who have pain, these correlations are explained in part by the effects of stressors on limbic areas of the brain (in particular, the cingulate cortex) that are associated with pain regulation. For example, a history of physical and sexual abuse is associated with increased reports of pain in people who have IBS, and increased pain correlates with enhanced activation of the midcingulate cortex, an area at the interface of pain regulation and emotional input (Ringel et al., 2008). In addition, peripheral inflammatory states associated with increased cytokine activation may in turn alter brain functioning, producing “sickness behavior.” These phenomena may help to explain the emotional distress and increased symptom awareness associated with CMI (Dantzer et al., 2008). That putative mechanism is illustrated in Figure B-1, which demonstrates that somatic and visceral sensations (for example, muscle pain, fatigue, and abdominal pain) are experienced as symptoms only when the signal amplitude is above the brain’s perception threshold. Thus, peripheral neural signals arising from an injury might be above the perception threshold and be experienced as a symptom, and other regulatory signals (for example, increased gut signals after eating) might be received in the brain but not experienced as a symptom unless one overeats or has a gastrointestinal disorder, such as functional dyspepsia. In addition, the brain’s ability to downregulate incoming signals (that is, to raise the threshold level) will depend on regulatory processes and the person’s cognitive and emotional state. Thus, injuring oneself might not be experienced as a symptom when one is distracted during a sports event until the event is


FIGURE B-1 Putative mechanism by which the body perceives symptoms.

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