Vascular Dementia - Introduction to Geriatrics - Lecture Slides, Slides of Geriatrics

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Definition

 VaD 1st^ described by Binswagner and Alzheimer in 19th

century, and thought to be due recurrent stroke ’MID’

 Doesn’t comply with usual definition of dementia which is in context

of AD, the memory deficit is late.

 This led to concept of ‘Vascular cognitive impairment’ or

VCI by National Institute of Neurological Disorders and Stroke-Canadian Stroke

Network Vascular Cognitive Impairment Harmonization Standards

 VCI that does not meet the Criteria of dementia is labelled "vascular

cognitive impairment, no dementia" (vCIND).

 VCI represents a syndrome, with the spectrum of cognitive disorders,

which often includes executive dysfunction. The most severe form of VCI s VaD and the Milder form is VaMCI

Stroke 2011, 42:2672-

Risk factors

 Variable association of conventional risk factors with VCI

 Post stroke dementia

 Clinical stroke

 Multiple studies shows incidence between 6-32%

 Mild cognitive impairment before stroke increases the likelihood of post-stroke dementia

 Age increase the risk of dementia after stroke

 Timing of assessment after stroke.

 Other factors, Severity of stroke, AF, WMLs, Multiple events, HTN, obesity,

elevated homocysteine or high density lipoprotein levels, and DM, Lt sided stroke

with aphasia

 Subclinical stroke

Etiology

 Large artery infarctions

 Small artery infarctions or lacunes

 Exclusively subcortical, in the distribution of small penetrating arteries, affecting the

basal ganglia, caudate, thalamus, and internal capsule as well as the cerebellum and

brainstem

 Due to lipohyalinosis or microatheroma affecting the small penetrating arteries,

elderly with HTN/or DM

 Another study shows association with microbleed/retinopathy with dementia

 Gad MRI shows diffuse BB dysfunction/Possible Binswagner

 Chronic subcortical ischemia

 Occurring in the distribution of small arteries in the periventricular white matter and

leading to neuronal loss. Doubles the risk of dementia.

 Anatomic distribution: Strategic sites

 Cortical (hippocampus, angular gyrus,,frontal lobe) and subcortical (thalamus, fornix, basal ganglia)

Clinical feature

 Cortical syndrome

 Medial frontal : executive dysfunction, abulia, or apathy. Bilateral medial frontal lobe

infarction may cause akinetic mutism.

 Left parietal : aphasia, apraxia, or agnosia.

 Right parietal : hemineglect (anosognosia, asomatognosia), confusion, agitation,

visuospatial and constructional difficulty.

 Medial temporal: anterograde amnesia

 Subcortical syndrome

 Focal motor signs

 Early presence of gait disturbance (marche a petit pas or magnetic, apraxic gait or

Parkinsonian gait)

 Early urinary frequency, urgency, and other urinary symptoms not explained by urologic

disease

 Pseudobulbar palsy

 Personality and mood changes, abulia, apathy, depression, emotional incontinence

 Cognitive disorder characterized by relatively mild memory deficit, psychomotor

retardation, and abnormal executive function

Diagnosis

 All Diagnostic criteria based on

 Congnitive impairment on Neuropsych testing

 Clinical stroke or vascular disease Neuro imaging

 Neuroimaging

 White matter lesions (WML)

 WML and the presence of dementia

 Anatomic distribution

 periventricular rather than subcortical WML

Feature Value

Abrupt onset 2

Stepwise deterioration

Fluctuating course 2

Nocturnal confusion 1

Preservation of personality

Depression 1

Somatic complaints 1

Emotional incontinence

Hypertension 1

History of stroke 2

Associated atherosclerosis

Focal neurologic symptoms

Focal neurologic signs 2

Hachinski ischemic score Dementia Defined by cognitive decline from a previously higher level of functioning and manifested by impairment of memory and of two or more cognitive domains (orientation, attention, language, visuospatial functions, executive functions, motor control, and praxis), preferably established by clinical examination and documented by neuropsychological testing; deficits should be severe enough to interfere with activities of daily living not due to physical effects of stroke alone.

Exclusion criteria: Cases with disturbance of consciousness, delirium, psychosis, severe aphasia, or major sensorimotor impairment precluding neuropsychological testing. Also excluded are systemic disorders or other brain diseases (such as AD) that in and of themselves could account for deficits in memory and cognition.

Cerebrovascular disease Defined by the presence of focal signs on neurologic examination, such as hemiparesis, lower facial weakness, Babinski sign, sensory deficit, hemianopia, and dysarthria consistent with stroke (with or without history of stroke), and evidence of relevant CVD by brain imaging (CT or MRI) including multiple large vessel infarcts or a single strategically placed infarct (angular gyrus, thalamus, basal forebrain, or PCA or ACA territories), as well as multiple basal ganglia and white matter lacunes, or extensive periventricular white matter lesions, or combinations thereof. A relationship between the above two disorders Manifested or inferred by the presence of one or more of the following:

(a) onset of dementia within three months following a recognized stroke; (b) abrupt deterioration in cognitive functions; or fluctuating, stepwise progression of cognitive deficits.

NINDS-AIREN

Treatment

 Risk factor management.

 Antihypertensive

 A meta-analysis combining the results of the Syst-Eur, PROGRESS, SHEP, and HYVET-

Cog studies found that blood pressure lowering resulted in relative risk reduction for

incident dementia of 0.87 (95% CI: 0.76-1.00). Lancet Neurol. 2008;7(8):.

 Diabetes , limited literature, higher BS and A1c- increased cog decline.

 Statins. Interest b/o CV risk and pleiotropic effect on vasculature, RCT of lipid lowering does not show effect on cog.  Antiplatelet agents_. No study to show benefit in dementia_

 Homocysteine lowering- CV risk factor, again on efffect on dementia

 Healthy lifestyle –smoking cessation , alcohol use, physical activity, and diet are associated with improved cognitive function.

 DISEASE MODIFYING THERAPY

 Acetylcholinesterase inhibitors- beneficial in cognition, functional improvement and clinical assessment.

 N-Methyl-D-aspartate receptor antagonists -memantine

 Calcium channel blockers