Background and PurposeWe wanted to establish independent associations of various clinical variables, computed tomographic (CT) scan features, presenting stroke subtypes, and outcome with the presence of silent infarcts on CT.Methods We studied 755 consecutive patients in a prospective registration of patients with first-ever supratentorial atherothrombotic, cardioembolic, or lacunar stroke or stroke of undetermined cause by multiple logistic regression analysis.Results Two hundred six patients (27%) with a first symptomatic territorial or small deep ischemic stroke had one or more silent infarcts on CT. Of all silent lesions, 169 (82%) were small and deep. Silent infarcts were significantly more strongly associated with a lacunar than atherothrombotic (odds ratio [OR], 1.59; 95% confidence interval [CI], 1.02 to 2.47; P=.O39) or cardioembolic (OR, 1.89; 95% CI, 1.2 to 2.99; P=.OO5) index stroke. Silent territorial lesions were more strongly associated with cardioembolic than with lacunar stroke but not with atherothrombotic stroke. In this respect, no differences were found between the atherothrombotic and undetermined-cause group. Advanced age and hypertension were the only risk factors that were significantly associated with silent infarcts (OR, 1.76; 95% CI, 1.14 to 2.71; P=.0U; and OR, 1.58; 95% CI, 1.13 to 2.21; P=.001; respectively), mainly because of a strong independent association of these risk factors with silent small deep infarcts (OR, 1.75; 95% CI,

Controversies exist concerning factors that contribute to the occurrence of epileptic seizures after stroke. Therefore, we studied prospectively the occurrence of seizures in 322 patients with a first-ever CT-confirmed symptomatic territorial brain infarct involving the cortex. We also studied potential risk factors for seizures, and gave special attention to cortical infarct location. Fifty-four patients developed post-stroke seizures. We distinguished between early- and late-onset seizures, occurring within two weeks following stroke-onset, or later than two weeks, respectively. We found that patients of 65 years or older with a cardioembolic brain infarct involving the middle temporal or post-central gyrus, had an almost eight times increased risk of early-onset seizures, whereas patients with a large brain infarct involving the supramarginal or superior temporal gyrus, had a five times increased risk of late-onset seizures. We conclude that risk factors and epileptogenic cortical areas for post brain infarct seizures can be identified, which however, differ between early- and late-onset seizures. These two seizure types may also differ in terms of seizure mechanism. Our findings may influence the decision on prophylactic treatment with antiepileptic drugs in stroke patients.

Acute isolated hemiataxia is in most cases due to infratentorial (cerebellar) stroke. It has only twice been described in supratentorial stroke-namely, after thalamic infarction and a capsular haemorrhage. Three patients with isolated hemiataxia after a supratentorial brain infarct are described. These patients were seen in a period of five years during which 899 patients with a first supratentorial brain infarct were registered. Clinically the hemiataxia was of the cerebeilar type. In two patients, CT and MRI showed a small, deep (lacunar) infarct restricted to the posterior limb of the internal capsule, a site not previously reported in isolated hemiataxia. The third patient had a small, deep (lacunar) infarct in the thalamus extending into the adjacent posterior limb of the internal capsule. Isolated hemiataxia after a supratentorial brain infarct is a very rare clinical stroke syndrome. The cerebellar type hemiataxia was most likely caused by interruption of the cerebellar pathways at the level of the internal capsule. Our cases confirm prior observations that the cerebellar pathways run through the posterior part of the posterior limb of the internal capsule separately from the motor and sensory pathways. (JNeurolNeurosurg Psychiatry 1994;57:742-744)

We evaluated the hypothesis that if hypotension or hypoperfusion is a major cause of border zone brain infarction, infarcts following cardiac surgery will be likely to be located in the vascular border zone areas, whereas cerebral perfusion would be lower compared with non-border zone infarcts. Ten of 37 patients with brain infarction following cardiac surgery had an infarct in one of the vascular border zones on CT. Haemodynamical characteristics and clinical features did not differ between border zone infarcts and remaining infarct subgroups. We conclude that compared with stroke series brain infarcts following cardiac surgery are more frequently located in one of the vascular border zone areas, but peri-operative haemodynamic compromise alone does not sufficiently explain this difference. Other possible mechanisms, such as showers of (micro-)emboli, should also be considered.

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