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Biomedical subjects

Herman M van Praag

Publications and source records attributed to Herman M van Praag.

6 recordsLinked to original sources
PubMed2005

Can stress cause depression?

The central issue raised in this paper is: can stress cause depression? Phrased more precisely: can stress cause brain disturbances thought to underlie (certain forms of) depression or particular components of the depressive syndrome. Focussing on 5-HT and the stress hormones, this question was answered in the affirmative, based on the following two considerations: (1) changes in the 5-HT and stress hormone systems produced by sustained stress, mimic to a substantial extent the disturbances in these systems that may be observed in depression; (2) substantial evidence indicates that the 5-HT and stress hormone disturbances in depression are of pathophysiological significance and not merely a consequence of the depressed state or a product of stress generated by the depressed state. Furthermore, the question was raised whether a depression type could be identified particularly stress-inducible. This question, too, was answered in the affirmative. The depression type in question was named anxiety/aggression-driven depression and characterized on three levels: psychopathologically, biologically and psychologically. Preferential treatment of this depression type was discussed. In studying stress-inducible depression biological depression research should shift focus from depression per se to the neurobiological sequelae of stress. Treatment of stress-inducible depressions and particularly its prevention should be geared towards reduction of stress and stress sensitiveness, utilising both biological and psychological means.

Adrenocorticotropic Hormone↗
PubMed2004

The debit balance of present day stress research.

Stress often precedes psychiatric disorders. This holds particularly for the group of mood disorders. A crucial question is whether stress is an epiphenomenon or a decisive factor in the causation of (certain forms of) mood disorder. Certainty about this question can only be obtained when it can be demonstrated that stress phenomena may induce changes in brain functioning similar to the ones supposedly associated with (certain forms of) depression. Since the phenomenology of stress syndromes, as well as their emotional intensity, are highly variable, careful diagnosis is a first requirement. In studies into the significance of stress in the occurrence of depression this degree of finesse has not been achieved. The major shortcomings are discussed. Those should be systematically addressed to provide this type of research with the necessary acuity

Diagnostic and Statistical Manual of Mental Disord↗
PubMed2003

[Depression after first myocardial infarction. A prospective study on incidence, prognosis, risk factors and treatment].

In these studies patients with first myocardial infarction (MI) were selected for studies focusing on epidemiology, risk factors and treatment of depression post-MI. Two consecutive cohorts of first MI patients were included. The first cohort was selected between May 1994 and May 1997 (n = 206), and the second between May 1997 and October 1999 (n = 206). All patients were screened every 3 months for depression using the SCL-90 and the Zung (cohort 1) or SCL-90, BDI and HADS (cohort 2) until 12 months post-MI. Patients scoring above the cut-off of one of the questionnaires were interviewed using a standardised interview in order to evaluate whether DSM-IV criteria for major depression were met; patients of the second cohort were also interviewed 1 month post-MI, independently of the score of the questionnaires. Of both cohorts data concerning major cardiac events and increased health care consumption were assessed during a 1 to 6 years follow-up period. Patients with major depression were offered treatment in the double-blind placebo-controlled trial with fluoxetine (n = 54). Depression appeared to be a predictor of increased health care consumption, but not of major cardiac events such as cardiac death and recurrent infarction in first myocardial infarction (MI) patients up to 6 years post-MI. This finding is in contrast to findings in the literature indicating that in patient populations with mixed first and recurrent MI, depression is a risk factor for cardiac mortality. In contrast to depression, symptoms of anxiety do predict cardiac mortality and recurrent MI in patients following first MI independently of other risk factors of cardiac mortality. Recognition of risk factors for post-MI depression may help the cardiologist to identify patients at risk for depression. Examples of such risk factors are, according to our studies, complications during admission, such as arrhythmic disorders and recurrent angina pectoris, and prescription of benzodiazepines. Patients at risk can be screened for depression using a 4-item questionnaire, and, if scoring is positive, be referred for psychiatric evaluation. Although the effectivity of antidepressive treatment in MI patients has as yet not been proven, we found that fluoxetine is a cardiac-safe antidepressive agent, but only in mild depression more effective than placebo. The positive effect of antidepressive treatment on cardiac prognosis has as yet not been shown.

Antidepressive Agents, Second-Generation↗
PubMed2002

Neuroendocrine response to meta-chlorophenylpiperazine and ipsapirone in relation to anxiety and aggression.

The aim of this study was to establish the association of trait anxiety and anger with hormonal responses to acute challenges with two different 5-HT agonists in a mixed group of patients with depressed mood. Fifteen patients and 16 normal controls received single oral doses of 0.5 mg/kg meta-chlorophenylpiperazine (MCPP), a 5-HT(2C) agonist, and 10 mg of ipsapirone, a 5-HT(1A) agonist, according to a double-blind, placebo-controlled, cross-over design. Dutch-adapted versions of the Spielberger Trait-Anxiety Inventory and the Spielberger Trait-Anger Scale administered assessed at study entry. Hormonal responses, expressed as drug-placebo differences, to MCPP and ipsapirone (changes in cortisol, ACTH and prolactin) were measured. Blood levels of MCPP and ipsapirone were also measured. MCPP and ipsapirone elevated cortisol, ACTH and prolactin. In the patient group, there was a significant correlation between trait anxiety and the cortisol response to MCPP. No significant correlations between the ACTH and prolactin responses to MCPP and levels of anxiety/anger were observed in the patients. No significant correlations could be established between levels of anxiety/anger and hormonal responses to ipsapirone. This study provided evidence for an association between measures of anxiety/aggression and the hormonal response to MCPP. Thus, in subjects with depressed mood, high levels of anxiety suggest a higher probability of 5-HT(2C) disturbances.

Adolescent↗
PubMed2002

Atypical cognitive profile in patients with depression after myocardial infarction.

BACKGROUND: We evaluated the cognitive profile of 48 patients with major depression following their first myocardial infarction (MI). METHODS: The cognitive performance of the patients was compared with the performance of 48 non-depressed MI patients and 48 healthy controls. RESULTS: Depressed MI patients performed slower on a simple cognitive speed related measure compared with non-depressed MI patients and healthy controls. Attention and speed-related aspects of cognitive functioning were not affected. Surprisingly, (depressed) MI patients showed even better performances with respect to memory function. LIMITATION: No patients with non-MI-related depression were included. CONCLUSIONS: The cognitive profile of major depression after MI differs from that of non-cardiac-related depressive disorder, as described in the literature. This may reflect a different etiology of post MI depression from non-cardiac-related depression.

Adult↗