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)

Determination of serum prolactin can help distinguish between epileptic and pseudo-epileptic attacks since generalized tonic-clonic and complex partial seizures frequently are accompanied by a transient rise in prolactin. In status epilepticus, however, serum prolactin levels are well within the normal range: cellular depletion due to the prolonged seizure activity has been suggested as a mechanism for this finding. The control of prolactin secretion is complex. Among several possible regulators, inhibitory dopamine and stimulatory thyrotropin-releasing hormone (TRH) may take part in the regulation of prolactin levels in connection with epileptic activity. There may be subpopulations of prolactin-producing cells that react differently in response to various regulators. A dopamine receptor blocker given during status epilepticus brings forth a distinct increase in prolactin levels. In order to add to the understanding of prolactin changes in connection with status epilepticus, we injected TRH i.v. during status epilepticus in seven consecutive patients. All patients had prolactin levels within the normal range (< 25 micrograms/l) before injection of TRH which resulted in at least a two-fold increase in prolactin levels. Our results contradict the hypothesis of cellular depletion of prolactin in connection with status epilepticus. The mechanism behind prolactin values within the normal range after prolonged seizure activity remains unknown.
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PMID:Serum prolactin response to thyrotropin-releasing hormone during status epilepticus. 816 88

In order to more precisely define a syndrome of medial temporal lobe epilepsy, histories and physical findings were evaluated in 67 patients studied with intracranial electrodes who had medial temporal seizure onset and became seizure free following temporal lobectomy. Patients with circumscribed, potentially epileptogenic mass lesions were excluded. Fifty-four patients (81%) had histories of convulsions during early childhood or infancy, 52 of which were associated with fever. Complicated febrile seizures occurred in 33 (94%) of the 35 patients in whom detailed descriptions of the febrile seizures were available. Bacterial (5) or viral (2) central central nervous system infections were present in 7 patients with seizures and fevers. Other less common, but probably significant, risk factors included head trauma (10%) and birth trauma (3%). Only 5 patients had no apparent risk factors. The mean age at habitual seizure onset was 9 years. All patients had complex partial seizures, with half having only complex partial seizures. The other half also had secondarily generalized tonic-clonic seizures, but these were never the predominant seizure type. Only 3 patients had histories of convulsive status epilepticus and no patient had a history of nonconvulsive status epilepticus. All but 3 patients reported auras before some or all of their seizures, with an abdominal visceral sensation being by far the most common type of aura (61%). Of the 60 patients with identified risk factors, all but 2 had an interval between the presumed cerebral insult and the development of habitual seizures, with a mean seizure-free interval of 7.5 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characteristics of medial temporal lobe epilepsy: I. Results of history and physical examination. 825 May 25

The amino acids L-glutamate and L-aspartate have been shown to be excitatory neurotransmitters in mammalian central nervous systems. Antagonists acting selectively at excitatory amino acid receptors have shown antiepileptic properties in several animal models. We report the results of the first therapeutic trial of the competitive NMDA antagonist, D-CPP-ene (SDZ EAA-494), in eight patients with intractable complex partial seizures. All patients withdrew prematurely because of side-effects, including poor concentration (8), sedation (7), ataxia (6), depression (3), dysarthria (2), amnesia (2) and unilateral choreo-athetosis in a patient with contralateral Sturge-Weber syndrome. Seizures were unchanged in four patients and worse in three. A further patient with apparent improvement in seizures in the first week developed complex partial status epilepticus on withdrawal of DCPP-ene. EEG on treatment (5) or in the immediate post-treatment period (2) showed slowing of background activity and, in five cases, an increase in epileptiform activity. Serum concentrations of DCPP-ene were found to be unpredictable and higher than expected from pharmacokinetic data on normal subjects. There was no clear relationship between serum concentrations and the severity of side-effects. Preliminary experience with DCPP-ene in patients with refractory partial seizures is not promising. Evaluation of related compounds is warranted.
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PMID:The excitatory amino acid antagonist D-CPP-ene (SDZ EAA-494) in patients with epilepsy. 826 15

This review emphasizes clinical manifestations, recognition of specific epileptic syndromes, use of antiepileptic drugs, and surgical evaluation and outcome. Juvenile myoclonic epilepsy is increasingly recognized but still underdiagnosed. Good evidence exists for a relationship between Landau-Kleffner syndrome (acquired epileptic aphasia) and electrical status epilepticus during sleep, which reflects the course of the aphasia. In focal onset seizures, the type of aura may be as valuable for determining the lobe of seizure onset as electroencephalographic and neuroimaging techniques. In temporal lobe seizures, postictal language assessment was used to determine the side of origin, and hippocampal and temporal volumetry using magnetic resonance imaging proved reliable indicators of the side of involvement. Valproate sodium and carbamazepine were equally effective for secondarily generalized tonic-clonic seizures, but carbamazepine was superior to valproate for complex partial seizures. One study suggests that in children, increased daytime sleep tendency persists 4 to 5 months after discontinuation of antiepileptic drugs and that neither drugs nor seizure activity are necessarily involved. Many recent publications were devoted to surgical treatment. The main issues reviewed concern patient selection and correlation between preoperative parameters and outcome after surgery.
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PMID:Clinical aspects of epilepsy including diagnosis, management, pharmacotherapy, and surgery. 848 66

Serum levels of prolactin may increase as a consequence of epileptic seizures. The hormone release is caused by the propagation of epileptic activity, usually from the temporal lobe to the hypothalamic-pituitary axis. Due to the intensity of the epileptic afterdischarge, a rise is seen in approximately 60% of complex partial seizures. Prolactin usually fails to rise after psychogenic seizures, therefore, postictal prolactin levels can be used to differentiate between epileptic and psychogenic seizures. However, a subclassification of epileptic seizures by means of prolactin measurement is not possible. In repetitive seizures, prolactin may show a decrease in its postictal release. This is more common in status epilepticus, probably as a result of a diminished propagation of ictal activity during the course of status epilepticus. The influence of chronic epileptic discharges and anticonvulsant medication on prolactin release is moderate.
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PMID:Epilepsy and prolactin in adults: a clinical review. 880 Jun 30

Sixty-three children with new-onset temporal lobe epilepsy (TLE) underwent extensive clinical, EEG, and neuroimaging investigation as part of a prospective, community-based cohort study of the natural history of TLE in childhood. Complex partial seizures occurred in 94% of the children, and tonic-clonic seizures occurred in 14%. Developmental, behavioral, or learning problems were present in 38%. Eighteen children (29%) had a significant illness/event prior to the onset of TLE, including febrile status epilepticus in seven, meningitis in four, respiratory arrest in two, and head injury in one. Magnetic resonance imaging or computed tomography revealed structural abnormalities of the temporal lobe in 24 children (38%), including hippocampal sclerosis (HS) in 13 and tumor in eight. There was a strong association between HS and a history of significant illness/event prior to the onset of TLE (p < 0.001). Analysis of past history and neuroimaging findings led us to propose three etiologically defined subgroups of TLE; developmental TLE (10 children with long-standing, nonprogressive temporal lobe tumors and malformations), TLE with HS/significant antecedents (18 children with HS or a history of a significant illness/event), and cryptogenic TLE (34 children with normal neuroimaging findings and no significant past history). Etiologic differences between children with new-onset TLE may confer prognostic information that will be useful for counselling families and planning treatment.
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PMID:Temporal lobe epilepsy in childhood: clinical, EEG, and neuroimaging findings and syndrome classification in a cohort with new-onset seizures. 933 74

This study analyzes the relative frequency and age of onset of the different seizure types in a 20-year cohort of a pediatric neurology outpatient clinic of an urban hospital that serves the majority of the city's population (Tel Aviv Medical Center). Only patients with two or more unprovoked seizures were included. Neonatal seizures were excluded from the analysis. The different seizure types in descending order of frequency were: partial seizures secondarily generalized (20.6%), complex partial seizures (12.5%), West syndrome (9%), simple partial seizures (8.6%), benign rolandic epilepsy of childhood (8%), absence seizures (7%), generalized tonic-clonic seizures (6.6%), generalized tonic seizures (5%), myoclonic seizures (2.2%), benign occipital epilepsy of childhood (2%), mixed type seizures (1.8%), Lennox-Gastaut syndrome (1.5%), juvenile myoclonic epilepsy (0.9%), atypical absence (0.6%), Landau-Kleffner syndrome, Ohtahara syndrome, myoclonic astatic epilepsy, electrical status epilepticus in sleep and startle epilepsy (0.2% each), and unclassified seizures (12%). The findings of this study confirm that there are more pediatric patients with partial seizures (52%) than primary generalized seizures (33%) and that partial seizures secondarily generalized is the most frequent seizure type in this age group.
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PMID:Epidemiology of epilepsy in childhood: a cohort of 440 consecutive patients. 949 91

1. Rats with spontaneous recurrent seizures (SRS) were obtained by injection of kainic acid (KA; 10 mg/kg SC) to drug-naive rats that regularly developed wet-dog shakes followed by complex partial seizures and status epilepticus. Three to five weeks later, the rats with manifest SRS were selected. 2. The SRS rats were challenged with KA (10 mg/kg SC). The seizures induced in SRS rats by KA were similar to SRS regarding their clinical stage and duration (mean duration of seizures: 44 sec and 43 sec, respectively). The frequency of seizures was, however, increased compared with the frequency of SRS in control, vehicle-treated SRS rats (mean frequency of seizures: 12.9 and 0.4 per 3 hr, respectively). The KA-induced seizures in SRS rats differ behaviorally from KA-induced seizures in naive rats-namely, neither wet-dog shakes nor the status epilepticus could be induced. 3. Repeated injection of an equal dose of KA, applied to the SRS rats 1 day after the previous KA challenge, did not induce seizures. The loss of seizure susceptibility to KA was only temporary, as shown after a 7-day drug-free period, when the repeated injection of KA regained its seizure-triggering capacity. 4. The results indicate that reactivity to the seizure-inducing agent kainic acid changes in rats with spontaneous recurrent seizures.
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PMID:The effects of kainic acid in rats with spontaneous recurrent seizures. 970 17

This is a case study in managing refractory status epilepticus under long-term usage of secobarbital (SB). The patient is a 26-year-old woman with viral encephalitis. Fifteen days after the onset of the disease, status epilepticus with complex partial seizures began. The seizures were so refractory to conventional anti-epileptic drugs, such as valproate, carbamazepine, phenytoin, phenobarbital, clonazepam, lorazepam and lidocaine, that we had to put her on anesthesia with SB for approximately 10 months. Finally, we stopped the administration of SB and support for ventilation; we reduced the dose of SB extremely slowly, using zonisamide at the same time. After trial and error, we found that a reduction of the dosage after long-term anesthesia with high-dose administrations of barbiturate should be made very slowly.
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PMID:[Experience in managing refractory status epilepticus caused by viral encephalitis under long-term anesthesia with barbiturate: a case report]. 980

Kainic acid-induced multifocal status epilepticus in the rat is a model of medically intractable complex partial seizures and neurotoxicity. The exact mechanisms of kainic acid epileptogenic and neurotoxic effects are unknown, but enhanced glutamate release seems to be an important factor. PNU-151774E ((S)-(+)-2-(4-(3-fluorobenzyloxy) benzylamino) propanamide, methanesulfonate) is a broad-spectrum new anticonvulsant with Na+ channel-blocking and glutamate release inhibiting properties. We have examined the effect of pretreatment with this compound on both seizure activity and hippocampal neuronal damage induced by systemic injection of kainic acid in rats. Lamotrigine, a recently developed anticonvulsant with similar glutamate release inhibitory properties, was tested for comparison, together with diazepam as reference standard, on the basis of its anticonvulsant and neuroprotectant properties in this animal model. PNU-151774E, lamotrigine (10, 30 mg/kg; i.p.) and diazepam (20 mg/kg; i.p.) were administered 15 min before kainic acid (10 mg/kg; i.p.). In the vehicle-treated group, kainic acid injection caused status epilepticus in 86% of animals. Hippocampal neuronal cell loss was 66% in the CA4 hippocampal area at 7 days after kainic acid administration. Diazepam inhibited both seizures and neurotoxicity. Lamotrigine reduced hippocampal neuronal cell loss at both doses, even when it did not protect from seizures, although it showed a trend toward protection. On the other hand PNU-151774E protected from both hippocampal neurodegeneration and status epilepticus. Thus, these data support the concept that seizure prevention and neuroprotection might not be tightly coupled. Glutamate release inhibition may play a major role in neuroprotection, but an additional mechanism(s) of action might be relevant for the anticonvulsant activity of PNU-151774E in this model.
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PMID:PNU-151774E protects against kainate-induced status epilepticus and hippocampal lesions in the rat. 983 Dec 89


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