Background and Purpose-An increasing body of literature suggests a role for clinically "silent" cerebrovascular disease in the pathogenesis of cognitive impairment. Such pathology commonly occurs in the absence of stroke. The main aim of the study was to examine neuropsychological impairment associated with cerebrovascular and peripheral vascular disease (PVD) and to compare cognitive deficits with a nonvascular control group. The main hypothesis was that older people with both transient ischemic attack (TIA) and PVD would demonstrate greater cognitive impairment than controls. Methods-A battery of neuropsychological tests was administered to 4 groups of community residents older than 65 years. The groups comprised 25 patients with carotid stenosis and TIA, 25 nonamputees with PVD, 25 patients with stroke, and 25 matched (with the stroke group) controls. Results-Stroke patients showed greater impairment than controls in all tests. PVD patients did not perform significantly worse (PϽ0.05 after Bonferroni correction) than control subjects on any of the neuropsychological tests. However, 25% of PVD patients had scores lying within the bottom 5% of control group scores for attention, calculation, and 1 test of frontal lobe function. TIA patients were more impaired in general intellectual impairment and frontal lobe function than controls. Frontal lobe impairment, suicidal thinking, and age were all independent predictors of global cognitive impairment in the TIA group. Frontal lobe impairment was the only predictor of global cognitive impairment in the PVD group. Conclusions-TIA and PVD patients showed similar patterns of neuropsychological impairment, but TIA may result in more prolonged cognitive impairment, particularly in frontal lobe function. This group may be at increased risk of vascular dementia as well as impulsivity and suicide. (Stroke. 1999;30:2167-2173.)

A diagnosis of alcohol use disorder is associated with a higher risk of dementia, but a dose–response relationship between alcohol intake consumption and cognitive impairment remains unclear. Alcohol is associated with a range of effects on the central nervous system at different doses and acts on a number of receptors. Acute disorders include Wernicke's encephalopathy (WE), traumatic brain injury, blackouts, seizures, stroke and hepatic encephalopathy. The most common manifestations of chronic alcohol consumption are Korsakoff's syndrome (KS) and alcohol‐related dementia (ARD). There is limited evidence for benefit from memantine in the treatment of ARD, but stronger evidence for the use of high‐dose parenteral thiamine in the progression of neuropsychiatric symptoms for WE.Accumulating evidence exists for pharmacological treatment in the prevention of hepatic encephalopathy. Rehabilitation of people with ARD may take several years, and requires an approach that addresses physical and psychosocial factors.

Objectives To examine the relationship between depression and cerebrovascular disease in three distinct settings: depression in established cerebrovascular disease, cerebrovascular disease in established depression and depression in vascular dementia. Methods Medline, EMBASE, PsychLit and PsychInfo databases were scanned to locate relevant articles. Data were also extracted from other articles, cited by those articles generated from the above databases. Results Using operational criteria, the prevalence of depression is higher than controls only within the first year after stroke, but most studies have not employed control groups. The prevalence of depression in vascular dementia compared with Alzheimer's disease is higher in the majority of studies, but matching for sociodemographic factors and severity of cognitive impairment has been inconsistent. An association between frontal/subcortical cerebrovascular lesions and depression in later life has been observed, but there may be methodological flaws underlying this observation in some computerized tomography studies. Conclusion There is some evidence that cerebrovascular disease has an aetiopathological role in late life depression. The increased likelihood of damage to frontal/subcortical brain circuitry following stroke, transient ischaemia and hypertension may explain the high prevalence of depression in older people with vascular risk factors. More valid definitions of lesion location and the use of appropriately matched control groups would seek to clarify this issue. The extrapolation to care settings from the high prevalence of depression accompanying cerebrovascular disease and the prolongation of disability in depressed people with stroke, suggests closer liaison between old age psychiatrists, neurologists and physicians caring for the elderly. Copyright © 2000 John Wiley & Sons, Ltd.

Baby boomers are the population at highest risk