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

From a larger series of autopsies with subarachnoid hemorrhage (SAH), 20 cases were selected for the known complication of cerebral vasospasm. Evidence for vasospasm was radiological and pathological in 17 cases and pathological alone in three. A systematic histological examination of the large arteries in places known formerly to have been in spasm showed that, in the 12 early cases (death before 3 weeks), there were relevant changes in all the layers of the arterial wall, the most significant being evidence of necrosis in the tunica media. In the eight late cases (death after 3 weeks), in addition to the sequelae of the earlier acute changes, there was marked concentric intimal thickening by subendothelial fibrosis, again located in the segments of arteries formerly in spasm. Changes were also found in the small arteries, capillaries, and veins, both in the early and late cases but these changes, although striking, were thought to be caused by the ischemia due to the vasospasm; similar changes were also seen in the control cases with ischemia from arterial occlusion.
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PMID:Cerebral artery spasm. A histological study at necropsy of the blood vessels in cases of subarachnoid hemorrhage. 63 76

A group of 20 necropsies of subarachnoid hemorrhage (SAH) were selected because of the known complication of cerebral vasospasm. Evidence for vasospasm was radiological and pathological in 17 cases and pathological alone in 3 cases. A histological examination of the large arteries in areas known formerly to be in spasm showed that in the 13 early cases (death before 3 weeks) there were relevant changes in all layers of the arterial wall, the most significant being a degeneration of the media and elastica. In the 7 late cases (death after 3 weeks), in addition to the sequelae of the acute changes, there was marked concentric intimal thickening; and the localization was again in the particular segments of arteries formerly in spasm. Changes found in the small arteries, capillaries, and veins in the early and the late cases were thought to be caused by the ischemia due to the vasospasm. These changes were also seen in control material.
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PMID:Cerebral artery spasm: histological changes in necropsies of cases of subarachnoid hemorrhage. 67 16

31P-NMR spectroscopic studies were performed in vivo on brains of rats administered cocaine. Cocaine.HCl (1-5 mg/kg) administered systemically to lightly anesthetized rats resulted in significant and progressive deficits in whole brain intracellular free Mg ([Mg2+]i). Intracellular pH (pHi) also fell in a progressive manner but only after a significant fall in brain [Mg2+]i was noted. Both [Mg2+]i and pHi returned to normal in most rats. Brains of rats that exhibited stroke-like events, however, demonstrated continued intracellular acidosis associated with progressive loss of phosphocreatine and elevation of Pi up until death. These observations are consistent with the tenet that injection of cocaine can result in severe cerebral vasospasm, ischemia and rupture of cerebral blood vessels as a consequence of depletion of brain [Mg2+]i.
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PMID:Cocaine induces intracellular free Mg deficits, ischemia and stroke as observed by in-vivo 31P-NMR of the brain. 142 Feb 62

The efficacy and possible side effects of thromboxane A2 (TXA2) synthetase inhibitor in the treatment of cerebral vasospasm after subarachnoid hemorrhage (SAH) were assessed for 24 patients who presented with grades I to IV of the Hunt and Hess classification. All patients underwent aneurysmal clipping within 48 hours after SAH. Postoperatively, TXA2 synthetase inhibitor, Cataclot [sodium (E)-3-[p-(1H-imidazol-1-ylmethyl)phenyl]-2-propenoate] was administered to 13 patients by continuous drip infusion at a dose of 1 microgram/kg/min for 8 to 14 days (group A). The remaining 11 patients did not receive this drug (group B). Of the 13 patients in group A, seven patients (54%) showed no symptomatic vasospasm after SAH. Four patients (31%) developed a transient deterioration of consciousness and/or motor disturbance. Three of these patients fully recovered, while one of them showed a mild neurological deficit on discharge. One patient (8%) developed permanent dysphasia and hemiparesis as a result of ischemic brain damage due to vasospasm. One patient (8%) died of the side effect. On the other hand, of the 11 patients in group B, only three (27%) showed no symptomatic vasospasm. One (9%) patient presented a transient neurological deficit but fully recovered upon discharge. Four patients (36%) showed permanent neurological deficits, although they all could lead an independent life after discharge. The three remaining patients developed a severe disturbance of consciousness caused by ischemia due to vasospasm, and two of them died within 1 month after the onset of SAH. In the group treated with Cataclot, two patients developed an epidural hematoma late during the administration of the drug. Of these two, one patient died of increased intracranial pressure that was accelerated by the complication. These results indicate that TXA2 synthetase inhibitor is effective in not only decreasing the occurrence of symptomatic vasospasm but also reducing the neurological deterioration due to vasospasm after SAH. However, this drug has a hazardous side effect in that it may promote a tendency to bleed, which caused death in one of our patients.
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PMID:Efficacy and toxicity of thromboxane synthetase inhibitor for cerebral vasospasm after subarachnoid hemorrhage. 189 55

In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain, which, depending on a multitude of factors, can result in cerebral infarction. It is highly likely that the erythrocyte is the most important blood element in the pathophysiology of this process. The exact mechanism by which the blood vessel is forced into this destructive spasm remains to be elucidated. Significant steps have been taken to avoid the consequences of vasospasm by using hypertension and hypervolemia (or at the very least avoiding iatrogenic hypotension and hypovolemia). These measures have resulted in a reduced incidence of delayed ischemia. Because clot has been shown to cause vasospasm, it has seemed only logical that the early removal of clot would be efficacious in its prophylaxis. Experimental and clinical evidence to support this view has been gathered. Therapeutic measures based on it have been shown to be effective in the experimental situation but await controlled clinical evaluation. In the past decade, thanks to such trials, one of the calcium antagonist drugs has been shown to be effective in improving the outcome following subarachnoid hemorrhage, probably on the basis of reducing the frequency and extent of infarction by small vessel dilatation or neuronal protection. Although patients still die from this lethal complication of subarachnoid hemorrhage, it is difficult not to have some measure of optimism, based on the history just reviewed, that cerebral vasospasm will be a treatable disease within a few decades.
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PMID:The history of cerebral vasospasm. 213 40

Many patients survive aneurysmal SAH with minimal neurological deficits, but are at risk for developing further neurological insult from ischemia resulting from cerebral vasospasm. Nimodipine has proven to be effective in preventing this complication in a majority of patients studied, with hypotension the most severe adverse effect. Nimodipine alone, or in combination with other methods of therapy, may significantly improve the neurological outcome in this select patient population.
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PMID:Nimodipine: the use of calcium antagonists to prevent vasospasm following subarachnoid hemorrhage. 214 68

Cerebral vasospasm (specifically, intracranial arterial spasm) is variously defined as: (1) an arteriographically evident narrowing of the lumen of one or more of the major intracranial arteries at the base of the brain due to contraction of the smooth muscle within the arterial wall, or due to the morphological changes in the arterial wall and along its endothelial surface that occur in response to vessel injury; (2) the delayed onset of a neurological deficit following subarachnoid hemorrhage, thought to be due to ischemia or infarction of a portion of the brain; or (3) the combination of these two features (symptomatic vasospasm). The arterial contraction of intracranial arterial spasm typically develops a few days after the rupture of an intracranial aneurysm and lasts 2 to 3 weeks. Such arterial spasm can also occur in other conditions such as head trauma. If it is severe enough it can lead to cerebral infarction. The pathogenesis of this condition is still unclear. Many ingenious attempts have been made to prevent or treat cerebral vasospasm, but most have failed. The best current approach is to ensure adequate blood volume, and to elevate the patient's blood pressure (especially if the aneurysm has been secured by an early operation). The continuing investigation of drugs such as calcium channel blocking agents to improve the cerebral circulation has begun to provide additional help.
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PMID:Cerebral vasospasm. 222 95

In 13 patients who had ruptured intracranial aneurysms, serial transcranial Doppler (TCD) and cerebral blood flow (CBF) examinations were performed in order to evaluate the degree of cerebral vasospasm. All patients showed some extent of vasospasm on angiography, which was performed between Day 7 and 10. The flow velocities of either the middle cerebral arteries or the anterior cerebral arteries, measured by TCD, began to increase on post hemorrhage Day 5, and maximum flow velocities were recorded between Day 9 and 13, with normalization occurring within the following 2 weeks. In 5 cases of symptomatic vasospasm, a rapid increase of flow velocities preceded clinical manifestation of the vasospasm. Maximum flow velocities of the 5 cases were at a higher level in the range of 119-184cm/sec (mean 149cm/sec) that the cases where there were no symptoms. Consequently, serial TCD examinations were very useful for the early detection of vasospasm after subarachnoid hemorrhage. And it was confirmed that the change of flow velocities was more important than the value itself, and that the rapid increase of flow velocities indicated severe ischemia. However, for judging when vessel narrowing was resolving, the usefulness of the TCD examinations were doubtful. This is because flow velocities measured by TCD are thought to be fairly much influenced by multiple factors such as the change of blood pressure, blood volume, which were caused by the active treatment for the vasospasm. Serial measurements of CBF were also made 2-7 times (mean 3.1 times) during the first two weeks following subarachnoid hemorrhage using the 133Xe intravenous injection method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Combination of serial transcranial Doppler examinations and cerebral blood flow studies in the management of cerebral vasospasm after subarachnoid hemorrhage]. 223 91

Traumatic cerebral vasospasm is a relatively frequent occurrence after an individual suffers a severe head injury, and therefore poses a real threat for these individuals. Although vasospasm is a physiologic defense response, it can cause a decrease in CBF, ischemia, infarction, and death. A review of the literature has indicated that hypervolemic and/or hypertensive therapy can increase cerebral perfusion and CBF pressure during cerebral vasospasms. Hypervolemic and hypertensive therapies, as well as the neurologic, pulmonary, and cardiovascular changes that can occur during traumatic cerebral vasospasms, pose a real challenge for the critical care nurse. The nurse must be a skilled clinician, able to detect subtle changes in the patient's condition, and also must constantly evaluate the current therapy.
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PMID:Traumatic cerebral vasospasms and secondary head injury. 235 10

Recent evidence supports the concept that cerebral vasospasm is involved in the pathogenesis of eclampsia. Magnesium, which has a beneficial effect in eclampsia, may act by opposing calcium-dependent arterial constriction, thereby relieving vasospasm. Magnesium may also antagonize the increase in intracellular calcium concentration caused by ischemia and thus prevent cell damage and death. Magnesium might have a role in the treatment of cerebral vasospasm and ischemia, such as occurs in subarachnoid hemorrhage, ischemic stroke, and brain trauma.
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PMID:Action of magnesium sulfate in the treatment of preeclampsia-eclampsia. 267 28


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