On November 28, Psychiatric Times published an article titled Psychiatric Diagnosis and Treatment of Somatizing Neuropsychiatric Disorders. The authors are Daniel T. Williams, MD, and Alla Landa PhD, both from Columbia University Psychiatry Department.
The article’s lead-in states:
“Although the somatizing disorders cover a vast array of symptomatic domains across many medical specialties, this article addresses the broad topic conceptually.”
The so-called somatizing disorders have an interesting history in psychiatry. DSM-III-R (1987) states:
“The essential features of this group of disorders are physical symptoms suggesting physical disorder (hence, Somatoform) for which there are no demonstrable organic findings or known physiologic mechanisms, and for which there is positive evidence, or a strong presumption, that the symptoms are linked to psychological factors or conflicts.” (p 255)
DSM-IV (1994) states:
“The common feature of the Somatoform Disorders is the presence of physical symptoms that suggest a general medical condition (hence, the term somatoform) and are not fully explained by a general medical condition, by the direct effects of a substance, or by another mental disorder (e.g., Panic Disorder).” (p 445)
DSM-5 (2013) states:
“All of the disorders in this chapter [Somatic Symptom and Related Disorders] share a common feature: the prominence of somatic symptoms associated with significant distress and impairment.” (p 309)
Note that the requirement that the symptoms are not fully explained by a general medical condition has been dropped from DSM-5. In this latest edition of the manual, the only requirements are that the symptoms are distressing, disruptive, and excessive, the assessment of which is inevitably subjective.
Note also that Drs. Williams and Landa refer to these “diagnoses” as neuropsychiatric disorders, essentially begging the question that they involve neurological pathology. There is no evidence to support this position. Nor is there any rational support for the notion that worries and concerns about medical matters should be conceptualized as illnesses, even if the individual’s level of distress and preoccupation is extreme. But a detailed critique of this matter is beyond the scope of this post.
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The Williams and Landa article is detailed and comprehensive. It addresses the phenomenology, epidemiology, and developmental course of the so-called somatization disorders. Under the heading “Postulated pathogenic influences,” the authors present working hypotheses from psychoanalytic theory, learning theory, behavior analysis, social-affective neuroscience, autoimmune sensitization, and theories of dissociation.
On the topic of social-affective neuroscience, the authors state:
“Recent advances in social-affective neuroscience suggest that early interpersonal environment may interact with genetic predisposition and epigenetic changes to affect the neural circuits involved in interpersonal emotions and physical pain. This type of predisposition makes a person particularly sensitive to emotional stressors and presents difficulties in regulating emotional and somatic distress 12. This could explain the variable vulnerability to somatization under similar stressors among different individuals. It also points to the need to carefully evaluate these relevant vulnerabilities in psychotherapeutic exploration of each patient’s unique biographical narrative.”
The essential point being expressed here is that people develop “excessive” concern about their health or “excessive” sensitivity to pain, because of neural circuitry anomalies. These anomalies, in turn, stem from the interaction of a hypothesized genetic predisposition and the individual’s early interpersonal environment.
Aberrant neural circuits are fast replacing the discredited chemical imbalances that constituted the cornerstone of biopsychiatry until effectively debunked by psychiatry’s critics. At present, the aberrant circuits are being postulated with a measure of caution; note the terms “suggest” and “could explain” in the above quote. But in general, the circuitry hypothesis is being actively promoted, and is gathering a good deal of traction.
Incidentally, reference # 12, cited in the above quote, is to an article by Dr. Landa and two other Columbia researchers. Here’s the final statement from the abstract:
“Specifically, the proposed theory and research review suggest that psychotherapeutic and/or pharmacological interventions that foster the development of affect regulation capacities in an interpersonal context will also serve to more effectively modulate aberrantly activated neural pain circuits and thus be of particular benefit for the treatment of somatoform pain.”
Note: “…psychotherapeutic and/or pharmacological interventions…”, and particularly the suggestion, which is also becoming common in psychiatric circles, that psychotherapy and drug treatment have essentially the same effect: the modulation of “aberrantly activated” neural circuits.
Certainly psychotherapy affects people’s brains. All human activity affects the brain. But the notion that talking to a person empathically and sincerely (whether in a professional capacity or simply as a friend) is on a par with the ingestion of psychiatric drugs makes a mockery of human interaction.
The authors discuss the treatment implications of these various “postulated pathogenic influences,” including the need to restructure learned patterns and the establishing of therapeutic rapport. Under the heading “Approach to treatment,” the authors stress the importance of psychosocial factors:
“…do the symptoms serve to avoid a constellation of stressors with ensuing functional impairment, by allowing the patient to retreat into ‘the sick role’? Moreover, might the symptoms be the body’s reaction to overwhelming stress?”
“Many patients may not be able to articulate the complex environmental stressors that produce feelings of shame or inadequacy. They may cling to the identity of the medically ill patient as a ‘safer’ refuge from life’s adversities. Therefore, the psychiatrist should present the diagnostic hypothesis of SSD tentatively and supportively, noting that it is not mutually exclusive of coexisting physical illness.”
Under the heading “Treatment options,” Drs. Williams and Landa list and discuss:
- Reassurance, placebo, suggestion and psychoeducation
- Individual or family psychotherapy
- Psychodynamic strategies
- Behavior modification
- Cognitive-behavioral therapy
- Group psychotherapy
- Mindfulness, meditation, progressive relaxation, deep breathing
All of this, apart from the unwarranted implications of neurological illness, sounds fairly encouraging. But then there’s this:
“Psychopharmacological agents may have specific therapeutic benefit for comorbid psychiatric disorders, including anxiety, depression, obsessive-compulsive disorder, and psychosis, all of which may coexist with and complicate SSDs. In addition, these agents may have nonspecific (placebo) benefits. For patients who have difficulty in grasping the concept of somatization, who have discomfort with psychotherapy, or who want a ‘medicine’ to legitimize the validity of their physical illness and recovery, a supportive discussion of the role of these medications in normalizing brain neurotransmitter function can be helpful. The medicine can be the needed aid that helps the psychotherapy go down.” [Emphasis added]
The fact is that there are no psychiatric drugs that normalize brain neurotransmitter function. Indeed, the opposite is the case. Every psychiatric drug on the market today produces abnormal brain function. So either Drs. Williams and Landa aren’t aware of this, or they are advocating that therapists should deceive their clients on this very fundamental issue.
Unfortunately, but perhaps inevitably, this kind of patronizing disrespect is still widespread in psychiatry, and is fundamentally incompatible with the lofty rapport-building and therapeutic sentiments expressed earlier in the article. Therapeutic rapport and systematic deception are mutually exclusive.
The very eminent psychiatrist Ronald Pies, MD, has written that the chemical imbalance theory is a kind of “urban legend” – never promoted by well-informed psychiatrists. Well, Dr. Williams, according to his bio, has been on the faculty at Columbia University for forty years! He has authored more then 60 publications in peer-reviewed journals and standard textbooks in the fields of psychiatry and neurology. I think it is reasonable to suppose that he would meet Dr. Pies’ standards for being well-informed, and yet here he is advocating the promotion of the spurious chemical imbalance theory!
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