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

Four young adults with spontaneous dissection of the vertebrobasilar system are reported. Clinically, two patients presented with subarachnoid hemorrhage and two with brain-stem ischemia. In two cases of ruptured arterial dissection of the posterior cerebral artery, angiography demonstrated fusiform and "sausage-like" dilatation of the involved vessel. In two cases of occlusive dissection of the basilar artery, angiography revealed the typical "string sign." All four patients were treated conservatively: three survive in good clinical condition and one remains disabled. Follow-up angiograms showed spontaneous healing of the lesion with return to an almost normal arterial configuration in two cases; residual narrowing corresponding to the dissection was the most notable finding in the other two. It is recommended that, in a subset of neurologically stable patients, angiographic monitoring is undertaken to assess the tendency for spontaneous repair before surgical intervention is planned.
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PMID:Benign arterial dissections of the posterior circulation. 159 Aug 47

The authors present three cases of dissecting aneurysms of the posterior inferior cerebellar artery (PICA). A literature search revealed only three previous cases. Analysis of these six cases showed a unique clinical picture. Three patients developed subarachnoid hemorrhage, and the other three had ischemia. All patients complained of occipital headache or neck pain, regardless of the initial symptoms. Heralding episodes were recorded in four cases. Angiography showed a characteristic fusiform dilatation of the PICA and a narrowing proximal to and distal to the lesion. Various surgical treatments were performed in five cases. Intraoperative observation showed a sausage-like swelling of the PICA or one of its branches with various discoloration depending on the age of the intramural clot. The outcomes were favorable.
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PMID:Dissecting aneurysms of the posterior inferior cerebellar artery. 206 17

The therapeutic effectiveness of calcium channel antagonists (CCA) in hypertension and angina are well established. More recently, CCAs have also been demonstrated to ameliorate neurologic dysfunction that often accompanies ischemia associated with subarachnoid hemorrhage and stroke. We have hypothesized that retinal degeneration associated with ischemia may also result from the accumulation of calcium intracellularly, so-called "Ca++ overload". To test this hypothesis, a rat model of acute retinal ischemia, produced by direct occlusion of posterior ciliary and central retinal arteries, was developed. The extent of retinal dysfunction induced by ischemia was evaluated by electroretinograms (ERGs). Occlusion of the retinal arteries resulted in the disappearance of both a- and b-waves during the occlusion period (30 minutes) in vehicle-treated rats. Total retinal ischemia did not produce any significant change in magnitude of ERG a-wave amplitude during three-hours of reperfusion. However, ERG b-waves amplitudes were significantly reduced by more than 60%. In rats, pretreatment with nifedipine (0.33 to 3.3 mg/kg, i.p.) 30 minutes prior to the occlusion of the retinal vessels produced a significant dose-dependent increase in the recovery of b-wave amplitude when compared to vehicle-treated rats. These data support the idea that "Ca++ overload", resulting from the deregulation of intracellular Ca++ homeostasis, is a primary factor involved in ischemic retinal degeneration and that CCAs can protect the retina from ischemic damage.
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PMID:Effect of the calcium antagonist, nifedipine, on ischemic retinal dysfunction. 209 13

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

Although vasospasm remains a common cause for morbidity and mortality following subarachnoid hemorrhage, new therapeutic approaches and diagnostic studies offer the hope that injury caused by this disorder can be further lessened. Current CBF technologies can help to determine whether new symptoms are caused by ischemia, as well as define the often unpredictable manner in which ischemia occurs in this disorder. The CBF measurements may also help identify the best time for surgical intervention following subarachnoid hemorrhage. In addition, CBF studies may delineate when aggressive medical therapies are indicated and when they are potentially harmful. Despite the inherent limitations, as new technologies for CBF determination become more widely available, they should play an important role in the management of patients with aneurysmal subarachnoid hemorrhage.
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PMID:Cerebral blood measurements in vasospasm. 213 43

The relationship of time of surgery and vasospasm is influenced by three factors: (1) the time course of vasospasm, (2) the effectiveness of clot removal at surgery, and (3) the choice of medical management to prevent rebleeding and to treat vasospasm. Data to date demonstrate that angiographic vasospasm and vasospasm-related deficits occur in the period from 4 to 14 days after subarachnoid hemorrhage. Surgical intervention in the period of risk for vasospasm is associated with higher morbidity and mortality rates. Morbidity and mortality rates are lowest following surgery in patients who have delayed surgery; however, morbidity and mortality rates for overall management are equivalent for patients with early surgery because of vasospasm and rebleeding in patients waiting for delayed surgery. The surgical removal of the clot may be accomplished in only a limited number of patients, and most series do not reflect a large change in vasospasm occurrence following early surgery. Changes to more aggressive medical therapy in terms of prevention or reversal of ischemia from vasospasm rendered after the aneurysm is clipped and rebleeding is prevented have been initiated during the past decade. The effectiveness and safety of these treatments may play an important future role in the choice of time of surgery and the relationship of time of surgery to vasospasm-related deficits.
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PMID:The timing of surgery and vasospasm. 213 46

The role of antifibrinolytic drugs in the management of patients with aneurysmal subarachnoid hemorrhage continues to remain uncertain. Recent controlled studies suggest that although these agents may alter the course of the illness, they confer no benefit in terms of overall outcome. Confronted with these data, clinicians in North America have radically altered their management of patients with ruptured aneurysms in the last decade. In the Timing of Surgery Study (1980-1983), 54% of patients were treated with antifibrinolytic drugs and only 32% underwent surgical clipping of the aneurysm on days 0-3 from the subarachnoid hemorrhage. In contrast, only 13% of the patients in the Randomized Trial of Nicardipine in Subarachnoid Hemorrhage (1987-1989) received antifibrinolytics, whereas 53% had early surgery (unpublished observations). Further study will be required to determine if this strategy has resulted in an improvement in overall outcome. Some observers have suggested that as effective therapy for symptomatic vasospasm evolves (e.g., with hypertensive or hypervolemic therapy or calcium antagonists), the adverse effects of antifibrinolytic drugs on brain ischemia may be ameliorated. This idea must be confirmed by further evaluation of the combined use of these treatments. In the interim, antifibrinolytic drugs, if used at all, should be used with caution, and their use should be restricted to those patients judged not to be candidates for early surgery. If therapy cannot be started before day 7 after subarachnoid hemorrhage, it should not be started at all, as the reduced rate of rebleeding after the first 7 days does not justify the increased risk of brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antifibrinolytic therapy and cerebral vasospasm. 213 47

The diameters of pial arterioles of mice were monitored in vivo with an image-splitting technique and television microscopy. Concentrations of leukotriene C4 as low as 10(-7) M constricted the arterioles. The leukotriene C4-D4 receptor blocker ICI 198615 (10(-8) M) inhibited the response. Endothelial injury by helium-neon laser/Evans blue technique eliminated the constriction and unmasked a slight but consistent relaxation that was not inhibited by 10(-8) M ICI 198615. Since leukotrienes are produced by the brain and enter the cerebrospinal fluid in ischemia, head trauma, and subarachnoid hemorrhage, the possibility that leukotrienes C4 and D4 contribute to decreases in cerebral blood flow during these conditions should be considered. However, the present data makes such a possibility far less likely because the endothelium is frequently injured in these conditions, and therefore the ability of leukotrienes to constrict vessels would be severely curtailed.
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PMID:Leukotriene constriction of mouse pial arterioles in vivo is endothelium-dependent and receptor-mediated. 217 72

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


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