Genetic Factors

Somatization clusters in families. This is particularly true for somatization disorder, which occurs in 10%-20% of first-degree relatives of patients with this disorder. Somatization disorders show a concordance rate of 29% in monozygotic twin studies (Kaplan et al. 1994). Rates of anxiety and depression are also higher in family members of somatiz-ing children and adolescents, suggesting a possible genetic etiology (Fritz et al. 1997). Mothers of children who somatize are more likely to report an excess of functional abdominal pain, anxiety, depression, and other somatic symptoms and are more likely to have a history of irritable bowel syndrome, chronic fatigue, and somatoform disorder (Campo et al. 2007). A study by Marshall et al. (2007) suggests that compared with children of parents with long-term medical illness, children of parents with somatoform disorders tend to demonstrate higher levels of "problematic health cognitions," as do their parents. Some studies indicate that parental physical illness may be associated with childhood soma-tization (Kaplan et al. 1994).

Recent imaging studies have the potential to help explain some of the neural mechanisms involved in somatization. Functional magnetic resonance imaging studies with conversion disorder have shown decreased or absent activation in the contralateral sensorimotor cortex during sensory or motor tasks (Ghaffar et al. 2006; Vuilleumier 2005). Lower rates of cerebral glucose metabolism have also been demonstrated in patients with somatization disorder (Hakala et al. 2006). Debate continues as to whether these neuroimaging studies suggest an exclusion of sensorimotor representations from awareness through attentional processes or whether the findings might better be explained by the modulation of such representations by primary affective or stress-related factors (Vuilleumier 2005). Researchers have also proposed that serotonergic amino acids, specifically decreased plasma concentrations of tryptophan (a precursor of serotonin), or perhaps elevated plasma levels of bradykinin, may be implicated in somatization (Fukuda 2003; Rief et al. 2004).

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