Rehabilitation Of The Older A... Health Article

Other Causes Of Stroke

The work-up for an older adult with stroke may be quite different from that of a young person. It is generally accepted that a hypercoagulable work-up in an elderly person with otherwise obvious stroke etiology, such as carotid stenosis, has a low yield. The differential diagnosis in young adults may include hematologic abnormalities and drug abuse, whereas advanced age may boast its own specific causes for stroke that warrant further investigation. The differential diagnosis of an elderly stroke patient may include such causes as hyperhomocysteinemia, amyloid angiopathy, and multi-infarct dementia.

Hyperhomocysteinemia is now established as a major risk factor for stroke [24]. It has been attributed to dietary deficiency of vitamin B 6 , vitamin B 12 , or folic acid, especially in older patients with poor nutritional intake. The interplay of folate, vitamin B 12 , and vitamin B 6 helps control blood levels of homocysteine. Some individuals may have an inherited deficiency and develop premature atherosclerosis and often experience a stroke early in life. The use of antiepileptic drugs, such as phenytoin, has also been shown to increase the level of homocysteine in the blood [25]. Patients with stroke can have homocysteine levels 1.5 times those of age- and sex-matched controls [26]. Two large randomized multicenter trials, the Vitamin Intervention for Stroke Prevention and the Vitamins to Prevent Stroke studies, are designed to determine if, in addition to best medical and surgical management, high-dose folic acid, vitamin B 6 , and vitamin B 12 supplements reduce recurrent stroke or transient ischemic attack [27].

Cerebral amyloid angiopathy is caused by deposition of β-amyloid sheets in media and adventitia of small to mid-sized arteries of the cerebral cortex and the leptomeninges. Vessels become more rigid and fragile increasing the risk of rupture. Advanced age increases the incidence of cerebral amyloid angiopathy, which has been reported as 5% of those in the seventh decade of life, and up to 50% of those older than 90 years. Fifteen percent of all intracerebral hemorrhages in patients older than 60 years and about 50% of nontraumatic lobar intracerebral hemorrhages in those older than 70 years are attributable to cerebral amyloid angiopathy. Incidence remains elusive because definitive diagnosis is made only by histologic examination or postmortem brain biopsy. The most common symptoms are headache, occurring 60% to 70% at onset, followed by dementia, transient neurologic symptoms, or coma. The most common and devastating effect of cerebral amyloid angiopathy is lobar intracerebral hemorrhages, but it is associated with a lower mortality rate and a better functional outcome than hypertensive deep ganglionic bleeds. It is estimated that at least 40% of patients with intracerebral hemorrhages–related hemorrhage have some degree of dementia. Although patient management is unchanged from standard intracerebral hemorrhages, priority should be given to reversing anticoagulation. Blood thinners, such as warfarin, and antiplatelet agents, such as aspirin, should be avoided if possible. If these medications are required for other conditions, such as heart disease, the potential benefits must be carefully weighed against the increased risks.

Multi-infarct dementia, or vascular dementia, is the second most common cause of dementia in the elderly after Alzheimer's disease. The diagnosis requires (1) cognitive loss, often subcortical; (2) imaging studies demonstrating vascular brain lesions; and (3) exclusion of other causes of dementia, such as Alzheimer's disease [28]. It affects people between the ages of 60 and 75 with a slight predilection for men. Multi-infarct dementia is caused by small, multiple cerebral infarcts with the progression of cognitive impairment being insidious, stepwise, or both, usually affecting executive dysfunction, memory loss, or aphasia. A familial form of dementia associated with cerebrovascular disease is observed in a rare genetic condition, cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy. This condition is less common in the elderly because recurrent strokes usually begin before the age of 50.

Effective rehabilitation of the stroke patient with dementia is dependent on motivation and cognitive ability even more than on remaining motor or sensory function. Specifically, there should be a meaningful engagement with the therapist. Neuropsychologic evaluation commonly identifies impairment in executive dysfunction, memory, and language. Given its strong vascular component, the diagnosis of multi-infarct dementia is believed to be more preventable and offers a better likelihood for cognitive improvement compared with Alzheimer's disease [29]. Treatment often involves control of risk factors, such as hypertension, diabetes, smoking, hyperfibrinogenemia, hyperhomocysteinemia, orthostatic hypotension, and cardiac arrhythmias and pharmacologic management. Medications currently being used are similar to Alzheimer's disease. Anticholinergic medications, atypical antipsychotic agents, and antidepressants (eg, selective serotonin reuptake inhibitors) may be useful in some patients [28]. Pentoxifylline has been studied to slow the progression of dementia in patients who meet Diagnostic and Statistical Manual-III criteria for multi-infarct dementia and have clinical and neuroradiologic evidence of cerebrovascular disease [30]. Small open-label studies using rivastigmine, a second-generation acetylcholinesterase inhibitor, have shown improved attention, executive function, and apathy in vascular dementia [31]. Memantine is an N -methyl- d -aspartate receptor antagonist, approved in October 2003 by the US Food and Drug Administration for treatment of moderate to severe Alzheimer's disease. In Alzheimer's disease it has been shown to promote less cognitive deterioration with early benefit on mood and behavior with a low incidence of adverse effects [32]. All of these medications seem to be promising agents in vascular dementia, but their effects need to be established in double-blind, placebo-controlled clinical trials.