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Aetiology of somatization disorder

Childhood learning

Somatization may have its roots in early childhood experiences. There are several retrospective studies indicating that adults who report high levels of somatic symptoms are more likely to have witnessed illness in family members than is the norm. These include:

excessive somatic complaints by parents

excessive illness or complaints of illness from other family members

excessive family complaints of pain.

In one study of this phenomenon, Craig et al. (2002) compared the (self-reported) history of three groups of women who were either chronic somatizers, had a long-term illness, or were healthy.

Somatizing mothers were three times more likely than the other women to have witnessed a parent having a physical illness. The children of these somatizing mothers were, in turn, more likely to report health problems than were the children of the medically ill or healthy women, and had more consultations with family doctors. In a second study with the same women, Craig et al. (2004b) demonstrated the subtle way in which parents can focus on healthrelated issues. In their study, they observed the women playing with their 4 – 8-year-old children in a structured play setting. Somatizing mothers were emotionally flatter and gave their children less attention than the other mothers during both play tasks. However, they were more responsive to their child than the other mothers when they played with a medical box. Craig and colleagues suggested that childhood experience of illness is most likely to result in somatization if it is associated with a lack of parental care (Craig et al. 2002) or sexual abuse (Modestin et al. 2005). However, the role of severe trauma was questioned by Lackner et al. (2004), who found that low-level, long-term neglect may be a more important precursor than specifi c traumas. Integrating these various strands of evidence, Craig et al. (1993) suggested a two-stage process to the development of somatization disorder:

lack of care or neglect increases risk of an emotional disorder such as anxiety or depression

high levels of illness behaviour among parents predispose children to interpret their emotional symptoms as indicative of physical illness.

Psychoanalytic explanations

Classic Freudian explanations of physical symptoms focus on sudden, inexplicable presentations of physical symptoms – conversion disorder – and are considered later in the chapter. Some post-Freudian explanations of somatization are not dissimilar to the explanation considered in the previous section. According to Guthrie (1996), deficiencies in the early motherchild relationship leave the individual with an inability to use their imagination and language to describe and control stress and distress. This results in a limited fantasy life, difficulties in processing emotional experiences, and a susceptibility to somatic complaints. This leads to difficulties in developing appropriate relationships in adulthood. Any relationships the individual does develop are either chaotic or symbiotic. In the latter, they form a relationship with someone who adopts the role of carer – and they adopt the role of invalid. The physical symptoms they report therefore act both as a way of coping with intolerable emotional feelings and as a means of eliciting the care of their partner. An alternative psychoanalytic understanding was proposed by Bucci (1997), who argued that as a child we establish representations of events or objects (such as people) across all modalities. These include memories of the event or object, their symbolic interpretations and related somatic, emotional, and even motoric associations. According to Bucci, somatization occurs when dissociation occurs within our emotional schema between the symbolic representation of objects and their associated somatic elements.

As a consequence, the individual may experience significant emotional responses to particular individuals or situations, but not understand why these emotional responses occur or have the language to describe or resolve them. As an example of this process, an individual who was emotionally abused as a child by a parent may have experienced intense fear in the presence of that individual, but as they were totally dependent on them and could therefore not avoid them, the child could not develop appropriate links between feelings of fear, cognitive representations of fear, and behaviours typically associated with fear such as avoidance. In adulthood, interpersonal fear and discomfort would therefore be felt at a somatic level only – unconnected to thoughts that would help make sense of these feelings to the individual concerned. As a consequence, they would not develop appropriate strategies to resolve the problems causing their fear, and continue to experience the somatic experience over a sustained period of time. This would eventually be interpreted as an illness or set of symptoms with no obvious psychological cause.

A psychobiological model

The simplest biological model of somatization suggests that people with the disorder have a biological sensitivity to physiological activity within the body, which they report as ‘symptoms’. The biological pathways through which this may occur are not clear – and not all evidence supports the notion of this hypersensitivity (e.g. Sherman et al. 2004). Nevertheless, Rief et al. (2004) speculated that dysregulation of amino acids and serotonin may contribute to somatization. They compared levels of various amino acids including tryptophan (a precursor to serotonin) in patients with somatization disorder, with and without depression, and normal controls and found that low levels of tryptophan were associated with high levels of somatization independently of the presence of depression. They took these data to suggest that the serotonergic system may be involved in a process of sensitization of neurons (including those in the muscles) that leads to a state of hyperalgesia, which forms the basis of chronic somatization. In their perception-fi lter model (see Figure 6.1), Rief and Barsky (2005) hypothesized that all our body organs continually produce sensory information that is forwarded to higher cortical structures.

The healthy nervous system learns to filter out this ‘sensory noise’, preventing over-stimulation of the upper cortical structures with irrelevant information: we experience higher levels of physical sensations if this fi ltering process is distorted. Rief and Barsky contend that a number of physical and psychological factors can increase or decrease both the need for the fi lter to operate and its effectiveness. Factors that increase the physical signals, and thereby increase the risk of experiencing unexplained symptoms, include high levels of sympathetic activity, stress, and neural sensitization. Factors that decrease the effectiveness of the fi lter include high levels of health anxiety, which may result in the individual interpreting any physical sensations in a catastrophizing manner. That is, they may misperceive body sensations as evid ence of dangerous somatic processes. They may also selectively choose to attend to any sensations they experience. These beliefs and attentional processes may arise from the childhood experiences considered in the previous section.

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