Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between MR patterns of brain damage and type or timing of perinatal hypoxia-ischemia was studied. MR images of 104 children with evidence of bilateral posthypoxic-ischemic brain damage and neonatal records were reviewed. Three different MR patterns were found. Periventricular leukomalacia occurred in 73 children, in 82% after a history of subacute or chronic hypoxia-ischemia, in 71% after preterm birth. Predominant lesions of basal ganglia and thalamus occurred in 21 children, in 95% preceded by acute profound asphyxia, in 85% after term birth. Multicystic encephalopathy occurred in 10 infants, in 70% preceded by mild signs of hypoxia-ischemia, followed by an unexpectedly severe encephalopathy, in 60% after term birth. Statistical analysis showed that the patterns of injury were primarily related to the type of hypoxia-ischemia. We conclude that the type of hypoxia-ischemia, rather than the postconceptional age at occurrence determines the pattern of brain injury.
 ...
PMID:MR patterns of hypoxic-ischemic brain damage after prenatal, perinatal or postnatal asphyxia. 1096 99

Ischemic/hypoxic brain damage induced in 7-day-old rats was significantly attenuated in a dose-dependent manner by intracerebral injection of glial cell line-derived neurotrophic factor (GDNF; 2 or 4 microg) within 30 min after the insult. Whereas the great majority of the vehicle-treated animals showed massive infarction involving more than 75% of the affected cerebral hemisphere, GDNF injection resulted in a remarkable reduction in both the incidence and severity of the brain damage (incidence ranging from 76% to 93% in controls to 34% to 64% in the 2.0-microg group and 7% to 29% in 4.0-microg group). The induction of immunoreactive 70-kDa heat shock protein (HSP70) in cerebral cortical neurons was also significantly reduced in GDNF-treated animals as compared to controls. The mechanisms responsible for the neuroprotective effects of GDNF remain unknown, although it has been speculated that these may be endogeneous. The higher expression of GDNF and its mRNA in developing brains may be one of the factors responsible for the relative resistance to ischemia of fetal and neonatal as opposed to adult brains. GDNF may possibly act by protecting against oxidative stress or by scavenging free radicals generated during ischemia. The results of our study strongly suggest that GDNF may prove to be an effective and potent protective agent against perinatal ischemic/hypoxic encephalopathy.
 ...
PMID:Glial cell line-derived neurotrophic factor protects against ischemia/hypoxia-induced brain injury in neonatal rat. 1096 63

Cerebral hypoxia-ischemia (asphyxia) occurring in the fetus and newborn infant is a major cause of acute mortality and chronic neurological disability in survivors. This review highlights many practical aspects of perinatal hypoxic-ischemic brain damage, including neuropathological features, obstetrical antecedents, and clinically important aspects of identification, management, and prognosis. Diagnostic techniques, including neuro-imaging, to diagnose hypoxic-ischemic encephalopathy also are discussed. A thorough knowledge of the clinical spectrum of perinatal hypoxic-ischemic encephalopathy should enable neonatologists to undertake appropriate management strategies and prognostic indicators.
 ...
PMID:Hypoxic-ischemic encephalopathy. 1101 34

Cryoglobulinemia is a rare cause of encephalopathy. The authors report three patients with strikingly similar clinical features of recurrent encephalopathy accompanied by symptoms of gastrointestinal ischemia. In only one patient was cryoglobulinemia ascertained in life during the final illness. The autopsy examinations all showed diffuse cerebral, enteral, and systemic small vessel lesions immunoreactive for immunoglobulins and typical of mixed essential cryoglobulinemia. This unusual relapsing clinical syndrome is readily misinterpreted as of nonorganic origin despite its potentially fatal prognosis.
 ...
PMID:Relapsing ischemic encephaloenteropathy and cryoglobulinemia. 1109 22

Birth asphyxia is O2i CO2 exchange disorder during the labour, with consequent hypoxia and ischemia. The term "asphyxia" has been used unprecisely quite often. The most frequently used criteria for birth asphyxia have been: fetal bradycardia, meconium stained amniotic fluid, fetal acido-base status with umbilical artery pH value below 7.10, low Apgar score and need for endotracheal intubation. The correct Apgar score quantification depends on the examiner. Fetal acido-base status measured in umbilical artery could be useful biochemical parameter of birth asphyxia. Only if the fetal oxygen supply during the labour is severe and long enough disturbed, the neurological abnormalities will develop later. Our study has enrolled 70 children with various degree of motor impairment, detected during neonatal period and/or infancy. They have been followed up till 24 months chronological age for term neonates and 24 months corrected age for prematures. 34 children out of them have developed clear clinical signs of cerebral palsy. Birth asphyxia as a possible cause of cerebral palsy has been documented in 10 cases, e.g. 29.4%. The criteria for birth asphyxia have been low Apgar score, meconium stained amniotic fluid and clinical signs of hypoxic-ischemic encephalopathy. Fetal blood gas and acido-base measurements obtained from umbilical artery at delivery have been an important parameter of intrapartal asphyxia. Those measurements should be introduced as a routine method in our practice, in the cases of fetal heart deceleration, to asses the extent of fetal acidosis.
 ...
PMID:[Birth asphyxia as a cause of cerebral palsy]. 1121 10

A 73-year-old man recurring hepatic encephalopathy due to a congenital splenorenal shunt concomitant with early gastric cancer was successfully treated by surgical intervention. The portal pressures before and after the shunt resection were 13.5 and 18 cm H2O, respectively. The liver was slightly atrophic and the histological specimen showed slight fibrosis and mild infiltration of lymphocytes in the portal area. After the operation, the encephalopathy was improved and the several factors of liver function also recovered. Interestingly, the liver volume estimated by abdominal CT clearly increased 1 month after the shunt resection. The encephalopathy in congenital portosystemic shunt might result from chronic liver ischemia and atrophy. Moreover, the shunt resection may enlarge the functional liver volume by increasing the portal blood flow.
 ...
PMID:Resection of spleno-renal shunt resulting in enhanced liver volume in a patient with congenital portosystemic shunt concomitant with early gastric cancer. Review of Japanese cases. 1124 65

Free radical release plays an important role in the development of brain injury following hypoxic-ischemic encephalopathy. It causes endothelial cell damage and anomalies in NMDA receptors, synaptosome structure and astrocyte function. Mitochondrial dysfunctions caused by asphyxia, reperfusion after ischemia, arachidonic acid cascade, catecholamine metabolism and phagocyte activation are known sources of reactive oxygen species, particularly the superoxide anion (O2(-)). O2(-) mainly induces peroxidation by the Fenton/Haber Weiss reaction or via iron-oxygen complexes. Since both reactions require reactive heavy metals, non-protein-bound iron (NPBI) is essential for the induction of lipid peroxidation. Experimental studies have demonstrated the neurotoxicity of iron in ischemia-reperfusion. Normal axonal transport of brain iron is also reported to be disrupted in hypoxia-ischemia, leading to a buildup of iron in the white matter. The free iron content of erythrocytes (ICRBC) is considered a marker of oxidative stress. Free iron release is accompanied by the oxidation of membrane proteins and the appearance of senescent antigen, as measured by autologous IgG binding. Our preliminary results suggest a significant positive correlation between plasma free iron and the number of nucleated red cells in cord blood, currently considered a reliable index of lasting intrauterine asphyxia but also possessing a high predictive value for poor neurodevelopmental outcome. The rate of erythropoiesis and the entity of ICRBC are related to the degree of asphyxia and the probability of neurological impairment. Since even an increase in NPBI during asphyxia is related to a poor outcome, iron released by red cells could possibly also contribute to NPBI levels.
 ...
PMID:Red blood cell involvement in fetal/neonatal hypoxia. 1127 53

Diffusion-weighted imaging provides novel and interesting insights into normal development and pathologic processes occurring in neonates and infants. Both myelinated and unmyelinated white matter show restricted diffusion. Focal infarction in perinatal stroke and more global injury associated with hypoxic ischemia encephalopathy produce high-signal lesions in the brain, in the acute phase. Diffusion-weighted imaging also demonstrates abnormalities of a variety of other diseases, when conventional imaging is relatively uninformative.
 ...
PMID:Diffusion-weighted imaging of the brain in neonates and infants. 1127 84

The ventricular assist device (VAD) is a mechanical pump that has been shown to be an effective modality of cardiac support in patients with heart failure refractory to pharmacologic intervention and who are awaiting cardiac allograft transplantation. Neuropathologic findings in these patients have not been well described. We retrospectively reviewed 2,632 autopsy reports (between 1990 and 2000) and found 64 patients who received VADs. Of these 64 patients, brain and spinal cord tissue was available for review in 33 patients (25 males and eight females; age range, 4 to 69 years; mean age, 52 years). The study group was composed of these 33 patients. Ventricular assist devices were in place from one to 603 days (mean 49 days). Twenty-five patients had left VAD, three had right VAD, and five had biventricular VADs. Brain weights ranged from 928 g to 1,740 g (mean 1,325 g). The most common central nervous system pathologic findings included infarct (N = 23; 70%), acute neuronal necrosis (N = 22; 67% focal and N = 1; diffuse anoxic encephalopathy), hemorrhage (N = 14; 42%), and herniations (N = 7; 21%). Two patients had no neuropathologic findings at autopsy. Cause of death was central nervous system-related in eight patients (24%) including six with massive parenchymal hemorrhage and herniations, one with brainstem infarction, and one with air embolism (radiographically diagnosed). The most common causes of death in the remaining 25 patients included sepsis (n = 10; 30%), pneumonia (n = 4; 12%), and embolic events with widespread infarcts (n = 4; 12%). The most common neuropathologic findings in patients with VAD were related to ischemia and infarction. In a significant subset of patients, central nervous system pathology, particularly hemorrhage with herniation, was the primary cause of death. Ann Diagn Pathol 5:67-73, 2001.
 ...
PMID:Neuropathology associated with ventricular assist devices: an autopsy series of 33 patients. 1129 90

This study was done to determine the effects of hyperglycemia or hypoglycemia on brain cell membrane function and energy metabolism during the immediate reoxygenation-reperfusion period after hypoxia-ischemia (HI). Forty-five newborn piglets were divided randomly into four experimental groups: normoxia control (NC, n=9); HI/reoxygenation-reperfusion (RR) control (HC, n=11); HI/RR hyperglycemia (HE, n=12); and HI/RR hypoglycemia (HO, n=13) group. Animals were subjected to transient HI for 30 min followed by 2 h of RR. Cerebral HI was induced by temporary but complete occlusion of bilateral common carotid arteries with surgical clips and simultaneous breathing with 8% oxygen. Glucose was unregulated in HC group, and controlled by modified glucose clamp technique immediately after HI in HE (350 mg/dl) and HO (50 mg/dl) groups. During HI, heart rate, base deficit, glucose and lactate level in the blood and cerebrospinal fluid increased, and arterial pH, oxygen saturation and blood pressure decreased significantly in HC, HE and HO groups. During RR, these abnormalities returned to normal values, but lactic acidosis persisted especially in HO group. Cerebral Na(+),K(+)-ATPase activity decreased, and lipid peroxidation products increased significantly in HC group than in NC group, and these abnormalities were significantly aggravated in HE, but not in HO, group. Brain ATP and phosphocreatine levels in HE group were significantly reduced compared to the corresponding values in NC, HC and HO groups. In summary, hyperglycemia, but not hypoglycemia immediately after HI interfered with the recovery of brain cell membrane function and energy metabolism. These findings suggest that post-hypoxic-ischemic hyperglycemia is not beneficial and might even be harmful in neonatal hypoxic-ischemic encephalopathy.
 ...
PMID:Effects of hyperglycemia or hypoglycemia on brain cell membrane function and energy metabolism during the immediate reoxygenation-reperfusion period after acute transient global hypoxia-ischemia in the newborn piglet. 1136 56


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>