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F Thibaut

Publications and source records attributed to F Thibaut.

At least 55 records · Page 3Linked to original sources
PubMed1994

[Drug modulation of libido and sexual activity. Behavior effect of GnRH analog in man].

Libido and male sexual behaviour are under the control of complex testosterone-dependent neuro-endocrine mechanisms. Better knowledge of these mechanisms has allowed to modulate sexual behaviour using drugs. Indeed, it is possible to block spontaneously uncontrollable sexual pulsions of aggressive hypersexual men by dropping testosterone secretion and consecutively decreasing androgen effects on target cells. From now, mutilating neurosurgery and treatment with either estrogens or antigonadotrophic progestagens are withdrawn. Cyproterone acetate, acting as a competitive inhibitor of testosterone action through its binding to androgen receptors, has been used with efficacy in 80% of cases studied. However, the therapeutic use of cyproterone acetate is limited by three drawbacks: i/potential side effects, ii/exclusive oral route of administration and iii/lack of available biological criteria as a control of the good observance of the treatment. We studied the efficacy of a GnRH analogue (Triptoreline), which induces a reversible hormonal castration and of which both the formulation and the route of administration avoid the inconveniences linked to a treatment with cyproterone acetate. 3.75 mg triptoreline injected intramuscularly once a month had been very effective on clinical and biological parameters in 5/6 aggressive hypersexual patients. In 3 of them a previous treatment with cyproterone acetate had been uneffective. Such a reversible hormonal castration suppressing sexual addiction, would lead to favourable conditions for psychotherapy.

Adolescent↗
PubMed1993

Effect of a long-lasting gonadotrophin hormone-releasing hormone agonist in six cases of severe male paraphilia.

Six men with severe paraphilia had been treated with depot gonadotrophin luteinizing releasing hormone analogue (GnRHa) (triptorelin 3.75 mg per month intramuscularly). In 5 cases, the treatment ended their deviant sexual behavior and markedly decreased their sexual fantasies and activities without further significant side effects than those related to hypoandrogenism. This clinical improvement was parallel to the gradual decrease of plasma testosterone level to castration values within the first month. The beneficial effect of this treatment had been maintained at follow-up varying from 7 months to 3 years. One patient interrupted the treatment at the end of the first year and relapsed within 10 weeks. GnRHa treatment, which leads to reversible castration, may constitute a promising treatment of paraphilic behavior and may favor the possibility of concurrent psychotherapy.

Adolescent↗
PubMed1992

SPEM impairment in drug-naive schizophrenic patients: evidence for a trait marker.

Smooth-pursuit eye movements (SPEM) were assessed in healthy subjects and in drug-naive, chronic, and residual schizophrenic patients. SPEM gain was found to be decreased in all the schizophrenic patients who also exhibited a significant increase in the rate of saccades. The frequency of square-wave jerks was the same in schizophrenic patients and normal controls, suggesting that the primary abnormality in schizophrenic patients was a low gain rather than a defect of the saccadic system. Patients were retested 1 month later, and stability of gain was high even in formerly drug-naive subjects who had been treated for 1 month with neuroleptic drugs. Altogether these results confirm the conclusions of most previous studies, extend them to drug-naive schizophrenic patients, and favor the hypothesis that SPEM impairment is a trait marker in schizophrenia.

Adult↗
PubMed1990

Microtopography of D1 dopaminergic binding sites in the human substantia nigra: an autoradiographic study.

The autoradiographic distribution of D1 dopaminergic binding sites was studied in the human ventral mesencephalon using the D1 antagonist [3H]SCH 23390. [3H]SCH 23390 binding was characterized by a single class of sites with a Kd of 2.5 nM and a Bmax of 31 fmol/mg of tissue. The density of [3H]SCH 23390 binding sites was high in the substantia nigra, moderate in the ventral tegmental area and low in the peri- and retrorubral field (catecholaminergic region A8). Binding densities were similar in pars compacta and pars reticulata of the substantia nigra, except for a peak value of high [3H]SCH 23390 in the pars reticulata, at a level just ventral to a zone of hyperdensity of melanized dopaminergic neurons in the pars compacta. The anatomical organization of the human ventral mesencephalon was analysed on adjacent sections stained for acetylcholinesterase histochemistry and tyrosine hydroxylase, substance P, dynorphin B, somatostatin and methionine-enkephalin immunohistochemistry, respectively. The similarity in distribution of [3H]SCH 23390 binding sites and substance P or dynorphin B immunoreactivity suggests that D1 binding sites are mainly located on the striatonigral projections. In accordance with these results: (1) the density of [3H]SCH 23390 binding sites was reduced in the substantia nigra of a patient with Huntington's chorea, a disease associated with a degeneration of striatonigral neurons; (2) the density of [3H]SCH 23390 binding sites was unaffected in the substantia nigra of a patient with Parkinson's disease, a disorder characterized by a marked loss in nigral tyrosine hydroxylase-positive neurons. [3H]SCH 23390 binding sites showed a characteristic, heterogeneous distribution within the human ventral mesencephalon, confirming data obtained in other species. The preferential localization of D1 dopamine receptors on striatonigral projections in human brain suggests that pharmacological manipulation of these receptors modulates the activity of striatonigral pathways, thereby affecting the various outputs of the nigral complex.

Acetylcholinesterase↗
PubMed1989

Time course of postmortem modifications in synaptosomal [3H]dopamine uptake and [3H]GBR 12783 binding to the dopamine uptake complex in the rat striatum.

The present study focuses on the changes of two biochemical markers of the striatal dopaminergic innervation evaluated after different postmortem storage periods of rat heads either at room temperature (21 degrees C) or at 4 degrees C: (i) the uptake of [3H]dopamine (DA) into striatal synaptosomes and (ii) the specific binding of [3H]GBR 12783, a selective ligand for the neuronal dopamine uptake sites, to a striatal membrane fraction. The uptake of [3H]DA was completely abolished after 24 and 72 h storage of the tissue at 21 degrees C and 4 degrees C, respectively, whereas in the same conditions, the binding of [3H]GBR 12783 was slightly decreased. The Km and Kd of these two processes were virtually unchanged after the different storage periods considered, whereas the Vmax and Bmax were markedly decreased.

Animals↗
PubMed1989

Continuous and intermittent levodopa differentially affect basal ganglia function.

The effects of continuous and intermittent levodopa treatment on behavioral and biochemical indexes of basal ganglia function were compared in rats with unilateral 6-hydroxydopamine lesions of the nigrostriatal dopamine pathway. Animals treated for 30 days with intermittent levodopa exhibited behavioral sensitization manifested by an enhanced rotational response to apomorphine; the rotational response of rats treated with an equivalent dose of levodopa by continuous infusion did not differ from that of saline-treated controls. Dopamine receptor up-regulation in the denervated striatum relative to the intact striatum was statistically significant for D1 but not D2 receptors: This asymmetry in dopamine receptor levels was diminished following intermittent levodopa treatment. Glutamic acid decarboxylase activity, modestly elevated in all groups in the denervated striatum relative to the intact striatum, increased substantially over control values bilaterally as a result of intermittent, but not continuous, levodopa treatment. These findings suggest a relation between the schedule of chronic levodopa administration and the development of behavioral sensitization, possibly as a consequence of alterations in neuronal systems located downstream from striatal dopamine receptors. The behavioral sensitization induced by chronic, intermittent dopaminomimetic treatment may serve as a model for motor fluctuations in Parkinson's disease.

Animals↗
PubMed1979

[Post-radiotherapy pericarditis. 5 cases (author's transl)].

These cases represented 2.8% of the patients admitted for pericarditis during the same period. The cause of irradiation was a carcinoma of the breast in three cases and a carcinoma of the oesophagus in two cases. Acute forms of pericarditis occured 8 and 13 months after irradiations, and chronic forms after 1, 8 and 13 years. Three clinical forms were observed; two patients had an acute form; the first one with a slight effusion was easily cured, the second with cardiac tamponnade recovered after surgical evacuation, two others patients had a chronic latent effusion; after surgical evacuation, one recovered but the other one developped an occult constrictive pericarditis diagnosed by rapid volume expansion. The fifth case was a constrictive pericarditis which was effectively traited by pericardectomy. The difficulty of etiological diagnosis varies with the time and the amount of effusion. When the effusion is moderate the distinction must be made with an acute idiopathic pericarditis; when effusion is large the distinction must be made with a tuberculosis and specially a tumoral recurrence; in three cases pericardial biopsy was carried out and eliminated these diagnosises; lesions were similar: pericard was sclerous and little in cells, inflammatory signs were slight or absent. The postoperative prognosis in constrictive pericarditis may be agravated by associated myocardial lesions.

Acute Disease↗
PubMedDate not supplied

No evidence for involvement of KCNN3 (hSKCa3) potassium channel gene in familial and isolated cases of schizophrenia.

Several studies have reported in schizophrenia a decrease of age of onset in successive family generations, and this observation is consistent with anticipation. Anticipation is known to result from expansion of CAG repeats in several neurodegenerative disorders. Longer alleles of the KCNN3 gene, which contains a highly polymorphic CAG repeat, and encodes a neuronal small conductance calcium-activated potassium channel, have recently been shown to be over-represented in sporadic cases of schizophrenia. In this report, we tested the hypothesis of an association between longer alleles of CAG repeat in the KCNN3 gene and schizophrenia in 20 families with clinical evidence for anticipation and in 151 unrelated schizophrenic cases. No significant difference in the distributions of allele frequencies was observed between familial cases of schizophrenia and controls, and between unrelated cases and controls. Furthermore, no intergenerational CAG repeat instability was detected in the 20 families. Our results do not support the involvement of the KCNN3 (hSKCa3) gene in the etiology of schizophrenia.

Adult↗
PubMedDate not supplied

[Carbamazepine and aggressive behavior: a review].

Carbamazepine which has been used as an anticonvulsivant for many years, has more recently been advocated for the control of aggressive behavior in epileptic and non epileptic populations. Carbamazepine is the drug of choice for patients whose aggressive outbursts are related to epilepsy. It appears that carbamazepine may also be affective in aggressive individuals with varying diagnoses (especially schizophrenic patients) but additional double-blind studies are needed. Patients experienced good control of aggressive behavior on carbamazepine in doses of 600 to 1,200 mg per day but the relationship of carbamazepine responsiveness to carbamazepine blood levels and concurrent medication (neuroleptic treatment) requires further studies. No significant problem has been encountered in the majority of patients receiving carbamazepine. However, it can rarely cause bone marrow suppression and hepatotoxicity so that blood counts and liver functions require monitoring.

Aggression↗
PubMedDate not supplied

[Lithium and aggression in adults].

The use of lithium as an antiaggressive agent independently of its action in bipolar illness is now well documented. It appears particularly effective in the control of aggressive behavior in chronically aggressive prisoners and mentally retarded patients. Approximately 70-75% of these patients are likely to show a positive response to lithium therapy. No convincing features have been identified as being predictive of a good response. The clinical effect of lithium is to reduce the frequency and the severity of both hetero and auto aggressive outbursts. The use of lithium for aggressive behavior remains controversial in epileptic disorders and inconclusive in chronically psychotic patients. Careful monitoring of lithium blood levels is necessary to ensure adequate therapeutic efficacy without toxicity. A caution is needed in patients with brain damage especially when concurrent neuroleptic treatment is used. The antiaggressive effect of lithium seems rather specific and may be associated with a serotoninergic effect.

Adult↗
PubMedDate not supplied

[Anti-aggressive effect of beta-blockers].

Since the first report in 1977, many studies have reported the efficacy of beta blockers for the treatment of violent and aggressive behavior. Propranolol had mainly been reported to be effective in aggressive patients with organic brain syndromes of diverse etiologies. Doses of propranolol had varied ranging from 60 to 1,440 mg per day with means also varying from 250 to 400 mg per day. Propranolol was in most cases added to existing neuroleptic treatment but sometimes it had been the only medication used. Treatment response required 4 to 6 weeks of maintenance therapeutic doses. The utility of propranolol in aggressive patients with other diagnoses and the efficacy of other beta blockers remain unclear and require further studies.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[The dopamine transporter: characterization and physiopathologic implications].

The dopamine transporter (DAT) is the carrier protein that transports dopamine across the presynaptic membrane. The DAT terminates the action of dopamine (DA) in the synapse via reuptake and thus regulates DA neurotransmission. The transporter has been studied by direct binding techniques using a variety of ligands which are inhibitors of DA transport. DAT binding, both in vivo (positron emission tomography) and in vitro (post mortem) may serve as a presynaptic marker to measure altered DA innervation in several neuropsychiatric diseases such as idiopathic Parkinson's disease, Tourette's disease, schizophrenia or cocaine addiction. In Parkinson's disease, a reduction in the density of binding sites could be due either to a degeneration of the terminal dopaminergic projections or to a compensatory readjustment in the level of dopamine synaptic transmission. This dopaminergic cell specific marker could also aid in attempts to elucidate the rate at which dopaminergic cells are lost in this disease. MPTP (a neurotoxin which induces a parkinsonian-like syndrome after conversion in MPP+) uses DAT to enter the neuron and exert its toxic effect which may be prevented by pretreatment with DA uptake blockers. In cocaine abuse, DAT mediates the addictive properties of cocaine. Cocaine binding sites on the carrier may be distinct from DA binding sites allowing the development of medication sparing the DA function but impairing the cocaine effects. In schizophrenia, functional DA uptake was reported to be increased in the striatum in post mortem brains, whereas the kinetic parameters of the uptake sites were unchanged using different transporter labeling ligands. Thus, this marker does not provide any evidence for the dopaminergic hypothesis, but an impairment of the DAT itself could possibly be involved in the etiology of schizophrenia. However, the possible interaction of drugs such as L-Dopa or neuroleptic treatment with transporter binding may be taken into account in the results analysis. Finally, the DAT gene is also an important candidate gene for psychiatric diseases such as schizophrenia or cocaine abuse.

Brain↗