Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.11.1.6 (catalase)
 55,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two subjects affected by various types of epilepsy have been studied as follows: 1) from the clinical point of view with careful case history or by direct observation of the seizures; 2) from the EEG point of view by means of prolonged recordings during wakefulness and nocturnal sleep or with pharmacological activations; 3) from a radiological point of view with standard skull radiography, air-encephalography (PNX), brain scanning and, when necessary, with cerebral angiography, mono or bilateral. Furthermore, all the patients underwent a CAT at least once; in the majority of cases this examination was repeated after administration of contrast medium. The following results were obtained by comparing the various examinations: 1) anatomo-elector-clinical correlation was present only in some cases; 2) only in patients with cerebral neoplasms was there proof of an agreement in site between EEG, CAT and PNX; 3) it was not possible to detect in a definite manner epileptic glial lesions with CAT; 4) the EEG analysis, when repeated several times with different methods of investigations, whoed epileptic foci in a higher number compared to the anatomical focal lesions proved by CAT; 5) compared with air-encephalography and morphological brain scanning, CAT usually pointed out a higher number of focal and/or diffused cerebral lesions with a higher degree of precision; viceversa cerebral angiography proved to be irreplaceable in cases where it was necessary to study possible circulatory alterations.
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PMID:[Preliminary observations on computerized axial tomography (CAT) in 32 patients with various epileptic syndromes (author's transl)]. 61 41

A total of 5,401 electroencephalograms performed in the Seizure Unit at Children's Hospital Medical Center over a 12-month period were analyzed for the presence of paroxysmal beta activity. Nine examples were found in patients under the age of 10 years, each of whom had a clinical seizure disorder. Seven patients showed abnormalities such as tumor, cerebral dysgenesis, or hydrocephalus on CAT scans or skull roentgenograms. Paroxysmal beta activity should be considered a manifestation of a seizure disorder. Furthermore, the finding of paroxysmal beta activity on an electroencephalogram in the young child should lead to further evaluation for a possible structural lesion.
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PMID:Paroxysmal beta activity in the pediatric electroencephalogram. 70 81

A patient is described with the dermatological features of blue rubber bleb nevus syndrome (BRBNS), focal seizures, and lateralized neurological signs. CAT scan demonstrated a nonenhanced density in the region of the vein of Galen. Neuropathological examination showed that this density was a clot within a vein of Galen malformation. Hemangiomas that grossly resembled the skin lesions of BRBNS were seen on the cerebral surface. Many of these hemangiomas were thrombosed and overlay patchy zones of infarction. Numerous vascular malformations of varying histological types were also found within the brain and systemic organs. Bluish, compressible, often raised hemangiomas of the skin should alert physicians to the BRBNS and the potential for vascular malformations ot occur within the brain as well as systemic organs. Diagnosis of BRBNS involving the brain may assist in interpretation of radiographic findings. The tendency of these malformations to thrombose may account for focal neurological deficits.
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PMID:Blue rubber bleb nevus syndrome with CNS involvement and thrombosis of a vein of galen malformation. 72 30

Twenty critically ill infants with abnormal head growth and/or seizures underwent CAT of the brain. Signs of birth asphyxia or respiratory distress were present in all. Six out of ten infants with abnormal size of the head had abnormal CAT scans. Nine out of ten infants with seizures had abnormal scans. Abnormalities included hydrocephalus, intraventricular hemorrhage, cerebral edema, subarachnoid hemorrhage and porencephaly. Six infants required neurosurgical procedures. Development at two to 15 months of age in the 19 surviving infants was normal in nine, suspect in eight, and severely delayed in two patients. Until the prognosis of the various CNS disorders discussed is clearly defined, aggressive management appears indicated.
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PMID:Computerized axial tomography of the brain in neonates and young infants. 88 78

Postoperative neurological deficit may result from ischaemic or hypoxic hypoxaemia. Postural cerebral hypoperfusion may ensue when a pre-existing asymptomatic vascular anomaly in combination with rotation of the head for surgical positioning compromises cerebral blood flow. CASE REPORT. A 30-year-old man was referred for recraniotomy for glioblastoma. Following uneventful induction of anaesthesia, increased diuresis and progressive hypothermia were observed. The postoperative period was complicated by a seizure, followed by apnoea requiring reintubation of the trachea. A CAT scan revealed global cerebral oedema with subtotal compression of the third ventricle. Intracranial pressure was 60 mm Hg as measured by an epidural probe. On the 1st postoperative day clinical and electroneurophysical signs of brain death were observed; the patient underwent organ explantation the next day. PATHOLOGY. Pathological examination revealed pronounced global hypoxaemic lesions and an S-shaped internal carotid artery with intimal proliferation (Fig. 1). The diagnostic conclusion was cerebral ischaemia following carotid occlusion caused by carotid kinking and completed by surgical positioning (rotation of the head). CONCLUSION. Carotid kinking is a rare abnormality, and patients at risk may not be identified preoperatively. Though it is questionable whether this disaster could have been prevented at all, electroneurophysiological monitoring would have been the only early monitoring system capable of detecting diminishing cerebral blood flow. Although a request for routine intraoperative neurophysiological monitoring seems unrealistic at present, it has to be acknowledged that only such monitoring could have provided the information needed to save this patient.
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PMID:[A fatal intraoperative cerebral ischemia following kinking of the internal carotid artery?]. 163 22

One to two per cent of children and up to 11% of adolescent have arterial hypertension. In most cases children and adolescent are not recognized to be hypertensive because physicians do not routinely measure blood pressure. Often the diagnosis is recognized only when the pediatric patients develop a complication: seizure, stroke, heart failure or paraplegia. Renovascular hypertension in children and adolescents is more common than all of the other causes combined, except for coarctation of the aorta. The diagnosis is not so easy and includes the usual history, physical examination (signs and symptoms of coarctation of the isthmic or abdominal aorta or of an abdominal mass or of one of the adrenal causes of hypertension), laboratory studies, abdominal ultrasound study and chest x-ray. Sometime a CAT can be usefull. The next steps are the early and rapid-sequence IVP, renal angiography and peripheral and renal renin activity. The management of renovascular hypertension in children and adolescent includes a conservative approach (percutaneous transluminal renal angioplasty or renal embolization), rarely used in pediatric age, and the surgical treatment. This latter includes all the surgical procedures of renal revascularization and, in unilateral renal parenchymal diseases, the nephrectomy or a partial nephrectomy. The postoperative results are very good in a high percentage of cases. In bilateral cases, the revascularization surgical procedures improve or normalize also the impaired renal function.
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PMID:[Renovascular hypertension in childhood]. 182 81

A boy born to healthy, unrelated parents, presented at birth with hypotonia and seizures. Very long chain fatty acids in the plasma were strongly elevated; bile acid intermediates and plasmalogen biosynthesis were normal. Acyl-CoA oxidase activity was normal. The patient died at the age of 3 months. The cerebellum and medulla oblongata showed neuronal migration defects. The specific biochemical basis for the impaired peroxisomal beta-oxidation has not been found. The three immunoreactive peroxisomal beta-oxidation enzymes and catalase were localized in the hepatocellular peroxisomes. Aberrant features of the peroxisomes included: a subpopulation of organelles larger than 1 micron, an amorphous nucleoid in many organelles, and invaginations of the peroxisomal membrane into the matrix. Peroxisomes in the proximal renal tubules also contained the three immunoreactive beta-oxidation enzymes. Regularly spaced trilamellar inclusions were seen in hepatic macrophages; they were much more abundant in adrenocortical macrophages. The inclusions were birefringent and resistant to acetone extraction. Distinct hepatic fibrosis had developed over a period of 2.5 months. We speculate that the impaired beta-oxidation is due to a defect at the level of the peroxisomal carnitine octanoyl or -acetyl transferase, responsible for the export of beta-oxidation products.
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PMID:Peroxisomal localization of the immunoreactive beta-oxidation enzymes in a neonate with a beta-oxidation defect. Pathological observations in liver, adrenal cortex and kidney. 194 12

In 15 patients we hypothesized the origin of epilepsies to be 'extratemporal' based on videotaped seizures and surface EEG. Neuropsychological tests and neuroimaging (CAT, MRI, and PET scans) were then compared to the hypothesized ictal sites. Neuropsychological tests were abnormal in 86.6% and FDG-PET scans were abnormal in 73%. The neuropsychological tests and PET localized or lateralized areas of dysfunction to the same sites as electroclinical characteristics did in 85% of patients (P less than 0.01, Fisher exact test). No statistically significant correlation between lesion sites on CT and MRI and the ictal origin was observed due to the high proportion of normal or non-specific scans. These observations should be verified in a larger series of extratemporal seizures.
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PMID:Multidisciplinary analysis of patients with extratemporal complex partial seizures. I. Intertest agreement. 210 81

Epilepsy complicates severe head trauma. Development of persistent seizures appears to correlate with the extent of trauma. Although early reports suggested that prophylactic administration of antiepileptic drugs would prevent epileptogenesis, controlled studies have failed to corroborate this assumption. Head trauma initiates a sequence of responses that includes altered blood flow and vasoregulation, disruption of the blood-brain barrier, increases in intracranial pressure, focal or diffuse ischemia, hemorrhage, inflammation, necrosis, and disruption of fiber tracts. The presence of an intracranial hematoma has a robust association with the development of post-traumatic epilepsy. Extravasation of blood is followed by hemolysis and deposition of heme-containing compounds into the neuropil, initiating a sequence of univalent redox reactions and generating various free radical species, including superoxides, hydroxyl radicals, peroxides, and perferryl ions. Free radicals initiate peroxidation reactions by hydrogen abstraction from methylene groups adjacent to double bonds of fatty acids and lipids within cellular membranes. Intrinsic enzymatic mechanisms for control of free radical reactions include activation of catalase, peroxidase, and superoxide dismutase. Steroids, proteins, and tocopherol also terminate peroxidative reactions. Tocopherol and selenium are effective in preventing tissue injury initiated by ferrous chloride and heme compounds. Treatment strategies for prevention or prophylaxis of post-traumatic epilepsy must await absolute knowledge of mechanisms. Antioxidants and chelators may be useful, given the speculation that peroxidative reactions may be an important component of brain injury responses. However, potential treatment strategies involving gamma-aminobutyric acid (GABA) agonists, NMDA receptor antagonists, and barbiturates need further scientific assessment.
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PMID:Post-traumatic epilepsy: cellular mechanisms and implications for treatment. 222 73

Adult female, Fischer-344 rats were exposed to 275 mg/kg of tris(2-chloroethyl)phosphate (TRCP) by gavage. TRCP produced consistent signs of convulsive activity within 60-90 min after dosing and extensive loss of CAT hippocampal pyramidal cells when examined 7 days after dosing. At the light microscopic level, toxic effects of TRCP on pyramidal cells in the CA3 and CA4 regions and on granule cells in the dentate gyrus were less severe than those on the CA1 cells. The seizure-related and neurohistological effects of TRCP were significantly attenuated by pretreatment with atropine or chlordizepoxide, suggesting that the hippocampal damage was related to the seizures produced by TRCP. In a second experiment designed to assess the potential health risk associated with TRCP, exposed rats were mildly impaired in the acquisition of a reference memory task in a water maze. However, TRCP-exposed rats were consistently impaired in performing a repeated acquisition task in the water maze. These data underscore the potential health risk associated with exposure to TRCP and support the conclusion that the hippocampus is intimately involved in spatial memory in rats.
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PMID:Acute exposure to tris(2-chloroethyl)phosphate produces hippocampal neuronal loss and impairs learning in rats. 225 15


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