Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent investigations at several institutes have demonstrated extensive acute brain pathology in experimental animals exposed to single subcutaneous doses of the chemical warfare nerve agents soman or sarin. Lesions include neuronal and neurophil degeneration, necrosis, and in animals that survive for several weeks, a degenerative encephalopathy characterized by mineralization, encephalomalacia, atrophy, and hydrocephalus. The cerebral cortex, amygdaloid complex, hippocampus, and multiple thalamic nuclei are consistently affected. This pattern of injury resembles that described for epilepsy and ischemic brain injury. Some animals have cardiac lesions characterized by acute necrosis with subsequent mild inflammation and fibrosis. Anticonvulsants protect experimental animals from lesion development. In rats, this encephalopathy causes long-range behavioral changes characterized by hyperactivity during routine handling and variances in traditional behavioral tests. The histopathologic features and distribution of lesions in nerve agent-poisoned animals support the hypothesis that epileptiform seizure activity is a major factor in nerve agent pathology. Other localized insults such as ischemia and hypoxia probably contribute to the pathogenesis.
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PMID:Pathology of nerve agents: perspectives on medical management. 409 82

In infants who die during the first months of life necrotic foci are almost invariably found. They are, as a rule, located in border zones between vascular territories, suggesting cerebral ischemia as a pathogenetic mechanism. Normally, the brain is protected against changes in perfusion pressure by autoregulation of cerebral perfusion. In utero, this mechanism is extremely fragile, and normal birth is a sufficient hypoxic insult to abolish autoregulation. Abolished autoregulation has been demonstrated in distressed newborns: Even mild hypotension, which is a common occurrence in these infants during the first few hours of life, is sufficient to induce ischemia. Follow-up studies at the ages of one and four years have shown neonatal ischemia to be the decisive factor in the development of atrophic encephalopathy and motor and cognitive dysfunction. This clarification of the pathogenetic process has important implications for prevention, which is briefly discussed.
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PMID:Perinatal cerebral ischaemia and developmental neurologic disorders. 619 41

Hereditary hemorrhagic telangiectasia (HHT) is a familial angiodysplastic disorder. Dermal, mucosal, and visceral vascular lesions of this disorder are well known. However, central nervous system (CNS) manifestations, occurring in as many as one-third of patients, have not been well appreciated until recently. The etiology of neurologic symptomatology includes hypoxemia or ischemia secondary to pulmonary arteriovenous shunting, vascular lesions of the brain and spinal cord ranging from aneurysms to arteriovenous malformations, brain abscesses secondary to pulmonary arteriovenous fistulas, and portal systemic encephalopathy. Angiographic and computed tomographic findings in four patients with CNS involvement in HHT are reported.
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PMID:CNS manifestations of hereditary hemorrhagic telangiectasia. 643 22

Neurologic complications of systemic lupus erythematosus (neuro-SLE) are common. The most frequent manifestations of neuro-SLE are seizures, encephalopathy, and behavioral changes, but a wide variety of other neurologic abnormalities affecting the central and peripheral nervous system and muscle also occur. Although the prevalence of neuro-SLE is high, the diversity of clinical presentations, the multiple potential etiologies, and the absence of sensitive and specific diagnostic tests render diagnosis difficult. Recent advances in understanding mechanisms of neuronal dysfunction combined with advances in imaging techniques, including functional imaging, should help in diagnosis and management. The mechanisms of neurologic injury can be divided into three broad categories. First, neuronal dysfunction may result from direct effects of the immune system on brain cells such as autoantibody binding to cell surface, immune complex deposition with secondary inflammation, and effects of cytokines. Second, immune- mediated injury to supportive structures such as the vasculature may also affect the nervous system by producing ischemia. Finally, the neuraxis may be affected by any one of several immune and non- immune effects of infection, toxins, and metabolic disturbances.
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PMID:Systemic lupus erythematosus: immunopathogenesis of neurologic dysfunction. 748 26

The case of an obese patient who developed massive centrilobular liver cell necrosis, severe coagulopathy, acute renal failure, and encephalopathy is presented. Hypovolemia and heart failure were absent, but the acute liver disease was associated with severe arterial hypoxemia due to obstructive sleep apnea that was shown by the nocturnal blood oxygen desaturation, the results of the polysomnographic study, and normal baseline pulmonary function tests. In this obese patient, liver cell necrosis was caused by severe liver cell hypoxia secondary to severe arterial hypoxemia as a consequence of obstructive sleep apnea associated with a Pickwickian syndrome. This observation is consistent with the hypothesis that liver ischemia was directly related to severe arterial hypoxemia.
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PMID:Ischemic hepatitis due to obstructive sleep apnea. 755 54

Connatal thalamic calcifications in apparently uneventful pregnancies have been described in various case reports and in a single report in two sibs. On the other hand, this lesion is known to occur after a hypoxic-ischemic accident in the immature brain. In the present report infantile encephalopathy with symmetrical thalamic calcifications is observed in one sib of a monozygous twin pair. This observation adds to the evidence that the condition is acquired, most probably on the basis of hypoxia-ischemia, and provides strong evidence against autosomal-recessive inheritance.
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PMID:Discordant infantile encephalopathy with symmetrical thalamic calcifications in identical twins. 780 12

The aim of the present study was 2-fold: (1) to determine the ratio between the amount of GAD67 and GAD65 (two isoforms of the GABA synthetizing enzyme glutamic acid decarboxylase) in nerve endings in the mature rat cerebral cortex damaged by hypoxia-ischemia during early postnatal life; and (2) to compare two different computer-assisted procedures developed for quantitative analysis of immunofluorescence images obtained with a confocal laser scanning microscope (CLSM). One procedure was based on a program present in the standard Leica CLSM software packet for full-field analysis, the other on a specially written program for object-oriented analysis run on a Kontron IBAS-KAT image analysis system. To this end, rat pups were unilaterally exposed to hypoxic-ischemic conditions and, after a survival period of 6.5 months, sacrificed by perfusion fixation. After dissection of the brain and vibratome sectioning, three animals with substantial damage on one cortical side were selected. Sections of these animals were double-stained with primary antibodies against GAD67 and GAD65 and fluorophore-conjugated secondary antibodies and subsequently sampled with a CLSM. Analysis of the CLSM images with both computer-assisted procedures showed for all three animals a clear tendency to higher GAD67/GAD65 ratios in cortical GABAergic nerve endings on the hypoxia-damaged side than in matched areas on the contralateral side. This outcome led to the following conclusions. (1) The correspondence between the outcome of both analysis procedures indicates that both procedures are valid for quantification of immunofluorescence images of nerve endings obtained with a CLSM. (2) The outcome lends further support to our view that hypoxic-ischemic encephalopathy, sustained during early postnatal life, may result in an unstable cortical network generating abnormal synchronizations and oscillations which can be amplified and propagated as true epileptic discharges. In such a network both excitatory and inhibitory processes are tonically enhanced, the latter probably as a homeostatic reaction tending to keep abnormal excitation within physiological limits.
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PMID:Quantitative immunofluorescence data suggest a permanently enhanced GAD67/GAD65 ratio in nerve endings in rat cerebral cortex damaged by early postnatal hypoxia-ischemia: a comparison between two computer-assisted procedures for quantification of confocal laser scanning microscopic immunofluorescence images. 782 Jun 25

Pattern of neurosonographic (NSG) abnormalities in 150 term newborn infants with hypoxic ischemic encephalopathy (HIE) was studied. Sonographic abnormalities, presumably indicating cerebral edema and or ischemia, were observed in 86% (n = 129) cases. Obliteration of the ventricles occurred as the sole abnormality in 30 (20%) cases. Eighty (53%) patients had diffusely increased echogenicity of the brain parenchyma (DPE) in addition to the compression of the ventricles, sulci and the interhemispheric fissure. Focal parenchymal echodense (FPE) lesions occurred in nine (6%) neonates with HIE. Ten (6.6%) patients, however, had increased periventricular echogenicity (PVE). Two patients, one with focal parenchymal lesions and the other with PVE had obliterated ventricles in addition. Regarding temporal sequence earliest NSG abnormalities were DPE or slit like ventricles that were observed on day-1 itself. Focal or periventricular echogenic lesions, however, made their first appearance on day-3 of life. Twenty one patients had normal scans. Fifty patients with abnormal scans died. None of the infants with normal scans, however, died (p < 0.001). At 4 weeks of age, scans performed in 100 survivors revealed no abnormality in 51 cases. Others showed development of cerebral atrophy (n = 21), multicystic encephalomalacia (n = 2), porencephalic cyst (n = 1), or persistence of PVE without cystic changes (n = 4). The results of this study highlight the diagnostic efficacy of neurosonography in cases of HIE. We suggest that it should be incorporated in the routine evaluation of patients with hypoxic brain injury.
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PMID:Neurosonographic abnormalities in neonates with hypoxic ischemic encephalopathy. 789 Mar 38

The case of a 67-year-old woman with terminal renal insufficiency, who developed extensive encephalopathy with predominant involvement of the white matter is reported. The encephalopathy was the consequence of preexisting hypertensive alterations, acidosis, hypoxia, ischemia, bacteremia and varicella-zoster meningoencephalitis. The vasculitic alterations associated with meningoencephalitis had a major influence on the development and the extent of the leukoencephalopathy.
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PMID:Vasculitic, hypoxic-ischemic leukoencephalopathy. 792 81

We present the clinical, morphological and neuropathological findings in a 44-year-old male suffering from the acquired immunodeficiency syndrome (AIDS) (CDC stage IV C2) who presented with rapidly progressive right-side hemiparesis and developed hemianopia and aphasia. Scans showed multiple, not contrast-enhancing, not space-occupying echo-intensive lesions in T2-weighted MR-imaging. No hint for an opportunistic infection, necrotizing vasculitis or vascular disease was found. All therapeutic regimens failed and 8 weeks after onset of neurological symptoms the patient died because of cardiorespiratory arrest. Post-mortem examination excluded opportunistic infection, progressive multifocal leukoencephalopathy, lymphoma, vasculitis and ischemia of the brain. In the presence of an unusually high amount of HIV-infected macrophages at immunohistochemical examination, the overall pathological findings were atypical both for HIV encephalitis and HIV leukoencephalopathy. We describe a pathologically distinct new form of HIV associated encephalopathy.
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PMID:A pathologically distinct new form of HIV associated encephalopathy. 815 18


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