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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy patients with cerebral ischemia (21 with transient ischemic attack and 49 with stroke) were studied with short-latency median nerve somatosensory evoked potentials to characterize the evoked potentials in all ischemic patients and to investigate their efficacy for prognosis in stroke. Within 72 hours of symptom onset, all 70 patients received a scaled neurologic function score, with a maximum of 50 points. Somatosensory evoked potential abnormalities were found in 10% (2/19), 42% (15/36), and 93% (14/15) of all patients with initial neurologic examinations who had normal (50 points), mild-moderate (30-49 points), and severe deficits (less than or equal to 29 points), respectively. Thirty-seven of the 49 stroke patients were available for a follow-up neurologic assessment. Eight-nine percent (8/9) of the stroke patients with poor outcome had somatosensory evoked potential abnormalities; 82% (9/11) of the stroke patients with severe neurologic deficits at onset had poor outcome. Results demonstrate that somatosensory evoked potential abnormalities are common in patients with cerebral ischemia but that somatosensory evoked potential findings are not significantly better than a detailed neurologic examination in predicting outcome from stroke.
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PMID:Assessment of median nerve somatosensory evoked potentials in cerebral ischemia. 238 96

In the Oxfordshire Community Stroke Project 14 patients were notified with lone bilateral blindness, defined as rapid onset of dimming or loss of vision over all of both visual fields simultaneously, lasting under 24 hours, without associated symptoms of focal cerebral ischaemia, epilepsy, or reduction in consciousness. The age of these patients was close to that of the 184 patients who presented with transient ischaemic attacks and they had a similar high prevalence of vascular risk factors. During a mean follow-up of 2.4 years, 5 of the 14 had a first-ever stroke (0.31 expected). In view of their 16 times (95% CI 7-39 times) excess risk of stroke such patients should be included, for practical purposes, under the diagnostic heading of transient ischaemic attack.
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PMID:Lone bilateral blindness: a transient ischaemic attack. 256 98

Frontal, central and parietal short and middle latency somatosensory evoked potentials (SEPs) arising after stimulation of the contralateral median nerve were studied in 10 normal adults. Stable SEPs were recorded: a frontal P21-N30 complex and an N20-P23-P28-N35-P42 complex in the centro-parietal region. The use of a chin reference electrode allowed identification of (the thalamic) P15 and N18. SEP studies of 20 patients with unilateral cerebral ischaemia were also performed, about 4 and 18 days after the stroke. In 13 out of 18 patients with a minor stroke (TIA, RIND and PNS) abnormalities of the frontal and/or parietal SEPs were demonstrated. Improvement in these SEPs occurred in 5 cases. In two patients who suffered from a major ischaemic deficit, the SEPs were highly abnormal and did not show any change in the course of time. SEP studies may be useful for the diagnosis of minor cerebral ischaemia as well as quantification of recovery; an even more important indication for this neurophysiological method might be detection of subclinical lesions in patients who have suffered from transient cerebral ischaemia even weeks before the SEP studies are carried out.
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PMID:Somatosensory evoked potentials in minor cerebral ischaemia: diagnostic significance and changes in serial records. 257 77

Diagnostic procedures for cerebral ischemia make clear strategies mandatory. Careful recording of case history, internal and neurological investigation either substantiate or make unlikely TIA and stroke. CT scan not only differentiates bleedings, tumors etc from ischemia but also can give very valuable information about the underlying vascular pathology. Multiple lacunes are characteristic of cerebral microangiopathy. Territorial and branch occlusion infarcts mostly indicate embolic occlusion of pial vessels from either cardiac or arterial sources. Endzone and borderline infarctions are seen with high grade stenosis or occlusion of the internal carotid artery. The identification of embolic sources necessitates cardiological (including echocardiography) and angiological (Doppler sonography and in selected cases angiography) investigations. Therapeutic and prophylactic measures depend on the etiology of TIA and stroke and are briefly dealt with.
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PMID:The value of diagnostic procedures in treating ischemic attacks and stroke. 267 95

The SEPIVAC study (Italian initials for "epidemiologic study of incidence of acute cerebrovascular disease") is a community-based epidemiologic survey of incidence and outcome of cerebrovascular disease in the territory of the 6th Local Health Unit, Umbria, Italy, where 49,101 people live. All cases were registered with the study either by notification from general practitioners or by check of hospital admission within the study area and in the two hospitals of Perugia. Death certificates were looked at as well. Patients were registered with the study when the clinical picture fulfilled the definition of stroke and transient ischemic attack (TIA) adopted for this study. Patients were followed up at approximately 30 days and 6 months. During the first year of the study (September 1, 1986 to August 31, 1987), 189 cases were registered: 108 suffered a "first ever in a lifetime" stroke, 30 a recurrent stroke, and 51 a "first ever in a lifetime" transient ischemic attack. Sixty-one percent of patients (71% of first strokes) had a computed tomography scan. For our study, the crude annual incidence rate of first stroke was 2.2 per 1,000 (confidence intervals 1.81-2.66); the standardized rate to the European population was 1.36 (confidence intervals 1.06-1.74). At least 83% of first strokes were due to cerebral ischemia; in 26 cases a clinical diagnosis of lacunar ischemia was made. The 30-day case fatality rate was 21%; 25% of our patients had recovered completely or almost completely after 1 month.
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PMID:First-year results of a community-based study of stroke incidence in Umbria, Italy. 274 44

We report on the results of combined carotid endarterectomy and coronary artery bypass grafting in 82 patients. Vascular pathology was severe in these cases: 94% of patients had extensive multivessel coronary artery disease, 29% had unstable angina, 30% had severe left main stem stenosis and all patients had hemodynamically significant stenosis of at least one carotid artery, 13% had an additional occlusion of the contralateral internal or common carotid artery and 26% had severe bilateral carotid artery stenosis. The carotid lesion was asymptomatic in 64% of cases, 24% of the patients experienced previous transient cerebral ischemia and 12% of the patients had a history of completed stroke. Hospital mortality was 7.3%. Neurological deficit occurred in 7.3% but functional impairment was not permanent. Late results have been obtained for 76 survivors at a mean postoperative interval of 29 months. Five year life table survival rate was 86%. Follow-up showed that 3 patients (4%) have died and that 3 patients (4%) experienced a late neurologic event (one TIA; two strokes) but none of these events involved the cerebral cortex on the side of the carotid endarterectomy. The cumulative 5 year stroke free survival rate is 91%. We conclude that combined carotid endarterectomy and coronary artery bypass grafting can be done with an acceptable mortality rate in these critically ill patients and that the postoperative incidence of neurological events is low.
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PMID:Combined myocardial and cerebral revascularization. A ten year experience. 280 89

We describe a series of experiments in which a subhuman primate model was used to create temporary and permanent cerebral ischemia by three separate mechanisms. In the first group of five baboons, a hemodynamic model was produced by creating unilateral and bilateral carotid stenotic lesions of varying degrees with and without associated reduction in systemic perfusion pressure. Only global ischemic changes and no focal changes resulted. In the second group of three baboons, a macroembolic model was produced by introducing solid particulate material into the extracranial circulation. No reversible contralateral focal neurologic changes resulted. In the third group of 11 baboons, cerebral ischemia was produced by introducing agents known to cause platelet aggregation (arachidonic acid, adenosine diphosphate, and collagen) into the extracranial arterial circulation. Arachidonic acid caused seizures, adenosine diphosphate caused severe postural hypotension, and only collagen fibrils produced a picture resembling a transient ischemic attack. We propose a theory that intravascular activation of the prostaglandin cascade by chemical initiation may result in the pathophysiologic changes of transient cerebral ischemia.
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PMID:Pathogenesis of transient ischemic attacks and stroke in baboons. 292 78

The results of Holter monitoring in 100 patients with transient and focal cerebral ischemia were studied retrospectively. Atrial fibrillation (AF) was found in five patients compared with two from a group of 100 age and sex-matched control patients. Four of these had a previous history of AF or showed AF on the standard electrocardiogram. Episodic forms of sick sinus syndrome, which have also been related to cerebral embolism, were found in 32 of the TIA patients against 13 of the controls (p less than 0.0025). Sick sinus syndrome was of the bradyarrhythmia-tachyarrhythmia type in 14 of the TIA patients and in three of the controls (p less than 0.01). The relationship between TIAs and transient sinus node dysfunction could not be explained by concomitant heart disease. It is not yet clear whether the relationship is causal or indirect.
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PMID:Holter monitoring in patients with transient and focal ischemic attacks of the brain. 293 8

Vasoactive arachidonic acid metabolites are postulated to play a role in the pathogenesis of cerebral ischemia. In order to characterize the local generation of cyclooxygenase and lipoxygenase metabolites of arachidonic acid in transient ischemia with reperfusion, Mongolian gerbils were studied for regional cerebral blood flow (CBF), using the hydrogen clearance technique, and for cerebral levels of the thromboxane metabolite TXB2, and prostaglandins 6-keto-PGF1 alpha and PGE2, as well as the leukotriene LTB4. The gerbils were anesthetized with pentobarbital, and half of the animals were pretreated with the cyclooxygenase inhibitor indomethacin. All received 10 or 20 minutes of dense forebrain ischemia followed by reperfusion of 10 minutes, 50 minutes, or 100 minutes. A separate control group received no ischemic lesion. Regional CBF decreased significantly from 23.7 +/- 2.6 to 4.3 +/- 1.7 cc/100 gm/min during ischemia (p less than 0.01). Reperfusion resulted in initially normal flows (22.5 +/- 5.1 cc/100 gm/min) followed by a progressive hypoperfusion (11.3 +/- 2.7 cc/100 gm/min). All metabolites showed parallel significant (p less than 0.05) increases after transient ischemia and reperfusion compared to baseline levels (values (in pg/mg protein) were: TXB2 45.5 +/- 7.1 vs 23.3 +/- 3.6; 6-keto-PGF1 alpha 262.8 +/- 47.9 vs 175.8 +/- 26.8; PGE2 256.5 +/- 35.6 vs 112.5 +/- 11.2; and LTB4 37.8 +/- 4.6 vs 24.6 +/- 6). These levels were all significantly decreased (p less than 0.05) by pretreatment with indomethacin except for the leukotriene LTB4, which was increased. Transient cerebral ischemia results in a reperfusion abnormality and the local generation of cyclooxygenase products, which are reduced by pretreatment with indomethacin; however, cyclooxygenase inhibition may result in increased substrate availability for the lipoxygenase system. Studies of such an interaction may lead to new understandings of the pharmacological modification of detrimental vascular changes after transient cerebral ischemia.
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PMID:Development of cyclooxygenase and lipoxygenase metabolites of arachidonic acid after transient cerebral ischemia. 300 Dec 48

A lupus inhibitor paradoxically prolongs phospholipid-dependent coagulation assays, but may increase risk of thromboembolism. We studied seven patients with cerebral infarcts and one with TIA who had lupus inhibitor. The average age at onset of cerebral ischemia was 41 years. Three patients had multiple cerebral ischemic events. The activated partial thromboplastin time was longer than that of controls, but usually within normal limits. Other abnormalities included biologic false-positive VDRL, antinuclear antibodies, thrombocytopenia (three patients each), and deep vein thrombosis (two patients).
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PMID:Cerebral infarct, TIA, and lupus inhibitor. 309 32


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