Multiple strokes may result in extensive cerebral damage and dementia. Such patients mostly have severe atherosclerotic cerebrovascular disease.
Cerebrovascular disease is the third most common cause of dementia in old age after Alzheimer's disease and Lewy Body Dementia (1), accounting for 20% of cases compared to 50% from Alzheimer's. In another 10% of patients, it occurs in combination with Alzheimer's neuropathological changes.
Evidence suggests that 25-30% of ischaemic stroke survivors develop immediate or delayed vascular cognitive impairment (VCI) or vascular dementia (VaD) (2)
- cognitive impairment or dementia after stroke is predominantly defined by dementia that occurred within three months after stroke onset. Irrespective, many stroke survivors develop delayed dementia beyond three months or only after recurrent stroke(s).
States of cognitive dysfunction before the index stroke are described under the umbrella of pre-stroke dementia, which may entail vascular changes as well as insidious neurodegenerative processes (2)
Neuroimaging determinants of dementia after stroke comprise silent brain infarcts, white matter changes, lacunar infarcts and medial temporal lobe atrophy.
Dementia developing after stroke is thought to be a clinical entity to define any type of dementia occurring subsequent to stroke injury irrespective whether it involves vascular, neurodegenerative or mixed processes
- development of dementia after stroke depends on several factors including the location and volume of the stroke, degree of related neuronal damage, presence of pre-existing cognitive impairment or other cerebral pathology
- direct influence of any specific genetic factor(s) is not clear
- however, the heritability estimate for all ischaemic strokes was determined to be 38% but varied considerably by subtype with the greatest associated with large vessel (40%) and cardioembolic disease (33%) and lowest with small vessel disease (16%) (4)
Repeated cortical infarcts due to embolic disease of the heart or major cerebral vessels can cause progressive deterioration towards dementia and incapacitation. In classic multi-infarct dementia, cognitive deterioration is stepwise rather than smoothly progressive.
Risk factors for cognitive impairment and dementia after stroke are multifactorial including (2):
- older age,
- family history,
- genetic variants,
- low educational status,
- vascular comorbidities,
- prior transient ischaemic attack or recurrent stroke and
- depressive illness
Factors supporting the diagnosis of vascular cognitive impairment and dementia are (4):
1. History of hypertension
2. Previous cerebrovascular accidents (CVAs) or transient ischemic attacks (TIAs)
3. A progressive deterioration in mental status
4. The presence of abnormal neurological signs
5. Scattered cognitive defects, e.g. aphasia
6. Extensive ischemic changes on MRI scan
Multi-infarct Dementia (4)
- in classic multi-infarct dementia, the cognitive deterioration is stepwise rather than smoothly progressive
- cognitive changes vary, but memory loss is usually much less prominent than in Alzheimer's disease
- with each event (stroke) the patient suddenly worsens but then improves either completely or partially
- as the disease progresses, the patient develops an accretion of abnormal neurologic signs such as:
- asymmetric reflexes
- pseudobulbar changes (i.e. swallowing and speech difficulties along with emotional lability)
- pathologic reflexes (e.g. Babinski signs)
- sensory abnormalities
- condition is usually seen in hypertensive individuals and is caused by multiple small infarcts in the white matter of the brain as well as the basal ganglia and cortex
- until the 1980s, MID was characterized by cortical infarcts or gray matter lesions, and the extent of the volume affected was thought to correlate with the extent of dementia
- a variant of multi-infarct dementia is Binswanger subcortical arteriosclerotic encephalopathy in which the disease is confined to the white matter of the hemispheres and is usually reported as a fairly rapidly progressing dementia with significant neurologic and cognitive changes
Dementia With Extensive MRI Abnormalities
Without History of Stroke
- extensive use of MRI has revealed that many individuals have a significant amount of white matter change without having had a clinically recognized TIA or completed stroke
- the white matter lesions are a combination of lacunar infarcts, demyelination and gliosis, all due to small vessel disease and decreased blood flow and tissue perfusion
- occur in normal nondemented elderly individuals and in patients with Alzheimer's disease but are most prominently seen in patients with mixed and vascular dementia
- risk factors include hypertension or diabetes
- a combination of the extent of the lesions and the strategic location of these lesions seems to be involved in producing the mental changes
- mental status changes exhibited by this population of vascular dementia patients is characterized by (3):
- slowness in mental processes,
- problems with decision making,
- poor organizational ability,
- difficulty adjusting to change (impaired executive functions of the frontal lobe),
- difficulty sustaining attention,
- appearance of apathy
- these clinical features are due to the disconnection of pathways from the basal ganglia and ascending brainstem pathways to the frontal lobes - this syndrome has been called subcortical dementia
- memory function, while impaired, is not the principal and devastating feature that it is in Alzheimer's disease
- patients may have aspects of both degenerative brain disease (e.g., Alzheimer's disease) and evidence of either clinical strokes or significant changes on MRI scan
- approximately 35% of Alzheimer patients have autopsy-proven vascular infarcts and 60% have white matter lesions on MRI
- a high percentage (70%-90%) of Alzheimer patients have amyloid changes in their vessels that narrow the vessels and produce hypoperfusion
- McKeith IG, et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. Neurology. 1996;47:1113–1124.
- Kalaria RN et al.Stroke injury, cognitive impairment and vascular dementia. Biochim Biophys Acta. 2016 May; 1862(5): 915–925.
- Rothwell P.M., Coull A.J., Silver L.E., Fairhead J.F., Giles M.F., Lovelock C.E., Redgrave J.N., Bull L.M., Welch S.J., Cuthbertson F.C., Binney L.E., Gutnikov S.A., Anslow P., Banning A.P., Mant D., Mehta Z., Oxford Vascular S. Population-based study of event-rate, incidence, case fatality, and mortality for all acute vascular events in all arterial territories (Oxford Vascular Study) Lancet. 2005;366:1773–1783.
- Strub RS. Vascular Dementia. Ochsner J. Winter 2003;5(1):40-3
- Bevan S., Traylor M., Adib-Samii P., Malik R., Paul N.L., Jackson C., Farrall M., Rothwell P.M., Sudlow C., Dichgans M., Markus H.S. Genetic heritability of ischemic stroke and the contribution of previously reported candidate gene and genomewide associations. Stroke. 2012;43:3161–3167.
Last edited 05/2020 and last reviewed 05/2020