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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The author discusses the epidemiology, the diagnosis, the clinical and morphological aspects of cerebral vasospasm from his personal experience and a study of the literature. Prediction and diagnosis of vasospasm is possible by evaluation of the amount of blood on CT scan, measuring fibrin breakdown products in the CSF and the findings of early EEG and Transcranial Doppler Sonography. CBF measurement is helpful in following the process of ischemia and deciding the right moment for operation. Early surgery on cerebral aneurysms is advocated in order to prevent rebleeding and for early removal of blood clot from the basal cisterns. If vasospasm and ischemia do develop, energetic treatment with hypervolemia and induced hypertension can be started without fear of rebleeding. Prophylactic intravenous administration of Nimodipine is thought to be of real value. Since the introduction of early surgery by the author 80 patients have been operated within 3 days after S.A.H. The mortality was 11% and the morbidity 7.5%. Management mortality and morbidity for the total group of 209 patients with S.A.H. treated either medically or surgically were 23.5% and 6% respectively. If one excludes the 18 patients that died within 24 hours the mortality was 15.6%.
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PMID:[Vascular spasm and cerebral ischemia after meningeal hemorrhage caused by rupture of an aneurysm]. 351 64

Based on accumulating evidence of the role of xanthine oxidase (XO) in generating oxygen free radicals and causing tissue damage during ischemia, we examined the possible role of XO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). After inducing SAH in dogs by two autologous blood injections 2 days apart, chronic vasospasm of the basilar artery was reliably produced. There was a 3.5-fold elevation in uric acid (UA), the product of XO, in the cerebrospinal fluid (CSF) of these animals. Parenteral administration of allopurinol (i.v., 25 mg/kg, every 6 hours), a specific blocker of XO, successfully abolished the elevation in CSF uric acid levels due to SAH. However, angiographic vasospasm measured on Day 7, morphological changes observed by electron microscope, and elevated CSF prostaglandin levels were not altered by the treatment. It can be concluded that the observed activation of the enzyme XO, which is a well-known source of oxygen free radicals in ischemia in various organs, is not playing a major role in the pathogenesis of chronic cerebral vasospasm in this animal.
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PMID:Production of uric acid in cerebrospinal fluid after subarachnoid hemorrhage in dogs: investigation of the possible role of xanthine oxidase in chronic vasospasm. 361 2

Cerebrovascular spasm in the cynomolgus monkey does not appear to be modified by nimodipine. It is possible that cerebral arteries from this species are unusually resistant to the action of calcium antagonists. To test this hypothesis, parallel studies on the in vitro response of cerebral arteries from monkey, dog, and man have been carried out. Rings of basilar or middle cerebral artery were tested with potassium chloride, noradrenaline, 5-hydroxytryptamine, prostaglandin F2 alpha, and hemoglobin. The responses were then reexamined in the presence of various concentrations of nimodipine. There is a significant variation among species in sensitivity to nimodipine, the vessels from the monkey being more resistant to nimodipine than those from other species. There is, as expected, a considerable difference in the ability of nimodipine to block the different agonists. Responses to potassium chloride are blocked by low concentrations of nimodipine in all species, whereas noradrenaline and 5-hydroxytryptamine are more resistant. It is noteworthy that, in all species tested, hemoglobin and prostaglandin F2 alpha were antagonized poorly even by higher concentrations of nimodipine. If these agonists play a major role in the development of vasospasm and subsequent delayed ischemia, it may be that the calcium antagonists exert a beneficial effect by some mechanism other than dilation of spastic arteries.
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PMID:Effects of nimodipine on in vitro contractility of cerebral arteries of dog, monkey, and man. 373 87

Regional cerebral blood flow (rCBF) and regional cerebral metabolic rate of oxygen (rCMRO2) were measured by positron emission tomography (PET) in four patients with subarachnoid hemorrhage and hemiparesis due to cerebral vasospasm. With resolution of the vasospasm, two patients recovered and two remained hemiparetic. Contralateral to the hemiparesis, rCBF was slightly higher in the two patients who eventually recovered (15.0 and 16.2 ml/100 gm/min) than in the two who remained hemiparetic (12.0 and 11.7 ml/100 gm/min). The rCMRO2 measurements showed similar differences, with values of 1.34 and 2.60 ml/100 gm/min in the patients who recovered, and 0.72 and 1.66 ml/100 gm/min in those who did not. These preliminary findings indicate that with PET studies it may be possible to prospectively differentiate patients with neurological deficits due to reversible ischemia from patients with irreversible infarction.
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PMID:Regional cerebral blood flow and metabolism in reversible ischemia due to vasospasm. Determination by positron emission tomography. 387 46

This study was undertaken to determine the minimum CBF and CMRO2 required by the human brain to maintain normal function and viability for more than a few hours. Positron emission tomography (PET) was used to perform regional measurements in 50 subjects with varying degrees of cerebral ischemia but no evidence of infarction. There were 24 normal subjects, 24 subjects with arteriographic evidence of vascular disease of the carotid system, and two subjects with reversible ischemic neurological deficits due to cerebral vasospasm. Minimum values found in the 48 subjects with normal neurological function were 19 ml/100 g-min for regional cerebral blood flow (rCBF) and 1.3 ml/100 g-min for regional cerebral metabolic rate of oxygen (rCMRO2). Minimum values for all 50 subjects with viable cerebral tissue were 15 ml/100 g-min for rCBF and 1.3 ml/100 g-min for rCMRO2. Comparison of these measurements with values from 20 areas of established cerebral infarction in 10 subjects demonstrated that 80% (16/20) of infarcted regions had rCMRO2 values below the lower normal limit of 1.3 ml/100 g-min. Measurements of rCBF, regional cerebral blood volume, and oxygen extraction fraction were less useful for distinguishing viable from infarcted tissue. These data indicate that quantitative regional measurements of rCMRO2 with PET accurately distinguish viable from nonviable cerebral tissue and may be useful in the prospective identification of patients with reversible ischemia.
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PMID:Cerebral blood flow and cerebral metabolic rate of oxygen requirements for cerebral function and viability in humans. 387 67

Cerebral vasospasm is one of the most dreaded consequences of a ruptured intracranial aneurysm. Although exceptions may be found, the relationship between angiographic narrowing of cerebral arteries and deterioration of clinical status is supported by many authors. The cause of cerebral vasospasm still remains obscure. Several substances such as serotonin, prostaglandins, catecholamines appear to have a vasoconstrictive effect on the cerebral vessels. Recent evidence indicates that erythrocyte lysis within the subarachnoid spaces may play a major role in the genesis of delayed clinically relevant cerebral vasoconstriction following aneurysmal subarachnoid hemorrhage (SAH). The pathophysiology of brain ischemia following aneurysmal rupture, and the correlation between angiographic vasospasm, neurological condition, intracranial pressure (ICP) value, cerebral blood flow and CT findings are briefly discussed. It is concluded that, at present, blood volume expansion and/or induced hypertension, and pharmacological control of increased ICP provide the best basis for clinical management of the cerebral ischemic complications of SAH. Preoperative antifibrinolytic therapy and delayed surgical obliteration of the bleeding aneurysm, i.e. the policy at present most frequently adopted, are currently undergoing critical review in the light of the fact that antifibrinolytic therapy seems to be accompanied by a higher rate of ischemic SAH complications and vasospasm, whilst there are very recent suggestions that the results of early intracranial aneurysm surgery may be better than those of delayed surgery, if account is taken of the patients lost because of recurrent SAH or ischemia during the waiting period.
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PMID:Cerebral vasospasm as a complication of aneurysmal subarachnoid hemorrhage: a brief review. 388 14

The efficacy of the calcium channel blocker nimodipine in the prevention of chronic cerebral vasospasm (VSP) and delayed ischemia after subarachnoid hemorrhage (SAH) in monkeys was examined in a blind, randomized, placebo-controlled trial. The primate model developed in this laboratory reliably induces chronic cerebral vasospasm and can induce pathologically proven delayed ischemic neurological deficits (DINDs). With standard microsurgical procedures, an average 6.4-ml autologous hematoma was placed directly against the major anterior cerebral vessels in the right basal subarachnoid spaces of 24 monkeys. The monkeys were randomized to one of four groups and were treated orally q8h for 7 days with nimodipine (3, 6, or 12mg/kg)or placebo. An additional 2 monkeys underwent the surgical procedure without clot placement. Drug administration began between 14 and 20 hours after clot placement. Indices monitored before and after SAH included neurological status, angiographic cerebral vessel caliber, and cerebral blood flow. Significant VSP (25 to 100% reduction in vessel caliber) was present on Day 7 on the clot side in 83% of the animals (P less than or equal to 0.001). There was no significant difference (P greater than 0.05) in the incidence of VSP among the four groups. Similarly, there was no significant difference (P greater than 0.05) in the mean vessel caliber reduction after SAH among the four treatment groups. There was no VSP present on Day 7 in the sham-operated animals. One animal receiving high dose nimodipine (12 mg/kg p.o. q8h) developed a DIND on Day 5 after SAH. A second animal in the 12-mg/kg group developed a transient neurological deficit between Days 4 and 7.
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PMID:Nimodipine and chronic vasospasm in monkeys: Part 1. Clinical and radiological findings. 397 22

A leukotriene-like immunoreactivity was measured by radioimmunoassay in the gerbil forebrain following ischemia and reperfusion, subarachnoid hemorrhage (SAH), or nonlethal concussive brain injury. In each paradigm an increase in immunoreactivity levels was found. Peak levels were reached 15 to 30 minutes after each insult, and slowly returned to baseline over the next 24 hours. The study supports the suggestion that cerebral vessels and circulating blood are capable of producing leukotrienes, and that a major source of production is a nonvascular component within gray matter, possibly the cortical neuron. Leukotrienes may play a role in the pathophysiology of cerebral edema formation, cerebral vasospasm, seizure activity, and other central nervous system abnormalities. These studies are the first to demonstrate leukotriene production in gerbil brain following SAH or concussive brain injury.
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PMID:Leukotriene production in gerbil brain after ischemic insult, subarachnoid hemorrhage, and concussive injury. 399 37

The levels of two calcium-binding proteins, S-100 protein and calmodulin, were measured serially in the cerebrospinal fluid (CSF) of patients after subarachnoid hemorrhage (SAH) and aneurysm surgery. These two proteins have a similar molecular structure and are highly concentrated in the central nervous system (CNS). The levels of S-100 protein found in the earliest postoperative CSF samples correlated with the preoperative SAH grades. High S-100 protein levels in the CSF were found in patients with poor SAH grades. Moreover, the prognosis of the patients correlated with the S-100 protein levels in the CSF samples taken during the immediate postoperative period and with the daily changes of the S-100 protein levels. Severe diffuse cerebral vasospasm was followed by a sharp S-100 protein increase. These results suggest that S-100 protein levels in the CSF provide a useful index of organic damage in the CNS, and furthermore that S-100 protein levels and their changes may have prognostic value for patients after SAH. On the other hand, there was a lack of correlation between the calmodulin levels and the preoperative grade or outcome. It would be inappropriate, however, to speculate from the results of this study that these calcium-binding proteins in the CSF play any causative role in pathological processes such as cerebral vasospasm or brain ischemia after SAH, since changes in the levels of these proteins followed the onset of clinical signs of deterioration.
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PMID:S-100 protein and calmodulin levels in cerebrospinal fluid after subarachnoid hemorrhage. 402 Apr 69

Diltiazem, nifedipine, and verapamil inhibit calcium entry into cells via different mechanisms with different pharmacologies. They display different relative effects on different cardiovascular functions, a complex interplay of direct actions and adrenergic reflexes. Peripheral arterial vasorelaxation causes adrenergic reflex activity which opposes their direct negative chronotropic, dromotropic, inotropic, and hypotensive actions. Verapamil's most potent activity is electrophysiologic, and nifedipine's effects are hemodynamic; diltiazem acts like a less-potent combination of verapamil and nifedipine. All three drugs are efficacious in angina. These three drugs may not be interchangeable in all patients, but individualization of therapy is possible. Future indications for calcium channel blocker therapy may include hypertrophic cardiomyopathy, cerebral vasospasm, migraine headaches, pulmonary hypertension, asthma, esophageal spasm, intestinal ischemia, Raynaud's phenomenon, dysmenorrhea, and premature labor.
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PMID:Calcium channel blockers in emergency medicine. 638 Mar 52


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