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PubMed1990

[Course of recovery from motor aphasia in four patients with localized lesions in the vicinity of Broca's area].

The neuropsychological signs and prognosis of patients with localized lesions in the vicinity of Broca's area of the left inferior frontal gyrus have been controversial. We studied periodic changes in the neuropsychological signs of four patients who had relatively localized lesions in the vicinity of Broca's area and manifested aphasia of the non-fluent type. The ages of the four patients at the onset were 62, 66, 30 and 37 years. The localized lesions in their brains were the result of brain infarctions revealed by CT scans, and included so-called Broca's center in the left inferior frontal gyrus along with adjacent brain tissue. The neuropsychological signs of the four patients were periodically assessed by means of the standard language test of aphasia (SLTA). In the early stage of aphasia, they had moderate difficulties in speaking to explain test materials or recall words and mild difficulties in reading aloud, repeating and writing words. One year later, most of their neuropsychological signs disappeared except for mild difficulties in speaking fluently and recalling words. It should be noted, however, that all four patients were able to return to their previous occupations one or two years later, because they had recovered from aphasia. Based on the results of this study, we conclude that the neuropsychological signs of Broca's aphasia caused by relatively localized lesions in the left inferior frontal gyrus are mild and largely disappear within one or two years.

Adult↗

PubMed2006

Aprotinin to improve cerebral outcome after hypothermic circulatory arrest: a study in a surviving porcine model.

BACKGROUND: Aprotinin is a serine protease inhibitor, which is usually used during cardiac surgery to reduce blood loss. There is evidence that aprotinin has neuroprotective effects during ischemia. We planned this study to evaluate its potential neuroprotective efficacy during hypothermic circulatory arrest (HCA). METHODS: Twenty piglets with a median weight of 25.7 kg (interquartile range, 23.9-26.6) were randomly assigned to receive aprotinin or placebo prior to a 75-minute period of HCA at 18 degrees C. Brain microdialysis parameters and neurological and histological scores were the primary outcome measures. RESULTS: Changes in brain metabolic parameters and histopathological findings were favorable in the aprotinin group. Brain lactate concentrations were significantly lower in the aprotinin group during the experiment (P = .02) along with blood lactate concentrations in the aprotinin group (P = .023). Brain glucose was significantly higher during the experiment (P = 0.02). Intracranial pressure tended to be higher in the control group. Two of 10 animals in the aprotinin group and 4 of 10 in the control group failed to reach full recovery on the seventh postoperative day. Four animals of 10 in the aprotinin group and 6 animals of 10 in the control group had brain infarction (P = .40). CONCLUSIONS: The present data suggest that aprotinin mitigates cerebral damage and improves neurological outcome following a period of HCA.

Animals↗

PubMed2001

Connexin43 null mutation increases infarct size after stroke.

Glial-neuronal interactions have been implicated in both normal information processing and neuroprotection. One pathway of cellular interactions involves gap junctional intercellular communication (GJIC). In astrocytes, gap junctions are composed primarily of the channel protein connexin43 (Cx43) and provide a substrate for formation of a functional syncytium implicated in the spatial buffering capacity of astrocytes. To study the function of gap junctions in the brain, we used heterozygous Cx43 null mice, which exhibit reduced Cx43 expression. Western blot analysis showed a reduction in the level of Cx43 protein and GJIC in astrocytes cultured from heterozygote mice. The level of Cx43 is reduced in the adult heterozygote cerebrum to 40% of that present in the wild-type. To assess the effect of reduced Cx43 and GJIC on neuroprotection, we examined brain infarct volume in wild-type and heterozygote mice after focal ischemia. In our model of focal stroke, the middle cerebral artery was occluded at two points, above and below the rhinal fissure. Four days after surgery, mice were killed, the brains were sectioned and analyzed. Cx43 heterozygous null mice exhibited a significantly larger infarct volume compared with wild-type (14.4 +/- 1.4 mm(3) vs. 7.7 +/- 0.82 mm(3), P < 0.002). These results suggest that augmentation of GJIC in astrocytes may contribute to neuroprotection after ischemic injury.

Animals↗

PubMed1980

Cerebral embolism in Libman-Sacks endocarditis.

Left homonymous hemianopia, hemiparesis, left-body clonic seizures, and progressive deterioration of consciousness complicated the clinical course of a 57-year-old woman with systemic lupus erythematosus (SLE). Autopsy documented the presence of multiple brain infarcts and cerebral arterial emboli that originated from the verrucae of Libman-Sacks endocarditis. Clinicians and pathologists should consider this unusual vascular mechanism of cerebral injury in patients with SLE who develop strokes.

Brain↗

PubMed1998

Effects of mild hypothermia on the release of regional glutamate and glycine during extended transient focal cerebral ischemia in rats.

The present study is to determine the effect of mild hypothermia (MHT) on the release of glutamate and glycine in rats subjected to middle cerebral artery occlusion and reperfusion. The relationship between amino acid efflux and brain infarct volume was compared in different periods during MHT. Reversible middle cerebral artery occlusion was performed in Sprague-Dawley rats using a suture model. The rats were divided into four groups including (1) MHT during ischemia (MHTi), (2) MHT during reperfusion (MHTr), (3) MHT during ischemia and reperfusion (MHTi + r), and (4) a normothermic group (NT). Extracellular concentrations of glutamate and glycine in the cortex and striatum were monitored using in vivo microdialysis and analyzed using high-performance liquid chromatography. Morphometric measurements for infarct volume were performed using 2,3,5-triphenyltetrazolium chloride staining. The increase of glutamate and glycine in the ischemic cortex of the MHTi and MHTi + r rats during ischemic and reperfusion periods was significantly less than that of the NT rats (p < 0.05). However, there was no statistical difference among these groups in the peak of glutamate and glycine release in the striatum. Infarct volume paralleled the release of glutamate and glycine. The protective effect of MHTi and MHTi + r in reducing ischemia and reperfusion brain injury may be due to the attenuation of both glutamate and glycine release during ischemia and reperfusion.

Animals↗

PubMed2004

Prophylactic use of melatonin protects against focal cerebral ischemia in mice: role of endothelin converting enzyme-1.

Melatonin has previously been shown to be neuroprotective in rodent models of ischemic stroke. Herein, we tested whether this antioxidant may also be suitable for prophylactic use against stroke. To clarify this issue, melatonin was administrated orally for 9 wk (4 mg/kg/day) in mice and its effects on subsequent injury development after 90 min of intraluminal middle cerebral artery (MCA) occlusion were tested. To evaluate its neuroprotective properties, the protective actions of prophylactic melatonin were compared with both acute melatonin (4 mg/kg, i.p.) administration and with a diluent (sham)-treated control condition. MCA occlusion resulted in reproducible ischemia, as revealed by laser Doppler flowmetry; this was followed by a rapid restoration of blood flow immediately after reperfusion onset. Laser Doppler flow values after reperfusion onset were moderately elevated by melatonin, both when the indole was given prophylactically and when acutely administrated after stroke. In control animals, reproducible brain infarcts were observed 24 hr after reperfusion onset. Treatment with melatonin significantly reduced the infarct size by approximately 30-35%, independent of whether the indole was given prophylactically before or acutely after ischemia. To test whether brain protection involved vascular mechanisms, as suggested earlier, the effects of melatonin on endothelin converting enzyme-1 (ECE-1) levels were studied using Western blots. Interestingly, delivery of melatonin was accompanied by a marked inhibition of ECE-1 levels, which was similarly seen after both acute and chronic melatonin treatment. Our data suggest that melatonin, given at pharmacological doses, may be suitable as a prophylaxis against stroke. Tissue protection may involve an inhibition of ECE-1, which improves vasodilation, after ischemia.

Animals↗

PubMed2007

Reversible encephalopathy associated with cholesterol embolism syndrome: magnetic resonance imaging and pathological findings.

We describe a patient found to have acute diffuse and reversible encephalopathy on magnetic resonance imaging (MRI) associated with cholesterol emboli syndrome (CES). The initial MRI showed extensive white matter, basal ganglia and cortical damage without evidence of brain infarction. Dramatic clinical and MRI improvement was observed with corticosteroids. Pathologically, cholesterol crystal emboli were found in the lumen of skin and brain arteries and were associated with varying degrees of inflammation of the arteriole wall. This case suggests that CES may be responsible for extensive, acute and reversible encephalopathy underlined by an inflammation of brain arteries.

Acute Disease↗

PubMed1992

Cerebral infarction in a child. A case report.

Cerebral infarcts in children are rather rare and in most cases no precise etiology is established. The authors describe a case of cryptogenetic cerebral infarction in a 9-year-old boy. The child presented an acute onset of hemiplegia in the right arm and leg, central facial palsy, dysarthria and steppage. The infarction was proved by Computed Tomography (CT) and Magnetic Resonance Imaging (MRI). Laboratory and instrumental studies rule out all known causes of brain infarction. The only possible etiopathogenetic hypothesis was a varicella arteritis which occurred 45 days before the clinical manifestation.

Arteritis↗

PubMed1993

Altered cerebral hemodynamics and metabolism in Takayasu's arteritis with neurological deficits.

BACKGROUND AND PURPOSE: Takayasu's arteritis is a nonspecific arteritis involving major cerebral arteries. The aim of our study is to examine cerebral hemodynamics and metabolism in Takayasu's arteritis with neurologic symptoms. METHODS: We measured cerebral blood flow and metabolism using positron emission tomography in seven patients (14 to 59 years of age) with Takayasu's arteritis who developed transient ischemic attacks (2 patients), ischemic stroke (4) or putaminal hemorrhage with multiple brain infarction (1). RESULTS: All patients had severe stenosis or occlusion of one or more major cerebral arteries. There were no significant differences in the values of cerebral blood flow, oxygen extraction fraction, and cerebral blood volume in the infarcted and noninfarcted hemisphere. By contrast, the value of cerebral metabolic rate for oxygen in the infarcted hemisphere was markedly reduced (1.87 mL/100 mL per minute, P < .01) compared with controls. Mean transit time in the infarcted hemisphere was significantly greater than in the noninfarcted one, both in patients and controls (P < .01 and P < .05, respectively). CONCLUSIONS: Collateral blood flow to the hemisphere without brain damage may be relatively well developed in Takayasu's arteritis, although hemodynamic reserve as well as oxygen metabolism were impaired in the infarcted hemisphere with ischemic lesions.

Adolescent↗

PubMed2001

Ischemic stroke of unusual cause: clinical features, etiology and outcome.

The clinical features, etiology and neurological outcome of ischemic stroke of unusual cause (ISUC) have rarely been reported. We retrospective reviewed all patients with this stroke subtype entered in the Sagrat Cor Hospital of Barcelona Stroke Registry, which includes data from 2000 consecutive first-ever stroke patients admitted to the hospital between 1986 and 1995. Patients with previous ischemia and/or hemorrhagic stroke were excluded. Topographic, anamnestic, clinical and neuroimaging characteristics of ISUC were assessed. Predictors of this stroke subtype were determined by logistic regression analysis. Ischemic stroke of unusual etiology was diagnosed in 70 patients (32 men and 38 women), with a mean +/- SD age of 52 +/- 22.4 years. This stroke subtype accounted for 4.3% of all first-ever strokes and 6% of all first-ever brain infarcts. Etiologies included hematological disorders in 17 cases, infection in 11, migraine stroke in 10, cerebral infarction secondary to venous thrombosis in nine, primary inflammatory vascular conditions in six and miscellaneous causes in 17. In the multivariate analysis after excluding cerebral venous thrombosis (n = 9) and arterial dissection (n = 4), because of typical clinical and radiological features, independent predictors of ISUC included 45 years of age or less (odds ratio [OR] 14.8), seizures (OR 6.8), headache (OR 5.2), hemianopia (OR 2.6) and occipital lobe involvement (OR 3.0). Patients with ISUC presented a lower in-hospital mortality rate (7.1% vs. 14.4%; P < 0.05), were more frequently symptom free at discharge (35.7% vs. 25.80%; P < 0.05) and experienced a longer mean length of hospital stay (23.7 days vs. 18.2 days; P = 0.06) than non-ISUC patients. We conclude that ISUC is infrequent, etiologies are numerous and hematologic disorders are the most frequent cause. We emphasize the better prognosis and the need to distinguish it from other ischemic stroke subtypes which have a different treatment approach and outcome.

Adolescent↗

PubMed1997

Functional and metabolic analysis of cerebral ischemia using magnetoencephalography and proton magnetic resonance spectroscopy.

The details of the relationship between brain function and metabolism in brain infarcts have not been studied. Using magnetoencephalography (MEG) and proton magnetic resonance spectroscopic imaging (1H MRSI), we localized sources of abnormal magnetic activities in ischemic brain regions and biochemical changes in suspected lesions showing pathological characteristics. Twelve patients with ischemic stroke were examined and the results of MEG and 1H MRSI were superimposed onto the corresponding MR images. The signal intensities of N-acetyl (NA) and lactate (Lac) were measured in the lesions with highly concentrated dipoles of slow wave activity. Eleven of 12 cases had increased slow wave activity in the cortical areas adjacent to the infarcts; 1 case was excluded because the infarct was too small (<1 cm in diameter). The signal intensity of NA in the regions with the highest slow wave activity was significantly reduced and was well correlated with the dipole density of slow waves. Though Lac was mildly accumulated in the lesions, the Lac level had no correlation with slow wave magnetic activity. The remaining and metabolically active cortical tissue showing NA signal produced the abnormal slow wave activity under lactic acidosis (mild accumulation of Lac).

Adult↗

PubMed1994

[Arterial hypertension in the acute phase of cerebral infarction. Survey on the current practice in a university hospital].

PURPOSE: Evaluate current practice in a university hospital on management of high blood-pressure in patients in the acute phase of brain infarction (BI). METHODS: A case report of a lucid patient admitted 8 hours after onset of a BI with normal CT and high blood pressure (BP = 186/110 mmHg) was presented to staff members and resident physicians (departments of neurology and neurosurgery excluded). Responders were asked to decide as to the best therapeutic option: no treatment/reduction/elevation of BP. RESULTS: 27 of 44 responders (61%) considered BP reduction as the best treatment option. The same trend was observed among residents (16/27: 60%) and staff members (11/17: 65%); among surgeons (6/12: 50%) and clinicians (20/30: 67%). CONCLUSIONS: BP reduction in the hyperacute phase of BI may be harmful. This basic concept of BI management has not been adequately assimilated by physicians of our university hospital, including those recently graduated. The results of this study signal to the urgent need of a wide diffusion of current concepts on pathophysiology and treatment of BI. Organization of stroke units may contribute to better patient management, medical education and research.

Cerebral Infarction↗

PubMedDate not supplied

Ischemic stroke associated with anticardiolipin antibodies.

Anticardiolipin antibodies are a group of antiphospholipid autoantibodies seen primarily in patients with systemic lupus erythematosus and other autoimmune diseases. We report 3 patients, 2 without systemic lupus, who suffered ischemic brain infarction associated with these antibodies in the absence of detectable lupus anticoagulant activity. Anticardiolipin antibodies, possibly associated with a lupus anticoagulant-like thrombotic tendency, may be a newly recognized cause of ischemic stroke.

Adult↗

PubMed1993

Sequential neuronal and astrocytic changes after transient middle cerebral artery occlusion in the rat.

The temporal evolution and spatial distribution of ischemic cell injury was investigated after transient middle cerebral artery (MCA) occlusion. Male Wistar rats (n = 61) were subjected to 2 h of MCA occlusion induced by advancing a nylon monofilament into the right internal carotid artery. Animals were killed after different durations of reperfusion, ranging from 4 to 166 h (n = 6-11 for each group). Neuronal injury and astrocytic reaction were evaluated using hematoxylin and eosin (H & E) and glial fibrillary acidic protein (GFAP) immunohistochemistry, respectively. Eosinophilic neurons were detected at 4 h of reperfusion in the basal ganglia, and at 10 h of reperfusion in the cortex. Focal brain infarct developed by 46 h of reperfusion, both in the cortex and the basal ganglia, and the volume remained constant between 46 and 166 h of reperfusion. Significant differences in astrocytic reaction were detected between the lesion and the periphery of the lesion at reperfusion times from 46 to 166 h; GFAP staining decreased in the core of the lesion and increased in the peripheral areas. Our data suggest that, after 2 h of MCA occlusion, brain tissue progresses from isolated neuronal injury to infarct with a time course dependent on anatomical site; and astrocytic reactivity, expressed by GFAP staining, reflects the outcome of the ischemic injury.

Animals↗

PubMed1990

Isradipine in patients with acute ischaemic cerebral infarction. An overview of the ASCLEPIOS Programme.

Calcium-related mechanisms are an integral part of metabolic reactions during acute cerebral infarction. In an animal model of stroke, the calcium antagonist isradipine was shown to protect neurons against ischaemia. In order to improve the neurological and functional outcome of human stroke patients, a randomised, double-blind, placebo-controlled multicentre study was started in up to 600 patients with acute ischaemic brain infarction. Since early treatment is considered to be of great importance, patients must be recruited no more than 12 hours after stroke onset. Medical, ECG, laboratory, neurological and functional evaluations are conducted for up to 90 days after stroke.

Adult↗

PubMed2003

Interferon-beta blocks infiltration of inflammatory cells and reduces infarct volume after ischemic stroke in the rat.

The inflammatory response that exacerbates cerebral injury after ischemia is an attractive therapeutic target: it progresses over days and strongly contributes to worsening of the neurologic outcome. The authors show that, after transient ischemic injury to the rat brain, systemic application of interferon-beta (IFN-beta), a cytokine with antiinflammatory properties, attenuated the development of brain infarction. Serial magnetic resonance imaging (MRI) showed that IFN-beta treatment reduced lesion volume on diffusion-weighted MRI by 70% (P < 0.01) at 1 day after stroke. IFN-beta attenuated the leakage of contrast agent through the blood-brain barrier (P < 0.005), indicating a better-preserved blood-brain barrier integrity. Both control and IFN-beta-treated animals showed a similar degree of relative hyperperfusion of the lesioned hemisphere, indicating that neuroprotection by IFN-beta was not mediated by improved cerebral perfusion as assessed 24 hours after stroke onset. IFN-beta treatment resulted in an 85% reduction (P < 0.0001) in infarct volume 3 weeks later, as determined from T2-weighted MRI and confirmed by histology. This effect was achieved even when treatment was started 6 hours after stroke onset. Quantitative immunohistochemistry at 24 hours after stroke onset showed that IFN-beta almost completely prevented the infiltration of neutrophils and monocytes into the brain. Gelatinase zymography showed that this effect was associated with a decrease in matrix metalloproteinase-9 expression. In conclusion, treatment with the antiinflammatory cytokine IFN-beta affords significant neuroprotection against ischemia/reperfusion injury, and within a relatively long treatment window. Because IFN-beta has been approved for clinical use, it may be rapidly tested in a clinical trial for its efficacy against human stroke.

Animals↗

PubMed2001

Stroke prevention and treatment in sickle cell disease.

While the problem of stroke in the patients with sickle cell disease (SCD) has been known for more than 75 years, adequate preventive and treatment strategies are just now being tested. Recent data on prevalence and incidence have been obtained from the Cooperative Study of Sickle Cell Disease of more than 4000 patients with SCD observed in 23 US clinical centers over a 10-year period.1 The overall age-specific incidence of first stroke in SCD (homozygous sickle cell anemia) is low (0.13%) at ages younger than 24 months, increasing to just over 1% at ages 2 to 5 years, with only a slight decrement to 0.79% at ages 6 to 9 years. The risk of brain infarction declines until a second peak is seen at ages older than 50 years, when the incidence again increases to nearly 1.3%. Although intracranial hemorrhage does occur in young children with SCD, the risk is low compared with older children and adults. The Cooperative Study of Sickle Cell Disease reported risk factors for infarction to be prior transient ischemic attack, low steady-state hemoglobin values, and rate and recency of episodes of acute chest syndrome, as well as elevated systolic blood pressure. Risk factors for intracranial hemorrhage included low steady-state hemoglobin values and a high leukocyte count. The burden of cerebrovascular disease is even higher if subclinical magnetic resonance imaging (MRI) lesions, presumed to be ischemic, are included. The prevalence of such lesions is more than 22% in patients with SCD, and most of these patients have not reported symptoms, although specialized neuropsychological testing shows lower scores in children with silent lesions on MRI scans. Patients with a history of clinical stroke typically have infarcts in the cortex and deep white matter, whereas silent infarcts tend to be more limited to deep white matter. Common infarction patterns are characterized by wedge-shaped lesions of large-vessel territories; border zone infarctions, particularly of the middle and cerebral artery watershed region; and small punctate lesions of the deep white matter. Fat embolism to the brain and venous thromboses are encountered rarely.

Anemia, Sickle Cell↗

PubMed1997

Recurrent cerebral venous infarcts and superior vena cava obstruction: case report.

We report a patient with repeated venous infarcts in the occipital lobe and occlusion of the superior vena cava. The pathogenetic relationships between the superior vena cava occlusion and the brain infarcts are discussed. High pressure in the superior venous territory and incomplete patency of the transverse sinus are probably responsible for the venous infarcts.

Cerebral Infarction↗