PubMed Health⌕ Search

Biomedical subjects

H M van Praag

Publications and source records attributed to H M van Praag.

At least 109 records · Page 6Linked to original sources
PubMed1987

Therapeutic indications for serotonin-potentiating compounds: a hypothesis.

The original antidepressants, tricyclics and MAO inhibitors, increase the availability in the brain of both 5-HT and NA. Prompted by clinical findings suggestive of 5-HT disturbances in depression, drugs were developed that increase 5-HT selectively. Data are presented that suggest that broad-spectrum compounds may provide better conditions for antidepressant effects than the 5-HT-selective ones. The hypothesis is proposed that 5-HT potentiators are partial antidepressants, in that they predominantly reduce the anxiety/aggressive component of the depressive syndrome, and deserve to be tested in conditions with heightened anxiety and/or aggression irrespective of the nosological diagnosis. Tentative evidence relates diminished 5-HT metabolism to disordered impulse control. Based on these data, trials of 5-HT potentiators in impulse control disorders unrelated to aggressive drives seem warranted.

5-Hydroxytryptophan↗
PubMed1987

Interconvertability of five self-report measures of depression.

This article describes the construction of a new self-report scale based directly on the DSM-III criteria for major depressive disorder. It provides data on the interconvertability of scores on this scale with scores obtained on the Beck Depression Inventory, the Zung Depression Scale, the Center for Epidemiologic Studies-Depression (CES-D) Questionnaire, and the Minnesota Multiphasic Personality Inventory Depression Scale (MMPI-D). The article also examines the relation between physical principles of measurement as described by physicists and psychiatric measurement. It concludes with an analysis of the connection between the dichotomies typical of diagnostic statements and the continuous, probabilistic data typical of self-report instruments.

Adult↗
PubMed1986

Biological suicide research: outcome and limitations.

Empirical study of suicide began early in this century from the sociological (Durkheim 1951) and psychological (Freud 1956) perspective. A decade ago, a biological dimension was added, focusing on two major issues, i.e., are disturbances in brain functioning instrumental in the occurrence of suicidal behavior and/or do such disturbances increase the likelihood of suicidal behavior in an individual exposed to stressful events? Biological suicide research has developed as an offshoot of biological depression research. This is a logical development, as depression is a major precursor of both attempted (Weissman et al. 1973; van Praag 1982a) and completed (Guze and Robins 1970; Miles 1977) suicide. The major biochemical research targets are similar: monoamines and hormones. This paper will review the main findings in suicidal behavior, discuss the methodological shortcomings of this research, and indicate ways of avoiding them.

Aggression↗
PubMed1986

Influence of desmethylimipramine on natural killer cell activity.

Mounting evidence suggests that the central nervous system (CNS) and the immune system are extensively interconnected. One question that arises is whether there is cross-reactivity between psychotropic agents, which are active in the CNS, and immune system function. To explore this notion, we examined the in vitro effect of the tricyclic antidepressant, desmethylimipramine (DMI), on human natural killer (NK) cell activity in seven separate experiments. At concentrations greater than or equal to 625 ng/ml, DMI reliably inhibited NK activity. Preincubation of lymphocytes with DMI before assay did not increase the inhibitory effect. Furthermore, removal of the drug from preincubated cells immediately before assay completely eliminated the inhibitory effect. These results demonstrate that DMI reversibly inhibits NK activity at serum concentrations that are not uncommonly found in depressed patients receiving this medication.

Depression, Chemical↗
PubMed1986

Affective disorders and aggression disorders: evidence for a common biological mechanism.

Ever since the discovery that the classical antidepressants--tricyclics and MA oxidase inhibitors--exert an influence on central 5-HT, this neurotransmitter has been studied in depression, particularly in those forms responsive to this type of treatment. This chapter reviews the evidence in favor of a relationship between depression and central 5-HT dysfunctions. Most of the findings have been derived from patients with depression as the principal diagnosis. Some data have originated from patients suffering from a somatic illness and from depression as well. Both peripheral and central data are discussed. Although no single 5-HT-related finding in depression has so far been unequivocally established, the available evidence, in balance, justifies the tentative conclusion that disturbances in 5-HT metabolism can occur in depression. Lowered CSF 5-HIAA, the major indicator of disturbed central 5-HT metabolism in depression, has also been reported in aggression disorders, both in patients who had committed suicidal acts and in those with outward-directed aggression. The finding can not be explained by a concomitant state of depression. Rather than to discard the classical 5-HT-depression hypothesis, in favor of a 5-HT-aggression hypothesis, the hypothesis is launched that disturbances in serotonergic regulation can give rise to both mood and aggression disorders. This would provide a biological explanation for the clinical observation that those disorders frequently go hand in hand.

5-Hydroxytryptophan↗
PubMed1986

Pharmacokinetics and therapeutic efficacy of haloperidol decanoate after loading dose administration.

For this open study, we selected 21 chronic psychotic female in-patients (16 of them schizophrenics) who were being maintained on oral neuroleptics. After a wash-out period, they were treated by intramuscular depot injections of haloperidol decanoate, once a month for four months. The dose was calculated from the previous oral dosage, and the amount of the first injection was double that of the three following injections. Relatively stable plasma levels of haloperidol were achieved with the first injection, and corresponded to those observed with oral medication. A very significant correlation was found between plasma level and the dose administered, but not between plasma level and therapeutic effect. The clinical condition of about two-thirds of the patients remained unchanged or improved, compared with the period of oral treatment. During the first two months of treatment, there was more rigidity and tremor, but from the third month, the extrapyramidal symptoms were less pronounced than during the period of oral neuroleptics.

Adult↗
PubMed1985

The effect of stress on the dexamethasone suppression test.

The dexamethasone suppression test (DST) was studied in 40 presurgical subjects and 20 controls. Cortisol plasma concentrations were measured before and after a nocturnal dose of 1 mg dexamethasone. Nineteen of the 40 patients (47.5%) failed to show a suppression of plasma cortisol after dexamethasone. Nonsuppression on the DST was associated with a significantly higher baseline plasma cortisol concentration. Another putative indicator of emotional stress, the level of acute anxiety, was also studied. There was a significant difference in the level of acute anxiety among suppressors, nonsuppressors, and controls--the level of anxiety in nonsuppressors being significantly higher than in controls. It is concluded that stress associated with a physical danger can be a cause of nonsuppression on the DST.

Adult↗
PubMed1985

The effect of milenperone on the aggressive behavior of psychogeriatric patients. A double-blind placebo-controlled study.

The antiaggressive action and side effects of a new neuroleptic, milenperone, were evaluated in 20 non-psychotic psychogeriatric patients by means of a double-blind randomized pilot study in comparison with placebo. In this study, milenperone was added to the existing medication as an adjuvant. The test substance was administered in a dose of 2 X 5 mg daily for the first 3 weeks, in a dose of 2 X 10 mg daily for the following 3 weeks. The addition of milenperone to the preexisting medication decreased the aggressiveness scores, significantly on the Paranoid Belligerence Scale, not significantly on the Visual Analogue Line. The improvement of the aggressiveness scores on the Paranoid Belligerence Scale was only significantly apparent when the dose was doubled. In spite of the association with milenperone, the severity and frequency of the side effects did not increase during the investigation.

Aged↗
PubMed1985

The effect of milenperone on the aggressive behavior of oligophrenic patients. A double-blind placebo-controlled study.

The antiaggressive action and the side effects of a new neuroleptic, milenperone, were evaluated in 21 oligophrenic patients by means of a double-blind randomized pilot study in comparison with placebo. Only 3 patients appeared to be psychotic, 2 from the milenperone group and 1 from the placebo group. In this study, milenperone was added to the existing psychotropic medication as an adjuvant. The test substance was administered in a dose of 2 X 10 mg daily for 6 weeks. The results were evaluated by means of the Paranoid Belligerence Scale and the improvement of the target symptoms were visualized on the Visual Analogue Line. Although, in the last 3 weeks of the study, the aggressiveness scores had decreased more in the milenperone group than in the placebo group, the difference between both studied groups was not significant. This lack of clear result may probably be ascribed to the high standard deviations, together with the small number of patients per group. The severity and frequency of the side effects remained almost unchanged during the investigation and were independent of the substance administered: milenperone or placebo.

Adult↗
PubMed1984

Clinical, biochemical, and hormonal aspects of treatment with Des-tyr1-gamma-endorphin in schizophrenia.

Des-tyr1-gamma-endorphin (DT gamma E) was administered intramuscularly in a dose of 1 mg/day for 10 days to 18 neuroleptic-free schizophrenic patients in a double-blind crossover design. Six patients showed either a slight or no antipsychotic response; seven patients showed a moderate antipsychotic response; and the remaining five patients showed a marked antipsychotic response. DT gamma E led to a decrease of plasma prolactin levels in patients treated with DT gamma E in the first period of experimental treatment as compared to those treated with placebo. Neither plasma levels of growth hormone and cortisol nor cerebrospinal fluid concentrations of homovanillic acid, 5-hydroxyindoleacetic acid, and 3-methoxy-4-hydroxyphenylglycol were affected by DT gamma E. Patients suffering from a hebephrenic or paranoid type of schizophrenia and those presenting relatively fewer negative symptoms were most susceptible to treatment with DT gamma E. These data confirm and extend previous findings that DT gamma E has antipsychotic properties in a number of schizophrenic patients.

Adolescent↗
PubMed1984

Repeated naloxone administration in schizophrenia.

A double-blind study of repeated subcutaneous administrations of 20 mg naloxone was performed in 10 schizophrenic patients as part of a World Health Organization collaborative project. No clinically obvious treatment effects were observed. None of the analyzed psychopathological symptoms, including hallucinations and unusual thought content, showed a distinct improvement during the 4 consecutive days of naloxone treatment. A slight but statistically significant decrease of symptomatology was found shortly after placebo injection on the first 2 days of treatment. This effect was not present following naloxone treatment. These findings are discussed in view of the hypothesis that increased endorphin activity contributes to the symptomatology of schizophrenic syndromes.

Adult↗
PubMed1984

Depression type and depression severity in relation to risk of violent suicide attempt.

Low levels of cerebrospinal fluid 5-hydroxyindoleacetic acid and a blunted thyroid-stimulating hormone response to thyrotropin-releasing hormone have been reported in depressed patients--in particular in those who have made violent suicide attempts. There are at least two conceivable explanations for these findings: The biological abnormalities relate to (1) disturbed aggression regulation or to (2) disturbed mood regulation (either type or severity). The second alternative presupposes that violent suicide attempts occur differentially in a particular depression type or differentially in severe depression. This study demonstrated that violent suicide attempts are "depression-specific," i.e., they relate to a particular depressive syndrome, that of vital depression, but not to the severity factor. Therefore, it is impossible to decide whether the biological abnormalities in depressed, violent suicide attempters relate to a particular type of mood disorder or to a distorted regulation of aggression.

Depressive Disorder↗