Disease relevance of Epilepsies, Partial

• Comparative data strongly suggest that valproate is the drug of choice for patients with primary and secondarily generalized epilepsies and that it is as effective as other antiepileptic drugs in the treatment of less clearly defined or partial epilepsies beginning in adult life [1].
• In these patients, failure to have a response to valproate therapy appeared to be related to the type of seizure (simple partial seizures alone/complex partial seizures alone, without secondarily generalized tonic-clonic seizures) and longer duration of uncontrolled seizures [2].
• Immunoreactivity of sera from patients with Rasmussen encephalitis (RE) and patients with partial epilepsy (PE) was analyzed by immunohistoblot on rat brain sections and the staining pattern compared with that obtained with antibodies to a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid and NMDA receptors [3].
• CONCLUSIONS: In epilepsies associated with tuberous sclerosis, there may be an interrelation between generalized and localization-related epilepsies, as well as one between generalized and partial seizures [4].
• Valproate, one of the major antiepileptic drugs used today, has besides its wide use in both generalized and partial epilepsies, several new approved indications including the treatment of bipolar disorders, neuropathic pain, and as a migraine prophylaxis [5].

Psychiatry related information on Epilepsies, Partial

• Subclinical seizure activity may be responsible for a portion of the memory deficits found in patients with epilepsy [6].
• Results of experiments with novel inhibitors of GABA uptake, which were inactive in the maximal electroshock seizure test but highly potent against kindled seizures, suggest that such drugs might be more effective than current antiepileptic drugs for treatment of partial epilepsy [7].

High impact information on Epilepsies, Partial

• Here we describe identification of the causative gene in autosomal-dominant partial epilepsy with auditory features (ADPEAF, MIM 600512), a rare form of idiopathic lateral temporal lobe epilepsy characterized by partial seizures with auditory disturbances [8].
• INTERPRETATION: Vigabatrin seems less effective but better tolerated than carbamazepine, which is the first-choice drug for the treatment of partial epilepsies [9].
• Thus, the local release of adenosine resulting in adenosine concentrations <25 nM at the site of action is sufficient to suppress seizure activity and, therefore, provides a potential therapeutic principle for the treatment of drug-resistant partial epilepsies [10].
• We identified two large French-Canadian families segregating a familial partial epilepsy syndrome with variable foci (FPEVF) characterized by mostly nocturnal seizures arising from frontal, temporal, and occasionally occipital epileptic foci [11].
• Previous imaging studies using 11C-flumazenil in patients with mesial temporal lobe epilepsy and neocortical partial seizure disorders have found focal decreases in gamma-aminobutyric acid type A/benzodiazepine receptor binding [12].

Chemical compound and disease context of Epilepsies, Partial

• One or more interictal positron computed tomograms of 18F-fluorodeoxyglucose were obtained on 50 patients with partial seizure disorders [13].
• Benzodiazepine withdrawal delirium with catatonic features. Occurrence in patients with partial seizure disorders [14].
• Clonazepam has given better results than valproate in temporal lobe and other partial (focal) epilepsies, while valproate has given better results in grand mal seizures and atonic attacks [15].
• In PHT nonresponders, TPM significantly increased ADT, which is in line with its proven efficacy in patients with refractory partial epilepsy in whom phenytoin has failed [16].
• PURPOSE: Lamotrigine (LTG) is recognised as effective add-on therapy for focal epilepsies, but this is the first double-blind, placebo-controlled, crossover study in treatment-resistant generalised epilepsy [17].

Biological context of Epilepsies, Partial

• An iron induced model of posttraumatic chronic focal epilepsy in rats was studied with respect to extracellular amino acids, electrophysiology, and morphology, approx. 6 months after intracortical injection of ferrous chloride [18].
• Changes in expression of the immediate early genes, zif268 and c-fos, were investigated in chronic focal epilepsy induced by tetanus toxin (TT, 20-35 ng) injected in the rat motor cortex [19].
• Epileptic seizures and event-related potentials (P300) in childhood partial epilepsies [20].
• Somatosensory evoked potentials (SEP) to ipsilateral and contralateral median nerve stimulations were recorded from subdural electrode grids over the perirolandic areas in 41 patients with medically refractory focal epilepsies who underwent evaluation for epilepsy surgery [21].

Anatomical context of Epilepsies, Partial

• None of the five simple partial seizures (two of temporal and three of frontal lobe origin) was associated with a marked rise in prolactin levels [22].
• PURPOSE: Based on data from brain biopsy samples of patients with pharmacoresistant partial epilepsy, overexpression of the multidrug transporter P-glycoprotein (PGP) in brain capillary endothelium has recently been proposed as a potential mechanism of resistance to antiepileptic drugs (AEDs) [23].
• The potential for cardiac arrhythmia was studied in an experimental focal epilepsy induced in hemispherectomized rats by topical application of buffered penicillin G onto the thalamus [24].
• Familial aggregation studies are consistent in showing an increased risk of epilepsy in the relatives of patients with partial epilepsies that occur in the absence of environmental insults to the central nervous system [25].
• It was previously shown that pharmacoresistant partial epilepsy is associated with an increased expression of P-gp in brain capillary endothelium and astrocytes, leading to the hypothesis that increased P-gp expression may be involved in medically intractable epilepsy [26].

Gene context of Epilepsies, Partial

• Mutations in LGI1 (leucine-rich, glioma-inactivated 1 gene) have been found in a few families with the syndrome of autosomal dominant partial epilepsy with auditory features (ADPEAF) [27].
• Long-term alterations in somatostatin regulation could be components of focal epilepsies [28].
• Silent celiac disease in patients with childhood localization-related epilepsies [29].
• PURPOSE: To evaluate how many patients with a clinical picture of idiopathic childhood localization-related epilepsies may also have silent celiac disease (CD) [29].
• The CD34 epitope is expressed in neoplastic and malformative lesions associated with chronic, focal epilepsies [30].

Analytical, diagnostic and therapeutic context of Epilepsies, Partial

• The characteristics and prognostic significance of subclinical seizures and independent auras were studied in 40 patients with partial epilepsy who had long-term electroencephalographic (EEG) monitoring with intracranial electrodes [31].
• METHODS: Intermittent photic stimulation with wavelength-specific optical filters was performed in photosensitive epileptic patients: six patients had severe myoclonic epilepsy in infancy (SMEI), eight had localization-related epilepsy (LRE), and seven had symptomatic generalized epilepsy (SGE) [32].
• PURPOSE: Levetiracetam (LEV) is an interesting novel antiepileptic drug with proven efficacy in both animal models and patients with partial epilepsy [33].
• PURPOSE: To establish whether regional disturbances of the benzodiazepine receptor distribution in focal epilepsies can be detected by SPECT using 123-I-Iomazenil [34].
• [resulting in] a state of depression or exhaustion." Interestingly, Todd was the first to present an electrical theory of epilepsy, supported by his own animal experimentation, well before his better-known successor John Hughlings Jackson (1835-1911) (famous for his investigations of partial epilepsies and the eponymous "Jacksonian march") [35].

References