Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report an infant with Shaken Baby syndrome (SBS) who presented with status epilepticus. The initial evaluation with computerized axial tomography (CAT scan) of the head was normal, and there was no history or physical finding consistent with physical abuse or shaking. This prompted an extensive evaluation to determine the etiology of the seizures. An ophthalmology consultation revealed the presence of severe bilateral retinal hemorrhages, which raised the possibility of SBS. Magnetic resonance imaging (MRI) showed cerebral hemorrhages, hemorrhagic contusions, and bilateral subtemporal subdural hematomas. This is the first reported case of SBS diagnosed by magnetic resonance imaging following a normal initial CAT scan. MRI may be a valuable tool in the diagnosis of brain injury in SBS and may be particularly valuable when the CAT scan of the head is normal, the etiology of neurologic injury is unclear, and the presence of retinal hemorrhages raises the suspicion of SBS.
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PMID:Shaken baby syndrome diagnosed by magnetic resonance imaging. 269 92

Poisoning is an uncommon manifestation of child abuse. The intentional administration of water to a child as a form of punishment has rarely been reported as the responsible substance among children who have been poisoned. We describe a case of a 5-year-old girl presenting with severe hyponatremia due to acute water intoxication. The patient was brought to the emergency room in status epilepticus. A history was obtained from the child's mother stating that the patient had been playing outside when she collapsed. She had had no known prior illnesses. Laboratory evaluation included a hemoglobin of 10.1 mg%, glucose of 60 mg%, serum sodium of 107 mEq/l, potassium of 3.2 mEq/l and chloride of 71 mEq/l. A CAT scan obtained approximately 1 h after admission revealed generalized cerebral edema. Careful examination of the skin revealed multiple linear ecchymosis of varying ages on the back and thighs and a hand print on the right flank. In addition, the child demonstrated severe failure to thrive with height, weight and bone age compatible with a 2.5-year-old girl. Appropriate therapy for severe hyponatremia was successfully instituted. For the next 12 h she was deeply somnolent, but the following morning was alert and conversant. She stated that she "would be good if she didn't have to drink any more water". The child's mother subsequently admitted that she frequently used water ingestion as a form of punishment. The child stabilized metabolically and demonstrated rapid in-hospital weight gain. She was placed in foster care at discharge and has had no further hyponatremia or seizures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyponatremic seizures as a presenting symptom of child abuse. 395 93

Experimental data indicate that acute hyperglycaemia can aggravate the consequences of epileptic seizures on the permeability of the blood-brain barrier (BBB). The purpose of this study was to examine the effects of chronic administration of alpha -tocopherol (vitamin E) and acute catalase administration on the disrupted BBB during experimentally pentylenetetrazole-induced status epilepticus in acute hyperglycaemic rats. The integrity of the BBB was tested using the Evans Blue (EB) dye extravasation. The concentration of EB dye was measured in four regions of the brain. Epileptic seizures induced a significant increase in EB dye extravasation in the brain regions compared with that of the groups of rats treated with saline, glucose, catalase and alpha -tocopherol (P< 0.01). The content of EB dye in the brain regions of animals in the acute hyperglycaemia plus epileptic group was higher than that of the saline, glucose, catalase, alpha -tocopherol and epileptic groups (P< 0.01). The increased EB dye transfer from blood to the brain in status epilepticus and acute hyperglycaemia plus status epilepticus was attenuated by the treatment with catalase and alpha -tocopherol. These data suggest that a partial reduction in the production of reactive oxygen species by catalase and alpha -tocopherol contributes to decreases in the content of EB dye across the BBB during pentylenetetrazole-induced status epilepticus in acute hyperglycaemic rats.
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PMID:Catalase and alpha-tocopherol attenuate blood-brain barrier breakdown in pentylenetetrazole-induced epileptic seizures in acute hyperglycaemic rats. 1184 25

The mechanism underlying the vulnerability of the brain to status epilepticus (SE) induced by pilocarpine remains unknown. Oxidative stress has been implicated in a variety of acute and chronic neurologic conditions, including SE. The present study was aimed at was investigating the changes in catalase activity after pilocarpine-induced seizures and SE. The Control group was treated with 0.9% saline (NaCl, subcutaneously (s.c.)) and sacrificed 1h after the treatment. Another group was treated with pilocarpine (400 mg/kg, s.c., Pilocarpine group) and sacrificed 1h after treatment. The catalase activity in the cerebellum, hippocampus, frontal cortex and striatum of Wistar rats was determined. The results have shown that pilocarpine administration and resulting SE produced a significant increase in the catalase activity in the hippocampus (36%), striatum (31%) and frontal cortex (15%) of treated adult rats. Nevertheless, in the adult rat cerebellum after SE induced by pilocarpine no change was observed in the catalase activity. Our results demonstrated a direct evidence of an increase in the activity of the scavenging enzyme (catalase) in different cerebral structures during seizure activity that could be responsible for eliminating oxygen free radicals and might be one of the compensatory mechanisms to avoid the development of oxidative stress during the establishment of SE induced by pilocarpine. Our reports also indicate clear regional differences in the catalase activity caused by pilocarpine-induced seizures and SE and the hippocampus might be the principal area affected and cerebellum does not modify for this parameter studied during epileptic activity.
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PMID:Catalase activity in cerebellum, hippocampus, frontal cortex and striatum after status epilepticus induced by pilocarpine in Wistar rats. 1524 87

The role of oxidative stress in pilocarpine-induced status epilepticus was investigated by measuring lipid peroxidation level, nitrite content, GSH concentration, and superoxide dismutase and catalase activities in the hippocampus of Wistar rats. The control group was subcutaneously injected with 0.9% saline. The experimental group received pilocarpine (400 mg.kg(-1), subcutaneous). Both groups were killed 24 h after treatment. After the induction of status epilepticus, there were significant increases (77% and 51%, respectively) in lipid peroxidation and nitrite concentration, but a 55% decrease in GSH content. Catalase activity was augmented 88%, but superoxide dismutase activity remained unaltered. These results show evidence of neuronal damage in the hippocampus due to a decrease in GSH concentration and an increase in lipid peroxidation and nitrite content. GSH and catalase activity are involved in mechanisms responsible for eliminating oxygen free radicals during the establishment of status epilepticus in the hippocampus. In contrast, no correlations between superoxide dismutase and catalase activities were observed. Our results suggest that GSH and catalase activity play an antioxidant role in the hippocampus during status epilepticus.
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PMID:Oxidative stress in the hippocampus after pilocarpine-induced status epilepticus in Wistar rats. 1575 49

Catalase is one of the enzymes that convert hydrogen peroxide (H2O2) to H2O presenting a protective role against free radicals. In this study, catalase activity was determined in homogenates of striatum (ST) and prefrontal cortex (PFC) in order to examine the participation of oxidative stress (OS) on cocaine actions in mice brain. Male Swiss mice were injected (i.p.) with cocaine at low (10 and 30 mg/kg) and high doses (90 mg/kg), and observed for 1 h. After cocaine overdose (90 mg/kg) some animals presented only status epilepticus (SE) while others died after seizures. These animals were dissected and divided in two groups, SE and death. Catalase activity was also determined after pretreatment with the anticonvulsant drug, diazepam, alone or injected before cocaine 90 mg/kg, and after seizures induced by a high dose of bupropion, a known inhibitor of NE and DA reuptake used for comparison. Results showed a decrease in catalase activity of the PFC and ST after SE and death induced by cocaine and bupropion overdoses. Cocaine at low doses decreased the enzyme activity only in ST. Diazepam treatment alone and before cocaine overdose did not interfere with catalase activity. This reduction in catalase activity may reflect an increase in H2O2 content in PFC and ST. Previous data reports that H2O2 inhibits dopamine transporter activity, suggesting that the decrease in catalase activity may potentiate the toxic mechanism of drugs that inhibit monoamines reuptake. As far as we know, this is the first report showing an involvement of OS in the cocaine's central mechanism of action.
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PMID:Cocaine alters catalase activity in prefrontal cortex and striatum of mice. 1608 63

Pilocarpine is a cholinergic agonist capable to induce seizures and an epilepticus-like state in rodents. This status epilepticus (SE) is an useful animal model to study the development and understanding of the neuropathology, behavioural and electroencephalographic alterations of human temporal lobe epilepsy. It has been suggested a relationship between SE and reactive oxygen species (ROS) that can result in seizure-induced neurodegeneration. The aim of this study was to evaluate the existence of oxidative damage and the changes in the antioxidant system in cortex after administration of a high pilocarpine dose. Rats were injected with pilocarpine (350 mg/kg i.p.) or with saline as control and 2h after the animals were sacrificed. Malondialdehyde (MDA) levels, as marker of lipid peroxidation, significantly increased (64%) after pilocarpine treatment evidencing oxidative damage. Antioxidant enzyme activities--catalase (CAT), glutathione peroxidase (GP) and superoxide dismutase (SOD)--significantly increased in response to pilocarpine (28%, 28% and 21%, respectively). GP and Mn-SOD gene expression were induced by pilocarpine treatment. Vitamin E concentration in brain cortex decreased (15%) as result of pilocarpine administration. In conclusion, the high dose of pilocarpine, used in the present study, induces oxidative damage and increases antioxidant enzyme activities and expression in brain cortex. Moreover, increased lipid peroxidation produces the consumption of Vitamin E.
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PMID:Antioxidant response and oxidative damage in brain cortex after high dose of pilocarpine. 1720 54

Experimental manipulations suggest that in vivo administration of exogenous antioxidants agents decreases the concentration of free radical in the brain. Neurochemical studies have proposed a role for catalase in brain mechanisms responsible by development to status epilepticus (SE) induced by pilocarpine. The present study was aimed at was investigating the changes in catalase activities after pilocarpine-induced SE. Animals were treated with vitamin E (VIT E) 200 mg/kg (intraperitoneally (i.p.)) and, 30 min later, they received pilocarpine hydrochloride, 400 mg/kg, subcutaneous (s.c.) (P400). Other three groups received VIT E (200 mg/kg, i.p.), pilocarpine (400 mg/kg, s.c.) or 0.9% NaCl (control) alone. Animals were closely observed for behavioral changes, tremors, stereotyped movements, seizures, SE and death, for 24 h following the pilocarpine injection. The brains were dissected after decapitation. The results have shown that pilocarpine administration and resulting SE produced a significant increase in hippocampal catalase activity of (88%). In the group pre-treated which VIT E in hippocampal catalase activity was increase of 67% and 214% when compared with P400 and control group, respectively. Our results demonstrated a direct evidence of an increase in the activity of the hippocampal catalase of rat adults during seizure activity and after the pre-treated which VIT E that could be responsible by regulation of free radical levels during the establishment of SE.
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PMID:Effects of the vitamin E in catalase activities in hippocampus after status epilepticus induced by pilocarpine in Wistar rats. 1738 94

Vitamin C (VIT C) is an exogenous antioxidant able to alter the brain oxidative stress. Antioxidant properties have been showed in seizures and status epilepticus (SE) induced by pilocarpine in adult rats. This present study was aimed at was investigating the VIT C effects on latency to first seizure, in percentage of seizures, mortality rate, as well as hippocampal lipid peroxidation levels and catalase activity after seizures and SE. The VIT C effects were investigated after the pretreatment with dose 250 mg/kg, i.p., 30 min before pilocarpine administration (400mg/kg, s.c., pilocarpine group (P400)). The VIT C increase the latency to first seizure and decrease the mortality rate and lipid peroxidation levels. In P400+VIT C and VIT C groups were observed an increase in hippocampal catalase activity. Our results suggests that the vitamin C can exert antioxidant and anticonvulsive effects in adult rats, suggesting that this vitamin can be able by reduction of lipid peroxidation content and increased of catalase enzymatic activity which cerebral compensatory mechanisms in free radical formation during SE.
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PMID:Vitamin C antioxidant effects in hippocampus of adult Wistar rats after seizures and status epilepticus induced by pilocarpine. 1751 18

In the present study, we examined the neuroprotective effects of vitamin C in adult rats after pilocarpine-induced seizures. Vitamin C is an exogenous antioxidant that can be used in treatment of seizures. It can alter oxidative stress and damage neuronal induced by seizures. Its antioxidant properties can be proved in epilepsy models, such as pilocarpine-induced seizures in adult rats. In order to investigate neuroprotective effects of vitamin C, adult male rats (2 months-old) were pretreated with vitamin C (VIT C 250 mg/kg, i.p.) 30 min before receiving pilocarpine (400 mg/kg, s.c., P400 group). The other three groups were treated with vitamin C (VIT C group) and saline 0.9 (control group) alone. The pretreatment with vitamin C increased the latency to first seizures and reduced mortality rate after pilocarpine-induced seizures. Pretreatment with vitamin C alone decrease lipid peroxidation levels when compared to pilocarpine group and P400+VIT C. In P400, P400+VIT C and VIT C groups were observed an increased hippocampal catalase activity when compared to control group. Our results can suggest that neuroprotective effects of vitamin C in adult rats can be the result of reduced lipid peroxidation levels and increase of catalase activity after seizures and status epilepticus induced by pilocarpine.
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PMID:Neuroprotective actions of vitamin C related to decreased lipid peroxidation and increased catalase activity in adult rats after pilocarpine-induced seizures. 1809 15


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