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PubMed1976

[Frontal, or generalized, epilepsy].

The author studied the results of surgical treatment of 28 epileptic patients where the localization of the epileptogenic focus was on the medial surface of the hemisphere in the area of the frontal pole or on the lateral surface. Taking into consideration the theoretical premises, an analysis of literary data and the results of a comprehensive clinical study of patients the author comes to the conclusion that for a localization of the epileptogenic focus in the area of the pole and medio-basal parts of the frontal lobes primary generalized epileptic seizures and distant synchronous bioelectrical activity in the EEG without distinct focal changes are most characteristic.

Epilepsy↗
PubMed2006

Why does fever trigger febrile seizures? GABAA receptor gamma2 subunit mutations associated with idiopathic generalized epilepsies have temperature-dependent trafficking deficiencies.

With a worldwide incidence as high as 6.7% of children, febrile seizures are one of the most common reasons for seeking pediatric care, but the mechanisms underlying generation of febrile seizures are poorly understood. Febrile seizures have been suspected to have a genetic basis, and recently, mutations in GABAA receptor and sodium channel genes have been identified that are associated with febrile seizures and generalized seizures with febrile seizures plus pedigrees. Pentameric GABAA receptors mediate the majority of fast synaptic inhibition in the brain and are composed of combinations of alpha(1-6), beta(1-3), and gamma(1-3) subunits. In alphabetagamma2 GABAA receptors, the gamma2 subunit is critical for receptor trafficking, clustering, and synaptic maintenance, and mutations in the gamma2 subunit have been monogenically associated with autosomal dominant transmission of febrile seizures. Here, we report that whereas trafficking of wild-type alpha1beta2gamma2 receptors was slightly temperature dependent, trafficking of mutant alpha1beta2gamma2 receptors containing gamma2 subunit mutations [gamma2(R43Q), gamma2(K289M), and gamma2(Q351X)] associated with febrile seizures was highly temperature dependent. In contrast, trafficking of mutant alpha1beta2gamma2 receptors containing an alpha1 subunit mutation [alpha1(A322D)] not associated with febrile seizures was not highly temperature dependent. Brief increases in temperature from 37 to 40 degrees C rapidly (<10 min) impaired trafficking and/or accelerated endocytosis of heterozygous mutant alpha1beta2gamma2 receptors containing gamma2 subunit mutations associated with febrile seizures but not of wild-type alpha1beta2gamma2 receptors or heterozygous mutant alpha1(A322D)beta2gamma2 receptors, suggesting that febrile seizures may be produced by a temperature-induced dynamic reduction of susceptible mutant surface GABAA receptors in response to fever.

Animals↗
PubMed1986

Opioid receptor alterations in a genetic model of generalized epilepsy.

Autoradiography was used to examine opioid receptor binding in the Mongolian gerbil, a genetic model of the epilepsies. Coronal brain sections of seizure-resistant (SR) and seizure-sensitive (SS) (both pre- and post-seizure conditions) gerbils were labeled with [3H]dihydromorphine. SS (pre-seizure) gerbils demonstrated overall greater brain opioid binding when compared to SR animals. The periaqueductal gray, substantia nigra and medial geniculate body were specific areas in SS (pre-seizure) gerbils which demonstrated highly significant increases in opioid binding compared to SR animals (% increase vs SR were 98%, 91.3% and 42.9%, respectively). Scatchard analysis demonstrated that the increase in opioid binding was due to an increase in the total number of receptors without a significant change in receptor affinity (i.e. periaqueductal gray area: total number of binding sites was 12.7 (SR) and 18.0 fmol/mg tissue (SS pre-seizure), while Kd values were 4.0 (SR) and 4.0 mM (SS pre-seizure). Opioid binding was also increased in the SS (post-seizure) animals when compared to SR animals, especially in the substantia nigra. However, when compared to SS (pre-seizure) gerbils, there was a general but not significant, decrease in opioid binding in SS post-seizure gerbils. The increased opioid binding in the SS (pre-seizure) gerbil compared to SR gerbils could reflect an up-regulation due to a deficit in endogenous ligand (e.g. a deficit in synthesis or decreased release) which could underlie the seizure diathesis in the gerbil.

Animals↗
PubMed2003

Clinically important drug interactions in epilepsy: general features and interactions between antiepileptic drugs.

There are two types of interactions between drugs, pharmacokinetic and pharmacodynamic. For antiepileptic drugs (AEDs), pharmacokinetic interactions are the most notable type, but pharmacodynamic interactions involving reciprocal potentiation of pharmacological effects at the site of action are also important. By far the most important pharmacokinetic interactions are those involving cytochrome P450 isoenzymes in hepatic metabolism. Among old generation AEDs, carbamazepine, phenytoin, phenobarbital, and primidone induce the activity of several enzymes involved in drug metabolism, leading to decreased plasma concentration and reduced pharmacological effect of drugs, which are substrates of the same enzymes (eg, tiagabine, valproic acid, lamotrigine, and topiramate). In contrast, the new AEDs gabapentin, lamotrigine, levetiracetam, tiagabine, topiramate, vigabatrin, and zonisamide do not induce the metabolism of other AEDs. Interactions involving enzyme inhibition include the increase in plasma concentrations of lamotrigine and phenobarbital caused by valproic acid. Among AEDs, the least potential interaction is associated with gabapentin and levetiracetam.

Anticonvulsants↗
PubMed1984

Immunohistochemical localization of extravasated serum albumin in the hippocampus of human subjects with partial and generalized epilepsies and epileptiform convulsions.

Human serum albumin-like immunoreactivity was detected by the peroxidase-antiperoxidase method in histological sections of the hippocampus from epileptic and control brains obtained on routine autopsies. In the hippocampi of epileptic patients immunoreactive astrocytes were found, the number of which was increasing with the severity of the manifest convulsions. The highest numbers of immunoreactive astrocytes were observed in those patients who died in status epilepticus. Hippocampi from control patients with no neurologic disorders in life were devoid of immunoreactive astrocytes. The results are discussed in terms of the breakdown of the blood-brain barrier during epileptic seizures.

Adult↗
PubMed1990

Selective electroencephalograph-guided microsurgical callosotomy for refractory generalized epilepsy.

Between 1978 and 1985, 35 patients with medically refractory multiform seizures were submitted for sections of variable portions of the corpus callosum. Guided by intraoperative electroencephalographic and electrocorticographic monitoring, the section was carried out only in the portion of callosum that was involved in the maintenance of the bilaterally synchronous slow spike and wave discharge (as documented by intraoperative electrocorticography). In our patients, only part of the frontal corpus callosum needed to be sectioned to interrupt the bilateral synchrony of epileptic discharge. Of the 35 patients, operated on, 28 have had an adequate long-term follow up and are presented herein. All had significant improvement in seizure frequency and psychosocial functioning.

Adolescent↗
PubMed2006

Giant subcortical high-frequency SEPs in idiopathic generalized epilepsy: a protective mechanism against seizures?

OBJECTIVE: Recently, we found that high-frequency somatosensory evoked potentials (HF-SEPs), which are modulated by arousal-related structures, were abnormally enhanced during N-REM sleep in two seizure-free IGE patients [Restuccia D, Rubino M, Valeriani M, Della Marca G. Increase of brainstem high-frequency SEP subcomponents during light sleep in seizure-free epileptic patients. Clin Neurophysiol 2005; 116: 1774-1778]. Here, we aimed at verifying whether similar HF-SEP abnormalities were significantly correlated to the clinical outcome in a larger population of untreated IGE patients. METHODS: Patients were classified as Juvenile Myoclonic epilepsy (JME; six patients) and Childhood or Juvenile Absence epilepsy (CAE and JAE, six patients). They were untreated because newly diagnosed, or because seizure-free. HF-SEPs from patients were compared with those obtained from 21 healthy volunteers. RESULTS: HF-SEPs were abnormally enhanced in all seizure-free CAE-JAE patients, whereas they were normal in all JME patients and in CAE-JAE patients with frequent seizures. Not only scalp distribution, but also dipolar source analysis suggested a subcortical origin for these enhanced subcomponents, possibly in the brainstem. CONCLUSIONS: The enhancement of HF-SEPs might reflect the hyperactivity of arousal-related brainstem structures; such an enhancement was found in all seizure-free CAE-JAE patients, while it was never observed in JME patients. SIGNIFICANCE: We speculate that the hyperactivity of arousal-related brainstem structures might account for the different clinical outcome among IGE subsyndromes.

Adolescent↗
PubMed1999

Predictors for recurrence of epileptic seizures in a general epilepsy population.

The aim of our study was to identify predictors for recurrence of epileptic seizures in a large county hospital population. We identified 956 patients (18-67 years) with ICD 9 code 345 as primary diagnosis, seen at the Central Hospital of Akershus over 7 years (1987-1994). The diagnosis of epilepsy was confirmed for 696 of the patients. These were divided into two groups: (1) no seizures during the previous year (n = 485) and (2) seizures during the previous year (n = 184). To identify predictors for recurrence of seizures, we used neurologic deficit, number of AEDs used, CT-scan findings, EEG findings, aetiology, gender, age below and above 50 years and comorbidity as independent variables in a logistic regression model. In a univariate analysis, the strongest predictors for recurrence of seizures were: age above 50 years (OR = 5.2;P < 0.0001), known aetiology (OR = 1.4;P = 0.04) and use of two or more AEDs (OR = 5. 7;P < 0.0001). In the multivariate analysis age, more than 50 years (OR = 1.7;P = 0.0216) and use of two or more AEDs (OR = 5.6;P < 0.0001) were the only predictors for recurrence of epileptic seizures.

Adolescent↗