2.2.2 VASCULAR DEMENTIA
Vascular dementia is a condition produced by ischemic
or hemorrhagic brain injury. In its classic form, it is characterized by
an abrupt onset, stepwise deterioration, a patchy pattern of intellectual
deficits, focal neurologic symptoms and signs, a history of hypertension,
and evidence of associated cardiovascular disease (American Psychiatric Association, 2000). Vascular
dementia is most common after the age 50 and affects men more commonly (Askin-Edgar
et al., 2002). The risk factors for vascular dementia include both
modifiable (e.g., hypertension, diabetes mellitus, hyperlipidemia) and not
modifiable (e.g., age, gender, race, heredity) factors (Chui, 2000).
Etiologies of vascular dementia include hypertensive cerebrovascular
disease and thrombo-occlusive disease, multiple cerebral emboli, systemic
hypotension, intracerebral hemorrhage, and inflammatory and infectious
vascular disease (Cummings and Benson, 1992; Meyer et al., 1988).
Four criteria for vascular dementia that are
currently used include the State of California AD Diagnostic and Treatment
Centers criteria (Chui et al., 1992), the National Institute of Neurologic
Disorders and Stroke and the Association Internationale pour la Recherche
et l’Enseignement en Neurosciences (NINDS-AIREN) criteria (Roman et al.,
1993), the Hachinski Ischemic Score (HIS) as modified by Rosen (Hachinski
et al., 1974; Rosen et al., 1980) and those found in DSM-IV (American Psychiatric Association, 1994).
Rather than considering vascular dementia as simply present or absent,
some of the recent neuropathologic analyses (Holmes et al., 1999; Lim et
al., 1999) distinguished between "some or any" vascular lesions versus
"pure" vascular pathology, i.e., the circumstance in which vascular
pathology was both sufficient to account for cognitive symptoms and
unaccompanied by other pathology. Some vascular pathology exists in 29 to
41% of dementia cases coming to autopsy in population-based cohorts, even
though pure vascular pathology accounted for dementia in only 9 to 10%
(Holmes et al., 1999; Lim et al., 1999).
Clinical features of vascular dementia include motor
abnormalities, neuropsychological deficits, and neuropsychiatric symptoms.
Motor abnormalities may include weakness, spasticity, hyperreflexia,
extensor plantar responses, bradykinesia, parkinsonism, and pseudobulbar
palsy (Ishii et al., 1986). Neuropsychological abnormalities in patients
with vascular dementia are patchy, with preservation of some abilities and
mild to severe compromise of others. Personality changes are the most
common neuropsychiatric alterations in patients with vascular dementia;
and apathy, aspontaneity and abulia dominate the clinical syndrome. Other
neuropsychiatric symptoms include depression, lability of affect and
delusions (Askin-Edgar et al., 2002). Structural imaging studies usually
indicate multiple vascular lesions of the cerebral cortex and subcortical
structures.
Treatment
of vascular dementia consists of control of blood pressure in the upper
range of normal and administration of aspirin or other platelet
antiaggregants (Meyer et al., 1988). Nonaspirin antiaggregants may
be used in patients who are resistant to or intolerant of aspirin’s side
effects. Baclofen may be beneficial in managing spasticity in the
poststroke patient (Askin-Edgar et al., 2002).
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