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

Records of 248 patients undergoing aortoiliac reconstruction for occlusive disease between 1957 and 1975 were reviewed. Carotid bruits were ausculted in 35 patients (14%). Five of the patients with bruits also were thought to have symptoms of transient ischemia. Strokes occurred after operation in four of the 248 patients (1.6%). No patient with a previously noted bruit developed postoperative stroke. Two patients with transient cerebral ischemia and no confirmed bruit before operation did develop postoperative strokes. Cerebral angiography was performed in 18 of the patients with carotid bruits. Two of these patients underwent carotid endarterectomy prior to aortoiliac reconstruction. None of these 18 patients developed strokes following their carotid surgery of aortoiliac reconstruction. A third patient with no bruit but with retinal cholesterol emboli also underwent arteriography and endarterectomy without complication. The results suggest that the asymptomatic carotid bruit alone does not indicate an increased risk of stroke during aortoiliac reconstruction. The authors conclude that their experience does not support prophylactic carotid endarterectomy in the asymptomatic patient prior to aortoiliac reconstruction.
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PMID:Carotid bruit as a risk factor in aortoiliac reconstruction. 85 Aug 72

Cerebral blood flow (CBF) and metabolism were measured before and after withdrawal of 5 to 6 ml of cerebrospinal fluid (CSF) in 17 baboons. The measurements were made before and after infusion of tyrosine, the precursor amino acid of the putative neurotransmitters, dopamine and norepinephrine, in the brain. The same observations were made in another experimental group, i.e., before and after acute cerebral multiembolization induced by microfil emboli. In the steady state CBF was unaltered following reduction of intracranial pressure by removal of CSF. After infusion of tyrosine, CBF was decreased, and cerebrovascular resistance increased significantly on removal of CSF. Cerebral embolization did not influence changes in CBF at reduced intracranial pressure. It appears that the cerebral resistance vessels constrict following reduction of intracranial pressure by removal of CSF and that cerebrospinal fluid pressure-CBF autoregulatory mechanisms are resistant to cerebral ischemia induced by middle cerebral artery embolization.
Stroke
PMID:Effect of cerebrospinal fluid removal on cerebral blood flow and metabolism in the baboon: influence of tyrosine infusion and cerebral embolism on cerebrospinal fluid pressure autoregulation. 86 Feb 92

Platelet suppressant drugs have been suggested as beneficial for patients with transient cerebral ischemic attacks and these drugs have been shown to lengthen shortened platelet survival time. In the present study platelet survival time (autologous labeling with 51Chromium) was measured in 25 patients with transient cerebral ischemia involving a carotid distribution. Platelet survival was shortened in all patients (2.5 +/- 0.10 days; AVE t 1/2 +/- SEM; Normal 3.7 +/- 0.04 days P less than 0.001). Sulfinpyrazone increased platelet survival in 9 of 19 (47%) of patients (2.4 +/- 0.10 to 2.8 +/- 0.16 days; P less than 0.01). Of the 19 treated with sulfinpyrazone, 10 had a marked reduction in the frequency of transient ischemic episodes and an increased in platelet survival (2.6 +/- 0.16 to 3.1 +/- 0.22 days; P less than 0.01) was observed in all patients. Three patients had no benefit from sulfinpyrazone and alteration of platelet survival did not occur. Results suggest that platelet survival is shortened in patients with transient cerebral ischemia, that sulfinpyrazone increases platelet curvival and may decrease the frequency of ischemic episodes, and that there may be a relationship between clinical benefit and alteration of platelet survival time.
Stroke
PMID:Effect of sulfinpyrazone on platelet survival time in patients with transient cerebral ischemic attacks. 87 Oct 29

Cephalocervical or intracranial fibromuscular dysplasia (FMD) can be identified by its characteristic angiographic appearance. Most of these lesions occur adjacent to the C1-2 interspace, characteristically sparing the origins and proximal segments of the major extracranial vessels. Approximately 65% of our patients had bilateral involvement of the cervical internal carotid arteries. Thirty percent were associated with one or more intracranial aneurysms. The vertebral arteries were involved in 10% of the cases. Twenty-four of 25 cases were associated with symptoms of either subarachnoid hemorrhage or focal cerebral ischemia.
Stroke
PMID:Angiographic spectrum of cervical and intracranial fibromuscular dysplasia. 90 63

It is widely accepted that transient cerebral ischemia and permanent stroke frequently are caused by platelet and thrombotic cerebral emboli that originate from lesions at the carotid bifurcation. Microembolization from ulcerated atheroma during carotid dissection also offers a logical explanation for the incidence of intraoperative neurologic deficits during carotid endarterectomy. The risk of intraoperative embolization is obvious when ulcers are macroscopic; but focal cerebral ischemia associated with atheroma that appear smooth and nonulcerated usually has been attributed to decreased regional cerebral blood flow. Several endarterectomy specimens were submitted for scanning electron microscopic evaluation using X20 through X4,000 malignification. Results indicate that carotid atheroma may contain superficial ulcerations and thrombi that are not appreciated by direct inspection or conventional microscopic techniques. Electron microscopic ulcerations and intraluminal thrombi may be responsible for embolic transient ischemic attacks, spontaneous strokes, and intraoperative neurologic deficits in patients in whom gross ulcerations are absent.
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PMID:Ultramicroscopic ulcerations and thrombi of the carotid bifurcation. 92 36

Controlled cerebral ischemia was produced in rabbits by bilateral occlusion of the common carotid arteries and restriction of collateral blood flow by a decrease of the systemic arterial pressure to a desirable level (by hemorrhage into a pressurized reservior system). The following circulatory parameters were simultaneously monitored: systemic arterial pressure (SAP), pressure in the circle of Willis (Pcw), systemic venous pressure (SVP), and pressure in the sagittal venous sinus of brain (Pvs). The cerebral blood flow (CBF) was measured by means of the H2-clearance method, and the brain volume (BrV) changes were evaluated with a mechanical system of the sterotaxic device. It has been concluded that the pre-edematous changes in the brain tissue arise during deep ischemis but an important factor in the brain edema development is the recovery of the CBF with and increase of the intravascular pressure closely related to the brain blood volume augmentation. The latter may be pronouced because of diminution of the blood outflow from the brain when the SVP is increased. The compensation for the BrV increase (caused either by brain blood volume augmentation or by brain edema) is obtained by Pcw decrease probably due to resistance rise in the internal carotid and vertebral arteries. The brain edema may be additionally compensated by an active decrease of the systemic arterial pressure.
Stroke
PMID:Mechanisms of postischemic brain edema: contribution of circulatory factors. 96 Jan 63

A series of 58 operations on 56 patients, in whom a branch of the superficial temporal artery was anastomosed to a branch of the middle cerebral artery (STA-MCA bypass or Yasargil procedure), is reviewed. These operations were performed chiefly for occlussions or for inaccessible stenotic lesions of the internal carotid or middle cerebral arteries. Patency in eight patients operated on from April 1971 through November 1973 was low (25%). Patency in patients operated on since July 1974 has been high (95%). There have been no deaths and no major ischemic strokes attributable to the surgery. The rationale for this procedure is considered in relationship to the anatomy and physiology of the cerebral circulation and the pathogenesis of syndromes of cerebral ischemia. The operation appears to have a low morbidity in good-risk patients. The role of this operation in managing common manifestations of cerebral vascular disease such as focal transient cerebral ischemic attacks (TIAs) and amaurosis fugax, although not fully established, appears encouraging. The procedure seems useful for orthostatic cerebral ischemia caused by multiple occlusions of major extracranial (and intracranial) vessels and, occasionally, for progressing strokes related to internal carotid artery occlusion, both of which are relatively uncommon manifestations of cerebral vascular occlusive disease. It may have application in the rare "slow stroke." The procedure is probably of limited value, if any, in the management of large completed infarcts but may be indicated in selected patients with small infarctions who have preserved most of their cerebral function and who have had evidence of subsequent focal ischemic events. The procedure is useful for bypassing giant aneurysms or basofrontal tumors invading major vessels. It may have a role in the management of fibromuscular disease of the internal carotid artery.
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PMID:Bypass surgery for vascular disease of the carotid system. 99 50

Some patients who have transient ischemic attacks are denied operation because severe occlusive lesions in other extra-cranial arteries may be inappropriately interpreted as constituting an unacceptable surgical risk, or because the lesion is so distal as to make its removal hazardous. Failure of endarterectomy is usually due to incomplete removal of the lesion or to thrombosis upon the frayed intima. Such lesions require excellent visualization and meticulous surgical technique -- not always possible with a shunt. Among 130 consecutive carotid endarterectomies performed under general anesthesia, EEG changes consistent with cerebral ischemia appeared in only nine (7%). These patients required a shunt. In 11 patients normal EEG tracings were obtained during endarterectomy despite contralateral carotid occlusion. None of these patients had a neurological deficit. Continuous EEG monitoring is a reliable method of detecting changes in cerebral perfusion, permits a more meticulous endarterectomy in high-lying lesions without a shunt, and extends operability in high risk patients. Angiographical findings may be an unreliable predictor concerning risk of endarterectomy.
Stroke
PMID:EEG surveillance as a means of extending operability in high risk carotid endarterectomy. 100 27

Cyclandelate, a vasodilator, was administered to 24 patients with dementia. The dementia in these patients was presumed to be due to cerebral ischemia caused by atherosclerosis in cerebral vessels after other possible causes were ruled out. In a double-blind, cross-over study, patients received 200 mg of cyclandelate four times daily for six weeks and a placebo for six weeks. Six psychological tests, which reflect various aspects of higher cortical ability, were used to evaluate the effect of cyclandelate on the dementia. Cyclandelate was found to be no more effective than placebo in improving higher cortical function in these demented patients.
Stroke
PMID:Effect of cyclandelate on dementia. 110 57

Acute occlusion of the left middle cerebral artery (MCA) was accomplished without anesthesia and inside an intact cranium containing cerebrospinal fluid (CSF) in ten cats five to nine days after implantation of an occlusive device through the orbit. Immediate neurological deficits included forced ambuxlation, circling, and tonic deviation of the head and neck toward the side of the occluded artery; weakness of the opposite limbs; and an apathetic or akinetic state. Two cats died within 24 hours. The other eight cats improved but secondary deficits developed in two, causing death. In two of the remaining six cats no deficits were apparent seven days later. The cerbral infarcts regularly involved the basal ganglia, internal capsule, and cortical regions, and were larger and less variable than those produced by MCA occlusion through and open optic foramen or craniectomy with cranial decompression by drainage of CSF. This model of acute focal cerebral ischemia may be of value for studies of physiological and biochemical factors uninfluenced by sedatives, anesthesia, or recent surgical procedures.
Stroke
PMID:Immediate effects of cerebral ischemia: evolution and resolution of neurological deficits after experimental occlusion of one middle cerebral artery in conscious cats. 115 69


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