Trauma and medically unexplained symptoms: Towards an integration of cognitive and neuro-biological accounts
Introduction
Somatic symptoms are the leading cause of outpatient medical visits. At least 33% of somatic symptoms are medically unexplained (Kroenke, 2003). Medically unexplained symptoms (MUS) constitute an important public health problem that is associated with considerable personal suffering, loss of productivity, and decreased quality of life (Kirmayer, Groleau, Looper, & Dao, 2004). Many patients present with individual somatic symptoms, such as back pain, headache, dizziness, and dyspnoea. Others present with functional syndromes characterized by constellations of somatic symptoms, such as irritable bowel syndrome (IBS) or somatization disorder (SD).
Since the 18th century it has been recognized that MUS may have a psychological origin and already in many early accounts within medicine and psychiatry the experience of potentially traumatic events is mentioned as an important etiological factor in MUS (Shorter, 1992). In this paper we aim to systematically review the empirical evidence of a possible relationship of trauma with MUS and to critically discuss ideas about how exposure to psychological trauma may in some way lead to the formation of somatic symptoms.
In trying to explain the genesis of MUS a distinction should be drawn among MUS that are: (a) the physiological components of anxiety and depression (presenting somatization); (b) normal bodily sensations or minor pathological events that are misinterpreted as signs of serious illness (hypochondriacal somatization); and (c) subjectively compelling symptoms that cannot be attributed to either physical or psychiatric illness or hypochondriasis (functional somatization) (Kirmayer & Robbins, 1991). For several reasons the current review will primarily focus on the latter type of MUS: functional somatization. Because anxiety and depression are common sequelae of experiencing trauma and because the co-morbidity of MUS with anxiety and depression is very high (Kroenke, 2003), the association of trauma with MUS in the case of ‘presenting somatization’ may be related to the presence of these affective complaints. The concept of ‘hypochondriacal somatization’ predominantly refers to an extreme anxiety for disease, rather than the presence of complaints. It may, moreover, be particularly relevant for MUS occurring after traumatic experiences involving possible exposure to toxic substances, resulting in the attribution of normal and benign physical symptoms to an external, physical cause (Havenaar & Van den Brink, 1997). In sum, presenting and hypochondriacal somatization largely depend on affective complaints or health anxiety. In the case of ‘functional somatization’, however, the association of previous trauma with MUS that are independent of a mental or physical disorder necessitates specific mediational models that can explain the proposed relationship. For these reasons, the link between previous trauma and functional somatization has been, and to a great extent still is, a riddle for which various theoretical models have been proposed, and which will be the primary focus of the present paper. Consequently, the present paper does not involve an exhaustive review of all investigations that study the association of trauma with MUS. The focus of this selected review is more circumscribed and related to the following three aims.
The first purpose of the present review is to investigate whether there is indeed any evidence of a specific relationship of trauma with MUS. For this aim we will review the literature on the association of trauma with MUS in some well-defined patient groups which historically have played a prominent role in the discussions about a possible relationship of trauma with functional somatization (Shorter, 1992). To this end we choose to review the following samples in more detail: chronic pelvic pain (CPP) and irritable bowel syndrome (IBS) (two functional somatic syndromes in which it has long been assumed that childhood sexual abuse may play an aetiological important role), somatization disorder (SD) and conversion disorder (CD) (both historically subsumed under the diagnostic umbrella of hysteria and hypothesized to be related to child sexual abuse as well). The second aim of this paper is to critically review specific mechanisms proposed to explain the relationship of previous trauma with MUS. In this context, three major models (i.e. dissociation, conversion, and hierarchical cognitive models) will be critically discussed. Especially the latter model, which basically integrates existing dissociation and cognitive models, appears to be of specific explanatory value and will be expanded on in the remainder of the paper. Because cognitive models lack integration with recent neurobiological findings concerning trauma and MUS, the third and last aim of this paper is to review neurobiological stress research indicative of alterations in prefrontal functions and central stress-systems and to integrate this with cognitive accounts of MUS.
Section snippets
Review of the empirical evidence on the relationship of trauma with MUS
First, the association of trauma with MUS in chronic pelvic pain (CPP), irritable bowel syndrome (IBS), somatization disorder (SD), and conversion disorder (CD) was investigated. Although it has long been assumed that childhood sexual abuse may play an important role in the genesis of all four disorders, dissociation accounts have prevailed particularly for SD and CD. Given our goal to review the association of trauma with MUS in general and to discuss both dissociative and non-dissociative
Putative mediators of the relationship of trauma with MUS
As reviewed above, the empirical evidence suggesting a specific relationship of trauma with MUS is quite consistent and shows that for at least a subgroup of persons with MUS (childhood) trauma may have been a risk factor involved in the genesis of MUS. So the question arises how this association can be explained. Three different groups of explanatory models for the pathogenesis and persistence of functional somatization can be discriminated: dissociation, conversion, and hierarchical cognitive
Towards an integration of neurobiological and cognitive accounts of MUS
Although patients with MUS receive no medical diagnosis that can fully explain their symptoms, several plausible physiological mechanisms by which MUS may be generated have been identified. In general there are two important lines of evidence, namely brain imaging studies, which are strongly indicative of CNS modulation of symptom experience in various somatoform disorders, plus other studies indicating altered responsiveness of central stress systems, in particular the Hypothalamus Pituitary
A review of neurobiological findings in various MUS samples
Changes in HPA axis reactivity. The model by Mayer et al. (2001) draws significantly from previous studies in patients with PTSD who have been found to show hypocortisolism and increased feedback inhibition of the pituitary–adrenal level of the HPA-axis (Yehuda, Giller, Levengood, Southwick, & Siever, 1995). Also for patients with varying types of MUS, including CPP, IBS, burnout and fibromyalgia, indications for hypocortisolism have been observed (for reviews see Bohmelt et al., 2005, Heim et
General conclusions
The first purpose of the present review was to investigate systematically the evidence for the assumed relation between trauma and MUS in a subset of patient samples presenting with functional somatization. Second, we aimed to critically review three dominant models explaining the relation between trauma and MUS (i.e. dissociation, conversion and hierarchical cognitive models). The latter model appeared to be of particular explanatory value and was found to have a firm basis in contemporary
Acknowledgements
This work was supported by a VENI Grant (#451-02-115) from the Netherlands Organization for Scientific Research (NWO) awarded to Dr. K. Roelofs. The authors thank Hanane El Hachioui for helping with the literature search and Bernet Elzinga for her comments on an earlier version of the manuscript.
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