Biomedical subjects

M Leboyer

Publications and source records attributed to M Leboyer.

98 records · Page 6Linked to original sources

PubMed1983

[Serotoninergic depression--hypothesis or reality?].

Could we use the term "serotoninergic depression"? To answer this question various tests that seem to confirm the serotoninergic hypothesis of depression are described and their respective value ascertained. The measure of 5 HIAA (5 hydroxy indole acetic acid) in the cerebrospinal fluid has made it possible to isolate a population of depressed people with a low rate of this main metabolite of serotonin. This test seems to be linked with the frequency and the severity of attempts to commit suicide. The tryptophane, the direct serotonin's precursor, is reduced among some depressed people, for whom it could be used as a therapy. Blood platelet is used as a peripheral model of serotoninergic neuron; present research highlight among depressed people, decrease of serotonin uptake, of binding of tritiated imipramine, of monoamine oxidase, and of serum serotonin levels. Results analysis has been made difficult because of a lack of homogeneous methodologies: classification systems of depressions differ and the composition of test groups do not take into account physiological factors. In spite of these difficulties, we can try to describe the "serotoninergic depression" and consider this notion as a model for research.

Blood Platelets↗

PubMed1982

[Reduction of platelet serotonin in major depression (endogenous depression)].

Serum serotonin (5-HT) levels were measured in several patients with psychiatric disorders using high pressure liquid chromatography with electrochemical detection. A marked reduction in 5-HT levels was found in male and female patients with major depressive disorder, as compared to controls, but not in dysthymic disorder. These modifications may constitute biochemical changes suggestive of major depressive disorders; they could not be attributed to chronic antidepressant treatment.

Adult↗

PubMedDate not supplied

[Is age at onset associated with executive dysfunction in obsessive-compulsive disorder?].

In obsessive-compulsive disorder (OCD), clinical, neurobiological and genetic differences have been reported according to age at onset (AAO). Given the importance of identifying homogeneous subtypes in complex hete-rogeneous disorders such as OCD, it would be particularly useful to identify a specific cognitive profile associated with early-onset OCD. Although impaired cognition has repea-tedly been demonstrated in OCD patients, discrepancies between studies have hampered the identification of a precise cognitive dysfunction. Executive dysfunction has often been reported, but findings have not always been replicated. The aim of this study was to assess executive functions in 30 patients according to their AAO. The sample consisted of 15 early-onset and 15 late-onset OCD patients and 22 normal controls, matched for age, sex and socio-economic status. Various aspects of executive function were assessed with five neuropsychological tests: Tower of London, Trail Making Test, Verbal Fluency, Design Fluency and Association Fluen-cy. The 30 OCD patients obtained lower total scores than the controls in the Tower of London test and association fluen-cy task (p<0.05 and p<0.001, respectively). Impairments were more marked for the early-onset group, with no effect of gender or age at interview. Deficits in specific aspects of frontal lobe function were found in the OCD group and were particularly pronounced within the early-onset group. These findings confirm clinical data suggesting that OCD patients can be subtyped according to age at onset and that OCD patients present unusual cognitive characteristics. They also support the hypothesis that early-onset OCD might be a rele-vant subgroup characterised both by a particular clinical profile and by specific cognitive characteristics.

Adolescent↗

PubMedDate not supplied

[Familial forms of schizophrenia. Cytogenetic study].

As a preliminary step in the search for chromosomal location of a susceptibility gene predisposing to schizophrenia, cytogenetic screening of patients might be useful. Search for chromosomal aberrations has successfully directed and accelerated the identification of several disease genes, such as the Duchenne muscular dystrophy gene, retinoblastoma, Burkitt's lymphoma and chronic myeloïd leukemia. Although karyotypes abnormalities do not account for a large portion of cases of Schizophrenia, the two candidate regions predisposing to this disease resulted from observation of chromosomal abnormalities. First, the identification of a partial trisomy of the 5q11-q13 region (Basset et al., 1988) led Sherrington et al. (1988) to report a positive linkage with markers localized on the long arm of chromosome 5, which has not yet been replicated (Kauffman et al., 1989; Kennedy et al., 1988; St Clair et al., 1989). Second, on the basis of frequent cytogenetic abnormalities of the sex chromosome (DeLisi, 1985) in addition to epidemiological observations, Crow (1988) suggested that there could be a locus for psychosis within the pseudoautosomal region, a data which has been recently confirmed (Collinge et al., 1991). With the hypothesis that such aberrations could be more frequent among schizophrenics who have at least one affected first-degree relative, we undertook cytogenetic screening on a sample recruited from consecutive psychiatric admissions to a Psychiatric facility (Hôpital Saint Paul) involving patients living in a limited geographical area on the island of La Réunion, a French Department in the Indian Ocean.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromosome Aberrations↗

PubMedDate not supplied

[Is anxiety hereditary?].

Familial aggregation of anxiety disorders has repeatedly been reported: the estimated risk among the first degree relatives is of 15% to 18% compared to 3% in control groups. The most recent studies are focused on more homogeneous clinical subgroups. Thus, among agoraphobics first degree relatives, the risk is elevated not only for agoraphobia but also for panic attacks and other phobias. In families of panic attacks, the risk of panic attacks in the first degree relatives is specifically elevated. Thanks to the extremely fast development of genetic linkage and molecular genetics, progress is expected in the field of genetics and psychiatry. Linkage methods applied to anxiety disorders are discussed.

Agoraphobia↗

PubMedDate not supplied

[Endorphins. Physiological and pharmacological aspects, and research in psychiatry].

This article gives an overview of the biochemistry, physiology and pharmacology of endogenous opioid peptides. The role of endorphins in psychiatric pathology in the last ten years, has mainly been studied through two clinical research strategies: Pharmacological, administration of opiate agonists or antagonists, or substances altering endorphins metabolism. Biological, static or dynamic dosage of opioid activity in peripheral liquids, trying to correlate those measures either with a syndrome, or with a clinical trait. These methods applied to schizophrenia, affective disorders, anxiety, addiction, anorexia, and tardive dyskinesia are being reviewed. Results are very heterogeneous but support the involvement of the endogenous opioid system in some psychiatric pathology. Furthermore, this paper should help to underline some of the present day development of biological psychiatry.

Alcoholism↗

PubMedDate not supplied

[Cholinergic hypothesis of depression].

Is acetylcholine implicated in depressive disorders? Biochemical methods studying the cholinergic system are not well set up. Only indirect elements could confirm the cholinergic hypothesis of affective disorders. Cholinergic agonists induce depressive symptomatology. Moreover, a central, cholinergic dysfunction could be an explanation of sleep disturbances and of neuroendocrine abnormalities seen in affective disorders. These observations could be applied in two ways: a more precise choice of antidepressive drugs, and the use of new tests developed to detect population with high depression risk.

Acetylcholine↗

PubMedDate not supplied

[Opiate hypothesis in infantile autism? Therapeutic trials with naltrexone].

The opioid hypothesis suggests that childhood autism may result from excessive brain opioid activity during neonatal period which may constitutionally inhibit social motivation, yielding autistic isolation and aloofness (Panksepp, 1979). This hypothesis has now received strong support and is currently based on three types of arguments: (1) similarity between autistic symptomatology and abnormal behaviors induced in young animals by injections of exogenous opioids, such as increasing social aloofness and decreasing social vocalization; (2) direct biochemical evidence of abnormalities of peripheral endogenous opioids being reported in autism and (3) therapeutic effects of the long lasting opioid receptor blocking agent naltrexone in autism. In this article, we give description of open and double-blind studies of naltrexone in autism. Naltrexone has been tested in several open studies. We performed an open trial with naltrexone in 2 autistic girls, displaying serious self-injurious behavior, reduced crying and a marked preference for salty and spicy foods, symptoms that could be related to a dysfunction of the opioid system. With dosages of 1 mg/kg/day, we observed an immediate reduction of hyperactivity, self-injurious behavior and aggressiveness, while attention improved. In addition, social behaviors, smiling, social seeking behaviors and play interactions increased (Leboyer, Bouvard et Dugas, 1988). Campbell et al. (1988) has also reported a tranquilizing and a stimulating effect in 6 out of 8 children with autism. We did confirm these preliminary results in a double-blind study performed on 4 children with autism. In a cross-over double-blind study, three dosages of naltrexone (0.5, 1 and 2 mg/kg/day) and placebo were compared.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗