Articles: subarachnoid-hemorrhage.
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Subarachnoid hemorrhage (SAH) is an important cause of death and serious morbidity, accounting for about 10% of all cases of stroke. In spite of recent advances in the surgical treatment of aneurysms and arteriovenous malformations (AVMs), the overall morbidity associated with SAH has changed little over the last several decades. A greater awareness by the medical community of the warning signs of SAH is essential in effectively reducing the morbidity associated with this illness. With modern surgical techniques, most aneurysms and many AVMs can be obliterated safely and effectively if detected early, before they result in a major SAH.
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We studied the course of CSF xanthochromia after subarachnoid hemorrhage by serial spectrophotometric analysis of lumbar CSF in 15 patients without clinical or CT evidence of rebleeding. The xanthochromic index rose in some patients up to the seventeenth day, and the proportion of oxyhemoglobin or the absolute concentration of hemoglobin often fluctuated. Therefore, rebleeding can be demonstrated in lumbar CSF only by increased xanthochromia, if previous samples had shown a decrease. These criteria could be applied in only 6 of 17 consecutive patients with rebleeding as demonstrated by CT, and they were met in 5.
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General pharmacology · Jan 1983
Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates.
1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. ⋯ In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.
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Seventy-four patients with proved spontaneous subarachnoid haemorrhage were studied. Sixty-four underwent computed tomography and 55 underwent lumbar puncture. ⋯ Computed tomography of the brain could determine patients at risk of coning. It is suggested that computed tomography is the investigation of choice after spontaneous subarachnoid haemorrhage and that lumbar puncture, if still then necessary, should be avoided until computed tomography has been undertaken.