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

Acute ischemia of the brain induces a cascade of biochemical and physiological events. The final consequences depend on the fact whether ischemia is of transient or permanent, total or partial nature. Alteration of extracellular potassium concentration, intracellular calcium and potassium concentration, development of cytotoxic and vasogenic edema, postischemic hyperfusion and no-reflow phenomenon are important factors which decide about the final fate of functional capacity. CO2 reactivity, autoregulation and hemorheology must be considered when therapeutic approaches are used to influence basic flow during ischemic condition. At present there exists no therapy which has been fully accepted and is able to guarantee benefit to the hypoperfused tissue. Since the calcium metabolism is altered by ischemic processes, substances which act on this metabolism might be of value in the treatment of ischemia and its consequences. However, their beneficial effect on cerebral infarction has not been proven yet. In subarachnoid hemorrhage and migraine calcium antagonists are used to prevent and treat ischemia. In epilepsia calcium overload blockers have been tried by one group with promising results.
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PMID:Is there a need for alternative approaches in the therapy of cerebrovascular disorders? 375 10

The authors report their experience with the use of saphenous vein bypass grafts for treating advanced occlusive disease in the posterior circulation (77 patients, all of whom had failed medical management and showed severe ischemic symptoms), deteriorating patients with giant aneurysms of the posterior circulation (nine patients), progressive ischemia in the anterior circulation (26 patients, none of whom had a normal examination), and giant aneurysms in the anterior circulation (20 patients, all of whom presented with mass effect or subarachnoid hemorrhage). Graft patency in the first 65 cases treated was 74%. However, after significant technical changes of vein-graft preparation and construction of the proximal anastomosis, patency in the following 67 cases was 94%. Excellent or good results (including relief of deficits existing prior to surgery) were achieved in 71% of patients with advanced occlusive disease in the posterior circulation, 44% of those with giant aneurysms of the posterior circulation, 58% of those with ischemia of the anterior circulation, and 80% of those with giant aneurysms of the anterior circulation. Mean graft blood flow at surgery in the series was 100 ml/min for posterior circulation grafts and 110 ml/min for anterior circulation grafts. Experience to date indicates that this is a useful operation, and is particularly applicable to patients who are neurologically unstable from advanced intracranial occlusive disease in the posterior circulation or with giant aneurysms in the anterior circulation. The risk of hyperfusion breakthrough with intracerebral hematoma restricts the technique in patients with progressing ischemic symptoms in the anterior circulation, and the intolerance of patients with fusiform aneurysms in the posterior circulation to the iatrogenic vertebrobasilar occlusion limits the applicability of this approach to otherwise inoperable lesions in that system.
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PMID:Saphenous vein bypass grafts for giant aneurysms and intracranial occlusive disease. 376 Sep 51

Hemolysis of periarterial clots after subarachnoid hemorrhage may liberate large quantities of K+ into the vicinity of cerebral blood vessels and possibly change their sensitivity to endogenous vasoactive agents. The current study examined the influence of subarachnoid hemorrhage on the sensitivity of rabbit basilar arterial segments to K+ and Ca++. An analysis of K+ and Ca++ dose-response curves demonstrated that incubated arterial segments isolated from animals with subarachnoid hemorrhage were substantially more sensitive to these cations than were corresponding controls. We speculate that chronically elevated K+ levels in areas of periarterial clot lysis or brain ischemia might initiate vascular smooth muscle depolarization and vasospasm. Our data provide additional rationale for the use of calcium channel blockers in preventing or treating vasospasm in cases of subarachnoid hemorrhage.
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PMID:Reactivity of rabbit basilar artery to alterations in extracellular potassium and calcium after subarachnoid hemorrhage. 376 82

A patient who presented with multiple episodes of subarachnoid hemorrhage was diagnosed as having a large mid-basilar artery aneurysm that had no definable surgical neck. Balloon embolization was performed utilizing two detachable silicone balloons to occlude the mid-basilar artery and the aneurysm. The procedure was carried out with the patient fully awake and alert. One day after the procedure, the patient developed pontine and cerebellar ischemia which completely resolved after 5 days on heparin therapy. A follow-up angiogram performed immediately after the procedure and at 3 months demonstrated complete occlusion of the mid-basilar artery and the aneurysm. The patient was intact neurologically upon discharge 5 days after the embolization procedure and has since resumed his normal activities. Balloon embolization therapy may offer some advantages over surgical methods for the treatment of such therapeutically challenging aneurysms.
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PMID:Intravascular balloon embolization of a large mid-basilar artery aneurysm. Case report. 378 43

Neurologic accidents are today the first cause of mortality following bacterial endocarditis through ischemia or mycotic aneurysm rupture. Authors propose a protocol management by complete cerebral angiography and CT scan as soon as the least neurologic sign appears. A headache is the most frequent of these signs. 35 patients were explored during 3 years and 10 treated surgically. These authors conclude that: mycotic aneurysm must be detected aneurysm with subarachnoid haemorrhage must be operated on as soon as possible. With unruptured aneurysm, surgical decision is more difficult: sequential angiography after excision of the most dangerous aneurysm, demonstrates that an aneurysm can appear, enlarge, diminish or spontaneously resolve. Carrying on with this protocol should allow an answer to this question.
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PMID:[Should the aneurysms of Osler's disease be investigated and operated on prior to hemorrhage?]. 380 68

The prognostic significance of admission leukocytosis with respect to ischemic complications of subarachnoid hemorrhage was retrospectively investigated in a series of patients with recently ruptured intracranial aneurysms. The present study concerned 47 consecutive cases admitted within 72 hours following the last hemorrhage, in the years 1982-1984. There was no difference in the admission WBC counts between patients who subsequently deteriorated due to ischemic complications and those who did not. However, the cell count rose significantly at the time of the clinical manifestations of ischemia, possibly as a result of structural damage of brain tissue and/or increased sympathetic and adrenocortical activity. The possible contribution of leukocytes to the pathogenesis of ischemic damage following subarachnoid hemorrhage--perhaps through the release of leukotrienes--will require further investigation.
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PMID:Relationship between leukocytosis and ischemic complications following aneurysmal subarachnoid hemorrhage. 381 Apr 57

The potential interactive effects between subarachnoid hemorrhage (SAH) and blood brain barrier (BBB) disruption were studied in a rat model. Experimental subarachnoid hemorrhage was produced in twenty rats (experimental group) by the intracisternal injection of blood. In ten additional rats (control group), saline was administered in place of blood. Analysis of mean blood pressure (MBP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP) demonstrated an increase in ICP and MBP and a drop in CPP in all animals following intracisternal injection. Subsequent infusion of the left internal carotid artery with sodium dehydrocholate resulted in blood-brain barrier (BBB) disruption in both groups as evidenced by Evans blue staining of the infused cortex. The extent of BBB disruption was significantly greater in the control group than the experimental group. Analysis of the experimental group demonstrated that animals with the lowest pre-SAH MBP and the lowest CPP during the maximum blood pressure response to SAH demonstrated the greatest resistance to experimental BBB disruption. The possibility of ischemia as a contributing factor in BBB protection subsequent to SAH is discussed.
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PMID:The protective effect of experimental subarachnoid haemorrhage on sodium dehydrocholate-induced blood-brain barrier disruption. 381 38

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

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

Regional cerebral blood flow (rCBF), cerebral metabolic rate of oxygen (CMRO2), intraventricular pressure, and lactate/pH levels in the cerebrospinal fluid (CSF) were measured in 38 patients with ruptured intracranial aneurysms between the 3rd and 13th day after subarachnoid hemorrhage (SAH). Angiography was performed following the rCBF study and the degree of vasospasm was measured on the angiograms. The patients were graded clinically according to the system of Hunt and Hess. Cerebral vasospasm significantly influenced rCBF: global reductions and focal changes (ischemia, hyperemia, and tissue peaks) were commonly associated with vasospasm. Patients with severe diffuse spasm always had global ischemia (21 +/- 5 ml/100 gm/min), and cerebral infarctions were demonstrated subsequently, The CMRO2 was more reduced than rCBF, indicating an uncoupling between flow and metabolism. This relative luxury perfusion was associated with CSF lactic acidosis and intracranial hypertension. The arteriovenous difference of oxygen was equally reduced in all categories of patients, probably due to the primary insult of SAH. The CMRO2 decreased concomitantly with arterial caliber, indicating a secondary impairment of cerebral metabolism due to vasospasm.
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PMID:Regional CBF, intraventricular pressure, and cerebral metabolism in patients with ruptured intracranial aneurysms. 396 55


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