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VASCULAR NEUROCOGNITIVE DISORDER
 

Prediction: Chronic, Progressive

      Occupational-Economic:
  • Progressive cognitive deterioration (memory, concentration, executive functioning, learning)
      Social:
  • Eventually needs total nursing care
  • Negative emotion (anxiety, depression)
  • Antagonism (hostility)
  • Disinhibition (agitation, irresponsibility, impulsivity, dangerous risk taking)
      Medical:
  • History of stroke(s), focal neurological signs, impaired gait and balance, frontal release reflexes

SYNOPSIS

Vascular Dementia F01 - ICD10 Description, World Health Organization
Vascular dementia is the result of infarction of the brain due to vascular disease, including hypertensive cerebrovascular disease. The infarcts are usually small but cumulative in their effect. Onset is usually in later life.

    F01.0 Vascular dementia of acute onset

    Usually develops rapidly after a succession of strokes from cerebrovascular thrombosis, embolism or haemorrhage. In rare cases, a single large infarction may be the cause.

    F01.1 Multi-infarct dementia

    Gradual in onset, following a number of transient ischaemic episodes which produce an accumulation of infarcts in the cerebral parenchyma. Predominantly cortical dementia.

    F01.2 Subcortical vascular dementia

    Includes cases with a history of hypertension and foci of ischaemic destruction in the deep white matter of the cerebral hemispheres. The cerebral cortex is usually preserved and this contrasts with the clinical picture which may closely resemble that of dementia in Alzheimer disease.

    F01.3 Mixed cortical and subcortical vascular dementia

Vascular Neurocognitive Disorder - Diagnostic Criteria, American Psychiatric Association

An individual diagnosed with vascular neurocognitive disorder needs to meet all of the following criteria:

  • The criteria are met for major or mild neurocognitive disorder:

    • Major Neurocognitive Disorder

    • Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on:

      • Concern of the individual, a knowledgeable informant, or the clinician that there has been a significant decline in cognitive function; and

      • A substantial impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another quantified clinical assessment.

    • The cognitive deficits interfere with independence in everyday activities (i.e., at a minimum, requiring assistance with complex instrumental activities of daily living such as paying bills or managing medications).

    • The cognitive deficits do not occur exclusively in the context of a delirium.

    • The cognitive deficits are not better explained by another mental disorder (e.g., major depressive disorder, schizophrenia).

    • Mild Neurocognitive Disorder

    • Evidence of modest cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on:

      • Concern of the individual, a knowledgeable informant, or the clinician that there has been a mild decline in cognitive function; and

      • A modest impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another quantified clinical assessment.

    • The cognitive deficits do not interfere with capacity for independence in everyday activities (i.e., complex instrumental activities of daily living such as paying bills or managing medications are preserved, but greater effort, compensatory strategies, or accommodation may be required).

    • The cognitive deficits do not occur exclusively in the context of a delirium.

    • The cognitive deficits are not better explained by another mental disorder (e.g., major depressive disorder, schizophrenia).

  • 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 fronto-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.

  • Possible vascular neurocognitive disorder is diagnosed if the clinical criteria are met but neuroimaging is not available and the temporal relationship of the neurocognitive syndrome with one or more cerebrovascular events is not established.

This disorder shows cognitive decline from a previous level of performance in one or more cognitive domains of higher cortical functioning:
  • learning and memory
  • complex attention
  • executive function (e.g., impaired planning, organizing, sequencing, abstracting)
  • language (e.g., aphasia)
  • perceptual-motor (e.g., agnosia [failure to recognize or identify objects despite intact sensory function], or apraxia [impaired ability to carry out motor activities despite intact motor function])
  • social cognition
These cognitive deficits are consistent with a vascular etiology, and cause significant impairment in social or occupational functioning.

Cerebrovascular Disease

Unlike most other dementias, this disorder has focal neurological signs and symptoms (e.g., exggeration of deep tendon reflexes, extensor plantar response, psuedobulbar palsy, gait abnormalities, weakness of an extremity) or laboratory evidence indicative of cerebrovascular disease (e.g., multiple infarctions involving cortex and underlying white matter) that are judged to be etiologically related to the disturbance. The deficits do not occur exclusively during the course of a delirium.

Effective Therapies

For mild to moderate vascular dementia, the cholinesterase inhibitor, donepezil, been shown to improve cognition functioning and activities of daily living. With elderly demented individuals, atypical antipsychotic medications significantly increase mortality; thus they should only be used to treat aggressive or psychotic demented patients when there is severe distress or risk of physical harm to those living and working with the patient. Psychosocial interventions (supervised day activity programs, nursing home/extended care placement, disability pensions or government financial aid) and caregiver support are key to managing this disorder. Caregiver support groups are very beneficial to caregivers.

Ineffective Therapies

Cognitive training and cognitive rehabilitation haven't been shown to be effective.

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