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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five central nervous diseases are described and their relationships to previously recorded conditions are discussed. The conditions are congenital inclusion-body encephalopathy probably caused by a paramyxovirus infection, idiopathic neuraxial oedema of a newborn calf, focal symmetrical encephalomalacia of a young calf, yacca (Xanthorrhoea spp) poisoning of adult cattle leading to spinal demyelination, and focal demyelination and neuropathy in an adult cow.
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PMID:Encephalolopathies in cattle in Tasmania. 18 2

The CT features of 45 cases of delayed radiation encephalopathy (including radiation necrosis) following radiotherapy for nasopharyngeal carcinoma are reported. The brain lesions were uni- or bilateral and involved mainly the white matter and subsequently the gray matter of the lower portion of the brain included within the portals of irradiation and its vicinity. The lesions were edematous and hypodense on CT and showed postcontrast enhancement in 50% of the cases. Within the period of follow-up (1-5 years), the lesions showed remissions and exacerbations and in some cases stabilized. In addition, there was progressive cerebral atrophy, manifesting itself mainly as dilatation of the temporal horns, the neighboring cisterns, and sylvian fissures. In some cases that were followed for a long time, the cerebral lesions showed either foci of calcification or encephalomalacia and/or porencephaly.
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PMID:Delayed radiation encephalopathy after radiotherapy for nasopharyngeal cancer: a CT study of 45 cases. 200 93

One hundred neonates determined prospectively to be at risk for neurologic handicap underwent magnetic resonance imaging with a high-field (1.5 T) imager. Thirty-three demonstrated a total of 37 lesions consistent with hypoxic-ischemic encephalopathy, including periventricular leukomalacia (n = 12), basal ganglia hemorrhage (n = 5), multicystic encephalomalacia (n = 5), and focal parenchymal hemorrhage (n = 15). Diagnoses by ultrasonography and computed tomography were compared with those by magnetic resonance imaging in 29 and 17 infants, respectively. Ultrasonography agreed more frequently with magnetic resonance imaging than did computed tomography. Ultrasonography detected 79% of lesions demonstrated by magnetic resonance imaging whereas computed tomography detected only 41%. Periventricular leukomalacia was seen most often in preterm infants, basal ganglia hemorrhage and multicystic encephalomalacia primarily occurred in term infants, and focal parenchymal hemorrhage occurred at all gestational ages. Basal ganglia hemorrhage and multicystic encephalomalacia were strongly associated with histories of perinatal asphyxia, seizures, and early abnormal neurological status. All infants with basal ganglia hemorrhage (5/5) and multicystic encephalomalacia (5/5) and the majority with periventricular leukomalacia (9/12) and focal parenchymal hemorrhages (9/15) had developmental abnormalities at discharge.
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PMID:Prospective observations of 100 high-risk neonates by high-field (1.5 Tesla) magnetic resonance imaging of the central nervous system. II. Lesions associated with hypoxic-ischemic encephalopathy. 201 18

The neuropathologic findings of brains and spinal cords removed at autopsy from 26 infants and children with AIDS is described; in two cases, only the spinal cords were available. The most common finding in the brains was dystrophic calcification of blood vessels of all calibers in the basal ganglia and deep cerebral white matter (21 og 24 cases). The next most frequent finding was subacute encephalitis (SE) (15 of 24 cases) with microglial nodules and multinulceated giant cells. Immunocytochemical and in situ hybridization studies showed HIV antigen or genetic sequences only in the brains of cases with SE. Multinucleated giants cells (MGC) were the most frequent cells with reaction products. MGC were labeled with ricinus lectin (RCA), but not with leukocyte common antigen (LCA) or glial fibrillary acidic protein. Many cells in microglial nodules were labeled with RCA, but not LCA; cells in the perivascular compartment were labeled with LCA, but not RCA. Corticospinal tract degeneration was noted in 15 of 20 spinal cords. In six cases tract degeneration was consistent with delayed myelination, and the remaining cases had axonal injury consistent with Wallerian degeneration. Opportunistic infections were rare (three cases). Central nervous system lymphoma occurred in three children and was the most common mass lesion. In two cases lymphoma occurred in the setting of a systemic polyclonal immunoproliferation possibly related to Epstein-Barr virus infection. Cerebrovascular accidents were noted in seven cases. Two cases had hemorrhage associated with immune thrombocytopenia; one hemorrhage was catastrophic. Two children had large vessel arteriopathy with multiple encephalomalacias. Two children had a necrotizing encephalopathy with encephalomalacia and vascular changes suggestive of a mitochondrial cytopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Central nervous system pathology in pediatric AIDS: an autopsy study. 273 40

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

Chicks were fed a diet rich in oxidized oil and deficient in alpha-tocopherol. As soon as nutritional encephalopathy developed the animals were immediately put on to a normal diet, and kept alive for up to 166 days. Examination of the cerebellum showed multiple foci of healed encephalomalacia with EM appearance of basal membrane labyrinths between astroglial cells and around blood vessels. The possible origin of the basement membrane material in this conditions was considered and compared with similar formations in normal animals, in CNS tumour explants, and after portocaval anastomosis as well as after spinal cord lesions.
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PMID:Basal membrane labyrinths in the healing stages of chick nutritional encephalopathy. 737 10

Mitochondrial myopathy, encephalopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome is one of the mitochondrial encephalomyopathies that has distinct clinical features including stroke-like episodes with migraine-like headache, nausea, vomiting, encephalopathy and lactic acidosis. We report a 27-year-old woman who presented with partial seizure, stroke-like episodes including hemiparesis, hemianopia and hemihypethesia, sensorineural hearing loss, migraine-like headache, and lactic acidosis. Brain computed tomographic scan showed encephalomalacia in the right parieto-occipital area and recent hypodensity in the left temporoparieto-occipital area with cortical atrophy. Muscle biopsy revealed ragged-red fibers and paracrystaline inclusions in the mitochondria. Genetic study revealed an A to G point mutation at nucleotide position (np) 3243 of mitochondrial DNA. External ophthalmoplegia and ptosis were also found during two exaggerated episodes in this patient. Therefore, the overlapping syndrome of chronic progressive external ophthalmoplegia in the MELAS syndrome is considered in this case. Furthermore, we also found carnitine deficiency in this patient and she was responsive well to steroid therapy. Muscle biopsy also revealed excessive lipid droplets deposits. Therefore, the carnitine deficiency may occur in MELAS syndrome with the A to G point mutation at np 3243. We recommend the steroid or carnitine supplement therapy be applied to the MELAS syndrome with carnitine deficiency.
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PMID:CPEO and carnitine deficiency overlapping in MELAS syndrome. 748 81

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 most important neurodegenerative diseases of the horse are reviewed. In addition to the literature, neurodegenerative diseases occurring in patients (horses, Mongolian Przewalski-horses, and two zebras) referred to the Utrecht Veterinary Faculty are mentioned. Neurodegenerative diseases described are: I. ataxia associated with: A/ static stenosis, B/ dynamic stenosis, C/ lesions at various locations in the central nervous system, D/ equine herpesvirus infections, E/ equine degenerative myelo-encephalopathy, or F/ cerebellar abiotrophy; II. equine motor neuron disease; III. grass sickness or equine dysautonomia; IV. postanaesthetic myelomalacia; and V. equine leuko-encephalomalacia. The patient descriptions show, that mixed forms of some of the differentiated diseases can be diagnosed. Little is known with certainty about the aetiology of the neurodegenerative lesions found. In some patients vitamin E may play a role, possibly in combination with other factors. A mycotoxin known to interfere with myelin metabolism is involved in leuko-encephalomalacia.
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PMID:[Neurodegenerative disorders of the central nervous system in horses]. 794 Apr 76

Multiple cystic lesions in brain parenchyma supplied by the anterior cerebral circulation is a recognized pattern of cerebral injury associated with hypoxic-ischemic encephalopathy in the term infant. This report presents a series of seven infants (gestational age, 39.3 +/- 2.8 weeks; range, 36 to 44 weeks) who developed multicystic encephalomalacia in the distribution of the anterior cerebral circulation after severe neonatal asphyxia. Cerebral imaging and pathologic studies demonstrate relative preservation of the cerebellum, brain stem, and cerebral structures supplied by the vertebrobasilar circulation. Compared to the vertebrobasilar vasculature, the anterior cerebral vessels in the term infant have dense sympathetic innervation. Asphyxia, a potent sympathetic stimulator, may induce vasoconstriction in the anterior circulation and differentially accentuate the effects of hypoxia/ischemia on cerebral tissue.
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PMID:Differential involvement of the brain in neonatal asphyxia: a pathogenic explanation. 857 57


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