When the left brain is not right the right brain may be left: report of personal experience of occipital hemianopia.
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OBJECTIVES: To make a personal report of a hemianopia due to an occipital infarct, sustained by a professor of neurology. METHODS: Verbatim observation of neurological phenomena recorded during the acute illness. RESULTS: Hemianopia, visual hallucinations, and non-occipital deficits without extraoccipital lesions on MRI, are described and discussed. CONCLUSIONS: Hemianopia, due to an occipital infarct, without alexia, is not a disability which precludes a normal professional career. Neurorehabilitation has not been necessary. (+info)
Neuronal nitric oxide synthase activation and peroxynitrite formation in ischemic stroke linked to neural damage.
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Nitric oxide (NO) is a new intercellular messenger that occurs naturally in the brain without causing overt toxicity. Yet, NO has been implicated as a mediator of cell death in cell death. One explanation is that ischemia causes overproduction of NO, allowing it to react with superoxide to form the potent oxidant peroxynitrite. To address this question, we used immunohistochemistry for citrulline, a marker for NO synthase activity, and 3-nitrotyrosine, a marker for peroxynitrite formation, in mice subjected to reversible middle cerebral artery occlusion. We show that ischemia triggers a marked augmentation in citrulline immunoreactivity but more so in the peri-infarct than the infarcted tissue. This increase is attributable to the activation of a large population (approximately 80%) of the neuronal isoform of NO synthase (nNOS) that is catalytically inactive during basal conditions, indicating a tight regulation of physiological NO production in the brain. In contrast, 3-nitrotyrosine immunoreactivity is restricted to the infarcted tissue and is not present in the peri-infarct tissue. In nNOS(Delta/Delta) mice, known to be protected against ischemia, no 3-nitrotyrosine immunoreactivity is detected. Our findings provide a cellular localization for nNOS activation in association with ischemic stroke and establish that NO is not likely a direct neurotoxin, whereas its conversion to peroxynitrite is associated with cell death. (+info)
Carotid disease in acute stroke.
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BACKGROUND: the Oxfordshire Community Stroke Project (OCSP) devised a simple clinical classification for acute stroke which predicted mortality, functional recovery and patterns of recurrent stroke. We aimed to determine whether this could predict the presence of carotid disease and be used to select which patients with acute stroke should be referred for carotid imaging with a view to subsequent carotid endarterectomy. METHODS: we assessed patients with acute stroke admitted to seven hospitals over a 10-month period. Patients were classified according to the OCSP system and their carotid arteries investigated using portable continuous wave Doppler. Those with abnormal portable assessments had colour duplex Doppler imaging. RESULTS: of 305 patients with proven or probable cerebral infarction, severe (70-99%) ipsilateral carotid stenosis was found in 16 (16%) of the 101 with partial anterior circulation infarct (PACI), four (4%) of the 100 with total anterior circulation infarct (TACI), none of the 80 with lacunar infarct (LACI) and one (4%) of the 24 with posterior circulation infarct (POCI). Complete ipsilateral carotid occlusion was found in 25 (25%) of the TACI group, 11 (11%) of the PACI group, three (4%) of the LACI group and none of the POCI group. Severe carotid stenosis or occlusion was more common in the ipsilateral than the contralateral carotid artery for the TACI and PACI groups (chi2 P< 0.05), but there was no difference between ipsilateral and contralateral carotid disease in the LACI and POCI groups. If the OCSP classification is used to detect patients with 70-99% carotid stenosis, then the sensitivity is 76% and specificity is 70%. CONCLUSION: these findings suggest that ipsilateral carotid disease is an important cause of stroke for those with anterior circulation infarcts but not for those with LACI or POCI. Subjects with PACI should be referred for early carotid imaging to identify those with severe disease who may be suitable for elective carotid surgery. (+info)
Blockade of the mitochondrial permeability transition pore diminishes infarct size in the rat after transient middle cerebral artery occlusion.
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The mitochondrial permeability transition pore is an inducer of cell death. During the reperfusion phase after cerebral ischemia, calcium accumulates in mitochondria, and a burst of free radical formation occurs, conditions that favor the activation of the mitochondrial permeability transition pore. Here the authors demonstrate that a blocker of the mitochondrial permeability transition pore, the nonimmunosuppressive cyclosporin A analogue N-methyl-Val-4-cyclosporin A (10 mg/kg intraperitoneally), administered during reperfusion and at 24 hours of reperfusion, diminishes infarct size in a rat model of transient focal ischemia of 2 hours' duration. The mitochondrial permeability transition pore may be an important target for drugs against stroke. (+info)
Neuronal protection in stroke by an sLex-glycosylated complement inhibitory protein.
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Glycoprotein adhesion receptors such as selectins contribute to tissue injury in stroke. Ischemic neurons strongly expressed C1q, which may target them for complement-mediated attack or C1qRp-mediated clearance. A hybrid molecule was used to simultaneously inhibit both complement activation and selectin-mediated adhesion. The extracellular domain of soluble complement receptor-1 (sCR1) was sialyl Lewis x glycosylated (sCR1sLex) to inhibit complement activation and endothelial-platelet-leukocyte interactions. sCR1 and sCR1sLex colocalized to ischemic cerebral microvessels and C1q-expressing neurons, inhibited neutrophil and platelet accumulation, and reduced cerebral infarct volumes. Additional benefit was conferred by sialyl Lewis x glycosylation of the unmodified parent sCR1 molecule. (+info)
Necrotizing mycotic vasculitis with cerebral infarction caused by Aspergillus niger in a horse with acute typholocolitis.
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An 18-year-old Morgan mare was presented to the Veterinary Medical Teaching Hospital, University of Illinois, with a 10-day history of watery diarrhea, depression, and dysphagia. On admission, the animal was severely dehydrated, depressed, and unable to swallow and had no clinical signs of diarrhea. The respiratory and heart rate and body temperature were within normal limits. Following fluid therapy, the mare developed severe watery diarrhea and continued to be depressed, incoordinated, and dysphagic. The animal died on the fourth day after admission and was sent to the Laboratories of Veterinary Diagnostic Medicine for necropsy. Gross postmortem findings were consistent with an acute cerebral infarction in the right cerebral hemisphere, an acute necrotizing typhlocolitis, multifocal petechial and ecchymotic hemorrhages, enlarged and congested pars intermedia of the pituitary gland, and marked bilateral adrenocortical hyperplasia with multifocal areas of necrosis and hemorrhage. Histologic evaluation of the affected brain demonstrated an area of coagulative necrosis of the gray matter, with hemorrhage, vasculitis, and thrombosis. There were many fungal hyphae 3.5-6.0 microm, pale basophilic, septate, and occasionally branching at 45 degrees present in the arterial walls and throughout the necrotic tissue. Immunohistochemical analysis revealed Aspergillus niger as the etiologic agent responsible for the mycotic vasculitis and infarction in the brain. Bacteria culture and immunohistochemical staining of the colon and cecum failed to demonstrate specific pathogens. (+info)
Homocyst(e)ine and risk of cerebral infarction in a biracial population : the stroke prevention in young women study.
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BACKGROUND AND PURPOSE: Genetic enzyme variation and vitamin intake are important determinants of blood homocyst(e)ine levels. The prevalence of common genetic polymorphisms influencing homocyst(e)ine levels varies by race, and vitamin intake varies by socioeconomic status. Therefore, we examined the effect of vitamin intake, race, and socioeconomic status on the association of homocyst(e)ine with stroke risk. METHODS: All 59 hospitals in the greater Baltimore-Washington area participated in a population-based case-control study of stroke in young women. One hundred sixty-seven cases of first ischemic stroke among women aged 15 to 44 years were compared with 328 controls identified by random-digit dialing from the same region. Risk factor data were collected by standardized interview and nonfasting phlebotomy. Plasma homocyst(e)ine was measured by high-performance liquid chromatography and electrochemical detection. RESULTS: Blacks and whites did not differ in median homocyst(e)ine levels, nor did race modify the association between homocyst(e)ine and stroke. After adjustment for cigarettes per day, poverty status, and regular vitamin use, a plasma homocyst(e)ine level of >/=7.3 micromol/L was associated with an odds ratio for stroke of 1.6 (95% CI, 1.1 to 2.5). CONCLUSIONS: The association between elevated homocyst(e)ine and stroke was independent not only of traditional vascular risk factors but also of vitamin use and poverty status. The degree of homocyst(e)ine elevation associated with an increased stroke risk in young women is lower than that previously reported for middle-aged men and the elderly and was highly prevalent, being present in one third of the control group. (+info)
Measurement of initial N-acetyl aspartate concentration by magnetic resonance spectroscopy and initial infarct volume by MRI predicts outcome in patients with middle cerebral artery territory infarction.
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BACKGROUND AND PURPOSE: (1)H MR spectroscopy can be used to study biochemical changes occurring in the brain in stroke. We used it to examine the relationship between metabolite concentration (N-acetyl aspartate [NAA], lactate, cholines and creatines), size of infarct, clinical deficit, and 3-month clinical outcome in patients with middle cerebral artery (MCA) territory infarction. METHODS: Thirty-one patients with acute MCA territory infarction were recruited within 72 hours of the onset of symptoms. Single-voxel short echo time stimulated echo acquistion mode spectroscopy was used to obtain metabolite data from the infarct core. Metabolite concentrations were determined with use of variable projection time domain-fitting analysis. Infarct size was determined with T2-weighted images. Patient outcome groups at 3 months were "independent," "dependent," or "dead." RESULTS: All patients (100%; 95% CI 75% to 100%) who had an infarct >70 mL did poorly. Eighteen of 20 patients (90%; 95% CI 68% to 99%) with a core NAA concentration <7 mmol/L did poorly at 3 months, whereas 7 of 11 patients (64%; 95% CI 31% to 89%) with an initial NAA concentration >7 mmol/L did well. Combining these results showed that all patients who had an initial infarct volume >70 mL did poorly, irrespective of the NAA concentration. Of those patients with infarcts <70 mL, those who had a core NAA concentration >7 mmol/L did well (88%; 95% CI 47% to 100%), whereas those with a lower NAA concentration did poorly (80%; 95% CI 44% to 97%). There was no association between other metabolite concentrations and outcome. CONCLUSIONS: Infarct volume and NAA concentration can together predict clinical outcome in MCA infarction in humans. (+info)