Épilepsie temporale | EPFL Graph Search

L’épilepsie temporale est la forme d'épilepsie la plus fréquente chez l’adulte. La zone atteinte se trouve dans le lobe temporal du cerveau, plus précisément dans l’hippocampe. Elle entraîne une perte de contact avec la réalité (hallucinations, symptômes d'allure psychotiques) et une perturbation de la mémoire. Le traitement médical est efficace contre cette forme d’épilepsie. La chirurgie est possible, elle peut permettre une diminution des symptômes. Symptômes La crise du lobe temporal commence par une hallucination et des perturbations du système nerveux autonome. On observe chez le patient une altération de la mémoire, un état de conscience altéré ou un état de rêve. Les personnes épileptiques sont souvent confrontées à l'impression de « déjà-vu » avant une crise d'épilepsie temporale (épilepsie affectant la face interne du lobe temporal) comme il l'a été démontré dans plusieurs études scientifiques, provenant notamment de Nathan Illman et de Chris Moulin. Bien que l

Remodeling of brain morphology in temporal lobe epilepsy

Bogdan Draganski, Lester Melie Garcia

Background Mesial temporal lobe epilepsy (TLE) is one of the most widespread neurological network disorders. Computational anatomy MRI studies demonstrate a robust pattern of cortical volume loss. Most statistical analyses provide information about localization of significant focal differences in a segregationist way. Multivariate Bayesian modeling provides a framework allowing inferences about inter-regional dependencies. We adopt this approach to answer following questions: Which structures within a pattern of dynamic epilepsy-associated brain anatomy reorganization best predict TLE pathology. Do these structures differ between TLE subtypes? Methods We acquire clinical and MRI data from TLE patients with and without hippocampus sclerosis (n = 128) additional to healthy volunteers (n = 120). MRI data were analyzed in the computational anatomy framework of SPM12 using classical mass-univariate analysis followed by multivariate Bayesian modeling. Results After obtaining TLE-associated brain anatomy pattern, we estimate predictive power for disease and TLE subtypes using Bayesian model selection and comparison. We show that ipsilateral para-/hippocampal regions contribute most to disease-related differences between TLE and healthy controls independent of TLE laterality and subtype. Prefrontal cortical changes are more discriminative for left-sided TLE, whereas thalamus and temporal pole for right-sided TLE. The presence of hippocampus sclerosis was linked to stronger involvement of thalamus and temporal lobe regions; frontoparietal involvement was predominant in absence of sclerosis. Conclusions Our topology inferences on brain anatomy demonstrate a differential contribution of structures within limbic and extralimbic circuits linked to main effects of TLE and hippocampal sclerosis. We interpret our results as evidence for TLE-related spatial modulation of anatomical networks.

WILEY2020

Noradrenaline increases K-conductance and reduces glutamatergic transmission in the mouse entorhinal cortex by activation of alpha 2-adrenoreceptors

Pierre Magistretti, Emilie Pralong

The entorhinal cortex is a gateway to the hippocampus; it receives inputs from several cortical associative areas as well as subcortical areas. Since there is evidence showing that noradrenaline reduces the epileptic activity generated in the entorhinal cortex, we have examined the action of noradrenaline in the superficial layer of the entorhinal cortex, which is the main source of afferents to the hippocampus. In a previous study we showed that noradrenaline hyperpolarized layer II entorhinal cortex neurons and reduced global synaptic transmission via alpha 2-adrenoreceptors. Here we present a detailed analysis of the effect of noradrenaline on membrane resistance and on the pharmacologically isolated postsynaptic potentials in layer II entorhinal cortex neurons of mice. Noradrenaline (50 microM) hyperpolarized most layer II entorhinal cortex neurons. This hyperpolarization corresponded to an outward current with a reversal potential following the Nernst equilibrium potential for potassium. The hyperpolarizing effect of noradrenaline was blocked by 10 microM yohimbine. These observations suggest that noradrenaline activates a potassium conductance via an alpha 2-adrenoreceptor. Noradrenaline (10-50 microM) reversibly reduced the amplitude of the pharmacologically isolated excitatory potentials mediated by both NMDA and alpha-amino-3-hydroxy-5-methyl-isoxazole-propionic acid (AMPA) receptors, the former being more strongly affected. Again this effect was blocked by 10 microM yohimbine. In contrast, GABAA-mediated synaptic transmission was virtually unaffected by noradrenaline. Thus, noradrenaline appears to strongly inhibit the glutamate-mediated synaptic transmission in the entorhinal cortex without affecting inhibitory post-synaptic potentials. These observations suggest that alpha 2-adrenergic receptor agonists may exert a beneficial effect in the control of hyperexcitability in temporal lobe epilepsy.

1995

Noradrenaline modulates glutamate-mediated neurotransmission in the rat basolateral amygdala in vitro

Pierre Magistretti, Emilie Pralong

The entorhinal cortex and the amygdala are interconnected structures of the limbic system in which paroxysmal activity occurs during temporal lobe epilepsy. Conflicting evidence shows that noradrenaline (i) inhibits the spreading to other parts of the limbic system of paroxysmal activity generated in the amygdala or the entorhinal cortex, but also (ii) increases glutamatergic transmission in the basolateral amygdala. Given our previous work on the inhibitory effect of noradrenaline on entorhinal cortex neurons, we developed an in vitro slice preparation to study the synaptic transmission in the basolateral amygdala and its modulation by noradrenaline. Noradrenaline reduced the fast excitatory postsynaptic potential (EPSP) by approximately 40% at 100 microM and the slow EPSP by approximately 50% at 50 microM. A similar effect was obtained with the alpha2-agonist UK 14304 at 100 and 50 microM respectively. In contrast, the beta-agonist isoproterenol increased the fast EPSP by approximately 40% at 100 microM and the slow EPSP by approximately 20% at 50 microM. Accordingly, the effect of noradrenaline on the EPSPs was blocked by the alpha2-antagonist yohimbine (10 microM) but not by the alpha1-antagonist prazosine (10 microM) and the beta-antagonist propranolol (10 microM). Noradrenaline (50-100 microM) was ineffective on most (14/16) of the isolated inhibitory postsynaptic potentials (IPSPs). These experiments provide evidence that noradrenaline inhibits the excitatory synaptic response of basolateral amygdala neurons. A pharmacological analysis revealed that the noradrenergic modulation of the excitatory transmission in the basolateral amygdala can be dissected into a predominant alpha2-adrenoreceptor-mediated inhibition and a beta-adrenoreceptor-mediated excitation.

1997

Remodeling of brain morphology in temporal lobe epilepsy

Bogdan Draganski, Lester Melie Garcia

WILEY2020

Noradrenaline increases K-conductance and reduces glutamatergic transmission in the mouse entorhinal cortex by activation of alpha 2-adrenoreceptors

Pierre Magistretti, Emilie Pralong

1995