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P Baruch

Publications and source records attributed to P Baruch.

14 recordsLinked to original sources
PubMed1992

[Pathological gambling: literature revue].

This paper summarizes the current literature on pathological gambling. Interest in gambling has been present in every society but treated as an object of sociopolitical or literary interest. It is only from the beginning of this century that psychiatry began to look at pathological gambling, first with Freud and his writing on Dostoïevsky then with other theories like the learning theory, studies on substance dependence, the links with affective syndromes and the psychobiological studies. These studies are presented and discussed. Finally, the authors offer some guidelines for an approach to a pathological gambler.

Behavior, Addictive↗
PubMed1992

[Dysmorphophobia (body dysmorphic disorder)].

This article reviews the historical and terminological origins of dysmorphophobia from Herodotus to today. It explains the differences pointed out by many authors, including the DSM-III-R, between body dismorphic disorder and delusional disorder somatic type, which are referred to as monosymptomatic hypochondriacal psychoses in Europe. Epidemiological data, clinical characteristics and outcome are discussed. Explicative theories and neurobiological, developmental and analytical aspects of body image are presented. The association between body dismorphic disorder and other disorders is analyzed, and treatment possibilities are discussed. The authors suggest that body dismorphic disorder be classified with obsessive compulsive disorder, whatever the intensity of symptomatology, rather than with somatoform or delusional disorder, and treated with serotonin uptake inhibitors or neureptics that have been proven to be effective for the treatment of this disorder, such as pimozide.

Body Image↗
PubMed1992

The dimensional approach to clinical psychopharmacology: a polysemous concept.

The last decade has seen significant progress in the development and specific clinical application of selective psychotropes. The dimensional approach to clinical psychopharmacology views the behavioral targets of psychotropes as phenomena existing on a continuum and as components, in varying degrees, of most psychopathologies. The modern concept of dimension has been used in different contexts. In psychology it has a mathematical sense, whereas in biological psychiatry it is associated more with biological function. This paper reviews these two concepts and the recent models attempting to merge them into one. The heuristic value of the dimensional approach, as well as some of its pitfalls and new avenues of research, are discussed.

Adult↗
PubMed1991

Corpus callosum agenesis and psychosis in Andermann syndrome.

Recent illustrations by cerebral magnetic resonance imaging of anomalies of the corpus callosum in schizophrenics have kindled renewed interest in this association. We studied 62 patients affected by the Andermann syndrome, a polymalformative familial syndrome combining frequent congenital corpus callosum agenesis, mental retardation, psychotic episodes, peripheral neuropathy, and some dysmorphic features. Twenty of 62 patients presenting with psychosis were compared with 20 nonpsychotic patients matched according to sex and age. The psychotic patients presented an atypical psychosis as defined by the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, beginning in postadolescence. No significant relationship was observed between corpus callosum agenesis and psychosis. However, a significant association between posterior fossa atrophy and psychosis was established in our study. Although there are limitations in using cross-sectional data for this purpose, the findings suggest an association between cerebellar anomalies and schizophrenialike syndrome and rule out an implication of developmental callosal defects in such psychiatric disorders.

Adolescent↗
PubMed1989

[Essential arterial hypertension and quality of life. Comparative crossed double-blind study of labetalol and captopril].

The purpose of this multicenter randomised, double-blind and cross-over study was to compare the antihypertensive effects of labetalol (L) and captopril (C) in 42 moderate hypertensive patients (mean age: 52 years). The drugs were given during two 4-weeks periods at the end of which the systolic (SBP) and diastolic blood pressures (DBP) were measured at rest in supine and standing positions. The assessment of the quality of life was realized with 4 scales completed by the practitioner [anxiety, depression, well-being, visual analog scale (VAS)] and 4 scales of auto-assessment completed by the patient [2 VAS, well-being, sub-scale of pleasure]. At the end of the first treatment's period (D28), both drugs had decreased significantly supine SBP and DBP (p less than 0.001), standing DBP (L = p less than 0.01; C = p less than 0.05), while only L lowered supine SBP (p less than 0.01). The cross-over analysis was unable to conclude, due to the number of patients and a significant interaction which reduced its power. Thus the effect of the first treatment's period seemed to influence the efficacy of the second one. The percentages of patients with a controlled BP were respectively: after 4 weeks of treatment, L = 61 p. 100 vs C = 42 p. 100 and at the end of study (D56), L = 67 p. 100 vs C = 64 p. 100.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Substance P and neurokinin A regulate by different mechanisms dopamine release from dendrites and nerve terminals of the nigrostriatal dopaminergic neurons.

Numerous striatal neurons innervating the substantia nigra contain substance P and/or neurokinin A. In contrast to substance P or neurokinin A, little neurokinin B is found in the substantia nigra. This led us to compare the effects of nigral application of these tachykinins on the release of dopamine from dendrites and nerve terminals of nigrostriatal dopaminergic neurons. Experiments were made in halothane-anesthetized cats implanted with one push-pull cannula in the substantia nigra and another in the ipsilateral caudate nucleus [3H]Tyrosine was delivered continuously to each push-pull cannula and the release of newly synthesized [3H]dopamine measured in the superfusate. Unlike substance P or neurokinin A, neurokinin B (10(-8) M) applied for 30 min into the pars compacta of the substantia nigra was without effect on the release of [3H]dopamine from nerve terminals or dendrites. When either substance P (10(-8) M) or neurokinin A (10(-8) M) was applied into the pars compacta, the release of [3H]dopamine from nerve terminals was enhanced. While neurokinin A also stimulated the dendritic release of [3H]dopamine, this was reduced by substance P. At a lower concentration (10(-9) M), neurokinin A induced similar effects to those observed at 10(-8) M whereas substance P (10(-9) M) stimulated moderately [3H]dopamine release from nerve terminals but did not affect the dendritic release of the [3H]amine. When superfused into the pars reticulata, substance P (10(-8) M) still stimulated [3H]dopamine release from nerve terminals but not from dendrites while neurokinin A (10(-8) M) was without effect either in the caudate nucleus or the substantia nigra. Additional experiments were made to determine whether or not substance P (10(-8) M) or neurokinin A (10(-8) M) act directly on nigral dopaminergic neurons when applied into the pars compacta. The effects of substance P on [3H]dopamine release from nerve terminals and dendrites were prevented when 2-amino-6-trifluoromethoxy benzothiazole (10(-5) M), an antagonist of glutamatergic transmission, was applied continuously into the caudate nucleus. In contrast, the stimulatory effects of neurokinin A on [3H]dopamine release from nerve terminals and dendrites were insensitive to 2-amino-6-trifluoromethoxy benzothiazole (10(-5) M). These results suggest that neurokinin A, but not substance P, acts directly on dopaminergic cells. In the light of previous observations, we propose that the effects of substance P on dopaminergic transmission are mediated by a nigro-thalamo-cortico-striatal loop.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

[Depressions resistant to tricyclic antidepressive treatment and hypothyroidism].

The relationship between thyroid disorders and depression is well known. This type of endocrine disease is mainly observed in patients with depression resistant to appropriate antidepressor therapy. Three clinical forms of this association may be distinguished: hypothyroidism in a patient with depression but without a previous psychiatric history; a relapse of depression in a manico depressive patient who has developed hypothyroidism; the finding of slight thyroid dysfunction (increased TSH response after injection of TRH) in a patient with depression. The frequency of the association of hypothyroidism and resistant depression underlines the need to perform thyroid function tests in all depressed patients who do not respond normally to appropriate antidepressor therapy. The precise mechanism of the resistance of depressive symptoms to tricyclic antidepressors is unclear. Several arguments point to an effect of triiodothyronine on central noradrenergic receptors. In practice, significant hypothyroidism implies substitute therapy. Minor thyroid dysfunction (abnormal TRH test alone) may require the association of tricyclic antidepressors and thyroid hormone although the indications and precise dosages of this drug association have not been established.

Antidepressive Agents, Tricyclic↗
PubMed1986

In vivo presynaptic control of dopamine release in the cat caudate nucleus--II. Facilitatory or inhibitory influence of L-glutamate.

The local effects of various concentrations of L-glutamate (from 10(-8) M up to 10(-3) M) on the release of [3H]dopamine synthesized continuously from [3H]tyrosine were examined in the caudate nucleus of halothane-anaesthetized cats implanted with push-pull cannulae. When used at a concentration of 10(-8) M or 10(-7) M, L-glutamate stimulated the release of [3H]dopamine from nerve terminals of the nigrostriatal dopamine neurons. This effect was still observed in the presence of tetrodotoxin (5 X 10(-7) M) but it was antagonized by 2-amino 6-trifluoromethoxy benzothiazole (PK 26124) (10(-5) M), an antagonist dopamine nerve terminals. While no significant change in the release of [3H]dopamine was observed with 10(-6) M L-glutamate, higher concentrations (from 10(-5) M to 10(-3) M) of the amino acid produced a long-lasting reduction in the [3H]transmitter release. This latter effect was also antagonized by PK 26124 (10(-5) M) but, unlike that observed with 10(-8) M L-glutamate, it did not persist in the presence of tetrodotoxin (5 X 10(-7) M). On the contrary, a marked stimulation of the release of [3H]dopamine was seen in the presence of this neurotoxin. The reduction in the release of [3H]dopamine produced by 10(-4) M L-glutamate was also antagonized by bicuculline (10(-5) M) and moreover a marked stimulation of [3H]dopamine release took place in the presence of this gamma-aminobutyric acid (GABA) antagonist. Therefore, high concentrations of L-glutamate exerted an inhibitory presynaptic control on [3H]dopamine release which seemed to be indirect and mediated partly by GABAergic neurons. Since a sustained reduction in the spontaneous release of [3H]dopamine was seen in the presence of PK 26124, the corticostriatal glutamatergic neurons appeared to exert a tonic facilitatory presynaptic influence on dopamine release. This effect was important since it represented 40% of the tetrodotoxin-sensitive release of the [3H]transmitter. The direct (stimulatory) and indirect (inhibitory) presynaptic controls on dopamine release mediated by corticostriatal glutamatergic fibres are discussed in light of previous findings and of the anatomical organization of the caudate nucleus.

Animals↗
PubMedDate not supplied

[Blood pressure control and quality of life: a comparative multicenter double-blind and cross-over trial of labetalol and captopril].

The purpose of this multicenter randomised, double-blind and cross-over study was to compare the antihypertensive effects of labetalol (L) and captopril (C) in 42 moderate hypertensive patients (mean age: 52 years). The drugs were given during two 4-weeks periods at the end of which the systolic (SBP) and diastolic blood pressures (DBP) were measured at rest in supine and standing positions. The assessment of the quality of life was realized with 4 scales completed by the practitioner [anxiety, depression, well-being, visual analog scale (VAS)] and 4 scales of auto-assessment completed by the patient [2 VAS, well-being, sub-scale of pleasure]. At the end of the first treatment's period (D28), both drugs had decreased significantly supine SBP and DBP (p less than 0.001), standing DBP (L = p less than 0.01; C = p less than 0.05), while only L lowered supine SBP (p less than 0.01). The cross-over analysis was unable to conclude, due to the number of patients and a significant interaction which reduced its power. Thus the effect of the first treatment's period seemed to influence the efficacy of the second one. The percentages of patients with a controlled BP were respectively: after 4 weeks of treatment, L = 61 p. 100 vs C = 42 p. 100 and at the end of study (D56), L = 67 p. 100 vs C = 64 p. 100. The cross-over analysis didn't show any difference between the effects of L and C on the quality of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Carpipramine].

Explore the source record for details and available documents.

Adult↗
PubMedDate not supplied

[Perphenazine enanthate. Results of a 1-year open multicenter study].

The results of a one-year, open multicenter trial of perphenazine enanthate, a sustained-release neuroleptic drug, are reported. 240 patients (62% suffering from schizophrenia) were included in the study and 144 were followed during the 12-month period. The usual adverse reactions associated with sustained-release neuroleptic drugs were observed. Total and partial BPRS ratings showed that improvement (expressed as a percentage) after 12 months' treatment was similar for systematized chronic delusions, paranoid schizophrenia and hebephrenia. However, the onset of therapeutic activity was different in these three groups of patients. Maximum therapeutic activity, as defined by the BPRS rating, was obtained within 4 months in chronic delusions whereas schizophrenia improved more progressively. Such patients therefore require prolonged treatment before the therapeutic activity of a sustained-release neuroleptic drug can be assessed.

Adult↗