Ischaemic cerebrovascular diseases in an autopsy series Part 2. Prevalence, location, pathogenesis, and clinical course of cerebral infarcts
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AbstractAmong 994 consecutive autopsies, 320 cases of ischaemic cerebrovascular disease were found. In 196 of the cases the disease had given clinical symptoms; they constitute 76.3% of all patients with stroke. The median age for men with ischaemic cerebrovascular disease was 73.2 years, for women 75.6. The ratio of men to women was 1:1.04.Altogether there were 400 infarcts with a diameter over 0.5 cm. In addition, 155 cases had one or more deep-seated infarcts less than 0.5 cm in diameter (lacunar state). Thrombi or emboli in relevant arteries were found by gross examination in 89.0% of all large recent infarcts. Cases where no gross occlusion could be found were grouped as non-embolic or embolic. Whenever there was doubt as to the genesis of the lesion, the case was assigned to a group of unclassified lesions.The thrombotic and other non-embolic infarcts were evenly distributed in the brain. The infarcts due to embolism were preferentially located in the territory of the middle cerebral artery.Many of the infarcts without verified gross occlusion were probably due to thrombi or emboli which had been overlooked or had resolved. Alternatively, they could have been due to a combination of localized arterial stenosis and systemic factors. Overt hypotension was present only in a few cases.In patients with occlusion distal to the circle of Willis the extent of the infarct depended upon the efficiency of the circulation in the neighbouring arterial territory, and probably also upon the level of the systemic blood pressure. In the group of infarcts without gross occlusion, the embolic lesions were generally larger than the non-embolic ones.Platelet aggregates were frequently found in small leptomeningeal and intracerebral arteries. They were more prevalent in cases with verified thrombi and non-embolic infarcts than in cases of embolism.In 58 of 138 recent infarcts the brain lesions were haemorrhagic. The bleeding appeared to depend upon a renewed blood flow into the ischaemic area. Most haemorrhagic infarcts were due to embolism. Anticoagulant therapy did not appear to be the primary factor initiating haemorrhage but it had possibly aggravated the bleeding.In 211 instances the occlusions and infarcts had given rise to clinical symptoms. In addition, 7 patients had suffered a clinical stroke syndrome, but no relevant thrombo-embolic occlusion or infarct could be found. Patients with embolism had a shorter length of survival after the onset of the symptoms than patients with ischaemic lesions of other types.Sudden onset, followed by a steady course, was observed in 81.3% of the cases with known clinical course. The remaining cases, most of which had thrombi or non-embolic infarcts without gross occlusion, presented an intermittent, recurring, stepwise, or gradual course. In some of the cases with thrombi, repeated attacks of symptoms could be ascribed to periods of active extension of the thrombus. Platelet aggregates in small arteries were particularly frequent in cases with intermittent or recurring symptoms, but they occurred also in cases with all other types of course. Multiple, deep-seated infarcts or a lacunar state could at times give a clinical history similar to the cases with intermittent, recurring, or stepwise course. These cases should be separated from those in which the stuttering or progressive course was caused by one localized vascular lesion.

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