Vascular dementia Flashcards
What is the most widely cited diagnostic criteria for VaD?
NINDS-AIREN criteria.
What do the NINDS-AIREN criteria specify?
1) presence of dementia characterized by memory impairment and impairment in at least 2 additional cognitive domains
2) interference in ADLs not attributable to the physical effects of stroke alone, deliruim, psychiatric symptoms, or other dementias
3) Evidence of cerebrovascular disease
4) Presumed causal relationship between dementia and cerebrovascular disease, as suggested by onset of dementia within 3 months of stroke event and/or abrupt deterioration of, or stepwise progression, of cognitive impairment.
What is the DSM5 criteria for vascular dementia?
The criteria are met for major or mild neurocognitive disorder.
The clinical features are consistent with a vascular etiology, as suggested by either of the following:
Onset of the cognitive deficits is temporally related to one or more cerebrovascular events.
Evidence for decline is prominent in complex attention (including processing speed) and frontal-executive function.
There is evidence of the presence of cerebrovascular disease from history, physical examination, and/or neuroimaging considered sufficient to account for the neurocognitive deficits.
The symptoms are not better explained by another brain disease or systemic disorder.
Probable vascular neurocognitive disorder is diagnosed if one of the following is present; otherwise possible vascular neurocognitive disorder should be diagnosed:
Clinical criteria are supported by neuroimaging evidence of significant parenchymal injury attributed to cerebrovascular disease (neuroimaging-supported).
The neurocognitive syndrome is temporally related to one or more documented cerebrovascular events.
Both clinical and genetic (e.g., cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) evidence of cerebrovascular disease is present.
What is the underlying neuropathology of vascular dementia?
1) Multiple small vessel disease with leukoencephalopathy (aka white matter disease) or lacunar infarctions
2) Large vessel occlusive disease
3) Multiple hemorrhagic lesions
Any combination of these processes
Which infarct areas can have devastating effects on function? AKA strategic infarct locations
1) Left angular gyrus - can produce Gerstmann syndrome as well as constructional dysfunction.
2) Caudate nucleus, globus pallidus, and thalamus - May disrupt prefrontal-subcortical connections and affect executive and motor functions.
3) Thalamus - broad range of cognitive and behavioral disturbances that manifest as executive dysfunction, language impairment, memory dysfunction, and/or disorders of initiation, inhibition, and modulation of mood and emotional behavior.
Single infarctions in branches of posterior cerebral artery.
Memory deficits are common.
Single infarctions in branches of anterior cerebral artery.
See stroke section.
What is cerebral amyloid angiopathy?
CAA is caused by amyloid deposition in blood vessels and resulting in repeated hemorrhage (usually lobar), ischemic infarction, and cognitive loss. It usually has its onset after age 55, occurs in both sporadic and hereditary forms, and can lead to AD.
What is CADASIL?
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
Hereditary nonatherosclerotic angiopathy affecting small vessels and resulting in diffuse WM disease and small lacunar infarctions. Onset is typically middle adulthood. Stroke may occur in absence of other known risk factors. Usually affects frontal and subcortical areas. It is a rare disease.
Can cerebral WM disease occur from metabolic and toxic states?
Yes.
Can result from folate deficiency, vitamin B12 deficiency, hypoxia, and toxin exposure such as chemo, radiation, drug abuse, solvents, carbon monoxide poisoning.
What is mixed dementia?
Coexisting cerebrovascular disease (CVD) with AD, leading to uncertainty of what is causing dementia. CVD and AD may have additive effects in producing dementia, resulting in an earlier expression of cognitive impairment and dementia than would be seen with either cause alone. CVD and AD may actually be intertwined through impaired beta amyloid clearance secondary to hypoperfusion. The resulting beta amyloid accumulation may exacerbate cerebral amyloid angiopathy with increased changes of bleeding.
What are risk factors for VaD?
HTN, hyperlipidemia, DM, cardiac disease (afib, CAD, arrhythmias), congestive heart failure, coronary artery bypass grafting (CABG), OSA, TIA, recurrent stroke, APOE e4 allele.
Behavioral risk factors are smoking, sedentary lifestyle, poor diet (high fat, high sodium)
Demographic risk factors are age and African American ethnicity.
What is the prevalence of VaD?
It is difficult to determine, due to lack of consensus of which diagnostic criteria to use. It has been reported to be about 2% of ppl older than 70, which is likely an underestimate. Autopsy reveal pathology of dx of VaD in 18% of all dementia cases, behind AD and LBD., but usually the VaD was mixed with AD.
What neuropathological systems are commonly affected by VaD?
Deep frontal WM, frontal-subcortical circuitry, the basal ganglia, and the thalamus.
What is the survival rate for VaD?
There is no consensus on this. Some say there is as similar progression rate compared to AD and LBD. Other studies say there is shorter survival relative to AD and LBD. Hard to create a consensus when the etiology is often mixed and there are different medical comorbidities, including HTN, DM, and CAD.
