage from a stroke is a lesion: a zone of dead or severely damaged tissue. The location of this lesion determines which functions are affected:

  • Middle cerebral artery territory — contralateral weakness, speech and language deficits (if left hemisphere)
  • Posterior circulation — vision loss, balance problems, vertigo
  • Lacunar infarcts — small, deep lesions affecting motor or sensory pathways
  • Brainstem — potentially life-threatening effects on breathing and consciousness

The lesion itself is visible on MRI as a region of signal change (bright on FLAIR/T2, dark on T1).

Global consequences

Stroke does not confine its effects to the infarct zone. Research consistently shows that stroke accelerates brain-wide changes — independent of where the lesion sits:

  • Accelerated atrophy — both in the hemisphere of the stroke and in the contralateral hemisphere through diaschisis (loss of input to connected regions)
  • White matter changes — diffuse white matter lesions accumulate faster after stroke, reflecting underlying vascular vulnerability
  • Hippocampal shrinkage — even after strokes that do not directly involve the hippocampus
  • Network disruption — resting-state functional networks, including the default mode network, reorganise after stroke; some reorganisation supports recovery, but network-level fragmentation can persist

Stroke and brain age

Stroke is one of the strongest known accelerators of brain ageing. Studies using brain age models consistently find that stroke survivors have brain age gaps that are 5–10 years larger than age-matched controls without stroke — an effect that persists years after the event.

This accelerated ageing likely reflects both the direct tissue loss and the downstream global effects described above, as well as the shared vascular risk factor burden that often precedes stroke.

Silent stroke

Many people sustain small ischaemic lesions with no recognised symptoms — so-called silent infarcts. These are common in older adults (found in ~10–20% of community-dwelling people over 70) and contribute to cumulative vascular brain injury even without a clinical event.

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