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The aim of this study was to describe the clinical experience in 184 consecutive stroke patients first‐ever treated with recombinant tissue plasminogen activator (rt‐PA) at a single Dutch centre, with special emphasis on results among the very old. Outcome parameters were the modified Rankin scale (mRs) at 3 months and symptomatic intracranial haemorrhage (SICH). Outcome was related to age. A total of 184 patients were treated of whom 45 were 80 years of age or older (24%). Sixty two (45%) of 139 patients

Aims—To determine whether mitral annular calcification and aortic valve calcification, with or without stenosis, are expressions of atherosclerotic disease. Methods—The incidence of atherosclerotic risk factors was analysed in patients with mitral annular calcification and aortic valve calcification and in control patients from a prospective echocardiographic database of 8160 consecutive patients; 657 patients (8%) were identified with mitral annular calcification and 815 (9%) with a calcified aortic valve, of whom 515 (6.3%) had stenosis with a minimal aortic valve gradient of 16 mm Hg. In these patients, cardiac and vascular risk factors were compared with 568 control patients using multiple logistic regression analysis. Results—Age (odds ratio (OR) varying from 5.78 to 104, depending on age class), female sex (OR 1.75), hypertension (OR 2.38), diabetes mellitus (OR 2.85), and hypercholesterolaemia (OR 2.95) were strongly and significantly associated with aortic valve calcification without stenosis, as were age (OR varying from 8.82 to 67, depending on age class), female sex (OR 2.22), hypertension (OR 2.72), diabetes mellitus (OR 2.49), and hypercholesterolaemia (OR 2.86) with mitral annular calcification. Age (OR varying from 1.11 to 7.7), hypertension (OR 1.91), and hypercholesterolaemia (OR 2.55) were strongly and significantly associated with stenotic aortic valve calcification. Conclusions—Mitral annular calcification and stenotic or non-stenotic aortic valve calcification have a high incidence of atherosclerotic risk factors, suggesting they should be considered as manifestations of generalised atherosclerosis. Keywords: mitral annular calcification; aortic valve calcification; calcified aortic stenosis; risk factors

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 cerebellar 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.

To determine whether sensorimotor strokes should be considered as lacunar syndromes 34 consecutive patients with first-ever ischaemic sensorimotor stroke were evaluated and compared with 103 patients with non-lacunar infarcts and another 88 patients with lacunar infarcts. Potential thromboembolic sources were more frequent in patients with non-lacunar infarcts (p = 0.003, versus sensorimotor strokes). Although the overall prevalence of hypodense lesions at CT scan was not significantly different among the three groups, lacunar lesions were found in 47.1% of sensorimotor strokes, compared with 6.8% of non-lacunar infarcts (p less than 0.0001). In a mean follow up period of 28.7 months, the incidence of stroke and myocardial infarction among sensorimotor strokes was similar to that of patients with lacunar infarct, but significantly lower than in non-lacunar infarcts (p less than 0.05). These results demonstrate important differences between sensorimotor and non-lacunar infarcts, but quite similar findings in sensorimotor and lacunar strokes, and thus support the theory that sensorimotor strokes are commonly due to lacunar lesions.

The benefits of long term anticoagulant treatment of patients with non-rheumatic atrial fibrillation and cerebral infarction were studied by comparing two series of patients with stroke from centres with different policies on anticoagulant treatment. The long term prognosis of 50 patients from the Oxfordshire community stroke project, who did not receive anticoagulants, was compared with that of 70 similar patients from Maastricht, who were treated with anticoagulants. After a mean follow up of 27 months there was no significant difference in either the rate of survival or the rate of recurrent stroke between the two groups. These data suggest that any benefit of anticoagulation is modest. A large randomised trial is planned to establish whether long term anticoagulant treatment is of value and, if so, to what extent.