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)

Four prolonged episodes of partial complex status epilepticus were observed in a teenaged girl. During each there was an "ictal" phase, in which her mental state frequently fluctuated between mildly clouded consciousness and almost total unresponsiveness; once, she was also blind during this phase of impaired consciousness. With therapy, the periods of unresponsiveness became less frequent and less prolonged until a second, "postictal," phase occurred when she was alert, but with profound retrograde and anterograde amnesia that gradually resolved in several weeks. The "ictal" EEG pattern always consisted of lateral temporo-occipital fast and sharp waves continually alternating with slow activity. These cycled independently in the two hemispheres and correlated with the fluctuating behavioral state. During the "postictal" phase the EEG was diffusely slow with isolated bilaterally independent temporal spikes. The key to the diagnosis of partial complex status epilepticus may be the fluctuating mental state. Recognition and prompt treatment of this disorder are important since delay could result in prolonged or enduring memory impairment.
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PMID:Prolonged partial complex status epilepticus: EEG and behavioral observations. 56 60

Domoate, a glutamate analog, is believed to be responsible for a seafood poisoning incident that caused acute neurological disturbances and chronic memory impairment in some victims, with the incidence of mortality and neuropsychological morbidity being highest among the aged. Domoate expresses neurotoxic (excitotoxic) activity in vitro by an action at the kainate subtype of glutamate receptor, and when administered to adult rats, it mimics kainate in causing status epilepticus and a severe seizure-brain damage syndrome. Because domoate is exceedingly expensive, we explored the feasibility of using kainate to study the age-linked features of domoate neurotoxicity. We administered kainate subcutaneously in various doses to young (5-6 months), middle-aged (12-13 months), and old (22-25 months) rats and found the middle-aged and old rats significantly more sensitive than young rats to the neurotoxic actions of kainate. Low doses of kainate, which were nontoxic to young rats, frequently triggered status epilepticus, associated brain damage, and precipitous death in old rats. Middle-aged rats were more sensitive than young rats, but less sensitive than old rats to kainate neurotoxicity. These results suggest that the kainate-treated rat may be a useful model for studying mechanisms underlying age-related aspects of the human domoate neurotoxic syndrome.
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PMID:Age-related sensitivity to kainate neurotoxicity. 174 99

The authors report on the results of clinical investigations, treatment and follow-up of a 9-year old boy with complex partial status epilepticus (CPSE) which occurred after the first onset of partial secondary generalized epileptic seizures. Electroencephalografic recordings during status epilepticus showed a diffuse, generalized, high-voltage delta dysfunction and bilateral epileptiform activity, with local maximum over the posterior right temporal parietal regions. Parenteral administration of diazepam, phenytoin and phenobarbitone as choice anticonvulsant drugs, failed to stop CPSE in the patient. Only by continuous intravenous infusion of chlormethiazole (Heminevrin) status epilepticus was successfully controlled. Paroxysmal discharges on electroencephalogram disappeared and attenuation of slow wave activity was evident. Memory deficits and the elements of nominal dysphasia and tactile dysgnosia were apparent soon after cessation of CPSE and may be related to the signs of maximal local electroencephalographic dysfunction. Later testings after complete seizure control by chlormethiazole and phenytoin given orally, showed almost normal results. No side effects were encountered. A more common chlormethiazole administration as a useful therapeutic agent in the management of CPSE especially in children with refractory and long-time status, would be mandatory. Since chlormethiazole is free from serious side effects, its earlier use in the control of epileptic status may help to preclude some severe cognitive effects and to evade the use of barbiturate anesthesia as the last therapeutic resort.
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PMID:[Chlormethiazole in the treatment of complex partial epileptic status in childhood]. 178 23

Male Wistar rats were subjected to pilocarpine-induced status epilepticus and allowed to recover. After reaching the chronic state with spontaneous seizures they were tested in an 8-arm radial maze. During learning trials, epileptic rats made significantly more errors than controls. Even in the last trials epileptic rats did not improve their performance, indicating severe learning disability. These results suggest that spontaneous seizures after pilocarpine-induced status epilepticus are a useful model for studying the learning and memory impairment detected in some cases of symptomatic epilepsy.
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PMID:Learning impairment in chronic epileptic rats following pilocarpine-induced status epilepticus. 210 Oct 94

A 70 year-old-man with recurrent herpetic keratitis had a meningo-encephalitis with transient left hemiplegia and disorders of consciousness. EEG disclosed periodic slow waves on the right temporal region. Isotope and CT scans showed focal abnormalities in the same region. Antibodies to herpes simplex virus were demonstrated by complement fixation in serum and specific antiherpes IgG and IgM by immunofluorescence assay in serum and CSF. A year later the patient had a status epilepticus. CT scan showed a large right temporal hypodense area. CSF was abnormal with pleiocytosis, increased protein and IgG levels. High titers of antiherpes IgG persisted in serum and CSF. Neuropsychological tests did not demonstrate any memory impairment. The occurrence of persistent inflammation after herpes simplex encephalitis is discussed. The unusual benign course without antiviral therapy, may be related to the reactivation of a latent infection with an efficient immunological response. The unilateral temporal necrosis may explain the absence of amnestic sequelae.
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PMID:[Acute necrotizing herpetic encephalitis with a spontaneously improving clinical course]. 669 26

Tiagabine exerts its antiepileptic drug (AED) activity by selectively inhibiting the uptake of gamma-aminobutyric acid (GABA) onto the transporter molecules, and thus, increasing extracellular concentrations of GABA in the brain. The absorption and elimination of tiagabine follow linear pharmacokinetics. Tiagabine is metabolized by hepatic cytochrome P450 enzymes and enzyme-inducing AEDs increase tiagabine clearance by 50-65%. Tiagabine has shown no clinically important interactions with other drugs, including oral contraceptives. In the perforant pathway stimulation model of status epilepticus, tiagabine reduced the seizure number and severity, and also prevented the loss of pyramidal cells in the hippocampus as well as alleviated impairment of the spatial memory impairment associated with hippocampal damage. Tiagabine has both antiepileptogenic and anticonvulsant effects in the kindling model of epilepsy. Based on the data from the short- and long-term add-on studies, tiagabine is effective adjunctive therapy for all partial seizure types in adolescents and adults. Conversion to tiagabine monotherapy has been also possible in substantial amount of patients with partial seizures in three trials. Tiagabine is generally well-tolerated. The most common adverse events in controlled studies involve the central nervous system; for example, dizziness, asthenia, nervousness, tremor, depressed mood and emotional lability. Special safety analyses with formal neuropsychological testing suggest that tiagabine does not adversely affect cognition or mood. Tiagabine represents an important new therapeutic option for patients with treatment-refractory partial seizures. The role of tiagabine in the management of partial epilepsy of patients with intellectual disability is especially emphasized since tiagabine has a low side-effect profile in the cognitive area.
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PMID:Tiagabine: a new therapeutic option for people with intellectual disability and partial epilepsy. 1003 Apr 35

Previous studies have demonstrated that remacemide and its desglycinyl metabolite, AR-R 2495AA, reduce neuronal damage in animal models of ischemia, subarachnoid hemorrhage, and traumatic brain injury. The aim of the present study was to investigate whether remacemide hydrochloride also alleviates seizure-induced neuronal damage in a model of status epilepticus induced by the stimulation of the perforant pathway (PP) in the rat. Chronic oral remacemide treatment (3 x 25 mg/kg/day) was started either 2 days before or 2 h after the beginning of PP stimulation (2 mA, 20 Hz, 0.1 ms pulse duration for 60 min). The effects of remacemide treatment on the severity of seizures, electroencephalogram (EEG) parameters, seizure-induced neuronal damage in the temporal lobe regions, and memory impairment were compared to unstimulated and stimulated vehicle-treated controls, and carbamazepine-pre-treated (3 x 40 mg/kg/day) rats. Both remacemide and carbamazepine pretreatments, but not remacemide posttreatment, decreased pyramidal cell damage in the CA3 and CA1 subregions of the hippocampus (P < 0.05). In addition, overall neuronal damage in the extrahippocampal temporal lobe regions (the piriform cortex, entorhinal cortex, and the amygdaloid complex) was milder in remacemide-pretreated rats compared to stimulated control rats (P < 0.01). The neuroprotective effect was most evident on the side contralateral to stimulation. Remacemide or carbamazepine pretreatment had no evident effect on the number or duration of behavioral seizures during PP stimulation. Neither drug altered the spectral parameters of the baseline EEG or prevented status epilepticus-induced EEG slowing observed 2 weeks after PP stimulation. Nor did remacemide or carbamazepine treatment alleviate spatial memory impairment determined in a Morris water-maze task 2 weeks after PP stimulation. Our data provide evidence that pretreatment with remacemide has a moderate neuroprotective effect against status epilepticus-induced neuronal damage.
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PMID:Neuroprotective effect of remacemide hydrochloride in a perforant pathway stimulation model of status epilepticus in the rat. 1021 40

The aim of this study was to evaluate the influence of 7-acetyl-5-(4-aminophenyl)-8,9-dihydro-8-methyl-7H-1,3-dioxolo(4,5 H)-2,3-benzodiazepine (LY 300164), a selective non-competitive antagonist at alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptors, on the protection provided by diazepam against electrically- and chemically-evoked seizures in rodents. LY 300164 (2 mg/kg) was devoid of any significant action upon each seizure parameter in kindled rats (seizure severity, seizure duration, after-discharge duration). LY 300164 (5 mg/kg) exerted a significant anticonvulsive effect as regards seizure and after-discharge durations. Combined treatment with LY 300164 (2 mg/kg) and diazepam (0.3125-1.25 mg/kg) resulted in the clear-cut anticonvulsive activity. It is noteworthy that the antiseizure potency of the combined treatment (diazepam 1.25 mg/kg plus LY 300164 2 mg/kg) was comparable to that of diazepam (10-20 mg/kg) alone. The combination of diazepam (1.25 mg/kg) with LY 300164 (2 mg/kg) did not induce any significant motor impairment in the rotorod test or memory deficit in the passive-avoidance task. In contrast, diazepam alone (10-20 mg/kg) had pronounced adverse effects in kindled animals. LY 300164 (up to 2 mg/kg) did not influence the threshold for electro- and pentylenetetrazol-induced convulsions but potentiated the anticonvulsive action of diazepam in the maximal electroshock and pentylenetetrazol test in mice, the ED50s of the benzodiazepine being reduced from 13 to 8.7 and from 0.29 to 0.049 mg/kg, respectively. As shown in the passive-avoidance task, combination of LY 300164 (2 mg/kg) with diazepam (8.7 mg/ kg) produced significant motor and long-term memory impairment. Diazepam alone (at the dose equal to its ED50 against maximal electroshock) also caused motor and memory deficits in mice. Interaction at the pharmacokinetic level, at least in plasma, can be excluded, because LY 300164 (2 mg/kg) did not affect the free plasma diazepam concentration. In conclusion, LY 300164 potentiates the protective action of diazepam in some animal models of seizures. This profitable interaction may create a new approach for the treatment of drug resistant epilepsy or status epilepticus.
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PMID:The AMPA/kainate receptor antagonist, LY 300164, increases the anticonvulsant effects of diazepam. 1088 38

We investigated the repetitive manifestation of non-convulsive status epilepticus with an uncommon ictal electroencephalographic pattern observed in two patients suffering from epilepsy (aged 29 and 55 years). The patients had suffered from epilepsy since the age of 1 and 40 years, respectively. Interictal and ictal neurological, neuropsychological and electroencephalographic investigations were carried out. Non-convulsive status started and ended abruptly, clinically as well as electroencephalographically. The ictal electroencephalographic pattern was a monomorphic alpha activity with a generalized bilateral distribution. Altered responsiveness, sometimes eyelid myoclonia (in one patient) and amnesia were the most characteristic clinical findings during non-convulsive status. Intellectual development was delayed in the patient with early onset of epilepsy. However, this was not the case in the other patient, who developed memory impairment during the course of the disease. In both patients, lamotrigine added to valproate reduced the frequency of status epileptici significantly. Obviously, these patients suffer(ed) from a type of generalized non-convulsive status epilepticus with an uncommon electroencephalographic pattern.
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PMID:Ictal generalized rhythmic alpha activity during non-convulsive status epilepticus. 1113 66

Status epilepticus causes neuronal damage that is associated with cognitive impairment. The present study examined whether a novel antiepileptic drug, lamotrigine (LTG), alleviates status epilepticus-induced temporal lobe damage and memory impairment, and compared its efficacy with carbamazepine. Status epilepticus was induced by electric stimulation of the perforant pathway (PP) in rats. Treatment with LTG (12.5 mg/kg, twice a day) was started either 3 days before (preLTG group) or 1 h after (postLTG group) a 60 min PP stimulation. Treatment with carbamazepine (CBZ; 30 mg/kg, twice a day) was started 3 days before (CBZ group) a 60 min PP stimulation. All treatments were continued for 2 weeks. Thereafter, the severity of seizures, seizure-induced neuronal damage, quantitative electroencephalogram (EEG), and memory impairment were compared between vehicle-treated unstimulated and stimulated controls, LTG-treated rats, and CBZ-pretreated rats. Both in the preLTG and postLTG groups, damage to hilar somatostatin-immunoreactive neurons, hippocampal CA3b and CA3a pyramidal cells, and the piriform cortex was mild and did not differ from that in unstimulated controls. Furthermore, CA3c damage in the preLTG group did not differ from that in unstimulated controls. Vehicle-treated stimulated controls and CBZ-pretreated rats, however, had significant damage in the hilus, CA3 subregions, and piriform cortex compared with unstimulated controls (P<0.05 for the stimulated side, contralateral side, or both). Treatment with LTG or CBZ had no effect on the number or duration of behavioral seizures during PP stimulation. They did not affect the baseline EEG or status epilepticus-induced slowing of the EEG. Also, the status epilepticus-induced spatial memory impairment in the Morris water-maze was not attenuated by treatment with LTG or CBZ. Our data demonstrate that treatment with LTG has a mild neuroprotective effect on status epilepticus-induced neuronal damage in rats even when administered after the beginning of status epilepticus.
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PMID:Effect of lamotrigine treatment on status epilepticus-induced neuronal damage and memory impairment in rat. 1151 23


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