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

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

We studied neurologic morbidity and its evolution during hyperglycemia induced immediately after permanent unilateral common carotid artery ligation in Mongolian gerbils. A total of 60 animals were divided into five groups: one experiencing severe hyperglycemia for 1 hour after the onset of ischemia (brief hyperglycemia group, n = 13), a normoglycemic control group for the brief hyperglycemia group (n = 12), a group with severe hyperglycemia for 4 hours after the onset of ischemia (prolonged hyperglycemia group, n = 11), a normoglycemic control group for the prolonged hyperglycemia group (n = 13), and a hyperosmolar normoglycemic control group for the prolonged hyperglycemia group (n = 11). Neurologic morbidity and mortality were higher in the two hyperglycemic groups than in the three normoglycemic control groups. The neurologic deficit progressed according to the duration of severe hyperglycemia. In the three normoglycemic control groups neurologic status stabilized 120 minutes after the onset of ischemia, in the brief hyperglycemia group stabilization occurred at 210 minutes, and in the prolonged hyperglycemia group neurologic deficit progressed for approximately 360 minutes, coinciding with the death of all but one gerbil, in which the neurologic deficit remained stable until death 23 hours after ischemia. We suggest that hyperglycemia is another cause of progressing cerebral infarction.
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PMID:Progressing cerebral infarction in relation to plasma glucose in gerbils. 223 57

Ischemic neuronal damage has been believed to make rapid progress in the course of a few days even in delayed selective neuronal death, to say nothing of acute brain necrosis. In the present study, however, we demonstrate for the first time a new type of ischemia-induced neuronal damage which progresses in the course of several weeks or a few months and we tentatively call this process "slowly progressive neuronal damage". We have focused on the chronological changes of neuronal damage in the dorsolateral striatum and neocortex following various durations of transient middle cerebral artery occlusion, which does not cause cerebral infarction and is clinically designated "transient ischemic attack". In the rats subjected to 15 min middle cerebral artery occlusion, the neocortex and lateral striatum were rarely damaged, whereas the small to medium-sized neurons only in the narrow area restricted to the dorsal striatum showed slowly progressive neuronal damage. Prolongation of ischemic duration to 30 min accelerated the evolution of neuronal damage in the dorsolateral striatum and also extended the distribution of neuronal damage to the neocortex, especially to layer III and more superficial layers. Further prolongation of ischemic duration to 45 min resulted in more rapid progress of selective neuronal death in those areas described above, whereas no animal escaped 60 min ischemia, without acute total tissue necrosis in the middle cerebral artery territory. Ischemia-induced slowly progressive neuronal damage may be implicated in the pathogenesis of such slowly progressive neurologic deterioration as dementia or Parkinsonism in patients with cerebral arteriosclerosis.
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PMID:Ischemia-induced slowly progressive neuronal damage in the rat brain. 225 91

Focal cerebral infarction and edema were measured in rats (Wistar, Fisher 344, and spontaneously hypertensive strains) pretreated with nimodipine (2 micrograms/kg/min i.v.) or its vehicle and subjected to the tandem occlusion of the middle cerebral and common carotid arteries. Animals awoke from anesthesia 10-15 min after onset of ischemia and continued to receive treatment over a 24-h survival period. Cortical infarction and edema were quantified by image analysis of frozen brain sections processed for histology. Nimodipine-treated rats developed 20-60% smaller cortical infarct volumes than controls (p less than 0.002). Cortical edema was reduced proportionately to the decrease in infarct volume and constituted approximately 36% of the infarct volume. Nimodipine caused a mild hypotensive response that did not aggravate ischemic brain damage. The results indicate that continuous nimodipine treatment, started before induction of focal cerebral ischemia, can attenuate ischemic brain damage and edema as late as 24 h after the onset of ischemia.
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PMID:Continuous nimodipine treatment attenuates cortical infarction in rats subjected to 24 hours of focal cerebral ischemia. 229 39

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.
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PMID:Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases. 238 25

We reviewed the clinical and laboratory data of 128 patients with cerebrovascular disease and antiphospholipid antibodies. Cases were evenly divided between men and women, and the mean age of the study group was 46 years. Cerebral infarction occurred in 97 patients, and transient hemispheric ischemic attacks without stroke were recorded in 19; 12 suffered ocular ischemia. Systemic lupus erythematosus was diagnosed in 16% of all cases. Histories of systemic thromboembolic events and recurrent miscarriages were noted in 14% of the patients and in 19% of the women, respectively. Evidence of cerebral infarction preceding the index event was present in 30% of cases. During a mean follow-up of 16 months, nine of 96 (9%) patients sustained new cerebral infarctions. Of 72 echocardiographic studies, 16 (22%) showed valvular abnormalities. Cerebral angiography detected intracranial lesions in 24 of 49 patients (49%). These data indicate that antiphospholipid antibodies can be identified in stroke patients without known autoimmune disorders. They also suggest that antiphospholipid antibody-associated cerebrovascular ischemia may be recurrent and often occurs in patients with systemic thromboembolic events. Our findings should help design a prospective clinical trial that will assess the risk of recurrent thromboembolism in this population, identify stroke risk factors, and address therapy.
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PMID:Clinical and laboratory findings in patients with antiphospholipid antibodies and cerebral ischemia. The Antiphospholipid Antibodies in Stroke Study Group. 200 15

We have evaluated the use of 2,3,5-triphenyltetrazolium chloride (TTC) as an histopathologic stain for identification of infarcted rat brain tissue. The middle cerebral artery (MCA) of 35 normal adult rats was occluded surgically. At various times after surgical occlusion, rats were sacrificed and brain slices were obtained and stained with TTC or hematoxolin and eosin (H & E); the size of the area of infarcted tissue stained by each method was quantified. In rats sacrificed 24 hr after occlusion of the MCA, the size of the area of infarction was 21 +/- 2% of the coronal section for TTC, and 21 +/- 2% for H & E (mean +/- S.D., N = 13). The size of areas of infarction determined by either staining method was not significantly different in area by the paired test, and a significant correlation between sizes determined by each method was found by linear regression analysis (r = 0.91, slope = 0.89, and the y intercept = 4.4%). Staining with TTC is a rapid, convenient, inexpensive, and reliable method for the detection and quantification of cerebral infarction in rats 24 hr after the onset of ischemia.
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PMID:Evaluation of 2,3,5-triphenyltetrazolium chloride as a stain for detection and quantification of experimental cerebral infarction in rats. 243 17

Twenty-five patients with clinical and CT findings indicating supratentorial cerebral infarct were prospectively studied with MR. MR examinations were performed between the 3rd and 150th day after stroke. T2-weighted axial images were compared with T1-weighted sequences after i.v. administration of Gd-DTPA. T2-weighted images demonstrated parenchymal lesions in all 25 patients. Postcontrast T1-weighted images, however, displayed pathologic contrast enhancement in only 19 areas of infarction. In 5 of the 25 patients, the use of Gd-DTPA provided additional diagnostic information by demonstrating gyral contrast enhancement as a pattern typical for ischemia. In 2 of the 25 patients, pathologic contrast enhancement was observed in an area that was isointense to the surrounding brain tissue on the T2-weighted images. In one patient, Gd-DTPA improved differentiation between areas of subacute and chronic infarction. At present, in the patient with suspected cerebral infarction, MR imaging after i.v. administration of Gd-DTPA appears recommended when clinical findings and CT are equivocal.
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PMID:[Subacute cerebral infarct: native and contrast medium-enhanced MRT]. 255 31

Diffuse carcinomatous leptomeningeal metastases "carcinomatous meningitis") have the usual clinical course involving multifocal nerve root deficits and a variable diffuse encephalopathy. In contrast, we describe a patient with carcinomatous leptomeningeal metastases who presented with clinical signs of meningitis and focal cerebral infarction. Over an 8-month period, multiple cerebral infarctions and cranial neuropathies developed. Postmortem examination of the patient's brain revealed diffuse leptomeningeal infiltration by a signet-ring adenocarcinoma. The extensive involvement of the subarachnoid space with tumor was associated with dense neoplastic infiltration of the Virchow-Robin spaces. These perivascular tumor infiltrates were accompanied by multifocal mural invasion and, less frequently, by intravascular tumor cells obliterating the lumen. Focal hemorrhagic infarcts in the cerebral cortex corresponded to areas of microscopic vasculopathy. This case provides evidence that tumor-associated vasculopathy with resultant ischemia plays a role in the pathogenesis of focal cerebral infarctions in carcinomatous leptomeningeal metastases.
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PMID:Focal cerebral infarctions associated with perivascular tumor infiltrates in carcinomatous leptomeningeal metastases. 255 69

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


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