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C Marescaux

Publications and source records attributed to C Marescaux.

At least 73 records · Page 4Linked to original sources
PubMed1999

Cognitive development in benign focal epilepsies of childhood.

Benign focal epilepsy of childhood (BFEC) is the most common form of epilepsy, in children from 3 to 12 years. Its prognosis is always favourable as far as the epilepsy is concerned. Nevertheless, recent clinical data suggest that children affected by BFEC are more likely to show learning difficulties and behavioural disturbances than their peers. We report here the preliminary findings of a prospective study of 22 children affected with BFEC. Electroclinical and neuropsychological changes observed during the first 18 months of the follow-up strengthen the conclusion of recent neuropsychological studies stressing the correlation between epilepsy and cognitive performances. The cognitive deficits affecting mainly non-verbal functions were significantly correlated with the frequency of seizures and spike-wave discharges and to the lateralization of the epileptic focus in the right hemisphere, whereas frontal functions like attention control, response organization and fine motor speed, were impaired in the presence of active BFEC independently of the lateralization of the epileptic focus. Our results indicate that maturing cognitive functions subserved by a cortical area distant from the epileptic focus are susceptible to interference with epilepsy.

Brain↗
PubMed1999

[Benign familial neonatal convulsions: a model of idiopathic epilepsy].

Benign neonatal familial convulsions have been recognized as a distinctive epileptic syndrome since 1964. This rare epileptic syndrome was classified in the category of idiopathic generalized epilepsies. Recently, mutations of potassium channel genes (KCNQ2, KCNQ3) were identified as responsible for this autosomic dominant epileptic syndrome. Generalized tonico-clonic seizures start at the second or third day after birth in children with no prenatal or perinatal pathological history. Interictal EEG is normal. This epilepsy is age-dependent: less than ten percent of children present seizures later in life. Despite their rarity, BNFC represent a useful model to understand the pathophysiology of idiopathic age dependant epilepsies.

Electroencephalography↗
PubMed1999

Early dissociation of verbal and nonverbal gestural ability in an epileptic deaf child.

Studies of sign language aphasia in deaf adults have provided the evidence for two separable verbal and nonverbal manual gesture systems. We report a congenitally deaf child with a idiopathic focal epilepsy of childhood who showed specific language impairment in French sign language. The child's amazing performances in miming or sketching pictures she was unable to sign support the notion of an early dissociation of the two gestural systems.

Adult↗
PubMed1999

Basal ganglia involvement in rotational seizures.

Body rotation during partial epileptic seizures remains a poorly understood clinical feature, possibly related to the ictal involvement of specific cortical areas (e.g. vestibular cortex). However, there are both experimental and clinical arguments which support the hypothesis of basal ganglia asymmetric activation during such complex motor behavior. We report a patient exhibiting rotational seizures which proved to arise from right anterior temporal lobe structures and the orbito-cingular cortex, as demonstrated during stereotactic EEG recordings. An ictal 99mTc-ECD-SPECT study was performed during an electrically induced seizure, similar to the seizures usually experienced by the patient but without a rotatory component, showing a marked increase of cerebral blood flow in the lenticular nucleus, ipsilaterally to the epileptogenic area. This finding suggests that lenticulate involvement might be necessary to produce an ictal circling behavior. As circling behavior can be observed during epileptic seizures originating from areas widely distributed in the cortex, one may postulate that the basal ganglia involvement is the "final common pathway" underlying the rotational part of the clinical symptomatology.

Basal Ganglia↗
PubMed1999

Efficacy of lamotrigine in idiopathic generalized epilepsy syndromes: a video-EEG-controlled, open study.

PURPOSE: This prospective, open, video-EEG-controlled study examined the efficacy of lamotrigine (LTG) as add-on and monotherapy in idiopathic generalized epilepsy (IGE). METHODS: 47 patients received LTG either because of insufficient seizure control (n = 35) or serious side effects of prior antiepileptic drugs (AED). Long-term video-EEG recordings were performed before and after the introduction of LTG. The mean follow-up time was 25.5 months. RESULTS: Of 12 patients with refractory childhood absence epilepsy, 9 became seizure free; in one child with absences with eyelid myoclonia, absence frequency was reduced > 50%; in 2 children with absences with a mild atonic component, seizure reduction was only transient. Of 12 patients with juvenile absence epilepsy, 10 became seizure-free and, in 2, a > 50% reduction was obtained. In 15 patients with juvenile myoclonic epilepsy, complete seizure control was achieved in 7 patients, in 6 patients myoclonia persisted. In one patient generalized tonic-clonic seizures also persisted and another patient developed a rash, LTG was therefore stopped. Of 5 patients with grand-mal on awakening, 3 became seizure-free, and a reduction of > 50% was obtained in one patient; LTG was stopped in one patient because of poor compliance. Three patients with pure photosensitive epilepsy became seizure-free. At the end of the study, 11 patients were seizure-free on LTG monotherapy, and in most other patients concomitant AED dosage could be substantially reduced. CONCLUSIONS: Lamotrigine was effective and well tolerated in patients with various IGE syndromes, although differences were observed between individual syndromes and seizure types.

Adolescent↗
PubMed1998

C-Fos, Jun D and HSP72 immunoreactivity, and neuronal injury following lithium-pilocarpine induced status epilepticus in immature and adult rats.

In order to follow the maturation-related evolution of neuronal damage, cellular activation and stress response subsequent to Li-Pilo seizures in the 10- (P10), 21-day-old (P21) and adult rat, we analyzed the expression of the c-Fos protein as a marker of cellular activation, HSP72 immunoreactivity as the stress response and silver staining for the assessment of neuronal damage in 20 selected brain regions. The early wave of c-Fos measured at 2 h after the onset of seizures was present in most structures of the animals at the three ages studied and particularly strong in the cerebral cortex, hippocampus and amygdala. The late wave of c-Fos measured at 24 h after the onset of seizures and that was shown to correlate to neuronal damage was absent from the P10 rat brain, and present mainly in the cerebral cortex and hippocampus of P21 and adult rats. The expression of the stress response, assessed by the immunoreactivity of HSP72 at 24 h after the seizures was absent from the P10 rat brain and present in the entorhinal cortex, amygdala, hippocampus and thalamus of P21 and adult rats. The expression of Jun D at 24 h after the seizures was discrete and present in most brain regions at all ages. Neuronal injury assessed by silver staining at 6 h after the onset of seizures was very discrete in the brain of the P10 rat and limited to a few neurons in the piriform and entorhinal cortices. In older animals, marked neuronal degeneration occurred in the cerebral cortex, amygdala, hippocampus, lateral septum and thalamus. Thus the immediate cell activation induced by lithium-pilocarpine seizures which is present at all ages translates only into a late wave of c-Fos and the expression of HSP72 in P21 and adult animals in which there will be extensive cell damage.

Age Factors↗
PubMed1998

Role of the subthalamo-nigral input in the control of amygdala-kindled seizures in the rat.

The substantia nigra pars reticulata (SNpr) is a critical site for the control of epileptic seizures. Potentiation of the inhibitory GABAergic input from the striatum to the SNpr suppresses primary or secondary generalized seizures in the rat. The purpose of this study was to examine the possible involvement of the excitatory glutamatergic input from the subthalamic nucleus to the SNpr in the control of both the electroencephalographic and the motor components of amygdala-kindled seizures in the rat. Microinjections of either an N-methyl-D-aspartate (NMDA) antagonist in the substantia nigra or a GABAA agonist in the subthalamic nucleus, significantly reduced motor seizures but did not modified the afterdischarges. These results provide evidence for the involvement of the subthalamo-nigral projection in the modulation and the propagation of the motor components of amygdala-kindled seizures.

Amygdala↗
PubMed1998

Metabolic activity is increased in discrete brain regions before the occurrence of spike-and-wave discharges in weanling rats with genetic absence epilepsy.

In the present study, we measured basal local cerebral metabolic rates for glucose (LCMRglcs) in immature genetic absence epilepsy rats from Strasbourg (GAERS) at postnatal day 21 (P21), at which age no spike-and-wave discharges can be recorded. LCMRglcs in GAERS were compared to those in control non-epileptic (NE) rats of the same age selected from our breeding colony. LCMRglcs were measured in 60 structures by the quantitative [14C]2-deoxyglucose (2DG) autoradiographic technique. In P21 GAERS, LCMRglcs were similar to those of P21 NE rats in 46 areas. They increased over NE control levels in two groups of structures. First, metabolic increases were recorded in limbic structures such as entorhinal and piriform cortex, lateral septum as well as all hippocampal subfields and basolateral amygdala, although no spike-and-wave discharges can be recorded from those areas in adult GAERS. On the other hand, increases in LCMRglcs were also recorded in substantia nigra pars reticulata, superior colliculus and globus pallidus which are structures involved in the control of seizure activity. Finally, significant metabolic decreases in P21 GAERS were recorded in two posterior auditory regions, the inferior colliculus and the superior olive. In conclusion, our data show that the genetic mutation(s) underlying the cellular and molecular events responsible for the expression of spike-and-wave discharges in adult GAERS is(are) able to increase metabolic activity in limbic structures and in the nigral inhibitory system before the occurrence of absence seizures. Conversely, the full electrocortical maturation seems necessary for the expression of spike-and-wave discharges with the concurrent increase in LCMRglcs in adult GAERS.

Animals↗
PubMed1998

Intracellular recordings in thalamic neurones during spontaneous spike and wave discharges in rats with absence epilepsy.

1. In vivo extracellular and intracellular recordings were performed from thalamocortical (TC) neurones in a genetic model of absence epilepsy (genetic absence epilepsy rats from Strasbourg) during spontaneous spike and wave discharges (SWDs). 2. Extracellularly recorded single units (n = 14) fired either a single action potential or a high frequency burst of up to three action potentials, concomitantly with the spike component of the spike-wave complex. 3. Three main events characterized the intracellular activity of twenty-six out of twenty-eight TC neurones during SWDs: a small amplitude tonic hyperpolarization that was present throughout the SWD, rhythmic sequences of EPSP/IPSPs occurring concomitantly with the spike-wave complexes, and a small tonic depolarization at the end of the SWD. The rhythmic IPSPs, but not the tonic hyperpolarization, were mediated by activation of GABAA receptors since they reversed in polarity at -68 mV and appeared as depolarizing events when recording with KCl-filled electrodes. 4. The intracellular activity of the remaining two TC neurones consisted of rhythmic low threshold Ca2+ potentials, with a few EPSP/IPSP sequences present at the start of the SWD. 5. These results obtained in a well-established genetic model of absence epilepsy do not support the hypothesis that the intracellular activity of TC neurones during SWDs involves rhythmic sequences of GABAB IPSPs and low threshold Ca2+ potentials.

Action Potentials↗
PubMed1998

Age-dependent regulation of seizure activity by nitric oxide in the developing rat.

The role of nitric oxide (NO) on the age-dependent selective vulnerability to the consequences of epileptic seizures was studied in 10-day old (P10) and 21-day old (P21) rats. At P10, the NO synthase (NOS) inhibitor, NG-nitro-l-arginine (LNA), increased severity of seizures while l-arginine (l-Arg), the NOS substrate, had no effect. At P21, l-Arg improved the outcome of seizures while LNA had no effect. These results demonstrated the age-dependent role of NO in epilepsy.

Aging↗
PubMed1998

BDNF restores the expression of Jun and Fos inducible transcription factors in the rat brain following repetitive electroconvulsive seizures.

The expression of inducible transcription factors was studied following repetitive electroconvulsive seizures (ECS), c-Fos, c-Jun, JunB, and JunD immunoreactivities were investigated following a single (1 x ECS) or repetitive ECS evoked once per day for 4, 5, or 10 days (4 x ECS, 5 x ECS, or 10 x ECS). Animals were killed 3 or 12 h following the last ECS. Three hours after 1 x ECS, c-Fos was expressed throughout the cortex and hippocampus. After 5 x ECS and 10 x ECS, c-Fos was reexpressed in the CA4 area, but was completely absent in the other hippocampal areas and cortex. In these areas, c-Fos became only reinducible when the time lag between two ECS stimuli was 5 days. In contrast to c-Fos, intense JunB expression was inducible in the cortex and hippocampus, but not CA4 subfield, after 1 x ECS, 5 x ECS, and 10 x ECS. Repetitive ECS did not effect c-Jun and JunD expression. In a second model of systemic excitation of the brain, repetitive daily injection of kainic acid for 4 days completely failed to express c-Fos, c-Jun, and JunB after the last application whereas injection of kainic acid once per week did not alter the strong expressions compared to a single application of kainic acid. In order to study the maintenance of c-Fos expression during repetitive seizures, brain-derived neurotrophic factor (BDNF) was applied in parallel for 5 or 10 days via miniosmotic pumps and permanent cannula targeted at the hippocampus or the parietal cortex. Infusion of BDNF completely reinduced c-Fos expression during 5 x ECS or 10 x ECS in the cortex ipsilaterally to the cannula and, to a less extent, also increased the expression of c-Jun and JunB when compared to saline-treated controls. BDNF had no effect on the expression patterns in the hippocampus. ECS with or without BDNF infusion did not change the expression patterns of the constitutive transcription factors ATF-2, CREB, and SRF. These data demonstrate that various transcription factors substantially differ in their response to acute and chronic neural stimulation. Repetitive pathophysiological excitation decreases the transcriptional actions of neurons over days in the adult brain, and this decrement can be prevented by BDNF restoring the neuroplasticity at the level of gene transcription.

Animals↗
PubMed1998

Contribution of T2 relaxation time mapping in the evaluation of cryptogenic temporal lobe epilepsy.

In this study we compared the results of visual analysis of MR imaging with T2 relaxation time mapping of the mesial structures in a group of 97 patients with cryptogenic temporal lobe epilepsy. All patients underwent a clinical neurological examination, neuropsychological investigation, prolonged video-EEG monitoring, SPECT imaging, MR imaging, and T2 relaxation time mapping. T2 relaxation times were estimated with a Carr-Purcell-Meiboom-Gill pulse sequence with 48 echoes (15 to 720 ms). The mean T2 relaxation time value was 118.5 +/- 2 ms in the hippocampi and 120.3 +/- 1.9 ms in the amygdala of 21 healthy subjects used as controls. T2 relaxation mapping revealed mesial temporal sclerosis in 91.8% of the patients (often involving both the hippocampus and the amygdala) and evidenced bilateral involvement in 44.6% of the patients against 72.2 and 6.2%, respectively, for MR imaging. The ipsilateral and contralateral hippocampal T2 relaxation time values did significantly correlate with seizure frequency and the contralateral hippocampal T2 relaxation time value with the duration of epilepsy. In conclusion, this quantitative method is highly sensitive for the detection of mesial temporal sclerosis and permits a better evaluation of the apparently normal contralateral mesial structures.

Adolescent↗
PubMed1998

[Bilateral subdural hematoma following epidural anesthesia].

PURPOSE: The authors report a case of bilateral subdural hematoma (SDH) which occurred following epidural analgesia for labour, complicated by post dural puncture headache (PDPH). Physiopathological mechanisms are discussed. CLINICAL FEATURES: A 27-yr-old woman displayed typical PDPH following epidural anaesthesia. On the fifth day she was given a blood patch (BP) which proved immediately effective. Further developments were marked by late recurrence of PDPH and by administration of a second BP on the 24th day. With the aggravation of the headaches, the disappearance of their postural nature and with the appearance of transitory focal neurological signs on the 30th day, a CT-Scan was done and showed bilateral subdural haematoma. Following surgical drainage, the patient made an uneventful recovery. CONCLUSION: The presence of PDPH complicated by a typical neurological deterioration should prompt the anaesthetist to seek an immediate clinical and x-ray diagnosis in order to look for the existence of intracranial complications.

Adult↗
PubMed1998

Pathophysiological mechanisms of genetic absence epilepsy in the rat.

Generalized non-convulsive absence seizures are characterized by the occurrence of synchronous and bilateral spike and wave discharges (SWDs) on the electroencephalogram, that are concomitant with a behavioral arrest. Many similarities between rodent and human absence seizures support the use of genetic rodent models, in which spontaneous SWDs occur. This review summarizes data obtained on the neurophysiological and neurochemical mechanisms of absence seizures with special emphasis on the Genetic Absence Epilepsy Rats from Strasbourg (GAERS). EEG recordings from various brain regions and lesion experiments showed that the cortex, the reticular nucleus and the relay nuclei of the thalamus play a predominant role in the development of SWDs. Neither the cortex, nor the thalamus alone can sustain SWDs, indicating that both structures are intimely involved in the genesis of SWDs. Pharmacological data confirmed that both inhibitory and excitatory neurotransmissions are involved in the genesis and control of absence seizures. Whether the generation of SWDs is the result of an excessive cortical excitability, due to an unbalance between inhibition and excitation, or excessive thalamic oscillations, due to abnormal intrinsic neuronal properties under the control of inhibitory GABAergic mechanisms, remains controversial. The thalamo-cortical activity is regulated by several monoaminergic and cholinergic projections. An alteration of the activity of these different ascending inputs may induce a temporary inadequation of the functional state between the cortex and the thalamus and thus promote SWDs. The experimental data are discussed in view of these possible pathophysiological mechanisms.

Animals↗
PubMed1998

High-frequency stimulation of the subthalamic nucleus suppresses absence seizures in the rat: comparison with neurotoxic lesions.

High-frequency electrical stimulation of deep brain structures has recently been developed for the surgical approach of neurologic disorders. Applied to the thalamus in tremors or to the subthalamic nucleus in Parkinson's disease, high-frequency stimulation has been demonstrated to exert a local inhibiting influence, leading to symptoms alleviation. In the present study, bilateral high-frequency stimulations (130 Hz) of the subthalamic nuclei suppressed ongoing spontaneous absence seizures in rats. This effect was dissociated from motor side-effects and appears specific to the subthalamic nucleus. Bilateral excitotoxic lesions of the subthalamic nuclei only partially suppressed absence-seizures. These results confirm the involvement of the basal ganglia system in the control of generalized seizures and suggest that high-frequency stimulations could be used in the treatment of some forms of seizures.

Animals↗
PubMed1998

Local cerebral glucose utilization in adult and immature GAERS.

In the present study, we compared the basal local cerebral metabolic rates for glucose (LCMRglcs) both in Wistar rats with genetic absence epilepsy (GAERS: genetic absence epilepsy rats from Strasbourg) and in control non epileptic (NE) rats selected in our breeding colony. LCMRglc was measured both in immature rats at postnatal day 21 (P21) at which age no spontaneous spike-and-wave discharges can be recorded in GAERS and at the adult age (6 months) when GAERS fully express thalamo-cortical spike-and-wave discharges recorded on the EEG. LCMRglcs were measured in 24 structures by the quantitative [14C]2-deoxyglucose autoradiographic technique. In adults GAERS, LCMRglc underwent a widespread increase recorded in all brain structures except in mediodorsal and ventromedian thalamus, and in the nucleus accumbens. These metabolic increases ranged from 17 to 50% over control levels in adult NE rats. In P21 GAERS, LCMRglc was similar to that of P21 NE rats in 16 areas. It increased over control levels of NE rats in two groups of structures. Metabolic increases were recorded in four limbic structures (entorhinal and piriform cortices, hippocampus and basolateral amygdala) where no spike-and-wave discharges were recorded in adult GAERS. Increases in LCMRglcs were also located in the substantia nigra pars reticulata, superior colliculus and globus pallidus which are structures involved in the control of seizure activity. In conclusion, our data suggest that the consequences of the genetic mutation(s) underlying the cellular and molecular events responsible for the expression of spike-and-wave discharges in adult GAERS is (are) able to increase metabolic activity in both limbic structures and the nigral inhibitory system before the occurrence of spike-and-wave discharges.

Aging↗
PubMed1998

The role of basal ganglia in the control of generalized absence seizures.

During the last two decades, evidence has accumulated to demonstrate the existence, in the central nervous system, of an endogenous mechanism that exerts an inhibitory control over different forms of epileptic seizures. The substantia nigra and the superior colliculus have been described as key structures in this control circuit; inhibition of GABAergic neurons of the substantia nigra pars reticulata results in suppression of seizures in various animal models of epilepsy. The role in this control mechanism of the direct GABAergic projection from the striatum to the substantia nigra and of the indirect pathway, from the striatum through the globus pallidus and the subthalamic nucleus, was examined in a genetic model of absence seizures in the rat. In this model, pharmacological manipulations of both the direct and indirect pathways resulted in modulation of absence seizures. Activation of the direct pathway or inhibition of the indirect pathway suppressed absence seizures through disinhibition of neurons in the deep and intermediate layers of the superior colliculus. Dopamine D1 and D2 receptors in the nucleus accumbens, appear to be critical in these suppressive effects. Along with data from the literature, our results suggest that basal ganglia circuits play a major role in the modulation of absence seizures and provide a framework to understand the role of these circuits in the modulation of generalized seizures.

Animals↗