Inflammation at the intersection of behavior and somatic symptoms.

Somatization refers to the persistence of multiple physical complaints that cannot be attributed to a medical illness. Increasing evidence suggests that activation of the proinflammatory cytokine network can lead to a constellation of behaviors, “sickness behavior,” which might underlie the pathophysiology of certain psychiatric disorders. In particular, depressive disorders, as well as somatoform disorders, share any components of “sickness behavior,” including alterations in pain sensitivity uch as exaggerated pain response (hyperalgesia), sleep disturbance, and fatigue. It as recently been hypothesized that this overlap in symptoms between somatoform isorders and depression may be due to a common underlying biology, including ctivation of inflammatory biology dynamics. In this review, we characterize inflammation, describe the connections between the immune system and the brain, and discuss the influence of proinflammatory cytokine activity on certain aspects of this constellation of behaviors that have been commonly referred to as “sickness behavior.” In particular, we focus on 3 prominent behavioral complaints in somatic disorders: exaggerated pain sensitivity (hyperalgesia), sleep disturbance, and fatigue. Within this conceptual frame linking inflammation with altered bodily perceptions, we consider the possibility that activation of proinflammatory cytokines, possibly acting in concert with stress, might lead to increased sensitization of the central nervous system. It is thought that such sensitization serves as a possible neuronal substrate for amplification of normal bodily sensations so that these perceptions lead to distress, complaints, and somatic symptoms, along with impairments in social, occupational, and health functioning.