Articles: subarachnoid-hemorrhage.
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Wien. Klin. Wochenschr. · Sep 1982
Case Reports[Idiopathic medial necrosis of intracranial and cervical arteries. A report of 3 cases].
Two cases of stroke and one of subarachnoid haemorrhage are reported in women of child-bearing age, in which histological examination of the cervical and intracranial arteries revealed idiopathic medial necrosis. In the first case there was a dissecting aneurysm of a vertebral artery in the neck, caused by medial necrosis of this vessels. Two further dissecting aneurysms were found of the cervical arteries and partial rupture of the posterior cerebral artery, as well as focal medial degeneration of the aortic arch. ⋯ In the third case a massive subarachnoid haemorrhage occurred after several years of severe migraine. Histological examination of an "aneurysm" of a vertebral artery revealed complete rupture and focal medial necrosis. The scanty literature on this subject is reviewed and the significance of idiopathic medial necrosis in stroke and unexplained subarachnoid haemorrhage is emphasized.
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In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. ⋯ Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.