The body in the brain: towards a representational neurobiology of somatoform disorders

Physical symptomswhich are diagnosed as somatoform and related disorders are usually termed as ‘medically/organically unexplained’. This label is misleading as it denotes only one aspect: lack of significant structural damage in organ systems implied by the complaints of the patient (muscles, joints, heart, etc.). But medical explanations are rising in number in terms of the biological, especially neural and endocrine regulatory, processes that underlie the experience of enduring physical symptoms without such structural damage in peripheral bodily organs. It is the hypothesis of this paper that special attention to the higher-level representational features of central nervous processing may help us to understand better the biological basis of some relevant clinical aspects of this group of symptoms and disorders, especially the important influence of cognitive and affective factors on symptom experience and their highly context-dependent variability. In order to put this hypothesis into perspective, it is necessary, though, to start off with a short account of the types of approaches which are already being used for clarifying the biological basis of somatoform disorders. It is useful to divide such studies of the regulatory nervous, endocrine and immune systems into those that measure ‘central’ nervous processing per se versus processing of peripheral afferent sensory stimuli versus efferent influence on more peripheral functions in somatoform and related disorders (1). Some of the more consistent results have been obtained in studies demonstrating diminished activity in the efferent hypothalamus–pituitary– adrenal (HPA) axis in subgroups of patients with medically unexplained bodily symptoms (2, 3). This finding, which is in contrast to the wellestablished HPA hyperactivity in many patients with major depression, has recently been complemented by evidence for differences in immune activation between patients with somatization syndrome and major depression (4). With respect to the central nervous system control of efferent functions, lateralized hypoperfusions and an altered brain asymmetry in the control of neuroendocrine activity have been found to be associated with somatization and physical complaints (5,6). Nevertheless, the mechanism linking these putatively stressrelated changes in efferent functions to the subjective experience of bodily complaints is largely unclear, as is their potential causal relevance (3). On the afferent side, the new technologies for functional brain imaging provide tools to study alterations in sensory processing, especially in patients with functional somatic syndromes like fibromyalgia or irritable bowel syndrome (7–9). Although this is not the place to review all relevant studies, it may be fair to state two things: first, despite heterogeneous results, most studies converge on the fact that there is evidence for altered central nervous processing in these syndromes; and, secondly, the validity of most of these studies is limited as they report on the processing of peripheral, more or less painful stimuli in patients whose predominant clinical problem is not the processing of peripheral stimuli but the Blackwell Munksgaard 2003: 15: 157–160 Copyright # Blackwell Munksgaard 2003 Printed in Denmark. All rights reserved ACTA NEUROPSYCHIATRICA ISSN 0924-2708