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Biomedical subjects

C Marescaux

Publications and source records attributed to C Marescaux.

At least 145 records · Page 8Linked to original sources
PubMed1992

[Paroxysmal neurological manifestations disclosing panic attacks].

Thirty-seven patients presented with paroxysmal neurological manifestations attributed to anxiety attacks. The manifestations included loss of consciousness, focal sensorimotor deficits, diffuse dysesthaesiae, visual disorders and tremor. They lasted 10 to 45 minutes and occurred once per day to once per week. Organic pathology was dismissed on the basis of normal examinations and atypical course. In all patients questioning revealed symptoms that were those of acute anxiety. The fact that these attacks took place in suggestive (circumstances e.g. in crowds and car driving), and that they could be induced by challenge tests hyperpnoea, infusion of lactate) suggested that these disorders were consecutive to panic attacks.

Adult↗
PubMed1992

[Myelitis caused by toxocara canis (larva migrans)].

A young woman presented with recurrent myelitis associated with persistent eosinophilia in blood and CSF. Specific serological procedures in blood and CSF led to the diagnosis of visceral larva migrans. The patient recovered after 21 days of treatment with diethylcarbamazine. To our knowledge, this is the second report of myelitis in the course of visceral larva migrans.

Adult↗
PubMed1991

Intrathalamic injections of gamma-hydroxybutyric acid increase genetic absence seizures in rats.

The effects of intrathalamic injections of gamma-hydroxybutyric acid (GHB) and of NCS 382 85, a specific antagonist of GHB receptors, were evaluated in rats with spontaneous generalized absence epilepsy. Bilateral injections of GHB (25 and 50 micrograms/side) into the mediolateral thalamus increased spontaneous spike and wave discharges (SWD) in a dose-dependent fashion. This effect was suppressed by administration of NCS 382 85 (50 micrograms/side). Bilateral injection of NCS 382 85 alone (50 and 100 micrograms/side) into the same sites had no effect on SWD duration. Injection of GHB or NCS 382 85 into the midline thalamus and the area of reticular nuclei did not modify the SWD. These data suggest that GHB receptors in the mediolateral thalamus may be involved in the control of spontaneous SWD in this rat model of petit mal epilepsy.

Animals↗
PubMed1991

Evidence for a critical role of GABAergic transmission within the thalamus in the genesis and control of absence seizures in the rat.

The involvement of GABAergic transmission within the thalamus in the generation and control of spike and wave discharges (SWD) in generalized non-convulsive or absence epilepsy was studied in rats with spontaneous SWD and in non-epileptic rats. In epileptic rats, bilateral injections of gamma-vinyl GABA (GVG, 10 micrograms/side) or muscimol (10 ng/side) into the medial part of the ventral lateral thalamus, i.e. the specific relay nuclei, significantly increased spontaneous cortical SWD whereas similar injections into the most lateral part of the thalamus, i.e. the area of the reticular nuclei, significantly suppressed these seizures. Injections of GVG (20 micrograms) or muscimol (20 ng) into the midline thalamus had no direct effect on the spontaneous SWD. In non-epileptic rats, injections of GVG (25 micrograms/side) or muscimol (100 ng/side) into the thalamic relay nuclei produced short SWD on the cortical EEG. These results suggest that GABAergic neurons in the reticular nuclei and their projections to the specific relay nuclei of the thalamus are involved in the elicitation and control of generalized non-convulsive seizures.

Aminocaproates↗
PubMed1991

Local cerebral glucose utilization in rats with petit mal-like seizures.

The quantitative 2-[14C]deoxyglucose autoradiographic method was applied to the measurement of local cerebral metabolic rates for glucose in a model of genetic petit mal-like seizures in a strain of Wistar rats. During the experimental period, epileptic rats exhibited synchronous spike-and-wave discharges recorded from the cerebral cortex, whereas the electroencephalographic pattern of control animals was normal. An overall consistent increase in local cerebral metabolic rates for glucose was observed in epileptic rats as compared to nonepileptic control rats. This increase was statistically significant in 52 of the 59 cerebral structures studied and concerned all cerebral functional systems. These results are in accordance with positron emission tomography measurements in humans with typical childhood absence epilepsy. There is a lack of anatomical correlation between areas demonstrating hypermetabolism and areas where spike-and-wave discharges are recorded. Thus, the diffuse increase in cerebral energy metabolism in epileptic rats as compared to controls is not directly related to the occurrence of spike and wave discharges.

Animals↗
PubMed1991

Lesions of noradrenergic neurons in rats with spontaneous generalized non-convulsive epilepsy.

The role of noradrenergic neurons in the control of a spontaneous generalized non-convulsive epilepsy (GNCE) was investigated. In rats with genetic spontaneous absence seizures, we produced lesions using 2 neurotoxins: 6-hydroxydopamine (6-OHDA) and N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4). Lesions of noradrenergic neurons were made either in pups by neonatal 6-OHDA intraperitoneal (i.p.) injection (2 x 100 mg/kg) or in adult rats by i.p. administration of DSP4 (60 mg/kg) or bilateral microinjection of 6-OHDA in the locus coeruleus (LC) (4 micrograms/microliters, 2 microliters/side). Effectiveness of the lesions was controlled by measuring dopamine (DA) and noradrenaline (NA) contents in the brains. Neonatal 6-OHDA administration did not lead to any difference in seizures in adult animals, compared with control rats. DSP4 injections and LC lesions with local injections of 6-OHDA produced a transient increase of the seizures. Within one to two weeks, the seizure duration went back to prelesion levels. No seizure occurred when the same lesions were performed in non epileptic rats. These results suggest that NA is not involved in the genesis of this generalized non-convulsive epilepsy; they confirm that NA participates in the control of seizures in this model, but the rapid development of compensatory mechanisms shows that this control is not critical.

Animals↗
PubMed1991

Are rats with genetic absence epilepsy behaviorally impaired?

Absence seizures in humans are characterized by unresponsiveness to external stimuli and inactivity. However, in typical generalized non-convulsive epilepsy in children, intellectual capacities are considered to be normal. Wistar rats from an inbred strain with spontaneous absence-like seizures were compared with rats from the outbred control strain in various behavioral tasks in order to detect possible impairments related either to the absence epilepsy or to occurrence of spike and wave discharges (SWD). Spontaneous circadian locomotion, exploratory activity in an open field, social interactions with an unfamiliar conspecific and mouse killing behavior were similar in both strains. Avoidance learning in a shuttle box or food reinforced learning in a Skinner test were unimpaired or even improved in epileptic rats. During performance of a learned task either in the Skinner box or in a conditioned sound-bar pressing task, SWD were suppressed in epileptic rats as long as they were working for reinforcement. SWD reappeared when the motivation to perform the task had declined: unresponsiveness to a conditioned stimulus was then observed during SWD. These data are in agreement with observations commonly described in children with typical genetic absence epilepsy.

Aggression↗
PubMed1991

[Recurrent aseptic meningitis in periodic disease or Mollaret's meningitis?].

A 33 year-old Sephardic Jewish man with familial mediterranean fever (FMF), presented during a 7 year period, 6 episodes of aseptic meningitis, improving within less than 24 h after spinal tap. Cerebrospinal fluid analysis showed a mixed leucocytic pleocytosis ranging from 100 to 1,000 cell/mm3. Spinal fluid cultures for bacteria, viruses and viral antibodies were always negative. Our case supports other reports showing that recurrent aseptic meningitis, although rare, may occur in FMF. It usually responds to treatment with colchicine, like other manifestations of the disease. FMF meningitis has been compared to Mollaret's meningitis whose cause is undetermined. However, Mollaret's meningitis, unlike FMF, is sporadic and ubiquitous, is not transmitted genetically and affects men and women equally. Moreover, in Mollaret's meningitis transient neurological abnormalities, such as signs of encephalitis have often been reported: polyserositis or associated amylosis are absent, there is no biological inflammatory syndrome, and in 65% of the patients the CSF contains specific large mononuclear-derived cells called endothelial cells. Such abnormalities have not been described in FMF.

Adult↗
PubMed1991

[Postures and abnormal paroxysmal movements during sleep: hypnogenic paroxysmal dystonia or partial epilepsy?].

In recent years, a differentiation has been made between two syndromes that are characterized by brief abnormal paroxysmal movements occurring principally at night: 1, hypnogenic paroxysmal dystonia (HPD), sometimes considered a particular form of dystonia similar to paroxysmal kinesigenic choreoathetosis, and 2, mesiofrontal epilepsy. Whether HPD is a distinct syndrome is not clear. Twenty-three patients, 11 men and 12 women, were hospitalized between 1985 and 1989 for examination of this type of abnormal paroxysmal movements (APM) occurring at night. In order to clarify the physiopathology of these abnormal nocturnal movement as focal epilepsy or a particular form of dystonia, we analyzed the personal and familial antecedents of all 23 patients, the polygraphic records during waking and sleep periods, and the results of neuroradiological examinations. Four patients were examined by positron emission tomography (PET) using i8F deoxyglucose. Symptoms first appeared between 3 and 28 years of age (M, 10.1) and developed over 1 to 20 years (M, 10.1). APM clearly occurred more commonly (greater than 90%) during sleep, usually during phases of slow-wave sleep. The sleeping patient opened his eyes and the motor signs then variously associated affective facial expression; axial postural modifications; tonic, dystonic or choreic postural movements of the limbs; pedalling; automatisms; disordered agitation and vocalization. The seizure was abruptly interrupted after 10 to 60 seconds. There was usually no postictal confusion. Thirteen patients clearly had clear epileptic antecedents: in 9, generalized tonic-clonic seizures; in 4, focal epileptic status. During nocturnal polygraphic recording, 6 patients presented a generalized seizure following a period of APM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Mapping of spontaneous spike and wave discharges in Wistar rats with genetic generalized non-convulsive epilepsy.

Electrical activity was recorded in different parts of the brain in Wistar rats from a strain with genetic generalized non-convulsive epilepsy (GNCE or absence epilepsy). Movable bipolar electrodes were lowered stereotaxically by 1 mm steps into the brain in immobilized animals. Spontaneous spike and wave discharges (SWD) of the largest amplitude were recorded in the cortex and in lateral nuclei of the thalamus where they appeared occasionally to precede. Smaller amplitude SWD were recorded in the striatum, hypothalamus, tegmentum and substantia nigra. No SWD were recorded in limbic structures. Partial limbic seizures induced by the introduction of the electrode did not interfere with occurrence of cortical SWD. These results confirm the primacy of thalamocortical involvement in SWD of GNCE. The absence of spread to limbic structures and the implication of a precisely limited substrate in GNCE accounts for the clinical and pharmacological specificity of this particular kind of epilepsy.

Animals↗
PubMed1990

Potentiation of gamma-vinyl GABA (vigabatrin) effects by glycine.

Vigabatrin, because of its ability to increase brain GABA concentration, acts as an anticonvulsant on convulsive epileptic seizures and increases seizures in generalized non-convulsive epilepsy. Next to GABA, glycine is one of the most important inhibitory neurotransmitter amino acids. We studied the influence of glycine on the effects of treatment with vigabatrin in two rat models of generalized convulsive seizures and a rat model of spontaneous generalized non-convulsive seizures. Glycine (750 mg/kg i.p.) or vigabatrin (200 mg/kg i.p.), when given alone, provided partial protection against convulsive seizures, while combined treatment with the two drugs significantly suppressed the convulsive seizures in both the mercaptopropionic acid (MPA)-induced seizures and audiogenic seizures. In contrast to the response to treatment with each individual drug, the drug combination nearly abolished the appearance of isolated spikes on the EEG in MPA seizures. On the other hand, glycine also enhanced the aggravating effect of vigabatrin on spontaneous spike and wave discharges in a rat model of genetic absence epilepsy, whereas glycine or vigabatrin alone, at the above doses, produced only a slight, non-significant increase in spontaneous spike and wave discharges. The GABA-glycine interaction is the first example of a synergistic action of two inhibitory neurotransmitters on seizure-related pathological discharges.

3-Mercaptopropionic Acid↗
PubMed1990

The GABAergic nigro-collicular pathway is not involved in the inhibitory control of audiogenic seizures in the rat.

Involvement of the GABAergic nigro-collicular pathway in the control of audiogenic seizures was examined in genetically sensitive rats by studying the effects of bilateral injections into the substantia nigra of muscimol, a gamma-Aminobutyric acid (GABA) agonist, and those of bilateral injections into the superior colliculus of picrotoxin, a GABA antagonist, and of muscimol. Microinjections of muscimol (20-80 ng/side) into the substantia nigra and microinjections into the superior colliculus of picrotoxin (20 and 40 ng/side) both failed to suppress audiogenic seizures. Following injections into the superior colliculus, audiogenic seizures were in fact facilitated by picrotoxin and suppressed by muscimol. These results suggest that the nigro-collicular GABAergic pathway is not involved in the inhibitory control over audiogenic seizures. Conversely, a different GABAergic mechanisms may be involved in the superior colliculus in the control of this form of epilepsy.

Acoustic Stimulation↗
PubMed1990

Immediate effects of 14 non MAOI antidepressants in rats with spontaneous petit mal-like seizures.

1. Wistar rats of a strain presenting spontaneous petit mal-like seizures were injected intraperitoneally with graded doses of 14 non-monoamine oxidase inhibitor antidepressants and the immediate effects on behavior and the EEG were recorded. 2. Amineptine and nomifensine, the two drugs interacting with dopaminergic neurotransmission, reduced the duration of spontaneous spike-wave discharges (SWD) and were thus potentially antiepileptic. 3. Trazodone increased SWD duration. 4. The antidepressants, imipramine-like (imipramine, chlorimipramine, desipramine, metapramine and amitriptyline) and non-imipraminic (minaprine, maprotiline, viloxazine, mianserin, fluvoxamine and indalpine), and the 3 noted above, had potentially convulsive effects.

Animals↗
PubMed1990

Involvement of the nigral output pathways in the inhibitory control of the substantia nigra over generalized non-convulsive seizures in the rat.

Activation of GABAergic transmission within the substantia nigra has been shown to suppress several forms of generalized seizures in experimental models of epilepsy. More especially, such pharmacological manipulations suppress spontaneous and chemically-induced generalized non-convulsive seizures in the rat. The aim of the present study was to examine the role of the dopaminergic and GABAergic thalamic and collicular nigral outputs in this antiepileptic effect. For this purpose, we examined the effects of output destruction on the antiepileptic effect of intranigral injections of a GABA agonist or pharmacological blockade of the neurotransmission at the nerve terminal level in rats with spontaneous absence seizures. After selective destruction of dopaminergic neurons within the substantia nigra with 6-hydroxydopamine (5 micrograms/side) or hemisection of the ascending nigral output, bilateral intranigral injection of muscimol (2 ng/side) still significantly suppressed generalized non-convulsive seizures. Bilateral lesioning of the ventromedial nucleus of the thalamus did not abolish the antiepileptic effects of intranigral muscimol (2 ng/side) and the GABA antagonist, picrotoxin, when given into this thalamic nucleus (10 ng/side) also failed to induce suppression of spike and wave discharges. The antiepileptic effects of intranigral injection of muscimol (2 ng/side) was reversed by bilateral electrolytic lesions of the superior colliculus. Blockade of the GABAergic transmission at this level with picrotoxin (40 ng/side) significantly suppressed generalized non-convulsive seizures. Finally, excitation of collicular cell bodies with low doses of kainic acid (4 and 8 ng/side) also resulted in a suppression of spike and wave discharges. These results demonstrate that the GABAergic nigrocollicular pathway is critical for the inhibitory control of the substantia nigra over generalized non-convulsive seizures. The data further suggest that antiepileptic effects observed following potentiation of GABAergic transmission in the substantia nigra result from a disinhibition of collicular cell bodies.

Animals↗
PubMed1990

Suppression of spontaneous generalized non-convulsive seizures in the rat by microinjection of GABA antagonists into the superior colliculus.

Intranigral injections of GABA agonists suppress spontaneous and chemically induced generalized non-convulsive seizures in the rat. In order to examine whether the GABAergic nigrotectal pathway could be involved in this suppression, bilateral injections of GABA antagonists were performed in the superior colliculus of rats with spontaneous generalized non-convulsive seizures. Bilateral microinjections into this structure of the GABA antagonists picrotoxin (20 and 40 ng/side) and bicuculline methiodide (5 ng/side) suppressed spike-and-wave discharges for 40 min and 20 min post injection, respectively. Unilateral injections of picrotoxin (40 ng) into the superior colliculus as well as bilateral injections of a GABA agonist (muscimol; 80 ng) did not induce significant modifications. These results show that blockade of the GABAergic transmission at the level of the superior colliculus results in a suppression of generalized non-convulsive seizures. These data support the hypothesis that the suppressive effect of intranigral injections of GABA agonists over generalized non-convulsive seizures involves, at least in part, the nigrotectal GABAergic pathway.

Animals↗
PubMed1990

Increased gamma-hydroxybutyric acid receptors in thalamus of a genetic animal model of petit mal epilepsy.

The distribution and kinetics of specific binding sites for gamma-hydroxybutyrate (GHB), a naturally occurring compound known to produce absence-like seizures, was studied in the brains of Wistar rats with spontaneous, bilaterally synchronous spike wave discharges (SWDs), a model of petit mal epilepsy, and non-epileptic controls using [3H]GHB autoradiography. [3H]GHB receptor binding was increased 40-60% in lateral thalamic nuclei of the epileptic animals. Kinetic analysis showed that the increase in the binding was due to an increase in density of low affinity GHB binding sites in the epileptic animals. Given the ability of GHB to produce petit mal-like seizures when administered to animals, and the fact that the SWDs in the Wistar rat model seem to emanate from lateral thalamus, these data raise the possibility that GHB-mediated mechanisms may play a role in the pathogenesis of petit mal seizures.

Animals↗
PubMed1990

[Late diagnosis of congenital argininemia during administration of sodium valproate].

Congenital hyperargininaemia is a rare condition transmitted as an autosomal dominant trait. Following a one-year free interval, repeated vomiting, psychomotor regression and spastic paraparesis with talipes equinus progressively develop. The diagnosis, confirmed by arginine assays in blood and urine, is probably often missed. We report a case of homozygous arginase deficiency belatedly diagnosed at the age of 18 years, when treatment with sodium valproate (VPA) was instituted. This female patient presented with psychomotor regression since the age of 15 months and with paraparesis since she was 3 years' old. These symptoms rapidly became worse. At the age of 18 years, when she was bed-ridden, she was hospitalized for subintrant tonic seizures. EEG showed generalized, continuous spike-wave discharges at the rate of 3.5 c/s. Treatment with VPA was instituted. Five days later, she went into a state of stupor. Blood ammonia level was elevated at 362 mumol/l. VPA was discontinued, and this was followed by a regression of disturbances of consciousness and by a decrease in arterial ammoniaemia, although the ammonia levels remained high, fluctuating between 40 and 100 mumol/l. Several months after VPA treatment was interrupted, the patient had a second episode of stupor, and her ammoniaemia was 500 mumol/l. Serum amino acid chromatography showed hyperargininaemia at 501 mumol/l (N = 30-150 mumol/l). The diagnosis of arginase deficiency was confirmed by the rise of arginine in red cells, cerebrospinal fluid and urine and, above all, by the finding of a deeply depressed arginase activity in erythrocytes. In all cases of intolerance to VPA, arterial ammoniaemia should be measured after withdrawal of VPA, some time after the acute episode.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗