The most common causes of vascular coma are intracranial hemorrhage—usually deep in the hemisphere, less often in the cerebellum or brainstem, extensive subarachnoid hemorrhage, and basilar artery occlusion. After several days, brain edema surrounding a large infarction in the territory of the middle cerebral artery or adjacent to a hemorrhage may compress the midbrain and produce the same effect. Certain remedial surgical measures are still available in these circumstances: drainage of blood from the ventricles, shunting of the ventricles in cases of secondary hydrocephalus due to obstruction of the third ventricle or aqueduct, evacuation of a cerebral hemorrhage in cases of recent decline into stupor and coma, and hemicraniectomy in the case of massive stroke edema. Also, thrombolytic therapy and anticoagulants are sometimes successful in reversing the progression of basilar artery thrombosis that has caused coma by ischemia or infarction of the upper brainstem.
With the exception of infarction caused by cerebral venous occlusion, convulsive seizures following stroke are not a great problem. As mentioned earlier and in other chapters of the book, seizures are quite infrequent as the initial manifestation of an ischemic stroke, and when they do occur in this fashion, an embolus is usually the causative mechanism. More often, they are delayed by months or years after the infarction or hemorrhage. In the data presented by Lamy and colleagues (who were studying stroke in young patients with patent foramen ovale), when seizures occurred not at the outset but within the first week after stroke, as they did in 2 to 4 percent of their cases, about half had another seizure, usually single, during the next several years. However, the same was true for those with a first seizure after 1 week. Perhaps not surprisingly, the rate of seizures is higher after hemorrhagic than ischemic strokes and for the latter category, larger cortical strokes were more likely to result in a seizure disorder. An overview of the low rate of seizures that occurred soon after a stroke can be appreciated from the report by Beghi and colleagues, about 6 percent.
No satisfactory study has been conducted to determine if these patients benefit from antiepileptic therapy to prevent the second or subsequent seizures. Following the practice of most other neurologists, we prescribe one of the main epilepsy medications only if there has been a seizure, and continue it for about 12 months. If the EEG shows focal sharp waves or other epileptic activity at that time, we continue the drug; if not, we may discontinue the medication. It is also clear that prophylactic anticonvulsant treatment of all stroke patients is not necessary.
Dementia of the Alzheimer type is often ascribed, on insufficient and conceptually incorrect grounds, to the occurrence of multiple small strokes. If vascular lesions are responsible, evidence of an acute stroke episode or episodes and of focal neurologic deficits to account for at least part of the syndrome are evident. However, there is a process in which diffuse white matter changes on the basis of vascular disease lead to a less saltatory decline in cognitive function—vascular dementia. Complicating the understanding of this syndrome is the frequent coexistence, and possibly interdependence, of the lesions of both vascular and Alzheimer disease. There may be difficulty in determining to what extent each of them is responsible for the neurologic deficits. Several studies have shown an increased incidence or an acceleration of Alzheimer dementia if there are concurrent vascular lesions.
ACTIVE Investigators: Effect of clopidogrel added to aspirin in patients with atrial fibrillation. N Engl J Med 360:2006, 2009.
ACTIVE Writing Group, The: Clopidogrel plus aspirin versus oral anticoagulation for atrial fibrillation in the atrial fibrillation clopidogrel trial with Irbesartan for prevention of vascular events (ACTIVE W)—a randomized trial. Lancet 367:1903, 2006.