Researchers in France found that among 306 outpatients followed for a year, quality of life remained stable relative to subjects’ expectations and perceptions about position in life. Symptom improvement was not associated with quality of life improvement relative to patients’ expectations. Results will appear in European Psychiatry.
Note from Kermit Cole, “In the News” editor
In many of the articles I put up on “Mad In America” I notice that the authors seek to explain, justify, or warn against the results of their studies when they seem counter to mainstream thinking. As, in this article, the authors suggest that “caregivers should be aware of this result so as to deal with possible disappointments in patients receiving a new efficient treatment.” The suggestion seems to imply that patients might be disappointed when the alleviation of their symptoms does not translate into an improved quality of life.
When I put up such an article, I hope that the results rather than the authors’ interpretations will speak for themselves. I don’t feel it’s appropriate for me to point out precisely how or what I think the authors may be assuming or missing. I am mainly interested in the fact that they have found something that contributes to the big picture. and hope that a healthy discussion will take place to bring these points out without me having put my spin on it.
This has been very satisfying when, for instance, in response to this week’s “Pharmacologic Treatment of Schizophrenia: a Fifty-Year Review” Donna pointed out that the authors, from within their understanding of schizophrenia as a genetic and/or disease entity, seem hard pressed to understand their own conclusions that “the future of the pharmacotherapy of schizophrenia looks bleak.”
Donna also pointed out (with a hat tip to Peter Breggin) that the benefit proposed in “ECT Reduces Frontal Cortical Connectivity” might also be interpreted as brain damage.
Last week Arta suggested that the authors of the article “Cognitive and Perceptual Origins of Social Isolation and Psychosis in Schizophrenia” seem to assume that “cognitive deficits” in the study are pathophysiological in nature, rather than the result of trauma. I believe, even if this is the authors’ assumption, that the suggestions in the study of the neuroplastic consequences of perseverative thinking opens the door out of the disease model.
Similarly, Altostrata suggests that the study in “Childhood Adversity Promotes Neuroimmune Inflammation and Depression” attributes depression to inflammation and, as such, perpetuates a false assumption. She quotes from the abstract “There is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients’ vulnerability to comorbid medical conditions. However, research on depression and inflammation has yielded conflicting findings, fostering speculation that these conditions associate only in certain subgroups, such as patients exposed to childhood adversity.”
I believe that there is much yet to be found in the connections between trauma, inflammation, and mental health that has not been fully “fleshed out” by research that has been largely divided into balkanized camps of “trauma” and “schizophrenia.” There are, of course, researchers who explore these topics but until they have seized the mainstream it falls to readers such MIA’s to point out connections that might otherwise go unnoticed.
Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.
Mad in America has made some changes to the commenting process. You no longer need to login or create an account on our site to comment. The only information needed is your name, email and comment text. Comments made with an account prior to this change will remain visible on the site.