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

Recurrent retinal branch artery occlusions, carotid thromboembolism, cerebral venous thrombosis, transient brainstem ischemia, and massive brainstem and cerebral infarction complicated the course of inflammatory bowel disease in 5 patients. Three patients had ulcerative colitis and 2 had regional enteritis. The usual risk factors for stroke were absent. Neuropathological examination in 1 patient showed in situ thrombosis of small cerebral and brainstem arteries and veins. Coagulation studies showed thrombocytosis, short partial thromboplastin times, and elevation of fibrinogen and Factor VIII levels. Platelet counts and coagulation factors returned toward normal after control of intestinal inflammation in each of the 4 surviving patients. Inflammatory bowel disease can be accompanied by a hypercoagulable state that predisposes to stroke.
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PMID:Cerebral and retinal vascular complications of inflammatory bowel disease. 44 68

Ten patients with angiographically verified occlusion of the basilar or vertebral artery have been followed for an average of 2.75 years. None has developed further ischemia after the initial stroke, and 4 patients survived without any clinical deficit. In occlusive disease of the posterior circulation, the critical period for deficit acquisition is at the time of occlusion. Extent of the deficit depends on the rapidity of development of adequate collateral circulation, and the presence of distal embolization at the time of occlusion. Some patients survive basilar occlusion without permanent deficit.
Stroke
PMID:Occlusion of the vertebral or basilar artery. Follow up analysis of some patients with benign outcome. 46 13

EEG was monitored at bilateral scalp sites outside the operative field during hypotensive aneurysm surgery in 21 patients. Mean arterial blood pressure at axillary level was 50-60 mm Hg (average 55 mm) for 1.9-5.3 hours (average 3.6). Four new deficits were noted immediately post-operatively, all related to the operated site: these were attributable to intra-operative rupture with forced vascular clipping, vasospasm, or edema. In no instance was hypotension solely responsible for a new deficit. EEG showed persistent slowing in relation to surgery in only 1 patient, where aneurysmal rupture led to severe hypotension, forced clipping of 1 posterior cerebral artery, and subsequent brain stem infarction. In the 3 other patients with fresh focal postoperative deficits, no persistent intraoperative EEG changes were observed. EEG monitoring did not detect ischemia in these 3 patients because 1) hypotension was moderate and did not per se cause new deficit, and 2) EEG electrodes did not survey the area at maximal risk, namely the operative field. EEG scalp electrodes near but outside the operative site do not seem useful for monitoring cerebral function in the region of aneurysm surgery. Epidural or cortical electrodes in the operative field may prove to be more useful.
Stroke
PMID:EEG monitoring for induced hypotension for surgery of intracranial aneurysms. 46 16

The handling of patients with cerebral ischemia is reviewed, taking into consideration recent concepts regarding etiopathogenesis along with new diagnostic and therapeutic methods. A particularly important new diagnostic method is computerized axial tomography. The subject is divided into four sections in order to present a practical outline. The first section deals with the arterial circulatory system. Evaluation of patients with arteriosclerosis of the vessels in the neck and/or intracranial are reviewed in some detail, according to whether the clinical manifestation was transitory ischemia, progressive cerebral infarction, or complete cerebral infarction. Emphasis is placed on the proper selection of diagnostic tests and application of therapy in each case. The second part is a discussion of the changes in arterial blood pressure in the etipathogenesis of stroke. Arterial hypertension is an important factor in production of small infarctions. In the third section a review is made of the role of the heart in transitory ischemia and as a cause of cerebral infarctions. Lastly, the hematologic factors which might contribute to the development of cerebral ischemia, along with the other causes, are mentioned.
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PMID:[Practical considerations in dealing with cerebral ischemia (author's transl)]. 47 Apr 90

Twenty-four pigs were studied to assess the effect of potassium in a cardioplegic solution on the ability of the swine myocardium to maintain functional and metabolic integrity following induced ischemia. The pigs were evaluated on total and right heart bypass with measurement at normothermia and after a one-hour intervention of stroke volume (SV), coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and lactate extraction. Myocardial tissue gases (PmO2 and PmCO2) were continuously monitored and, at the conclusion of the procedure tissues were analyzed for adenosine triphosphate (ATP). There were five interventions: (1) hypothermic perfusion (28 degrees C) (Group 1); (2) hypothermic ischemia (28 degrees C) (Group 2); and hypothermic ischemia with a cardioplegic solution (nonlactated Ringer's solution, pH 7.4, 4 degrees C) using (3) normokalemia (4 mEq of potassium chloride/L, 300 mOsm/L (Group 3), (4) hyperkalemia (43 mEq of KCl/L, 390 mOsm/L) (Group 4), and (5) normokalemia with increased osmolarity (3.6 mEq of KCl/L, 400 mOsm/L) (Groups 5). A significant decrease in SV and elevation in peak PmCO2 were seen in all groups subjected to ischemia except those protected with hyperkalemic solution. We conclude that the presence of hyperkalemia in a cold root perfusion solution provides better myocardial protection than cold root perfusion alone. Furthermore, potassium arrest appears to be more protective than coronary perfusion at 28 degrees C.
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PMID:The importance of hyperkalemia in a cold perfusion solution: a correlative study examining myocardial function, metabolism, tissue gases, and substrates. 48 29

Twenty-three instances of internal carotid artery occlusion occurring with minimal neurological deficit in 22 patients are described. Although each of these patients was referred to the neurosurgical service for evaluation for an extracranial-intracranial microvascular bypass procedure, complete arteriographic evaluations of their cerebrovasculature suggested that alternative methods should be the treatment of choice. For each patient reported the ipsilateral external carotid artery was demonstrated by angiography to be an important source of collateral blood supply to the cerebral hemispheres or retinae distal to the occluded internal carotid arteries. Ten patients with no significant atherosclerotic narrowing or ulceration of the external carotid artery have remained free of symptoms of cerebral ischemia for 6 to 40 months. In twelve patients who developed delayed recurrent cerebral or retinal ischemia ipsilateral to their internal carotid artery occlusion, there were found obstructive and/or ulcerative plaques involving the common and/or external carotid arteries. Thromboendarterectomy in 11 of these patients gave complete relief of ischemic symptoms during the 4 to 36 months of postoperative follow up. One of these 12 patients refused operation and went on to develop a major cerebral infarction. Angiographic identification of a functionally important external carotid artery ipsilateral to an internal carotid artery occlusion carries considerable prognostic and therapeutic significance.
Stroke
PMID:External carotid artery in internal carotid artery occlusion. Angiographic, therapeutic, and prognostic considerations. 50 84

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
Stroke
PMID:Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability. 50 96

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.
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PMID:Ischemic optic neuropathy as a possible early complication of vascular hypertension. 51 8

A total of 289 carotid endarterectomies were performed in 204 patients. A decision to place a temporary shunt during carotid endarterectomy in this series was made entirely on the basis of intraoperative EEG monitoring. Retrospectively, the correlation between stump pressures and the results of intraoperative EEG monitoring in each case was determined. Evidence of ischemia developed in 6% of the total series on intraoperative EEG monitoring despite a stump pressure of greater than 50 mm Hg. The degree of disagreement between stump pressure and EEG varied according to clinical category in this series. In those endarterectomies performed for completed stroke, all cases requiring shunting had stump pressures less than 50 mm Hg. In those cases performed for symptoms of vertebral basilar insufficiency, however, 77% of the cases requiring an intraoperative shunt had stump pressures greater than 50 mm Hg. A review of the complication rate in the various study groups indicates that the use of intraoperative EEG is a safe indicator of cerebral ischemia during carotid endarterectomy regardless of stump pressure.
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PMID:Failure of carotid stump pressures. Its incidence as a predictor for a temporary shunt during carotid endarterectomy. 53 56

The results of a retrospective study of patients undergoing carotid endarterectomy for hemispheric and/or nonhemispheric symptoms of transient ischemic attacks are presented. During an approximately 3-year period of follow-up observation, recurrent cerebral ischemia following carotid endarterectomy was two to three times more frequent among patients with nonhemispheric transient ischemia than among those with hemispheric transient ischemia. Patients with symptoms of both hemispheric and nonhemispheric transient ischemia had the highest frequency of transient ischemic attacks and stroke during the follow-up period and also had the greatest surgical morbidity and mortality. The results of this study suggest that carotid endarterectomy has little or no therapeutic value in treating patients with vertebral-basilar ischemia.
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PMID:The value of carotid endarterectomy in treating transient cerebral ischemia of the posterior circulation. 55 76


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