A biological substrate for somatoform disorders: importance of pathophysiology

Abstract

Somatoform disorders are troubling to both patients and physicians. The diagnosis regrettably relies on the presence of subjective distress in the absence of objective findings. As a result, there is always the possibility that a diagnosis will be "missed." There is a clear underlying physiology of distress, which implies that there is a two-way street--both psychosomatic and somatopsychic in terms of production and experience of somatoform symptoms. Studies on communication pathways from the immune system to the brain provide exciting new information on the pathophysiology of inflammation-associated symptoms.

Figure 1

Symptom perceptions elicited by nails. The left panel exemplifies somatic amplification; reprinted from Fisher JP, Hassan DT, O’Connor N. Minerva. Br Med J 1995;310:70, with permission from BMJ Publishing Group Ltd. The right panel exemplifies somatic deamplification; reprinted with permission from Associated Press, Wide World Photos. 1/16/05.

Figure 2

Immune-to-brain communication. Proinflammatory cytokines are produced at the periphery by innate immune cells in response to pathogen-associated molecular patterns or to danger signals, such as heat shock proteins released by dying cells. Peripheral proinflammatory cytokines induced the production of the same proinflammatory cytokines in the brain. The brain proinflammatory cytokines acting on various brain areas induce nonspecific symptoms of sickness, such as fatigue, depressed mood, and altered cognition. The production and action of proinflammatory cytokines are regulated both at the periphery and in the central nervous system by a number of opposing molecules including anti-inflammatory cytokines, steroid hormones such as glucocorticoids and neuropeptides such as α-melanotropin (α-MSH) and vasopressin (AVP).