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Biomedical subjects

M Leboyer

Publications and source records attributed to M Leboyer.

At least 91 records · Page 5Linked to original sources
PubMed1991

The reliability of the SADS-LA in a family study setting.

The joint-rater and test-retest reliability study of two translated versions of the SADS-LA (Schedule for Affective Disorders and Schizophrenia--Lifetime version--modified for the study of anxiety disorders), one in French and the other in German, have been tested in family study settings, in a sample of patients and first-degree relatives. The test-retest reliability study demonstrated that identification of major affective disorders and schizophrenia was performed with sufficient reliability; however, diagnoses of subtypes of major disorders (e.g. bipolar II disorder) and identification of minor disorders was less reliable. The implications of these findings in phenotype identification during family studies in psychiatry are discussed.

Adult↗
PubMed1991

Absence of linkage between chromosome 11p15 markers and manic-depressive illness in a Belgian pedigree.

OBJECTIVE: The original finding of genetic linkage in an Old Order Amish pedigree has been contradicted by the results of several subsequent studies. Using the same genetic parameter values, diagnostic criteria, and 11p15 genetic markers as those used to study the initial Amish population, the authors performed a linkage study of a four-generation informative pedigree in Belgium. METHOD: Recombinant DNA technology was used to analyze three markers for the chromosome 11p15 location: the genes for tyrosine hydroxylase (TH) and insulin (INS) and the c-Harvey-ras oncogene (HRAS). Diagnoses of the relatives of a proband with bipolar affective disorder were determined with the Schedule for Affective Disorders and Schizophrenia--Lifetime Version and based on the Research Diagnostic Criteria. Relatives were considered affected if they had bipolar disorder, unipolar disorder, or cyclothymia; a diagnostic hierarchy was developed to include unipolar disorder and cyclothymia in the linkage analysis. RESULTS: Pairwise analyses of the disease locus and each of the three polymorphisms excluded the possibility of close linkage between manic-depressive illness and the three chromosome 11p15 markers. Multipoint linkage analysis combining the information from all three genes also excluded linkage. CONCLUSIONS: The conflict between the original results from the Amish study and the many negative reports on chromosome 11 linkage of manic-depression has been interpreted as indicating genetic heterogeneity, but heterogeneity has not been documented for the 11p15 locus. Conversely, the linkage approach has major drawbacks, so other genetic strategies should also be considered.

Adolescent↗
PubMed1990

Subtyping familial schizophrenia: reliability, concordance, and stability.

This report examines the reliability, concordance, and long-term stability of the subtypes of schizophrenia defined by four major diagnostic systems (DSM-III, DSM-III-R, ICD-10, and Tsuang-Winokur criteria) and rated both for the first hospitalization and for a best estimate diagnosis reflecting lifetime evolution of symptomatology. Schizophrenics studied belonged to two samples of multiply affected families, namely a sample selected in France and a sample of non-metropolitan French identified in the island of La Réunion. ICD-10 and DSM-III-R show opposite stringency regarding subtyping of schizophrenia, with DSM-III-R having a narrow and ICD-10 a broader definition of specific subtypes. Long-term stability of each subtype was fairly good, stability being the highest for hebephrenics and only intermediate for paranoid and undifferentiated subtypes. Comparison of two different cultural and geographical regions reveals an overall similarity of subtype frequencies in familial schizophrenia. The implications of the results for the choice of diagnostic procedures in family studies of schizophrenia are discussed.

Adolescent↗
PubMed1990

Sampling strategy in linkage studies of affective disorders.

Evidence of linkage in families of bipolar patients has so far been identified with genetic markers on chromosome X and 11. However, replications of these data have not consistently been reported in either case, which favours the hypothesis of genetic heterogeneity. Therefore, we have tried to outline a sampling strategy for linkage replication in affective disorders. We estimated the average number of nuclear families required to replicate X or 11 linkage as a function of the degree of heterogeneity as well as the number to prove heterogeneity given that linkage exists. The results are presented and discussed.

Bipolar Disorder↗
PubMed1989

Performance of linkage analysis under misclassification error when the genetic model is unknown.

Linkage analysis of complex diseases raises a number of important methodological problems. One of them concerns the clinical classification of disease phenotypes. In this study, we investigate the effects of false positive misclassification on the estimation of the recombination fraction and on the power and the robustness of tests for linkage. These effects are investigated 1) when the genetic model of the trait locus is known; and 2) when it is unknown, by maximizing the likelihood of the marker configuration given the disease status in the family. Results show that linkage analysis of misclassified data leads to an overestimation of the recombination fraction and a loss of power of the linkage test. The results are quite similar in both situations. However, the linkage test itself is robust to this kind of misclassification error.

Affective Disorders, Psychotic↗
PubMed1989

Hemisphere asymmetry of alpha burst sequential organization in depression.

A new quantitative EEG index based on the sequential variability of the frequency of occurrence of alpha bursts (alpha-BVI) was utilized for investigating the respective role of the two hemispheres in depression and their relationship with two clinical dimensions of this illness: psychomotor retardation and blunted affect. The EEG (at P3 and P4 referred to Fz) was recorded during rest periods in two groups of patients selected according to their scores on various clinical scales: one consisted of 12 patients characterized by psychomotor retardation (PMR group), the other of 9 patients characterized by blunted affect (BA group). A control group of 12 normal subjects was recorded in the same conditions. All subjects were dextral. The following main results were obtained: (1) in both groups of patients the right and the left alpha-BVI were, before treatment, significantly lower than those of the controls. (2) In controls, the sequential alpha burst variability was identical on both hemispheres. (3) In patients, before treatment, the right hemisphere alpha-BVI was significantly lower than the left. (4) Electro-clinical correlations were also observed: (A) in the BA group, before treatment, (a) between the degree of blunted affect and the decrease of the right alpha-BVI, (b) between ideoverbal retardation and the decrease of the left alpha-BVI (these correlations disappeared after treatment); (B) in the PMR group, ideoverbal retardation was, on the contrary, correlated to a right alpha-BVI decrease, this correlation persisting after treatment. These results are discussed according to the role of each hemisphere in depression.

Adult↗
PubMed1989

Effect of the Tfm mutation on handedness in mice.

The hyposthesis has been proposed that testosterone is involved in the determination of handedness in man: a high sensitivity to testosterone being associated with left handedness. Handedness in mice is tested according to Collins' paradigm: most mice present either a right or a left paw preference but others are ambilateral. The hypothesis that there is an association between a low neonatal imprinting by testosterone and a strong handedness (right or left) is tested here using Tfm male mice which are testosterone insensitive. Our results confirmed the hypothesis, since Tfm males were as well lateralized as their female siblings and significantly more strongly lateralized than their male siblings not carrying the mutation.

Androgen-Insensitivity Syndrome↗
PubMed1988

Is autism associated with anomalous dominance?

Geschwind and Galaburda (1985, 1985b) have advanced a theory of the development of anomalous dominance and its biological associations. The present article reviews existing literature in an attempt to apply this theory to the study of autism.

Autistic Disorder↗
PubMed1986

Pharmacological properties of acetorphan, a parenterally active "enkephalinase" inhibitor.

Acetorphan, i.e. N-[(R,S)-3-acetylmercapto-2-benzylpropanoyl]-glycine, benzyl ester, is a lipophilic derivative of Thiorphan, a potent inhibitor of "enkephalinase" (EC 3.4.24.11). On purified enkephalinase its inhibitory potency was approximately 1000 fold less than that of Thiorphan but became close to the latter (nanomolar) when it was incubated previously with cerebral membranes. After parenteral administration to mice and rats (1-10 mg/kg) extensive inhibition of cerebral enkephalinase was shown by the depressed enzyme activity in brain membranes from treated animals and the long-lasting potentiation of analgesia elicited by (D-Ala2,Met5)enkephalin (i.c.v.). This suggests that acetorphan easily enters the brain where the active Thiorphan is released. Parenteral acetorphan elicited a series of naloxone-reversible, opioid-like effects, most of which were described previously with intracerebral Thiorphan or other enkephalinase inhibitors. Antinociceptive effects were found in some tests (hot plate jump and phenylbenzoquinone-induced writhing) but not in others (hot plate licking and tail withdrawal). "Antidepressant" effect was found in the "mouse despair" test and antidiarrhoeal effect in the rat castor oil test. Acetorphan also elicited significant increases and decreases in turnover indexes of serotonin and noradrenaline, respectively, in mouse cerebral cortex. In mice chronically treated with acetorphan, the antinociceptive activity of the compound was not modified markedly and no overt withdrawal symptom could be observed after either treatment interruption or administration of naloxone.

Amino Acids, Sulfur↗
PubMed1984

Reduced platelet serotonin in depression.

Platelet serotonin levels were measured in several psychiatric disorders to determine whether they distinguish among major depressive disorder (one or more depressive episodes and no manic episodes), dysthymic disorder (depressive neurosis), and schizophrenic and paranoid disorders. Serotonin levels in 141 subjects were determined using high performance liquid chromatography with electrochemical detection. Serotonin (5HT) levels in control subjects were significantly lower in males than in females. A marked reduction in 5HT levels, as compared to controls, was found in male and female patients with major depressive disorder, but not in dysthymic disorder. A slight but significant reduction in serotonin levels was found in female schizophrenic patients. The reduction in serotonin levels found in major depressive disorder could not be attributed to chronic antidepressant treatment. Liquid chromatography with electrochemical detection used in the present study permits a large-scale investigation.

Adult↗
PubMed1983

[A case of dysthymic pathology in a 16-year-old adolescent].

Dysthymia in children and adolescents, illustrated by a sixteen-year-old-girl's clinical history, raises different diagnostic, therapeutic and prognostic problems. Diagnostic, since dysthymia in children and adolescents has specific peculiarities (often mixed manic episodes, variable expression of depressive affect according to age, problem of the meaning of "masked depression"; Diagnostic again, since it is difficult to collect clearcut evidence ascertaining the diagnosis of manic-depressive syndrome in children: genuine periodicity in the occurrence of dysthymic episodes, family history of psychoses (manic-depressive syndrome, periodic psychosis, or other types of psychosis) and effectiveness of lithium are reliable criteria; Finally, differential diagnosis with the two other types of childhood psychosis: affective psychoses and severe dysthymic disorders; Therapeutic: the problem is to know when and on what evidence treatment with lithium can be started and, if called for, discontinued.

Adolescent↗