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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating platelet aggregates formed in vivo were serially measured, and platelet-aggregation thresholds were determined in vitro in 82 patients with acute cerebral ischaemia. The percentage of aggregated platelets was increased in 53 patients with completed stroke (30.9% +/- 2.0) and in 29 patients with transient ischaemic attacks (34.1% +/- 2.3), all studied within 10 days of the acute event. These values were higher (P less than 0.001) than levels of aggregated platelets in 30 patients with non-vascular neurological disease (16.8% +/- 2.3). The percentage of aggregated platelets returned to normal 10 days to 6 wk after acute cerebral ischaemia. Aspirin and dipyridamole did not affect either the increase in or subsequent normalisation of circulating-platelet-aggregate levels in these patients. Platelet-aggregation sensitivity to adenosine diphosphate and adrenaline was also increased in patients with acute cerebral ischaemia, but this abnormally resolved during convalescence. Platelet activation is abnormal in acute cerebral ischaemia but usually returns to normal with or without anti-platelet therapy. This activation of platelets may contribute to the clinical manifestations of occlusive vascular disease.
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PMID:Platelet activation in acute cerebral ischaemia. Serial measurements of platelet function in cerebrovascular disease. 6 34

The protective effect of the (n-3) fatty acids in menhaden fish oil on acute cerebral ischemia was investigated in cats. Cerebral ischemia was produced by ligation of the left middle cerebral artery of cats fed either a basal diet of feline cat chow or the basal diet supplemented with 8% of the calories as menhaden oil for 18-24 days. Fatty acids esters of 20:5 (n-3) were increased and the 18:2 (n-6) decreased in the heart and liver of cats fed supplemental fish oil, but the brain lipid showed no effect of the diet. We found that the neurological deficit and the volume of brain infarction in the group treated with fish oil was less than that of the control group. The present findings suggest that moderate dietary supplements of fish oil may be beneficial in the prophylactic treatment of ischemic cerebral vascular disease.
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PMID:The protective effects of dietary fish oil on focal cerebral infarction. 55 Jan 56

A series of 58 operations on 56 patients, in whom a branch of the superficial temporal artery was anastomosed to a branch of the middle cerebral artery (STA-MCA bypass or Yasargil procedure), is reviewed. These operations were performed chiefly for occlussions or for inaccessible stenotic lesions of the internal carotid or middle cerebral arteries. Patency in eight patients operated on from April 1971 through November 1973 was low (25%). Patency in patients operated on since July 1974 has been high (95%). There have been no deaths and no major ischemic strokes attributable to the surgery. The rationale for this procedure is considered in relationship to the anatomy and physiology of the cerebral circulation and the pathogenesis of syndromes of cerebral ischemia. The operation appears to have a low morbidity in good-risk patients. The role of this operation in managing common manifestations of cerebral vascular disease such as focal transient cerebral ischemic attacks (TIAs) and amaurosis fugax, although not fully established, appears encouraging. The procedure seems useful for orthostatic cerebral ischemia caused by multiple occlusions of major extracranial (and intracranial) vessels and, occasionally, for progressing strokes related to internal carotid artery occlusion, both of which are relatively uncommon manifestations of cerebral vascular occlusive disease. It may have application in the rare "slow stroke." The procedure is probably of limited value, if any, in the management of large completed infarcts but may be indicated in selected patients with small infarctions who have preserved most of their cerebral function and who have had evidence of subsequent focal ischemic events. The procedure is useful for bypassing giant aneurysms or basofrontal tumors invading major vessels. It may have a role in the management of fibromuscular disease of the internal carotid artery.
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PMID:Bypass surgery for vascular disease of the carotid system. 99 50

In the cerebral ischemic pathophysiologic mechanism, lactic acidosis is a important factor to exacerbate cerebral damage. Our research showed that the lactic level of cerebral cortex in rats increased rapidly after the focal cerebral ischemia or during blood reperfusion after cerebral ischemia, 26.99 +/- 5.89 and 28.63 +/- 5.08 mumol/g brain wight respectively, it exacerbated significantly brain edema and pathological damage. The lactic level decreased rapidly to treat with dichloroacetate (50 mg/kg body weight) after cerebral ischemia or during blood reperfusion, 14.11 +/- 2.06 and 13.23 +/- 1.71 mumol/g brain wight respectively, brain edema and pathology improved significantly. It suggested that dichloroacetate might across blood-brain barrier into the cerebral ischemic region and lowered lactic level, improved brain internal environment, relieved cerebral damage after focal cerebral ischemia or during blood reperfusion. It may improve the prognosis of patient with ischemic cerebral vascular disease to be treated with dichloroacetate early.
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PMID:[Treatment of experimental ischemic cerebral lactic acidosis in rats with dichloroacetate]. 130

Per-operative use of S.E.P.s for vascular disease is based on: 1. The relationship between electrical cortical responses and cerebral blood flow. 2. The existence of a reversible threshold of cerebral ischemia. Intra-operative monitoring S.E.P.s were used during 30 procedures for aneurysms of the middle cerebral artery (M.C.A.). In 18 cases, a temporary occlusion of M.C.A. was necessary. Occlusion times ranged from 1 to 30 minutes. The central conduction time delay (C.C.T.), i.e. the delay N14-N20 and the cortical peak (N20) amplitude, elicited by median nerve stimulation was bilaterally monitored. A prolongation of the C.C.T. by 1 millisecond (compared with the baseline induction value) and a progressive decrease or a disappearance of the N20 peak were considered as "significant" changes. In response to these changes, immediate corrective actions (interruption of temporary M.C.A. occlusion (T.O.), repositioning of brain retractors, reapplication of aneurysm clips ...) were implemented. The reversibility of the S.E.P.s alterations during surgery was correlated with the post-operative outcome. Significant changes were found in 20 cases (including 13 T.O.). They were totally reversible in 11 cases: 5 of them developed a new but transient immediate post-operative deficit, none had a definitive deficit, and 6 patients had no new deficit. In 9 cases, the per-operative S.E.P.s alterations were not reversible: 3 cases (including 1 T.O.) had a transient deficit, 4 a permanent deficit, and 1 died (aneurysm rupture during craniotomy). An irreversible N20 peak disappearance predicted a permanent post-operative deficit in 4 of 4 patients (100%), whereas an isolated irreversible C.C.T. increase was only followed by a transitory deficit. Only 1 of 9 patients with no change in S.E.P.s (during a 15 min. T.O.), had a transient hemiparesis: this "false-negative" case will be discussed. This study confirms that S.E.P.s monitoring provides useful warning during aneurysm surgery. Median nerve S.E.P.s reflect the functional integrity of cortical M.C.A. territory; it is the pathway a risk during M.C.A. aneurysm surgery. S.E.P.s changes are not real-time information (an average of 500 responses need about 2 min), but these delays allow the surgeon to reverse the situation by immediate intra-operative adjustment, especially during temporary M.C.A. occlusion.
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PMID:[Monitoring of somatosensory evoked potentials during surgery for aneurysms of the sylvian artery]. 130 88

Coronary thrombolysis with streptokinase or tissue plasminogen activator is useful for the treatment of acute myocardial infarction in selected patients. This treatment is associated with local hemorrhagic complications and age-related cerebral hemorrhage. Coronary thrombolysis is contraindicated in patients with transient cerebral ischemia and stroke, arterial hypertension, cerebral trauma, cerebral aneurysms, and arteriovenous malformations, because of the risk of cerebral hemorrhage. We report the occurrence of a cerebral hemorrhage related to cerebral amyloid angiopathy in a patient who underwent thrombolysis and treatment with heparin for acute myocardial infarction. Despite normal coagulation parameters, the cerebral hematoma enlarged over 36 hours, as documented by sequential computed tomographic scans, to produce significant mass effect, which prompted surgical evacuation. Histological examination of the resected specimen demonstrated the strong affinity for Congo red and yellow-green birefringence that are characteristic of cerebral amyloid angiopathy. Hemostasis was difficult to achieve, as the divided or disrupted amyloid-laden cortical vessels failed to vasoconstrict, their contractile elements replaced by amyloid beta protein. The patient died of recurrent myocardial ischemia 3 days postoperatively. The incidence of cerebral amyloid angiopathy increases with advancing age. It must be considered as a potential source of cerebral hemorrhage in elderly patients undergoing thrombolysis for cardiac ischemia. Such an occurrence presents a difficult challenge because cardiac function is compromised, the coagulation profile may be altered, the cerebral hematoma is life threatening, and intracranial hemostasis is difficult to achieve.
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PMID:Cerebral hemorrhage from amyloid angiopathy and coronary thrombolysis. 140 40

We studied 23 patients suffering cerebral ischemia who also had laboratory evidence of either a lupus anticoagulant (LA) or an abnormal anticardiolipin antibody (ACA). Four patients had lupus or a lupus-like illness, three had drug-induced lupus, and 16 had no overt evidence of collagen-vascular disease. Cerebral ischemic events were multiple in 71% of the patients; two patients presented with multi-infarct dementia. Recognized cerebrovascular disease risk factors were present in 57% of the patients. The partial thromboplastin time was prolonged in only 35% of the patients. An LA was identified in 15 of 21 patients tested, and an elevated ACA titer was identified in 10 of 12 patients tested. Simultaneous assays for LA and ACA were discordant in eight of 10 patients tested. LA- and ACA-associated brain ischemia is often recurrent, but other risk factors for cerebrovascular disease are often present. The laboratory findings in such patients may display considerable heterogeneity.
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PMID:Lupus anticoagulants, anticardiolipin antibodies, and cerebral ischemia. 249 72

To assess whether a rigorous clinical classification, based on computerised tomography, of patients with cerebral ischaemia would identify subgroups at higher or lower risk with respect to cigarette smoking habits, a case-control study was carried out on 422 cases of first-episode cerebral ischaemia matched for age and sex with 422 community-based neighbourhood controls. Patients with ischaemic stroke due to extracranial or intracranial vascular disease were at higher risk from smoking than has previously been reported for stroke (relative risk 5.7, 95% confidence interval 2.8, 12.0) whereas those with stroke due to cardiac emboli had no excess risk associated with smoking (relative risk 0.4 [0.1, 1.8]). After cessation of smoking, the relative risk declined gradually over 10 years, at the end of which time a significant risk was still evident. This finding may imply that the risk incurred by smoking is due mainly to atheroma formation, rather than transient haematological effects. Exposure to smoking by a spouse was an independent risk factor for the whole group of cerebral ischaemia patients (relative risk 1.7 [1.1, 2.6]), but this was not so for smoking by either parent (relative risk 1.2 [0.8, 1.8]). These findings suggest that smoking is a more potent risk factor for the most common form of ischaemic stroke than has previously been appreciated. The persistent nature of the risk even after cessation of smoking and the possible risk associated with passive exposure strengthens public health arguments against smoking.
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PMID:Smoking as a risk factor for cerebral ischaemia. 257 46

We report two cases of traumatic cerebral vascular disease which were treated successfully with barbiturate. The first case sustained blunt trauma to the bilateral vertebral arteries, resulting in complete occlusion of both arteries. After ligation of the injured vertebral arteries, multiple cerebral infarction appeared. Cerebral angiography revealed dissection and stenosis of the bilateral internal carotid arteries. We treated this case with barbiturate (Thiamylal) in combination with administration of heparin. The second case sustained cerebral contusion and traumatic subarachnoidal hemorrhage as a result of a motor cycle accident. This patient deteriorated and cerebral angiography showed diffuse cerebral arterial vasospasms. When this was treated with induced hypertension, he developed recurrent subarachnoid hemorrhage. In order to protect the brain from ischemia without elevating blood pressure, we employed barbiturate therapy and the patient recovered without major neurological deficit. The condition of severe head injury with cerebral ischemia is complicated. Therefore it has been hard for neurosurgeons to cure the patient with this condition. But we treated it with barbiturate successfully. Barbiturate therapy in severe head injury with cerebral ischemia may decrease the mortality in that group of patients considered difficult to treat with the usual therapeutic modalities.
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PMID:[Barbiturate therapy in traumatic cerebral vascular disease: report of two cases]. 261 99

Late-onset focal epileptic seizures occurred in 8 patients with ischemic cerebro-vascular disease (ICVD) and were associated with TIAs in 6 of them. History, physical, laboratory, ancillary examinations and follow-up revealed no other disease which might be responsible for the seizures. Moreover, time of onset and appropriate signs of ICVD suggested that transient cerebral ischemia was the most likely cause of seizures.
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PMID:May focal epileptic seizures be considered a marker of TIAs? 311 50


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