[Are mental and neurological disorders related?] / Zijn zenuw- en zielsziekten familie van elkaar?

A recent article in Science reported the results of a genome-wide analysis of a variety of psychiatric and neurological conditions, conducted by an international consortium. Psychiatric disorders showed some degree of genetic risk sharing; conversely, the genetic risk profiles of neurological disorders lacked virtually any resemblance to each other as well as to mental diseases. Even though the spectrum of studied diseases was incomplete, the findings are unsurprising. Of course, neurological disorders and mental disorders share a common substrate in the brain, which has led to different methods attempting to discover the material basis of mental disorders. Yet, there is and continues to be an important difference regarding the causal role of the environment, viz. psychological and social factors. However, in terms of the way diseases manifest themselves, i.e. the symptoms experienced by patients, there is considerable overlap between psychological and somatic factors. Body and mind may be separated in medical textbooks, but not in the waiting room.

Dios y el cerebro. Una perspectiva judía / No disponible

La religiosidad es sobre todo, una capacidad experimental. Como tal no puede existir sin un sustrato biológico, sin circuitos neuronales cuya activación evoca experiencias religiosas. La investigación de la naturaleza de estos circuitos ha producido ya algunos resultados. ¿Se reduce de este modo la religiosidad a un fenómeno de determinación puramente psicológica? Rotundamente no. La religiosidad no está anclada en los circuitos cerebrales. No se encontrarán sus raíces en un nivel psicológico. Las funciones del cerebro son un intermediario; un intermediario entre las necesidades religiosidades y la satisfacción experimental. En otras palabras, el homo sapiens ha desarrollado una base física que hace posible el desarrollo de la religiosidad. Concluyo que la investigación neuroteológica no respalda la perspectiva atea. La susceptibilidad religiosa no puede ser vista como un sofisticado complejo de quimeras. Al contrario, los datos neuroteológicos respalda la visión teísta: la religiosidad es un componente normal y valioso de la psique humana. Tiene una firme fijación biológica, que es, en parte, intrísecamente genética(AU)

No disponible

Schizophrenia: it's broken and it can't be fixed. A conceptual analysis at the centenary of Bleuler's Dementia praecox oder Gruppe der Schizophrenien.

BACKGROUND: In 1911 Bleuler's Dementia praecox oder Gruppe der Schizophrenien served to launch schizophrenia as a group of nosological entities characterized by a "splitting of the psychic functions." Today, at the centenary of this opus magnum, we find that the term is still in force but not the concept originally envisaged by Bleuler. METHOD: For the sake of this conceptual analysis a literature search was carried out in PubMed, Embase, and the historical literature. RESULTS: The current schizophrenia concept, as operationalized in the DSM and other psychiatric classifications, is primarily indebted to Kraepelin and his degenerationist take on psychopathology. That approach is now obsolete, but the product still prevents us from moving beyond the notion of schizophrenia as a single-disease concept with multiple etiologies, multiple clinical expressions, and an unfavorable outcome. CONCLUSIONS: If we aim to investigate the biological underpinnings of psychotic symptoms, first a deconstruction of the schizophrenia concept will need to take place. In this paper we highlight a method--called functionalization--which allows for such a deconstruction. LIMITATIONS: Functionalization will probably require a new scientific language, which will be largely discontinuous with our current nosological and diagnostic systems.

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.

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

A stubborn behaviour: the failure of antidepressants to reduce suicide rates.

Over the past decades the rate of completed suicide has remained quite stable, that of suicide attempts even seems to have increased (to the extent it has been studied in defined regions). These are puzzling observations, since depression is the major suicide precursor and since antidepressants over the years have been increasingly used in the treatment of depression. These observations have not attracted sufficient attention, possibly because they do not accord with consensus opinions about depression treatment in psychiatry today. In this paper a number of possible explanations are discussed. They not only deserve but are definitely in need of systematic investigation.

[Depression after first myocardial infarction. A prospective study on incidence, prognosis, risk factors and treatment]. / Depressie na een eerste hartinfarct. Een prospectieve studie naar incidentie, prognose, risicofactoren en behandeling.

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.

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.

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.