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

In order to identify the brain lesions of symptomatic/cryptogenic partial epilepsies (S/CPEs) in infants and children, magnetic resonance imaging (MRI) studies, thorough encephalographic (EEGic) studies, and detailed clinical and neurologic evaluations were obtained in 300 infants and children who were diagnosed to have S/CPEs with onset before the age of 13 years during the past 7 years. The overall detection rate of brain lesions by MRI was 41.7% (125/300). Congenital malformations (18 cases), vascular malformations (9 cases), neurocutaneous syndromes (13 cases), and space-taking lesions (20 cases) constitute a large percentage of SPEs in infants and children. A variety of insults such as infection, ischemia, hemorrhage, trauma and metabolic disorders can result in destructive parenchymal loss lesions including porencephaly, focal atrophy, hemiatrophy, and diffuse brain atrophy (20 cases). Major etiologic factors leading to infarction, encephalomalacia, leukomalacia, included trauma, hvpoxicischemic encephalopathy (HIE), systemic lupus erythematosus (SLE), encephalitis, vasculitis, venous thrombosis, vasculopathies, and heart problems (22 cases). Mesial temporal sclerosis (MTS) could be evidenced in around 20% (18/95) of cases with temporal lobe epilepsy (TLE), which was strongly associated with past histories of febrile seizures and encephalitis complicated by status epileptics. However, cases with porencephaly, global atrophy or delayed myelination of unilateral temporal lobe on MRI were more related to HIE. With the advent of neuroimaging techniques, particularly MRI, a wide variety of underlying pathology can be detected as a cause of symptomatic partial epilepsies in pediatric patients. The occurrence of S/CPE indicates the presence of localized brain dysfunction, and many of the causes are potentially treatable. An orderly and thorough clinical and laboratory investigations, as well as neuroimaging studies should be made to diagnose and treat any underlying conditions.
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PMID:Magnetic resonance imaging in symptomatic/cryptogenic partial epilepsies of infants and children. 915 66

Small and large vessel occlusive disease leading to chronic cerebral ischemia and brain atrophy is a concept originating in the last century. The modern notion of acute brain infarct, however, appears to have eclipsed the idea of chronic hypoperfusion as an important factor in ischemic cerebral damage. We present a patient history featuring recurrent episodes of acute posterior circulation infratentorial ischemia in addition to a progressive cerebellar syndrome over a course of several years. Laboratory work-up including cerebral angiography, repeated CT and MR scanning revealed basilar artery occlusion, a pontine infarct and a subsequently developing cerebellar atrophy without signs of cerebellar infarction. Findings indicating causes of cerebellar atrophy other than ischemia could not be elicited. We offer the hypothesis that basilar artery occlusion, inducing subsequent chronic ischemia, is the most likely cause of the cerebellar atrophy observed in our case.
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PMID:Cerebellar atrophy with basilar artery occlusion. 942 61

Cerebral magnetic resonance imaging (MRI) has demonstrated a high prevalence of infarct-like lesions, white matter hyperintensities, and evidence of cerebral atrophy in older adults. While these findings are generally believed to be related to ischemia and atherosclerosis, their relationship to atherosclerosis in the carotid arteries remains to be explored. Study subjects were part of the multicenter Cardiovascular Health Study, a cross-sectional study of 3502 women and men >/=65 years of age undergoing cranial MRI and carotid ultrasonography. MRI infarcts were detected in 1068 participants (29.3%) and measurable carotid plaque in 2745 (75.3%). MRI infarcts, ventricular and sulcal widening, and white matter score were strongly associated with carotid intimal-medial thickness (IMT) and stenosis degree after adjustment for age and sex (all P<0. 01). Associations with plaque characteristics were less strong and less consistent; MRI infarcts were weakly associated only with surface irregularity, and ventricular size was weakly associated only with lesion density (both P<0.04). In contrast, sulcal widening was strongly related to plaque characteristics, with scores being higher in those with heterogeneous and irregular plaque (both P<0. 009). Adjustment for other risk factors, and for carotid IMT/stenosis, removed associations of MRI findings with plaque characteristics except for weak relationships remaining between MRI infarcts and surface irregularity and between sulcal score and heterogeneous plaque (both P<0.03). MRI abnormalities show strong and consistent relationships with increasing carotid IMT and stenosis degree but less strong associations with plaque characteristics, especially after adjusting for IMT and stenosis.
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PMID:Relationships of cerebral MRI findings to ultrasonographic carotid atherosclerosis in older adults : the Cardiovascular Health Study. CHS Collaborative Research Group. 997 19

Therapeutic result and pitfalls in the surgical treatment of cerebrovascular moyamoya disease are evaluated. During the recent 15 years, 268 patients with moyamoya disease have been treated in our clinic. Among them, 238 patients showed ischemic symptoms. Superficial temporal artery to middle cerebral artery anastomoses combined with temporal muscle grafting (encephalo-myo-synangiosis) were performed for most of the cases. Complete remission and clinical improvement were obtained in 34.0% and 64.2% of the patients, respectively. Symptomatic aggravation due to ischemic complication followed the operation in five patients (1.9%). Normocapnic control during general anesthesia with sufficient hydration is essential to avoid perioperative ischemic complications. Omental graft was performed in 16 patients. In 13 patients, omental graft was performed for the progressing ischemia in the posterior cerebral artery or anterior cerebral artery distribution. In the other three patients, omental graft was used for marked brain atrophy.
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PMID:Direct anastomotic bypass for cerebrovascular moyamoya disease. 1023 22

The aim of this study was to elucidate the neuropathological substrate of intestinal failure before and after small bowel transplantation (SBT). Retrospective analysis of complete autopsy or brain biopsy specimens of 17 patients with intestinal failure (12 children and 5 adults) were studied. Patients were divided into two groups. Group I (transplanted group; n = 13) included those patients who underwent intestinal transplantation under tacrolimus and steroids immunosuppressive therapy. Group II (control group) included 4 children with intestinal failure who were candidates for SBT and died while awaiting an intestinal allograft. Central nervous system (CNS) abnormalities were seen in 92% of the SBT recipients and in 100% of SBT candidates. The neuropathological lesions of SBT recipients included: (a) vascular lesions: global brain ischemia, infarcts, intracranial hemorrhage and edema (7 children/2 adults; 69%); (b) cerebral atrophy (6 children; 46%); (c) Alzheimer type II gliosis (5 children/4 adults; 69%); (d) infection (3 patients; 23%) due to cytomegalovirus (1 child), Aspergillus fumigatus (1 adult) and progressive multifocal leukoencephalopathy (PML)-like (1 adult); (e) Epstein-Barr virus-related cerebral post-transplant lymphoproliferative disorder (2 children; 15%); and (f) central pontine and extrapontine myelinolysis (1 child; 7.5%). The neuropathological lesions of SBT candidates were Alzheimer type II astrocytosis (4 patients), vascular changes (4 patients), brain atrophy (4 patients) and cerebral candidiasis (1 patient). CNS vascular, metabolic and infectious pathology are significant causes of morbidity and mortality in patients suffering intestinal failure, both before and after SBT. Brain atrophy was a frequent finding and may be related to nutritional and developmental inadequacy of long-term total parenteral nutrition.
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PMID:The neuropathology of intestinal failure and small bowel transplantation. 1033 88

The morphological changes in the brain of diabetic rats were examined up to 8 weeks after transient forebrain ischemia produced by transient occlusion of both carotid arteries. Using histochemistry, we also examined the extent and rate of development of atrophic changes in the brain, appearance of astrocytes, activated microglia, and glucose transporter 1 (GLUT1) in streptozotocin-treated rat brains after forebrain ischemia. Atrophic changes appeared in the hippocampus in both non-diabetic-- and diabetic--ischemic groups 4 weeks after ischemia. In diabetic--ischemic rats, the atrophic changes were more severe and progressed more rapidly in the hippocampus, and were also observed in the frontal, temporal and parietal cortices, but not in any cortical areas of the non-diabetic--ischemic rats and non-ischemic--diabetic rats. We observed reduced density of GLUT1 in all cortical regions and hippocampus in ischemic-diabetic rats at 4--8 weeks, when the number of activated microglias and astroglias increased in all cortical regions. Although severe atrophic changes were observed in the gray matter, no serious injury was noted in the white matter in the diabetic-ischemic group. Our results indicate that brain ischemia in the presence of diabetes causes more severe late-onset damage culminating in brain atrophy, compared with non-diabetics.
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PMID:Progressive cortical atrophy after forebrain ischemia in diabetic rats. 1124 74

To ascertain the effect of extreme hypercapnia on perinatal hypoxic-ischemic brain damage, 7-d-postnatal rats were exposed to unilateral common carotid artery occlusion followed by hypoxia with 8% oxygen combined with 3, 12, or 15% carbon dioxide (CO2) for 2 h at 37 degrees C. Survivors underwent neuropathologic examination at 30 d of postnatal age, and their brains were characterized as follows: 0 = normal; 1 = mild atrophy; 2 = moderate atrophy; 3 = cystic infarct with external dimensions <3 mm; and 4 = cystic infarct with external dimensions >3 mm. The width of the cerebral hemisphere ipsilateral to the carotid artery occlusion also was determined on a posterior coronal section and compared with that of the contralateral hemisphere to ascertain the severity of cerebral atrophy/cavitation. CO2 tensions averaged 5.08, 11.1, and 13.2 kPa in the 3, 12, and 15% CO2-exposed animals, respectively, during hypoxia-ischemia (HI). Neuropathologic results showed that immature rats exposed to 3 and 12% CO2 had similar severities of brain damage. In contrast, rat pups exposed to HI combined with 15% CO2 were significantly more brain damaged than littermates exposed to 3% CO2. Specifically, eight of 14 animals exposed to 15% CO2 showed cystic infarcts (grades 3 and 4), whereas none of 14 littermates exposed to 3% CO2 developed cystic infarcts (p < 0.01). Analyses of coronal width ratios at each CO2 exposure provided results comparable with those of the gross neuropathology scores. Cerebral blood flow (CBF), measured at 90 min of HI, was lowest in those immature rats exposed to 15% CO2 compared with control (p = 0.04), with higher values in those rat pups exposed to 3 and 12% CO2. The findings indicate that 7-d-postnatal rats exposed to HI with superimposed 12% CO2 are neither less nor more brain damaged than littermates exposed to 3% CO(2) (normocapnia). In contrast, animals exposed to 15% CO2 are the most brain damaged of the three groups. Presumably, extreme hypercapnia produces more severe cardiovascular depression than is seen in animals subjected to lesser degrees of hypercapnia; the cardiovascular depression, in turn, leads to greater cerebral ischemia and ultimate brain damage.
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PMID:Effect of extreme hypercapnia on hypoxic-ischemic brain damage in the immature rat. 1138 41

The aim of the present study was to demonstrate the usefulness of fetal magnetic resonance imaging (MRI) in ischemic brain injury. We report seven cases of fetal brain ischemia prenatally suspected on ultrasound (US) and confirmed by fetal MRI. Sonographic abnormalities included ventricular dilatation (n=3), microcephaly (n=1), twin pregnancy with in utero death of a twin and suspected cerebral lesion in the surviving co-twin (n=3). MRI was performed with a 1.0 T unit using half-Fourier acquisition single-shot turbo spin-echo (HASTE) sequences between 28 and 35 weeks of gestation. US and MRI images were compared with pathologic findings or postnatal imaging. MRI diagnosed hydranencephaly (n=1), porencephaly (n=2), multicystic encephalomalacia (n=2), unilateral capsular ischemia (n=1), corpus callosum and cerebral atrophy (n=1). In comparison with US, visualization of fetal brain anomalies was superior with MRI. The present cases demonstrate that MRI is a valuable complementary means of investigation when a brain pathology is discovered or suspected during prenatal US.
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PMID:Fetal magnetic resonance imaging (MRI) of ischemic brain injury. 1155 8

Hypoxia-ischemia (H/I) damages cells in the immature brain and interferes with subsequent brain development; the extent of the damage has been related to the severity, or duration, of the initial insult. This study examined the effects of both severe and moderate duration of H/I on the evolution of damage through 8 weeks of recovery. Seven-day-old rat pups were subjected to either 75 min or 2 h of 8% oxygen following a unilateral carotid artery ligation. Evaluation of brain damage included morphometric analysis of hemispheric diameter at 2, 4, and 8 weeks of recovery, and hematoxylin and eosin for evaluation of pathology at 8 weeks. Two hours of H/I produced severe infarction in the ipsilateral hemisphere in the majority of the survivors, apparent by 2 weeks of recovery with no change at 4 or 8 weeks. In marked contrast, 75 min of H/I produced no significant damage during the initial 2 weeks of recovery but resulted in progressive cerebral atrophy with delayed infarction such that the extent of damage at 8 weeks was not different from the 2-hour group. Thus, even a mild-moderate ischemic insult to the perinatal brain establishes a vulnerable region which ultimately dies without intervention.
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PMID:Delayed cerebral atrophy following moderate hypoxia-ischemia in the immature rat. 1159 17

Magnetic resonance imaging (MRI)-based volume measurements of brain structures are useful indicators of pending cognitive decline in humans suffering from neurodegenerative diseases. Transgenic mouse models that mimic the clinical conditions of these disorders have been developed. Noninvasive methods that can follow progression and regression of relevant pathology in these mice are therefore in great demand. In this study we tested whether high-resolution MRI (micro-MRI) in a mouse model of neurodegeneration (cerebral ischemia) could reliably track development of brain atrophy. We first established that diffusion imaging at a spatial resolution of 1.6 x 10(-3) mm(3) allowed superior visualization of forebrain, ventricles, and dorsal hippocampus in the mouse brain compared to either T2*- or T1-weighted MR imaging. Using this predetermined protocol we subsequently scanned C56BL/6J (C57) and ApoE-deficient (ApoE(-/-)) mice before and after ischemia. Four groups were studied: C57/sham (n = 9), ApoE(-/-)/sham (n = 9), C57/ischemia (n = 9), and ApoE(-/-)/ischemia (n = 11). All mice received a baseline 3D diffusion scan. One week later C57/ischemia and ApoE(-/-)/ischemia mice were exposed to 10 min of ischemia and scanned again on the 3rd and 30th postischemic day. The C57/sham and ApoE(-/-)/sham mice served as controls and were scanned at corresponding time points. Diffusion images of ApoE(-/-)/ischemia mice on the 3rd postischemic day revealed multiple localized high signal intensity areas. An increase in ventricle and a decrease in dorsal hippocampal volumes (which included the associated cortex laterally) at 30 days confirmed brain atrophy in C57 mice after ischemia. Excessive mortality of ApoE(-/-)/ischemia mice restricted statistical analysis, but ventricle enlargement postischemia was demonstrated. Our results show that volume changes in the brain of a 30-g mouse can be tracked by micro-MRI in a model of neurodegeneration. Clearly the ability to follow progression of pathology in mice will greatly aid our understanding of neurodegenerative diseases and facilitate the many possibilities to intervene pharmacologically.
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PMID:Tracking brain volume changes in C57BL/6J and ApoE-deficient mice in a model of neurodegeneration: a 5-week longitudinal micro-MRI study. 1170 81


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