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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aim of the study is the evaluation of therapeutic effectiveness of nimodipine in acute focal cerebral ischaemia. Thirty patients affected by minor ischaemic stroke divided in two randomized groups have been studied consecutively: all the patients were treated with standard therapy, nimodipine was delivered in addition only to the patients of the first group. Both clinical evaluation using Mathew scale, modified by Gelmers, and flowmetric evaluation with SPECT were performed at different times. The results haven't shown any significant statistical difference in the effectiveness of the therapy between the two groups even if a positive clinical trend was evidenced in the group treated with nimodipine. The flowmetric study has shown the poor homogeneity of the groups from a physiopathological point of view not-with-standing the two groups were similar for the clinical severity, sex, age and vascular risk factors. We conclude that is advisable to carry out further trials in which the comparison study groups are more numerous and balanced also from a physiopathological point of view.
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PMID:[The nimodipine therapy of acute focal cerebral ischemia (minor stroke). A clinical study with an assessment of regional cerebral blood flow by SPECT]. 150 26

The role of cerebral ischemia in the pathophysiology of traumatic brain injury is unclear. Cerebral blood flow (CBF) measurements with 133Xe have thus far revealed ischemia in a substantial number of patients only when performed between 4 and 12 hours postinjury. But these studies cannot be performed sooner after injury, they cannot be done in patients with intracranial hematomas still in place, and they cannot detect focal ischemia. Therefore, the authors performed CBF measurements in 35 comatose head-injured patients using stable xenon-enhanced computerized tomography (CT), simultaneously with the initial CT scan (at a mean (+/- standard error of the mean) interval of 3.1 +/- 2.1 hours after injury). Seven patients with diffuse cerebral swelling had significantly lower flows in all brain regions measured as compared to patients without swelling or with focal contusions; in four of the seven, cerebral ischemia (CBF less than or equal to 18 ml/100 gm.min-1) was present. Acute intracranial hematomas were associated with decreased CBF and regional ischemia in the ipsilateral hemisphere, but did not disproportionately impair brain-stem blood flow. Overall, global or regional ischemia was found in 11 patients (31.4%). There was no correlation between the presence of hypoxia or hypertension before resuscitation and the occurrence of ischemia, neither could ischemia be attributed to low pCO2. Ischemia was significantly associated with early mortality (p less than 0.02), whereas normal or high CBF values were not predictive of favorable short-term outcome. These data support the hypothesis that ischemia is an important secondary injury mechanism after traumatic brain injury, and that trauma may share pathophysiological mechanisms with stroke in a large number of cases; this may have important implications for the use of hyperventilation and antihypertensive drugs in the acute management of severely head-injured patients, and may lead to testing of drugs that are effective or have shown promise in the treatment of ischemic stroke.
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PMID:Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. 843 61

The neurometric method as introduced by John was used to study three groups of patients with cerebral ischemia, three groups of patients with renal disease and an additional normal control group. The traditional neurometric approach was slightly modified: relative band power values were not expressed as a percentage of the total power per derivation but as a percentage of the "global power"; frequency matrices were used in addition to power matrices. From the study of the three groups of patients with one-sided supratentorial ischemia it appeared that sensitivity and specificity are completely satisfactory when using neurometrics in patients with severe ischemia in the middle cerebral artery territory studied within 48 hours of the onset of the stroke. However, in ischemia patients with less pronounced clinical signs and especially in patients without persistent neurological deficit the sensitivity is much lower. In studying dialysed and non-dialysed renal patients signs of an (often subclinical) encephalopathy could be detected in approximately 37% of all patients. Follow-up studies of the ischemia patients and the renal patients over a period of several years revealed a parallelism between clinical scores and qEEG scores in the ischemia patients; almost all qEEG improvement occurred in the first three months after the stroke. The qEEG profile of the groups of dialysed patients tended to be more or less stable over a period of several years.
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PMID:Neurometrics in cerebral ischemia and uremic encephalopathy. 151 Aug 71

The mechanism of embolic stroke in young adults remains unidentified in about 35% of cases. In recent years defects in the atrial septum have been described as an important route for cerebral and retinal embolism. These include classical atrial septal defect and patent foramen ovale, as well as the less well-recognized entity of atrial septal aneurysm, with or without interatrial communication. The combined incidence of these defects in the general population is between 20-35%. The introduction of transesophageal echocardiography and the use of echogenic contrast have lead to significant improvement in identification. We describe 3 patients in whom atrial defects were identified as possible routes for cerebral embolism: The first presented with recurrent stroke and combined atrial septal aneurysm and patent foramen ovale. In the second, patent foramen ovale was found in a patient with 2 prosthetic values. The third was a soldier in whom patent foramen ovale was found following transient loss of consciousness. Based on our modest experience and review of the literature we believe that transesophageal and contrast echocardiography should be performed in every young patient with unexplained cerebral ischemia.
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PMID:[Atrial septal defects and embolic stroke in young adults]. 151 71

The goal of the current study was to determine whether treatment of hypertension reduces cerebral infarction after occlusion of the middle cerebral artery in stroke-prone spontaneously hypertensive rats (SHRSPs). Three-month-old SHRSPs received untreated drinking water or drinking water containing cilazapril, an angiotensin converting enzyme inhibitor, or hydralazine and hydrochlorothiazide. After 3 months of treatment, the left middle cerebral artery was occluded and neurological deficit was evaluated. Infarct volume was measured 3 days after occlusion using computer imaging techniques from brain slices. Cilazapril and hydralazine with hydrochlorothiazide were equally effective in reducing systolic blood pressure in SHRSPs. One day after occlusion of the middle cerebral artery, neurological deficit was decreased by both cilazapril and hydralazine with hydrochlorothiazide compared with untreated SHRSPs, and the deficit 3 days after occlusion was decreased significantly only by cilazapril. Infarct volume was 178 +/- 7 mm3 (mean +/- SEM) in untreated SHRSPs, and it was significantly reduced to 117 +/- 15 mm3 by hydralazine with hydrochlorothiazide and to 101 +/- 17 mm3 by cilazapril. Infarct volume in Wistar-Kyoto rats was 27 +/- 16 mm3. Thus, reduction in arterial pressure by hydralazine with hydrochlorothiazide or an angiotensin converting enzyme inhibitor is protective against focal cerebral ischemia in SHRSPs.
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PMID:Effect of antihypertensive treatment on focal cerebral infarction. 153 16

During the onset of heat stroke, rabbits displayed hyperthermia (42.8 degrees C), and decreased cerebral perfusion pressure and decreased cerebral blood flow (as reflected by a prolonged cerebral circulation time) compared to those of normothermic rabbits. On the other hand febrile rabbits, during the fever plateau did not show the above responses, although they had a similar level of hyperthermia (42.4 degrees C). The data support the concept that cerebral ischemia is the main cause for the onset of the heat stroke syndrome.
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PMID:Cerebral ischemia is the main cause for the onset of heat stroke syndrome in rabbits. 154 47

Primary CVT alterations and arrhythmias, occurring one hour after embolization were detected in several experiments about focal cerebral ischaemia in rabbits. 62 animals were fed on a standard diet and 15 on an atherogenic diet. Primary CVT alterations and arrhythmias occurred in 4 rabbits fed on a standard diet and in 6 rabbits fed on an atherogenic diet. These results gave statistic evidence of a relationship between more frequent and serious electrocardiographic alterations and an atherogenic diet. The information coming out of these experiments are discussed. Considering the data coming out of other experiments and the data of the literature it is supposed that the pathogenesis of "the cerebro-cardiac syndrome" is linked to several biohumoral alterations occurring after the stroke. If these alterations occur in animals (or in subjects) with damaged coronary arteries cardiac alterations occurring after the stroke are greater and more important than the cardiac alterations occurring in the same conditions in the animals in which coronary arteries are not jet damaged.
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PMID:[Early ECG changes after experimental focal cerebral ischemia. A pathogenetic hypothesis of the brain-heart syndrome]. 155 60

The occurrence of various forms of severe neurologic events has been increasingly reported in acute myocardial infarction patients receiving thrombolytic therapy. Strokes have long been known to complicate acute myocardial infarction. The recent attention on severe neurologic events has focused primarily on probable cerebral bleeds. The various forms of severe neurologic events that clinicians are confronted with have unique features and characteristics that will be delineated. The incidence of these events and patient risk factors for cerebral ischemia and cerebral hemorrhage will be outlined. Guidelines that should be adopted to minimize the chance of a patient's suffering a severe neurologic event while at the same time maximizing the number of patients who receive this lifesaving therapy are summarized.
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PMID:Prevention of severe neurologic events in the thrombolytic era. 155 77

Though the role of cerebral ischemia as an etiologic factor for epilepsy is accepted, the effect of seizures on stroke sequelae has received little attention. We describe 10 patients with poststroke partial epileptic seizures that were followed by persistent worsening of the previous neurologic deficit. Of 38 other patients with poststroke seizures who were examined during the same period, eight suffered transient neurologic worsening (Todd's phenomenon). Persistent worsening was associated with longer seizures and longer partial seizures before generalization. Risk factors, age, sex, other seizure features, and characteristics of previous stroke were irrelevant to developing persistent worsening of stroke sequelae. None of the patients with persistent worsening showed a new lesion or an extension of the previous ischemic area on computed tomography or magnetic resonance imaging, except one who had a first hemorrhage that spared the cortex and who suffered a second hemorrhage, which was lobar. Persistent worsening of a neurologic deficit following a seizure in patients with previous stroke may not be uncommon and may be due to a direct effect of the seizure itself on the infarcted area.
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PMID:Persistent worsening of stroke sequelae after delayed seizures. 155 20

To evaluate the prevalence and prognostic role of silent coronary artery disease (CAD) in patients with symptomatic high-grade carotid stenosis (70 to 99%) undergoing carotid endarterectomy, and with neither history nor symptoms of CAD, 106 patients (76 men, 30 women, mean age 58.7 years [range 42 to 71]) with recent cerebral ischemia were prospectively studied. Patients were stratified as to the presence (n = 27, 25%) or absence (n = 79, 75%) of silent CAD defined by concordant abnormal exercise electrocardiographic testing and thallium-201 myocardial scintigraphy. The male sex, the severity of the symptomatic carotid lesion (greater than 90%), and the coexistence of contralateral carotid disease identified patients with higher probability of coexisting CAD. The 106 patients underwent 121 operations (bilateral in 15). In the perioperative period, no deaths or cardiac events occurred, 1 patient suffered a recurrent stroke and 3 had a transient ischemic attack. During a mean follow-up period of 5.4 years, 9 patients died (1.7%/year): fatal myocardial infarction occurred in 5 (all in the silent CAD group), cancer in 3 and vertebrobasilar stroke in 1. Nonfatal events occurred in 9 patients: myocardial infarction in 1 (without silent CAD), unstable angina in 3 (with silent CAD), and cerebral ischemic attacks in 5. After 7 years, the Kaplan-Meier estimated survival free from coronary events was 51% in patients with silent CAD, and 98% in patients without CAD (p less than 0.01). In conclusion, among patients with symptomatic high-grade carotid stenosis undergoing carotid endarterectomy, even in absence of history or symptoms of CAD, a silent CAD is detectable in one fourth of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Frequency and prognostic significance of silent coronary artery disease in patients with cerebral ischemia undergoing carotid endarterectomy. 843 Jun 60


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