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date may produce an agitated delirium with few focal ndings This may be mistaken for a toxic or withdrawal state Parietal infarctions on either side (usually nondominant hemisphere) are often missed because the patient is entirely unaware of the problem or the symptoms create only a subtle confusional state, drowsiness, or only subtle problems with calculation, dialing a phone, reaching accurately for objects, or loss of ability to write Extinction of bilaterally presented visual or tactile stimuli gives a clue; marked asymmetry of the optokinetic nystagmus response is sometimes the only de nite sign A cerebellar hemorrhage may at rst be dif cult to recognize as a stroke An occipital headache and complaint of dizziness with vomiting may be interpreted as a labyrinthine disorder, gastroenteritis, or myocardial infarction A slight ataxia of the limbs, inability to sit or stand, and mild gaze paresis may not have been properly tested or have been overlooked Early intervention by surgery may be lifesaving; but once the syndrome has progressed to the point of coma with pupillary abnormalities with bilateral Babinski signs, surgery is most often useless Periventricular white matter changes (leukoareosis) correlate poorly with cerebrovascular disease and may be misinterpreted We prefer to ignore them unless they are extensive and obscure a new lacunar stroke The Comatose Stroke Patient 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: drain-

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age 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 These procedures are best carried out in centers with experience in cerebrovascular intensive care If coma persists or is deep and sudden, only supportive treatment is possible Seizures Following Stroke With the exception of infarction due to cerebral venous occlusion, epileptic 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 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 rst 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 rst seizure after 1 week No satisfactory study has been conducted to determine if these patients bene t from anticonvulsant therapy to prevent the second or subsequent seizures Following the practice of most other neurologists, we prescribe phenytoin or an equivalent drug only if there has been a seizure and continue it for about 18 months If the EEG continues to show 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.

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ADAMS HP JR, BUTLER MJ, BILLER J, TOFFOL GN: Nonhemorrhagic cerebral infarction in young adults Arch Neurol 43:793, 1986 ADAMS RD: Mechanisms of apoplexy as determined by clinical and pathological correlation J Neuropathol Exp Neurol 13:1, 1954 ADAMS RD, CAMMERMEYER J, FITZGERALD PJ: The neuropathological aspects of thrombotic acroangiothrombosis J Neurol Neurosurg Psychiatr 11:1, 1948 ADAMS RD, TORVIK A, FISHER CM: Progressing stroke: Pathogenesis, in Siekert RG, Whisnant JP (eds): Cerebral Vascular Diseases, Third Conference New York, Grune & Stratton, 1961, pp 133 150 ADAMS RD, VANDER EECKEN HM: Vascular disease of the brain Annu Rev Med 4:213, 1953 ADLER JR, ROPPER AH: Self-audible venous bruits and high jugular bulb Arch Neurol 43:257, 1986 ALAMOWITCH S, ELIASZIW M, ALGRA A, et al: Risk, causes, and prevention of ischaemic stroke in elderly patients with symptomatic internalcarotid-artery stenosis Lancet 357:1154, 2001 ALEMA G: Behcet s disease, in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology: Infection of the Nervous System Vol 34: Part II Amsterdam, North-Holland, 1978, pp 475 512 ALEXANDER MP, SCHMITT MA: The aphasia syndrome of stroke in the left anterior cerebral artery territory Arch Neurol 37:97, 1980 ALGRA A, VANGIJN J, ALGRA A, KOUDSTALL PJ: Secondary prevention after cerebral ischemia of presumed arterial origin: Is aspirin still the touchstone J Neurol Neurosurg Psychiatry 66:557, 1999 ALGREN E, AREN C: Cerebral complications after coronary artery bypass surgery and heart valve surgery: Risk factors and onset of symptoms J Cardiothorac Vasc Anesth 12:270, 1998 ALLEN GS, AHN HS, PREZIOSI TJ, et al: Cerebral arterial vasospasm: A controlled trial of nimodipine in patients with subarachnoid hemorrhage N Engl J Med 308:619, 1983 ALRAWI A, TROBE, JD, BLAIVAS M, et al: Brain biopsy in primary angiitis of the central nervous system Neurology 53:858, 1999 AMARENCO P, COHEN A, TZOURIO C, et al: Atherosclerotic disease of the aortic arch and the risk of ischemic stroke N Engl J Med 331:1474, 1994 AMARENCO P, HAUW J-J: Cerebellar infarction in the territory of the anterior and inferior cerebellar artery: A clinicopathological study of 20 cases Brain 113:139, 1990 AMES A, NESBETT FB: Pathophysiology of ischemic cell death: I Time of onset of irreversible damage: Importance of the different components of the ischemic insult Stroke 14:219, 1983 AMES A, NESBETT FB: Pathophysiology of ischemic cell death: II Changes in plasma membrane permeability and cell volume Stroke 14: 227, 1983 AMES A, NESBETT FB: Pathophysiology of ischemic cell death: III Role of extracellular factors Stroke 14:233, 1983 AMES A, WRIGHT RL, KOWADA M, et al: Cerebral ischemia: II The nore ow phenomenon Am J Pathol 52:437, 1968 ANDREW BT, CHILES BW, OLSEN WL, et al: The effects of intracerebral.

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