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Biomedical subjects

H M van Praag

Publications and source records attributed to H M van Praag.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1976

TRH by slow, continuous infusion: an antidepressant?

A slow, continuous infusion of 1000 mug TRH (thyrotropin releasing hormone) over a period of 4 h had a very faint and diffuse short-lasting beneficial effect on a group of 10 depressive patients. This was assessed in a double blind cross-over trial with placebo. The effect was of no therapeutic value. No difference was found between the depressive patients and a control group of normal subjects in TSH response, T3 resin uptake, T4 or free thyroxine index values as a consequence of the TRH infusion.

Adjustment Disorders↗
PubMed1976

An unexpected effect of L-5 hydroxytryptophan-ethyl-ester combined with a peripheral decarboxylase inhibitor on human serum prolactin.

While the 5-HT precursors tryptophan and 1-5-HTP cause an increase in serum prolactin concentration, a combination of 1-5-HTP with a peripheral decarboxylase inhibitor was found to reduce the serum prolactin concentration. This combination seemed to behave like a DA agonist. This effect is not produced by the decarboxylase inhibitor per se. A possible explanation is that 5-HTP is converted to 5-HT in CA-ergic neurons, that 5-HT supersedes the CA from the stores, and that some of the CA reach the synaptic cleft and stimulate CA receptors. Another possible explanation is that 5-HTP decarboxylase is centrally inhibited as well, and that an effect of 5-HTP itself is involved here. In view of the observations made it is doubtful whether the therapeutic effect of 5-HTP combined with a peripheral decarboxylase inhibitor in depressions and myoclonus can in fact be atributed to activation of central serotonergic systems.

5-Hydroxytryptophan↗
PubMed1976

Serum levels of 5-hydroxyindole derivates after administration of L-5-hydroxytryptophan ethyl ester.

Serum levels of 5-hydroxytryptophan ethyl ester, 5-hydroxytryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid (5-HTPE, 5-HTP, 5-HT and 5-HIAA, respectively), were measured after intravenous administration of L-5-HTPE in humans, premedicated with a peripheral decarboxylase inhibitor. Semi-automated methods for the estimation of the 5-hydroxyindole derivatives are described. Only serum levels of 5-HTP and 5-HIAA were found to be increased, indicating that the ethyl ester is rapidly hydrolyzed and that the decarboxylation of 5-HTP is in part inhibited. The levels of 5-HTP increased during the infusion, but dropped rapidly when the intravenous administration was terminated. Serum levels of 5-HIAA remained constant for at least 6 hours, although during the same period the levels of 5-HTP do change markedly. The persistently increased serum levels of 5-HIAA suggests, that this metabolite is formed from the 5-HT stored in peripheral or central tissue. Serum levels of 5-HIAA may therefore be indicative of changes of 5-HT metabolism during drug treatment. Levels of 5-HTP may be used for the estimation of the availability of the ethylester of 5-HTP.

Adult↗
PubMed1975

Central monoamine deficiency in depressions: causative of secondary phenomenon?

There are indications for a functional deficiency of 5-HT and DA in certain kinds of depression. The question arises if these biochemical disturbances are primary or secondary, whether they contribute to the pathogenesis of the depression or whether they result from it. From research with MA precursors we drew the tentative conclusion that they are presumabely primary and interrelated with the depression in a causal and/or predisposing way.

5-Hydroxytryptophan↗