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Chapter: Essentials of Psychiatry: Delirium and Dementia

Vascular Dementia

Vascular dementia usually results from multiple CVAs or one significant CVA.

Vascular Dementia


Vascular dementia usually results from multiple CVAs or one significant CVA. It is generally considered the second most com-mon cause of dementia after Alzheimer’s disease, accounting for about 10% of all cases. Men are twice as likely as women to be diagnosed with this condition. Vascular dementia is character-ized by a stepwise progression of cognitive deterioration with ac-companying lateralizing signs. It is always associated with evi-dence of systemic hypertension and usually involves renal and cardiac abnormalities. Risk factors for the development of a vas-cular dementia include those generally associated with obstruc-tive coronary artery disease, including obesity, hypercholestero-lemia, smoking, hypertension, stress and lack of exercise. The actual incidence of vascular dementia has decreased somewhat with better standards of care, improved diagnostic techniques and lifestyle changes.


Clinical Features


Vascular dementia is characterized by the early appearance of local-izing neurological signs. Spasticity, hemiparesis, ataxia and pseu-dobulbar palsy are common. Pseudobulbar palsy is associated with injury to the frontal lobes and results in impairment of the corticob-ulbar tracts. It is characterized by extreme emotional lability, abnor-mal speech cadence, dysphagia, hyperactive jaw jerk, hyperactive deep tendon reflexes and Babinski’s reflex. CT, MRI and gross spec-imens show cerebral atrophy and infarctions, with the radiological procedures showing multiple lucencies and the gross specimens revealing distinct white matter lesions (Figure 32.8). The EEG is ab-normal but nonspecific, and positron emission tomography reveals hypometabolic areas. Vascular dementia is differentiated from AD on the basis of its mode of progression, early appearance of neuro-logical signs, and radiographical evidence of cerebral ischemia.




Primary prevention and secondary prevention are important in the treatment of cerebrovascular disorders. Lifestyle changes are effective in arresting the progress of the disease; however, no known pharmacological treatment can reverse the effects of a completed stroke. Such interventions as anticoagulants for fre-quent transient ischemic attacks after a hemorrhagic lesion have been investigated but excluded; aspirin for decreasing platelet ag-gregation, and surgical removal of obstructing plaques probably do not reverse the mental state. Depression occurs in 50 to 60% of patients with CVAs and responds to traditional antidepressants. Tricyclic antidepressants, such as amitriptyline, in less than anti-depressant doses, improve both CVA depression and pseudobul-bar palsy. Physical rehabilitation is essential and often results in an improvement in mood and outlook.


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