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Biomedical subjects

H Cuche

Publications and source records attributed to H Cuche.

At least 19 recordsLinked to original sources
PubMed1994

[Antidepressive agents: benefits/risks].

In 1994, the risk/benefit ratio when using antidepressant drugs for the treatment of mood disorders has become very difficult to assess. From the medical standpoint, frequent nosographical modifications generated new clinical entities (brief recurrent depression, subsyndromal depression, mixed anxiety and depression according to the ICD 10, dysthymia). Within these entities, mood appears modified in duration and severity and belongs to extremely different structures. The obvious link between antidepressants and typical depression has to be thoroughly assessed for these new forms of illness. But the evolution of medical and economical assessment techniques progressively turns the attributed risk into a global index based on group results far from the dual patient-physician relationship in which the risk/benefit ratio is assessed according to idiosyncratic criteria. The development of a dimensional clinical field could, if misused, be reduced to an addition of "target treatments". Finally, some antidepressants are no longer presented for their main antidepressive effects (for which their use is authorized) but for peripheral properties: treatment strategies (particularly duration) remain unclear for these latter effects. From a sociological point of view, consequences of consumerism, social and economical crisis and modifications of the image of the psychiatry, play a role in the evaluation of this risk/benefit ratio.

Antidepressive Agents↗
PubMed1993

[Choice of antidepressant treatment after a major depressive episode].

The choice of an antidepressant is not necessary during the initial phase of only treatment (acute treatment), it can be reviewed after one or two months (continuation treatment) and a prophylactic treatment may be discussed after a 6 months period (long-term maintenance treatment). Many reasons explain the need to readjust the dosage of antidepressant treatment or to change it: the nature and the gravity of the depression, the family and personal history of affective disorders, the level of side effects and above all the quality of the recovery. Thus the modification of a treatment can be considered according to 4 methods: modification of the psychotropes associated to antidepressant treatment, association of a second antidepressant medication, change of antidepressant medication, institution of a prophylactic treatment. A special aspect concerns the decision and the choice of the antidepressant treatment after recovery by E.C.T. Two types of treatment can be considered: most often a maintenance treatment of antidepressant medication is suggested. Prolongation of ECT may be justified for consolidation: 6 or 8 sessions after recovery, or for prevention of relapse: session every 3-4 weeks after recovery, and for a period of 2-3 years.

Antidepressive Agents↗
PubMed1990

Conjugated catecholamines in human plasma: where are they coming from?

The origins of conjugated catecholamines remain poorly known. The aim of the present study was to see whether a major contribution comes from the sympathetic nervous system. We have assumed some kind of parallelism between the activity of the sympathetic nervous system, the amount of catecholamines released and taken up, and the amount of conjugated catecholamines circulating in plasma. Accordingly, an increase in sympathetic activity should be followed by an increase in the plasma level of conjugated catecholamines. The plasma levels of sulfoconjugated and glucuroconjugated catecholamines were measured in 10 patients with mental disease resistant to drug treatment, before and after electroconvulsive therapy. As expected, blood pressure, norepinephrine concentration, and epinephrine concentration in plasma were transiently increased. Neither sulfoconjugated nor glucuroconjugated catecholamines were significantly changed. Conjugated catecholamines were measured in 10 volunteers before and at the nadir of insulin-induced hypoglycemia. As expected, plasma levels of norepinephrine and epinephrine were drastically increased. Plasma levels of sulfoconjugates were decreased and glucuroconjugates increased; these were narrow but statistically significant variations. Data reported in the present article do not support a major role for the activity of the sympathetic system in fixing the level of conjugated catecholamines in human plasma. This is a negative, but nonetheless important, observation. In human subjects, currently available information suggests an important role for the intestinal wall and renal function in determining the level of circulating sulfoconjugates.

Blood Glucose↗
PubMed1983

[3H]spiroperidol binding on lymphocytes: changes in two different groups of schizophrenic patients and effect of neuroleptic treatment.

[3H]spiroperidol binding to lymphocytes was measured in untreated paranoid or disorganized and treated paranoid schizophrenic patients. An increase in the Bmax was detected in untreated paranoid patients but a decrease was found in the disorganized patients. No difference was detected in the KD value. Neuroleptic treatment produced a decrease in the Bmax without affecting the KD value. Such results did not comply with the down regulation but might be explained by a change in membrane viscosity as [3H]spiroperidol binding sites on lymphocytes were coupled to phospholipid methylation.

Adult↗
PubMed1982

[Biochemistry of schizophrenia and mechanism of action of neuroleptics].

Among the biochemical theories proposed for schizophrenia the best-founded appears to be the dopaminergic theory. Dopaminergic agonists exacerbate schizophrenic symptoms. Neuroleptics, which are the most effective drugs in schizophrenia, are dopaminergic-blocking agents. Other biochemical disorders have been demonstrated in some cases of schizophrenia but results are not always consonant. The presence of abnormal compounds, i.e. methylated derivatives or phenylethylamine, has often been mentioned. Several disorders of enzymes have also been reported, such as a defect in beta-dopamine hydroxylase or an abnormal activity of the MAO which metabolizes the indolamines and catecholamines. Disorders of the metabolism of noradrenaline and serotonin have also been suggested, mainly on experimental evidence. Other compounds have been incriminated, such as endorphins, gamma-aminobutyric acid, lysine-8 vasopressin or prostaglandins. The action of neuroleptics can be ascribed to dopaminergic respector blockade, as a safe approximation. However, the demonstration of several dopaminergic pathways and of several types of receptors makes the understanding of their mode of action all the more difficult that they interplay with many other neurotransmittors.

Antipsychotic Agents↗
PubMed1982

[3H-Imipramine binding to human platelets. A peripheral index in depressive syndromes (author's transl)].

3H-imipramine shows specific, high-affinity binding to human platelet sites. The characteristics of these specific binding sites are very similar to those previously described in the rat brain. The inhibitory effects of 11 tricyclic antidepressants on 3H-imipramine binding to human platelets were investigated. There was a significant correlation between the inhibition observed and the average therapeutic doses of antidepressants, which suggests that the binding sites may be involved in the mode of action of these drugs. The number of binding sites (Bmax) for 3H-imipramine was compared in 39 controls and in 37 hospital patients with untreated severe depressive syndrome and was found to be significantly smaller in depressed patients, without any modification of the affinity constant Kd. The significance of these findings and their changes under treatment are discussed.

Adult↗
PubMed1982

High doses of haloperidol in schizophrenia. A clinical, biochemical, and pharmacokinetic study.

The effects of high doses of haloperidol on clinical status and plasma neuroleptic and prolactin concentrations and CSF levels of homovanillic acid (HVA) and gamma-aminobutyric acid (GABA) were investigated in three paranoid schizophrenic patients over six weeks. The patients had been receiving haloperidol. Oral dosages were increased at weekly intervals from 10 to 200 mg/day and then reduced to 10 mg/day. The increase did not affect paranoid symptoms. Neurological side effects were slightly increased in two patients and moderately reduced in one. Plasma prolactin levels, initially high, increased when the dosage was increased to 100 mg/day but did not increase further. The CSF levels of HVA and GABA increased to day 7 but returned to initial values on day 28 in two patients; they were decreased to day 28 in one patient.

Adult↗
PubMed1982

[Use of haloperidol in high doses in schizophrenia. Clinical, biochemical and pharmacokinetic study].

The effect of high doses of haloperidol on the clinical status, plasma neuroleptic and prolactin concentrations as well as on CSF HVA and GABA levels was investigated in 3 paranoid schizophrenic patients over a 6 weeks period. When the study was initiated patients had been on haloperidol (10 mg a day) for 4-10 weeks. Oral doses were increased at weekly intervals from 10 (day 0) to 100 (day 7) and 200 (days 14 to 28) mg a day and then reduced to 100 (day 35) and 10 (day 42) mg/day. A linear relationship was observed between plasmatic levels and daily doses of haloperidol. In neither patient, the increase in haloperidol dosage affected paranoid symptoms. Neurological side effects were slightly increased in 2 cases and moderately reduced in one case. Prolactin plasma levels, already high at the onset of the study rose when increasing the dose to 100 mg a day but did not increase further despite increment in the haloperidol dosage. CSF levels of HVA and GABA rose from day 0 to day 7 but were back to the initial values on day 28 in 2 patients and were decreased from day 0 to day 28 in one patient. For the 3 patients a close correlation was observed between changes in CSF HVA and GABA levels. It is concluded that high doses of haloperidol, although causing biochemical changes compatible with the occurrence of dopamine target cell supersensitivity, do not lead to any clinical improvement in the 3 studied schizophrenic patients.

Adult↗
PubMed1981

Open clinical study of cis(Z)-clopenthixol.

The antipsychotic effect and tolerance of cis(Z)-clopenthixol were studied in 13 patients with acute exacerbation of chronic schizophrenia. Seven patients were with CGI registered as improved after 28 days of treatment while 2 did not complete test treatment and the remaining 4 patients were considered unchanged. Significant average reduction of the initial total BPRS-score were registered throughout, while with NOSIE-30 a significant score reduction was seen only at day 28. The frequency of single side effects fell progressively during the treatment period. Dosages were individual and ranged at day 28 from 30 to 350 mg.

Adult↗
PubMed1980

Psychiatric uses of beta-blockers.

Beta-blocking agents have been used for many years in psychiatry. But many are suspicious about their mechanisms and therapeutic effects. In this review, the most part of clinical trials is reported and criticized. With the exception of anxiolytic effects, the other therapeutic effects are still questionable for many reasons, such as the methodology of clinical trials. In this paper, others agents which interact with the noradrenergic system are envisaged. It is taking into account all these factors (alpha and beta receptors, alpha and beta agents) that we can looking for award for a real progress in the field of biochemical psychiatry.

Adrenergic beta-Antagonists↗
PubMed1979

Brain distribution and kinetics of 11C-chlorpromazine in schizophrenics: positron emission tomography studies.

The positron emitter 11C (20 minutes half-life) permits the labeling of chlorpromazine (CPZ) and the study of its distribution in humans by external counting. Trace amounts of 11C-CPZ were injected intravenously into 22 schizophrenic patients all untreated for several months with neuroleptics. The brain uptake was 6.04 +/- 1.6% of the injected dose 15 minutes after the injection, and it remained constant for 45 minutes. By positron emission tomography, the drug distribution was shown to be in the gray matter, and such structures as the cortex, caudate nucleus, thalamus and putamen could be identified. This new methodology will be helpful in studying specific receptors in humans in a noninvasive way.

Adolescent↗
PubMed1979

[Biochemical prospects in treatment of depressive illness (author's transl)].

Biochemistry of the brain has to avoid the dead-end where psychopharmacology is trapped at the present time. First of all it is needed to draw of the lack of efficacy of the antidepressants of today. Brain biochemical research must go beyond the moamine models and take into considerations the afferent and efferent influences. The sutdy of ECT and ions like lithium, rubidium, and cesium may open up new perspectives to the knowledge of new psychotropic drugs and to their mecanisms of action. Starting from clinical observations new indications for already known non psychotropic drugs could appear.

Antidepressive Agents↗
PubMed1979

[Classification of the antidepressants (author's transl)].

The antidepressants can be classified chemically. The standard division is between the tricyclic antidepressants and the chemically heterogeneous MAOIs. Many other compounds can be included among the antidepressants, e.g. the bicyclics and possibly also the beta-stimulants, the alpha-blockers and ions such as rubidium. As regards the mechanisms of action, we have the antidepressants which act selectively upon serotonin and those which act more particularly upon noradrenaline. This notion must be extended. Dopamine may be involved in certain depressive syndromes and also other systems may have a role, such as electrolyte systems, cell permeability and the multiple influences which have a bearing upon the monoamines. Finally, the effect upon receptors and their nature are discussed. A third type of classification refers to the therapeutic spectrum of the drug. We have the sedative antidepressants, active in agitated depression and the stimulant antidepressants which are active in retarded depression. However, the two categories of antidepressants have the same global antidepressant action.

Antidepressive Agents↗
PubMed1979

[Value of pharmacokinetic data during the treatment of psychoses with haloperidol].

Pharmacokinetic data of psychotropic drugs should allow a better understanding of therapeutic results and side effects. The different factors influencing liberation, absorption, protein binding, distribution, metabolism and excretion are reviewed. Then, the principal pharmacokinetic data of haloperidol are exposed with a special emphasis on the lack of information about the correlations between plasma levels and clinical effects. The role of pharmacokinetic informations in the interpretation of responses to treatment is detailed, wishing that the monitoring of haloperidol plasma levels will be more developped in a next future.

Haloperidol↗