Clinical Neuroscience

[Interhemispheric propagation of seizures in mesial temporal lobe epilepsy]

ERÕSS Loránd, ENTZ László, FABÓ Dániel, JAKUS Rita, SZŰCS Anna, RÁSONYI György, KELEMEN Anna, BARCS Gábor, JUHOS Vera, BALOGH Attila, BARSI Péter, CLEMENS Zsófia, HALÁSZ Péter

OCTOBER 20, 2009

Clinical Neuroscience - 2009;62(09-10)

[Objectives - To investigate interhemispheric propagation of mesial temporal lobe epilepsy seizures in patients undergoing long-term video-EEG monitoring with combined scalp and foramen ovale electrodes. Aim of the study - To reveal possible interhemispheric propagation patterns in mesial temporal lobe epilepsy, to improve presurgical evaluation of temporal epileptic patients. Methods - Sixty-five seizures from 20 patients were analyzed. We defined two contralateral seizure propagation patterns: Type I for those seizures that spread to the contralateral foramen ovale electrodes earlier than to the contralateral scalp electrodes, and type II for the opposite. Participants - Twenty drug resistant epileptic patients were investigated in frame of their presurgical evaluation. Results - The majority of seizures (80%) were classified as type I. Inter-foramen ovale electrode propagation time was significantly shorter for type I compared to type II seizures. Ninety percent of patients had either type I or type II seizures only. Patients with type I seizures significantly more often had mesiotemporal structural alterations evident on magnetic resonance imaging scans, and became more often seizure-free after surgery compared to patients with type II seizures whose surgical outcome was less favorable or surgery could not be indicated because of independent bilateral ictal seizure-onset. Conclusions - The two types of contralateral propagation patterns we are describing seem to represent two subtypes of mesial temporal lobe epilepsy with different morphological and prognostic features. The predominance of type I over type II seizures together with shorter propagation times for type I seizures indicate a role of a more direct and dominant interhemispheric pathway in mesial temporal lobe epilepsy.]

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Clinical Neuroscience

[The transcription of the amyloid precursor protein and tryptophan 2,3-dioxygenase genes are increased by aging in the rat brain]

KÁLMÁN Sára, PÁKÁSKI Magdolna, SZŰCS Szabina, GARAB Dénes, DOMOKOS Ágnes, ZVARA Ágnes, PUSKÁS László, BAGDY György, ZELENA Dóra, KÁLMÁN János

[Aging itself is considered as a major risk factor of dementia. The prevalence of the Alzheimer’s disease (AD) is increasing exponentially after the age of 65 and doubles every 5 years. The major aim of our present research was to examine the effect of aging on the transcription of certain genes associated with neurodegenerative disorders in the rat brain. The influence of the vasopressin (VP) hormone was also examined in the same experimental paradigm. Age dependent transcriptional changes of the following four genes were examined in the cerebral cortex: the first was the gene of the amyloid precursor protein (APP) which is abnormally cleaved to toxic beta-amyloid fragments. These aggregated peptides are the major components of the senile plaques in the AD brain. The second one was the mitogen-activated protein kinase (MAPK1) gene. The MAPK is involved in the abnormal hyperphosphorylation of the tau-protein which results in aggregated neurofibrillary tangles. The beta-actin gene was the third one. The protein product of this gene is considered to be involved in synaptogenesis, neuronal plasticity and clinical conditions like depression and AD. The last one was the gene of the tryptophan 2,3-dioxygenase (TDO2) enzyme. The activity of this enzyme is considered as a rate limiting factor in the metabolism of the neuro-immune modulator quinolinic acid (QUIN). The transciptional activity of young (2.5 months) and aged (13 months) Brattleboro rats with or without VP expression were compared by means of real time PCR technique. The cortical transciptional activity of the APP and TDO2 genes were increased in the aged animals as compared with the activity of the young ones, and this effect was independent on the presence of the VP. Our results indicate the importance of certain age dependent transcriptional changes might influence the mechanism of AD and other neurodegenerative disorders.]

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Clinical Neuroscience

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