Vasospasm

White, Richard P.

doi:10.1007/978-1-4612-5437-9_9

Cited by 13 publications

(1 citation statement)

References 173 publications

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“…Auch bei Grad Iund II liegt die Letalitfit noch zwischen 7 und 14% [1,4,8,41,84,110,111]. Die t6dlichen Verlriufe nach zunrichst komplikationslos erscheinenden F~illen h~ngen mit Blutungen wrihrend oder nach der Operation zusammen, insbesondere aber mit intra-und postoperativen Spasmen der intrazerebralen Arterien [2,7,41,118]. Die t6dlichen Verlriufe nach zunrichst komplikationslos erscheinenden F~illen h~ngen mit Blutungen wrihrend oder nach der Operation zusammen, insbesondere aber mit intra-und postoperativen Spasmen der intrazerebralen Arterien [2,7,41,118].…”

Section: Morphologie Der Aneurysmenunclassified

Zur Ph�nomenologie und Morphologie spontaner t�dlicher Hirnaneurysmablutungen

1986

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Hemorrhages from rupturing aneurysms in the main cerebral arteries are repeatedly the object of forensic dissection. The victims are often relatively young, death is sudden and unexpected, and there is no known history of serious illness. Of a total 62,888 dissections carried out by the Institut für Rechtsmedizin of the Free University of Berlin (1956-1984), the University of Hamburg (1970-1984), and the University of Munich (1964-1984), there were 246 such cases (0.39% of the dissected material); 122 were male and 124 female. To compare possible differences between these cases and clinically conducted autopsies with regard to localization and extent of the aneurysm, age and sex of the deceased, an evaluation of the dissected material of the Department of Neuropathology, University Hospital, Hamburg-Eppendorf (1960-1984) was carried out simultaneously in altogether 160 cases, 66 male and 94 female. The phenomena are discussed. In the morphological findings, particular attention is focused on the occasional difficulty in establishing the source of the hemorrhage, which is of crucial importance when differentiating from traumatically caused hemorrhages. Some specific, particularly problematic causes (e.g., where errors were made in medical treatment), are presented in the form of case histories.

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Section: Morphologie Der Aneurysmenunclassified

Zur Ph�nomenologie und Morphologie spontaner t�dlicher Hirnaneurysmablutungen

1986

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Cisternal and lumbar CSF levels of arachidonate metabolites after subarachnoid haemorrhage: An assessment of the biochemical hypothesis of vasospasm

et al. 1987

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Several naturally occurring compounds have been identified in human cerebrospinal fluid (CSF) after subarachnoid haemorrhage (SAH) as possible vasoactive agents involved in the biochemical mechanism of vasospasm. The authors have measured, in 30 patients admitted for SAH, CSF concentrations of two arachidonic acid metabolites. Prostacyclin and Prostaglandin D2, as representative of vasodilator and vasoconstrictor compounds. CSF samples were made available by lumbar punctures and intraoperative cisternal punctures. Nine patients presented with symptomatic vasospasm: lumbar CSF Prostaglandin D2 levels are significantly higher than in patients without vasospasm. The Cisternal Prostaglandin D2 level is significantly higher than the lumbar CSF concentration; CSF Prostacyclin levels do not significantly differ in the two groups of patients. These data suggest the presence of an imbalanced biochemical situation responsible for promoting vasospasm. The evaluation of cisternal levels of arachidonate metabolites support the hypothesis of the clotting phenomenon around the ruptured aneurysm wall as an important predictive pattern of vasospasm onset after SAH, as shown in computed tomography.

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Prostaglandin D2 monitoring in human CSF after subarachnoid hemorrhage: the possible role of prostaglandin D2 in the genesis of cerebral vasospasm

et al. 1986

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Experimental and clinical studies indicate that cerebral vasospasm following subarachnoid hemorrhage (SAH) may be caused by changed biochemical properties of the endothelium and vascular smooth muscle cell exposed to vasoactive substances synthetized by cerebral arteries and released in clotted blood. Many compounds have been identified in CSF from SAH patients: Thromboxanes A2 and B2, Prostaglandins F2 alpha, E2 and D2 are the major prostanoids incriminated in the causation of cerebral arterial spasm. We have monitored the CSF PGD2 concentrations with serial lumbar punctures at different intervals from the hemorrhage in 16 patients admitted for SAH: PGD2 was measured with radioimmunoassay as its 9-methoxy derivative. The lumbar CSF PGD2 concentration ranges from 0.11 to 1.53 ng/ml. In 7 cases vasospasm was angiographically demonstrated. 9 patients presented no clinical or radiological evidence of vasospasm. In 5 cases cisternal CSF samples were available at the operation by cisternal punctures. There was no correlation between CSF PGD2 concentration and clinical course. In the 7 cases with evidence of vasospasm a significant increase of CSF PGD2 corresponded to neurological deterioration. In all 9 cases without evidence of vasospasm CSF PGD2 concentration trend was in a steady-state. The cisternal CSF PGD2 concentration was higher than lumbar CSF concentration in cases with arterial spasm. This suggests the importance of the clotting phenomenon in vasospasm onset after SAH. PGD2 is one of the most important spasmogens in clotted blood. Although its role in the genesis of vasospasm onset remains to be defined, its vasospastic action, in addition to that of other analogous compounds, seems to be relevant.

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Vasospasm

Cited by 13 publications

References 173 publications

Zur Ph�nomenologie und Morphologie spontaner t�dlicher Hirnaneurysmablutungen

Zur Ph�nomenologie und Morphologie spontaner t�dlicher Hirnaneurysmablutungen

Cisternal and lumbar CSF levels of arachidonate metabolites after subarachnoid haemorrhage: An assessment of the biochemical hypothesis of vasospasm

Prostaglandin D2 monitoring in human CSF after subarachnoid hemorrhage: the possible role of prostaglandin D2 in the genesis of cerebral vasospasm

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