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Biomedical subjects

H M van Praag

Publications and source records attributed to H M van Praag.

At least 19 recordsLinked to original sources
PubMed1992

Cortisol response to intramuscular desipramine in patients with major depression and normal control subjects: a replication study.

The authors conducted a double-blind study evaluating the cortisol response to 75 mg of desipramine (DMI), administered intramuscularly to 20 patients with major depressive disorder (MDD) and 20 age- and sex-matched normal control subjects. A blunted placebo-corrected cortisol response to DMI was found in MDD patients in comparison with the normal control subjects. Since the behavioral/side effect and pharmacokinetic profiles of DMI were similar for patients with MDD and normal control subjects, these findings suggest that patients with MDD have an underlying biological insensitivity of the hypothalamic-pituitary-adrenal axis to DMI. It is hypothesized that these findings are consistent with a norepinephrine deficit, an alpha 1-adrenergic receptor insensitivity, or both. Further use of DMI as a neuroendocrine probe for the noradrenergic system is indicated.

Adolescent↗
PubMed1979

Improvement of schizophrenic patients treated with [des-Tyr1]-gamma-endorphin (DTgammaE).

It was postulated from animal experiments that gamma-endorphin and, in particular, the nonopiate-like peptide [des-Tyr1]-gamma-endorphin (DTgammaE, beta-lipotropin [beta-LPH]62-77) have neurolepic-like activity. To test this, 14 patients with long-lasting, relapsing schizophrenic or schizoaffective psychosis resistant to conventional neuroleptics were treated with DTgammaE. An open design was used first for six patients (study 1) and a double-blind, crossover design for the other eight (study 2). In study 1, all neuroleptic medication was discontinued and 1 mg of DTgammaE zinc phosphate was given daily intramuscularly for about seven days. In study 2, six patients were maintained with neuroleptic therapy and two patients were drug free; all eight received daily intramuscular injections of 1 mg of nonlasting DTgammaE in saline and solution for eight days. There was transient or semipermanent improvement in both studies in which the psychotic symptoms diminished or even disappeared. In study 2, there was a slight but significant improvement with the first treatment. Improvement continued and by day 4, the psychotic symptoms had almost disappeared. No toxic side effects were noted. These effects of DTgammaE may be a consequence of the normalization of beta-endorphin homeostasis in the brain.

Adult↗
PubMed1979

Effects of zimelidine, a selective 5-HT uptake inhibitor, on serum prolactin levels in man.

The levels of serum prolactin were studied both after an acute intake of zimelidine and during a treatment period of 3--7 weeks. No significant changes in basal serum prolactin levels were seen after single oral doses of zimelidine (100 mg) in healthy volunteers during an investigation period of 12 h. Serum prolactin concentrations remained well within the pretreatment levels also during a continuous treatment of depressive patients with zimelidine up to 150 mg orally b.i.d. It is concluded that clinical doses of the selective 5-HT uptake inhibitor zimelidine does not exert any significant effect on serum prolactin levels.

Adult↗
PubMed1979

Central serotonin metabolism and frequency of depression.

Central serotonin (5-hydroxytryptamine; 5-HT) metabolism can be disturbed in a subgroup of patients with vital (endogenous, primary) depression. Presumably these disturbances do not result from the depression and have a predisposing rather than a causative relationship to it. This latter statement is based on two observations. First, in a majority of patients, the 5-HT disturbances persist after depression has abated. Secondly, 5-hydroxytryptophan seems to have prophylactic value, in particular in patients with persistent abnormalities in central 5-HT metabolism. In this study we approached the hypothesis that 5-HT disturbances are a predisposing factor to the occurrence of depression from still another perspective. If this hypothesis is correct, then depressive patients with persistent 5-HT disturbances should have higher frequencies of depression than depressive patients without demonstrable 5-HT disturbances. This was indeed demonstrated. The same was true for family members of probands with low levels of 5-hydroxyindoleacetic acid. No cerebrospinal fluid data are available for family members. The reported findings strongly support the predisposition hypothesis.

Adult↗
PubMed1978

The effect of L-dopa and propranolol on human CSF cyclic nucleotides.

Human CSF cyclic AMP and cyclic GMP have been measured as possible indicators of activity of central neurotransmitter-sensitive adenylate or guanylate cyclase. In an attempt to help to identify the specific neurotransmitter systems of origin of human CSF cyclic AMP and GMP, we studied Parkinson patients with and without L-dopa therapy and schizophrenic patients before and after propranolol therapy. No effect of L-dopa or propranolol was found on CSF cyclic nucleotides. However, Parkinson patients had a 40-50% reduction of CSF cyclic AMP and a 80-90% reduction of CSF cyclic GMP compared with the schizophrenic patients. Implications of this finding are discussed.

Adult↗
PubMed1978

Amitriptyline plasma-concentration and clinical effect. A World Health Organisation Collaborative Study.

54 patients in five centres participated in a study of the relationship between steady-state plasma-levels of amitriptyline (AT) and its active metabolite nortriptyline (NT) and therapeutic response. The participants were inpatients who, after a 7-12 day period of assessment, were rated greater than or equal to 16 on the Hamilton rating scale for depression. They were given 75 mg of amitriptyline for 3 days and then 150 mg daily for an active-treatment period of 6 weeks. Clinical ratings and plasma-samples were obtained at baseline then at 2, 4, and 6 weeks after starting therapy. Contrary to the findings of three previous trials, no important correlations were found between steady-state plasma-levels and therapeutic outcome or corrected side-effects. Corrected side-effects correlated negatively with therapeutic outcome. There seems little advantage in routine monitoring of AT and NT, since variations in plasma-levels do not account for the considerable variation in therapeutic outcome.

Adult↗
PubMed1978

Neuroendocrine disorders in depressions and their significance for the monoamine hypothesis of depression.

This article discusses the results of recent neuroendocrinological research in depressions. The abnormalities found in a given category of vital depressive patients--cortisol hypersecretion, decreased growth hormone response to insulin hypoglycaemia and decreased luteinizing hormone secretion in menopause--are believed to be due to deficient noradrenalin-(NA)-ergic activity in the hypothalmus. Thus explained, they support the so-called MA (monoamine) hypothesis, which postulates that a functional NA deficiency in the brain plays a role in the pathogenesis of certain types of vital depression. Disorders in certain central MA-ergic systems are predictive of disorders in the hormone secretion of the anterior pituitary. Inversely, disorders in the hormone secretion of the anterior pituitary can be indicative of disorders in the MA-ergic transmission in the hypothalamus. Consequently we can expect a convergence of transmitter research and neuroendocrinological research--two lines of research which have so far been largely separated in studies of human individuals.

Catecholamines↗
PubMed1978

The scientific foundation of anti-psychiatry.

Anti-psychiatry has exerted a substantial influence on the thoughts of workers in the field of mental hygiene; on those of the psychiatrically trained, but even much more on those without psychiatric training. Consequently it seemed important to me to investigate the strength of the foundation of this school of thought. This has been the objective of this study. The point of crystallization of anti-psychiatry is the labelling theory on the origin of deviant behaviour. The scientific status of anti-psychiatry stands or falls with that of the labelling theory. Since this theory has not been formulated in verifiable hypotheses, I ventured to formulate "theses", and then tested these against empirical obtained data. The results of this study were largely negative. The empirical material does not support the labelling theory, and in many cases even contradicts it. Consequently anti-psychiatry--as a model to explain the development of psychological disorders--has not a leg to stand on. The labelling theory has had great merits as a "sensitizing theory". It has given momentum to innovative tendencies in psychiatry. Now that it has proved to be untenable on its principal points, however, it should be abandoned. It has become a rubber check, which has no scientific buying-power.

Attitude↗
PubMed1978

[Comments on the impossible concept of schizophrenia (author's transl)].

Schizophrenia is an impossible concept. Under this heading, a number of psychoses is being grouped which have the common characteristic that the patient is, as a rule, but by no means always, fully conscious. In all other respects, no other points agree, neither in respect of symptoms, nor in respect of etiology or prognosis. Hence, there are hardly any reasons to reduce these disease patterns to a common denominator, either as "schizophrenia" or as a "group of schizophrenic psychoses". Rather, it seems more probable that schizophrenic psychoses are individual disease patterns, instead of being variations of a basic type. What is principally needed at this stage, is a fair amount of empirical research to catalog the concept of schizophrenia. Such a catalog would have to be based on exactly defined and described syndromes to enable further study whether there are any other points besides these symptoms which characterize the syndrome in question, such as etiology, pathogenetic factors, course, or response treatment. The more characteristics are found, the greater the chance that the disease pattern under investigation is really a unit by itself. In the course of these studies, and in order to avoid terminological confusion, it is advisable to use, for the time being, the term "schizophrenic psychoses", under the condition that in each concrete case this term must be supplemented by a careful typification of the symptomatology, of the etiologic factors, and of the course of the disease.

Diagnosis, Differential↗
PubMed1977

Determination of clomipramine and desmethylclomipramine in plasma by means of liquid chromatography.

A method is presented for the determination of clomipramine and its major metabolite desmethylclomipramine in plasma. After extraction with n-hexane, the components are separated by high performance liquid-solid chromatography on silica gel and detected with a UV detector. The detection limits are 2 ng/ml for clomipramine and 10 ng/ml for desmethylclomipramine. Recoveries from plasma exceed 95% for both drugs. In routine analysis, 30-40 samples can be handled in one day. The practical use of the method is shown in plasma concentration-time curves after oral and intramuscular administration of clomipramine.

Chromatography, High Pressure Liquid↗
PubMed1977

The significance of dopamine for the mode of action of neuroleptics and the pathogenesis of schizophrenia.

Animal experiments have demonstrated the likehood that all known neuroleptics inhibit transmission in central CA-ergic systems, regardless of their chemical structure and via different mechanisms. For clinical psychiatry this fact prompts a number of questions: (1) is this phenomenon also to be found in human individuals; (2) if so, is it of importance for the clinical (side) effects of neuroleptics; (3) do patients with (schizophrenic) psychoses show signs of central CA-ergic hyperactivity? This article presents a survey of clinical research focused on these questions which, for the sake of brevity, is confined to DA metabolism. The available data indicate the plausibility of a correlation between inhibition of DA-ergic transmission on the one hand, and on the other hand the therapeutic effects of neuroleptics and the occurrence of hypokinetic-rigid symptoms. The hypothesis that DA-ergic hyperactivity is an important pathogenetic mechanism in schizophrenic psychoses can be based only on indirect arguments; direct studies of the DA metabolism have so far failed to reveal supporting evidence. The possible causes of this failure are discussed.

Dopamine↗