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Sarthak - Neurocognitive Disorders - Behaviour Dysfunction
Sarthak - Neurocognitive Disorders - Behaviour Dysfunction
Other Medications
If coping strategies do not work, a consultant psychiatrist can
prescribe risperidone or haloperidol, antipsychotic medicines,
for those showing persistent aggression or extreme distress.
Cognitive stimulation therapy: Cognitive stimulation therapy
(CST) involves taking part in group activities and exercises
designed to improve memory and problem-solving skills.
Cognitive rehabilitation: Cognitive rehabilitation works by
getting you to use the parts of your brain that are working to
help the parts that are not.
Reminiscence and life story work: Reminiscence work
involves talking about things and events from your past. It
usually involves using props such as photos, favourite
possessions or music.
Vascular (formerly arteriosclerotic) dementia, which includes
multi-infarct dementia, is distinguished from dementia in
Alzheimer's disease by its history of onset clinical features, and
subsequent course.
History of transient ischaemic attacks (a brief episode of
neurological dysfunction caused by loss of blood flow
(ischemia) in the brain, spinal cord, or retina, without tissue
death (infarction).) with brief impairment of consciousness,
fleeting pareses, or visual loss.
Some impairment of memory and thinking then becomes
apparent. Onset, which is usually in later life, can be abrupt,
following one particular ischaemic episode, or there may be
more gradual emergence.
This dementia is usually the result of infarction of the brain due
to vascular diseases, including hypertensive cerebrovascular
disease.
The infarcts are usually small but cumulative in their effect.
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: This is more gradual in onset
than the acute form, following a number of minor ischaemic
episodes which produce an accumulation of infarcts in the
cerebral parenchyma.
F01.2 Subcortical vascular dementia: There may be a history
of hypertension and focal point of ischaemic destruction in the
deep white matter of the cerebral hemispheres, which can be
suspected on clinical grounds and demonstrated on
computerized axial tomography scans.
F01.3 Mixed cortical and subcortical vascular dementia:
Mixed cortical and subcortical components of the vascular
dementia may be suspected from the clinical features, the
results of investigations (including autopsy), or both.
F01.8 Other vascular dementia
F01.9 Vascular dementia, unspecified
Major or mild vascular NCD is the second most common cause
of NCD after Alzheimer's disease.
In the United States, population prevalence estimates for
vascular dementia range from 0.2% in the 65-70 years age
group to 16% in individuals 80 years and older.
Within 3 months following stroke, 20%-30% of individuals are
diagnosed with dementia.
In neuropathology series, the prevalence of vascular dementia
increases from 13% at age 70 years to 44.6% at age 90 years or
older, in comparison with Alzheimer's disease (23.6%-51%) and
combined vascular dementia and Alzheimer's disease (2%-
46.4%).
Higher prevalence has been reported in African Americans
compared with Caucasians, and in East Asian countries (e.g.,
Japan, China).
Prevalence is higher in males than in females.
Environmental: The neurocognitive outcomes of vascular brain
injury are influenced by neuroplasticity factors such as
education, physical exercise, and mental activity.