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

We evaluated 183 patients with brain ischemia for an embolic source, using transesophageal echocardiography with extensive imaging of the thoracic aorta. There were mobile, frond-like projections of aortic plaque in seven (4%) patients. The plaque originated on a wide base on the posterior aspect of the ascending aorta at its junction with the transverse arch in six patients, and on the aortic root in one. The acute event was a cerebral infarction in five patients, and a transient ischemic attack in two. This type of aortic plaque could be a previously underdiagnosed source of cerebral embolism that is now easily visualized by transesophageal echocardiography.
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PMID:Aortic plaque in patients with brain ischemia: diagnosis by transesophageal echocardiography. 164 Nov 58

In order to clarify the effectiveness of extracranial- intracranial bypass in cases of vertebro-basilar occlusive disease, we investigated the operative complication, clinical course and follow-up study of 30 cases undergoing superficial temporal artery-superior cerebellar artery (STA-SCA) bypass surgery. Postoperative angiogram showed the patency of the anastomoses in all cases. No serious surgical complications were observed. The outcome on discharge was excellent, with no morbidity and one mortality which was due to cardiac infarction. In the follow-up study, there were four cases with ischemic symptoms, two with transient ischemic attack and two with completed stroke, one of which was a supratentorial infarction due to internal carotid artery occlusion and the other was a small infarction of pons. There were also two deaths due to cardiac infarction and diabetes mellitus. Favorable outcomes were obtained for the remaining cases. The present study suggests that, STA-SCA bypass, can be performed without surgical and systemic complications and used as an effective therapy for vertebrobasilar ischemia.
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PMID:Clinical analysis of STA-SCA bypass for vertebrobasilar occlusive disease. 175 11

Experimental ischemia models have shown the antitussive dextromethorphan to be an N-methyl-D-aspartate antagonist with neuroprotective properties. We treated 10 patients with a history of recent stroke or transient ischemic attack with oral dextromethorphan (60 mg q.i.d.) for 3 weeks in a placebo-controlled, double-blind, crossover tolerance study. We documented no clinical evidence of toxicity attributable to dextromethorphan in this preliminary study.
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PMID:Safety and tolerance of oral dextromethorphan in patients at risk for brain ischemia. 186 55

We analyzed existing research on the prognosis of patients who have had a transient ischemic attack to identify studies that adhere to basic methodological principles and to identify underinvestigated questions. Studies were eligible for analysis if they were published in peer-reviewed journals after 1950, written in English, and included at least 50 patients with transient ischemia. Studies that included patients with stroke were included only if they reported outcome rates separately for the subgroup of patients with transient ischemia. All eligible studies were extracted by one investigator who recorded adherence to six key methodological principles. Among 60 eligible studies, 54 were observational cohort studies and six were randomized trials. Adherence to the six methodological principles was as follows: eight studies included an adequate description of diagnostic criteria and of procedures used to assure adherence to the criteria, 54 used appropriate end points, two assembled inception cohorts, 10 included an adequate description of end point surveillance, 22 adequately reported and analyzed censored patients, and 10 included a multivariate analysis for predictive variables. No study adhered to all six principles, but two adhered to the three most important ones (appropriate end points, inception cohort, and adequate reporting and analysis of censored patients). Aspects of prognosis after transient ischemia that have not been completely investigated include the severity of subsequent strokes and methods for estimating the outcome risk for individual patients. We conclude that only a few published investigations on prognosis after transient ischemia are methodologically complete. This finding helps explain why it is difficult to interpret many studies. Further research is needed and should target underinvestigated topics.
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PMID:A methodological appraisal of research on prognosis after transient ischemic attacks. 192 53

In six patients, we observed remarkably unsteady blood flow and indications of vasospasms on the arteriolar level in connection with episodes of focal cerebral ischemia. The patients originated from a prospective consecutive study of 53 patients with stroke and transient ischemic attack who had been examined by cerebral angiography and rapidly repeated regional cerebral blood flow measurements using the intracarotid xenon 133 method. In 47 patients, regional cerebral blood flow values, flow patterns, and clinical condition were stable during the repeated regional cerebral blood flow measurements. In six patients, pronounced regional hypoperfusion and hyperperfusion developed during the course of examination. In the hypoperfused regions, flow was transiently reduced to values consistent with ischemia, and in four of these patients this was accompanied by transient neurological deficits. The arteriogram and isotope angiograms ruled out spasms of large arteries or thromboembolism. A condition of cerebrovascular instability on the arteriolar level probably was induced by the examination procedure. These patients were hypersensitive to the provoking stimuli either habitually or as a consequence of previous ischemic accidents. It is suggested that in some patients with focal cerebral ischemia, the primary cause might be spasms of the smallest resistance vessels rather than thromboembolism.
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PMID:Cerebrovascular instability in a subset of patients with stroke and transient ischemic attack. 192 93

The records of 483 patients admitted to the emergency room because of syncope were reviewed. Thirty seven patients (7.7%) were found to suffer from transient ischemic attack- (TIA) related syncope. This group is the subject of this report. Of these patients, 28 (76%) were men (mean age 71 years). Seven patients reported previous syncopal episodes. Past history revealed a high rate of ischemic heart disease (70%) and hypertension (68%). Concurrent neurologic symptoms, which led to the diagnosis of TIA-related syncope, included mainly vertebrobasilar symptoms: vertigo (in 55% of the patients), ataxia (46%), parasthesia (41%). Two patients most probably were presenting bilateral carotid artery disease. Various diagnostic tests (including electroencephalography, computed tomography, sonography, and cerebral angiography) were used to exclude other causes of syncope. During follow-up (mean 14.5 months) four patients (11%) had an additional episode of TIA and in three of them syncope reappeared. One patient had a complete stroke. We conclude that TIA is a much more frequent explanation for syncope than has been previously argued. These patients tend to be elderly males with high incidence of ischemic heart disease and hypertension. The concurrent neurologic symptoms, leading to the diagnosis, represent mainly vertebrobasilar territory ischemia.
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PMID:Transient ischemic attack-related syncope. 204 43

We studied delayed postischemic calcium accumulation and neuronal damage in the gerbil brain, using 45Ca autoradiography as a marker for detection of injured tissue and light microscopy. Transient cerebral ischemia was induced for 15 min. Sham-operated gerbils showed no abnormal calcium accumulation and neuronal damage throughout the brain. At 2 and 7 days following 15 min of ischemia, marked calcium accumulation and mild to severe neuronal damage were found in the selectively vulnerable areas such as neocortex, striatum, hippocampus and thalamus, and brainstem such as medial geniculate body, substantia nigra and inferior colliculus. After 1-2 months of recirculation, the calcium accumulation was not recognized in the brainstem. But, the accumulation was still detectable in the striatum, the hippocampus and the thalamus. Morphological study showed that marked proliferation of glia cells was rapid in the inferior colliculus and was relatively slow in the striatum and the hippocampus, although these structures were severely damaged after ischemia. The result suggests that the speed of restoration of injured tissue and the mechanisms for the damage after cerebral ischemia may be different between the selectively vulnerable areas and the brainstem. Furthermore, they suggest that 45Ca autoradiographic technique may provide a useful approach for diagnosis of the restoration of injured tissue at chronic stage following cerebral ischemia.
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PMID:Long-term observations on calcium accumulation in postischemic gerbil brain. 204 98

Eighty-three patients underwent 85 intracranial to extracranial pedicle bypass anastomosis procedures to the posterior circulation. There were 15 patients with occipital artery (OA) to posterior inferior cerebellar artery (PICA) anastomosis, 20 patients with OA to anterior inferior cerebellar artery (AICA) anastomosis, and 50 patients with superficial temporal artery (STA) to superior cerebellar artery (SCA) anastomosis. All patients had transient ischemic attacks (TIA's) suggestive of vertebrobasilar ischemia. Twenty-seven patients had crescendo TIA's or stroke in evolution and were considered to be clinically unstable. All patients had severe bilateral distal vertebral artery or basilar artery disease. Twenty-two patients had bilateral vertebral artery occlusion and three had basilar artery occlusion. In this series, 69% had complete resolution of symptoms; the mortality rate was 8.4% and the morbidity rate 13.3%. Clinically stable patients did better than unstable patients. The STA-SCA anastomosis was well tolerated and technically less demanding than the OA-PICA or OA-AICA anastomosis procedures. Patients with symptomatic severe bilateral vertebral or basilar artery disease have a grave prognosis and the option of a surgical arterial pedicle revascularization procedure should be offered to them.
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PMID:Superficial temporal and occipital artery bypass pedicles to superior, anterior inferior, and posterior inferior cerebellar arteries for vertebrobasilar insufficiency. 231 13

The authors investigated 100 patients (55 males and 45 females) aged 16 to 45 years who experienced cerebral ischemic attack, excluding venous thrombosis. Transient ischemic attacks accounted for 12% only. Attacks were related to usual causes of brain ischemia in 49 cases (premature atherosclerosis in 26, cardiopathy in 20 and lacunar stroke in 3). Thirty-eight events were attributed to most uncommon etiologies. Nonatherosclerotic arteriopathies (10 cases) such as spontaneous dissection, dysplasia or megadolichoarteries were easily diagnosed by angiography. Oral contraceptives (14 cases) and migraine (2 cases) were diagnosis of exclusion. Hematological disorders were a possible cause in 10 patients. Etiology remained undetermined in 13 cases. Four patients died acutely. Follow-up data were obtained in 93 survivors with a mean duration of 26 months (range, 6 to 60 months). Four subjects died during follow-up and 6 experienced recurrent stroke (annual recurrence rate: 3%). In activities of daily living, 64% of patients had complete autonomy while 13% had mild residual disability and 23% had severe handicap.
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PMID:[Cerebral arterial ischemic complications in young adults. Etiology and prognosis]. 232 55

Over a 24-month period, 291 patients were consecutively admitted to the West Haven Veterans Administration Medical Center with new ischemic neurological symptoms. Of these, 90 patients (31%) developed ischemic neurological symptoms while taking aspirin (aspirin treatment failure). Of those in whom aspirin treatment failed, 66 patients had ischemic symptoms in the distribution of the carotid artery. Aspirin treatment failed in 21 patients with severe carotid stenosis (greater than 75% stenosis). Eleven of these 21 patients had cerebral infarctions while taking aspirin, and 7 of these 11 infarcts occurred without the prior warning of transient ischemic attacks. Aspirin treatment failed in 45 patients with lesser degrees of carotid stenosis. Transient ischemic attack without permanent ischemia was the most common manifestation of failure in these patients. Infarction occurred in only 12 of these 45 patients and in only 4 patients did infarction occur without warning. We conclude that patients with symptomatic high-grade carotid stenosis (greater than 75%) in whom aspirin treatment failed are likely to suffer an infarct without warning as the first sign of treatment failure (P less than 0.033). We suggest that this subgroup of patients should be considered for alternative forms of therapy.
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PMID:Patterns of failure of aspirin treatment in symptomatic atherosclerotic carotid artery disease. 233 76


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