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

We experienced a patient with acute thrombosis of the unilateral internal carotid artery. We monitored the brain tissue temperature and intracranial pressure not only in both hemispheres simultaneously but also continuously throughout the process of brain death. The patient was a 73-year-old male who presented to our emergency room with right hemiparesis and aphasia. On admission to our department, no specific pathological findings were identified by brain CT. However a following investigation with left carotid arteriogram demonstrated a complete occlusion of the left internal carotid artery. Probes to monitor intraparenchymal temperature (Tip) and intracranial pressure(ICP) were inserted surgically into the bilateral hemispheres, and these two parameters were monitored continuously until the patient's death. Initially, Tip in the infarcted hemisphere was lower than that in the intact hemisphere, and the left hemisphere's ICP was significantly higher than that of the right one. When the ICP in the left hemisphere exceeded 40 mmHg, bilateral ICPs became equal. Brain herniation was confirmed when the ICP became progressively elevated thereafter. Subsequently the bilateral Tips became equal and lower than the bladder temperature following the brain herniation. In this case, we successfully monitored two parameters while the patient was in the process of brain death; i.e., brain ischemia, complete loss of brain circulation and subsequent decrease in the brain tissue temperature.
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PMID:[Neuromonitoring of acute internal carotid artery occlusion]. 1100 83

Acute incomplete brain ischemia in rats was induced by bilateral carotid artery occlusion(BCAO). BCAO results in severe suppression of EEG and increase of brain water content. Left middle cerebral artery occlusion(MCAO) in rats by electrical coagulation results in increase of brain water content of ipsilateral hemisphere and contralateral hemiparesis. The typical ischemic neuropathological damage emerges in both BCAO and MCAO models. Intraperitoneal injection of puerarin significantly helps improve all these brain ischemic disturbances.
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PMID:[Protective effect of puerarin on acute cerebral ischemia in rats]. 1124 76

Clinical trials for ischemic stroke have been characterized by a disappointing series of negative results, using a panoply of pharmacologic agents. This paper emphasizes five physiologic measures that can be taken to mitigate ischemic brain damage. These are (1) hypothermia, (2) insulin, (3) arterial hyperoxemia, (4) blood pressure control and (5) magnesium. Hypothermia is protective in both focal and global ischemia, even postischemically protecting against selective neuronal necrosis and infarction. The total equation for protection includes the (i) postischemic delay, (ii) depth, and (iii) duration of hypothermia. Insulin operates by lowering glucose levels to the normal range in focal ischemia. It is possible that very low glucose levels are detrimental in focal ischemia with paradoxical augmentation of the infarct size, and that spreading depression plays a role in this. Controlled arterial hyperoxemia seems effective experimentally in reducing infarct size, operating mechanistically by either a direct effect of oxygen, or vasoconstriction causing shunting of blood into the infarct, or both. Blood pressure is a critical determinant of infarct size, and raising blood pressure improves collateral blood flow and reduces stroke size. To be used clinically, however, hemorrhage must be ruled out. The most dramatic clinical effects of blood pressure are seen in aneurysm patients with vasospasm, where minor increases in blood pressure reverse temporary hemiparesis by reducing ischemia. Magnesium is likely the safest NMDA antagonist, with a long history of safe administration to pregnant women with eclampsia. There is potential interaction with insulin, in that magnesium causes hyperglycemia, which requires insulin to counteract it. Magnesium and insulin together have been shown effective in experimental brain ischemia. In the absence of safe and effective pharmacologic neuroprotection agents, clinical trials should be designed and launched to test these physiologic measures, singly and in combination, to reduce brain damage after ischemia.
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PMID:Non-pharmacologic (physiologic) neuroprotection in the treatment of brain ischemia. 1146 80

A 35-year-old male presented with basilar artery vasculitis secondary to sphenoid sinusitis manifesting as rapidly deteriorating symptoms including consciousness disturbance and right hemiparesis. Computed tomography (CT) on admission showed sphenoid sinusitis without intracranial lesion. Emergency angiography demonstrated basilar artery stenosis. The neurological deterioration was considered to be caused by ischemia of the perforating arteries branching from the stenotic portion of the basilar artery. The patient was treated with urokinase infusion through a microcatheter just proximal to the stenosis 3 hours after the onset of the symptoms. His consciousness level and right hemiparesis markedly improved immediately after the procedure. Magnetic resonance (MR) imaging on day 5 revealed that extension of the sphenoid sinusitis into the prepontine cistern had formed an abscess which was attached to the clivus. The basilar artery was embedded in the abscess at the angiographic stenosis. Cerebrospinal fluid (CSF) analysis showed white blood cell count of 601/mm3 with 82% neutrophils, 89.2 mg/dl protein, and 31 mg/dl glucose. No causative organism in the CSF could be identified by smear or culture. Early MR imaging and CSF examination are recommended when patients present with both ischemic symptoms involving the basilar artery and opacification of the sphenoid sinus on CT to identify basilar artery vasculitis secondary to sphenoid sinusitis.
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PMID:Basilar artery vasculitis secondary to sphenoid sinusitis--case report. 1159 74

We report a 12-year-old child with episodes of migraine-like headaches with visual and motor auras a year after the surgical resection and radiation therapy for medulloblastoma The patient presented with an episode of headache, prolonged aphasia, right hemiparesis, status epilepticus, and salt wasting. There was no evidence of a structural lesion. The neurologic deficits resolved over a period of 6 weeks. Because of the progressive deterioration in neurologic deficits, the patient underwent an extensive battery of laboratory tests and multiple neuroimages, all of which were normal. The unusually prolonged neurologic deficit in this patient without demonstrable structural lesions and his eventual complete recovery were most likely caused by ischemia in the left hemisphere secondary to vasospasm. This presentation mimics migraine headache. Evidence suggesting that this represents a long-term complication of treatment of children with central nervous system neoplasia is presented.
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PMID:Pseudomigraine with prolonged aphasia in a child with cranial irradiation for medulloblastoma. 1195 86

We report a case of bilateral internal carotid artery (ICA) stenosis treated with stenting. A 78-year-old man suffered from vascular dementia and left hemiparesis, and, by magnetic resonance angiogram (MRA), was diagnosed as having bilateral ICA stenosis. Cerebral angiogram showed severe, bilateral ICA stenosis (right; 88%, left; 93%) and xenon single photon emission tomography (SPECT) showed severely decreased cerebral blood flow (CBF) and cerebrovascular reactivity (CVR). We performed bilateral carotid angioplasty with self-expanding stents. Both CBF and CVR were improved bilaterally after the operation. The patient was discharged without neurological deficits. Carotid stenting may be an alternative treatment for severe ischemia caused by severe, bilateral ICA stenosis.
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PMID:[Bilateral carotid stenting for bilateral carotid artery stenosis improved vascular dementia]. 1213 74

The authors report a rare case in which a large cerebral arteriovenous malformation (AVM) located in the left parietooccipital region presented with venous ischemia in the contralateral hemisphere. A 74-year-old man was admitted to the hospital because he was experiencing a loss of appetite, disorientation, and left hemiparesis. Computerized tomography scans revealed a low-density area in the right temporal lobe. Angiography demonstrated a large AVM in the left parietooccipital lobe and dilation, stagnation, and meanders of cortical veins in the contralateral hemisphere. The authors speculated that the elevated sinus pressure caused by a huge venous return of blood from the AVM produced venous ischemia in the contralateral hemisphere.
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PMID:Large cerebral arteriovenous malformation presenting with venous ischemia in the contralateral hemisphere. Case report. 1240 94

A 58-year-old male presented with a dissecting aneurysm of the basilar artery manifesting as dysarthria, left hemiparesis, and numbness of the left side. Angiography revealed a double lumen at the midportion of the basilar artery which was consistent with a diagnosis of dissecting basilar artery aneurysm. The patient was treated conservatively, and remained neurologically stable for a 5-year period following initial presentation, but serial magnetic resonance imaging revealed growth of the aneurysm compressing the brain stem. His condition then worsened. Computed tomography revealed obstructive hydrocephalus. Ventriculoperitoneal shunting was performed and the patient's symptoms improved. However, he died of subarachnoid hemorrhage. Autopsy showed the patient had had a type 3 "dolichoectatic dissecting aneurysm." Surgical treatment should be seriously considered for treating the patients with dissecting basilar artery aneurysm causing brain stem ischemia, especially if the aneurysm is growing. High-flow bypass and proximal occlusion may be the choice in patients with poor collateral circulations.
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PMID:Dissecting basilar artery aneurysm growing during long-term follow up--case report. 1251 29

NS-7 is a novel, voltage-dependent Na(+) and Ca(2+) channel blocker. This study evaluated the in vivo neuroprotective effect of NS-7 in a rat transient focal ischemic model when administered during occlusion. Left middle cerebral artery occlusion was induced in adult male Sprague-Dawley rats for 120 min using an intraluminal thread method. The rats received a single intravenous injection of NS-7 or saline (control group) just after the onset of ischemia, and at 30, 60 and 120 min after ischemia. Their brains were removed after 48 h reperfusion, sectioned, and stained with hematoxylin and eosin. Animals were evaluated by neurological examination at 120 min ischemia and 48 h reperfusion. Infarcted cortex and striatum were measured quantitatively and infarction volumes were calculated. Cortical infarction volumes were 128+/-74 (NS-7) and 214+/-64 mm(3) (control) immediately after the ischemia group, 155+/-48 (NS-7) and 225+/-12 mm(3) (control) after the 30 min group, 160+/-54 (NS-7) and 225+/-48 mm(3) (control) after the 60 min group, and 176+/-43 (NS-7) and 223+/-38 mm(3) (control) after the 120 min group. Cortices in NS-7-treated groups were significantly less infarcted than in control groups at all treatment times. There was no significant difference in the striatal infarction volume between the treatment and control groups. Neurological examination showed that hemiparesis and abnormal posture of the NS-7 groups were significantly more improved at 48 h reperfusion than those of the control groups without posture examination in the 120 min group. These observations suggest that NS-7 may be a new potential therapeutic agent for the acute phase of cerebral infarction.
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PMID:Neuroprotective effect of NS-7, a novel Na+ and Ca2+ channel blocker, in a focal ischemic model in the rat. 1267 77

A 76-year-old man with left internal carotid artery occlusion developed a progressing right hemiparesis. Brain MRI presented reinfarctions in the left anterior border zone and terminal zone in the left deep white matter. Ambulatory blood pressure monitoring showed a decrease in systolic blood pressure by more than 20 mmHg one hour after starting meals, which is considered as postprandial hypotension. The recurrent stroke occurred probably by a hemodynamic mechanism with the presence of internal carotid artery occlusion and postprandial hypotension. Administration of voglibose, an alpha-glucosidase inhibitor, improved postprandial hypotension. In patients with severe carotid or intracranial artery disease, the postprandial hypotension should be carefully monitored for prevention of hemodynamic brain ischemia.
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PMID:[A case of hemodynamic brain infarction with postprandial hypotension]. 1273 87


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