Other Psychiatric Disorders and the Immune Response

Some evidence suggests that other stress-related neuropsychiatric conditions may be associated with immune activation, although these conditions are less well characterized than major depression. These disorders include posttraumatic stress disorder (PTSD), chronic fatigue syndrome (CFS), seasonal affective disorder (SAD), and fibromyalgia. Patients with combat-related PTSD have been reported to demonstrate increased plasma concentrations of IL-1 and increased CSF concentrations of IL-6 (Baker et al. 2001; Spivak et al. 1997). PTSD following civilian disasters appears to be associated with elevated plasma concentrations of IL-6 and its soluble receptor (Maes et al. 1999c). Although not found consistently (Maes et al. 1999c), both severity of symptoms and duration of illness have been reported to correlate positively with indices of immune activation in PTSD (Miller et al. 2001; Spivak et al. 1997).

A growing body of literature suggests that patients exposed to early life trauma may be especially vulnerable to the development of psychophysical disorders (e.g., CFS, fibromyalgia) that are characterized by complaints of chronic pain, fatigue, and cognitive difficulties of unknown etiology

(Heim et al. 1997). Consistent with this, these disorders have also been associated with evidence of increased inflammatory activity. For example, it has been reported that both CFS and fibromyalgia are accompanied by an increase in acute-phase reactants and increased plasma concentrations and/or peripheral blood mononuclear cell production of proinflammatory cytokines, including IL-1, IL-6, and TNF-k (Borish et al. 1998; Cannon et al. 1999; Gupta et al. 1997; Maes et al. 1999b). Of note, one report indicates that SAD, a condition with significant symptom overlap with CFS and fibromyalgia, may be characterized by increased plasma concentrations of IL-6 (Leu et al. 2001).

Finally, although the picture is far less clear, there has been speculation that immune system activation may contribute to the pathophysiology of psychotic disorders, including schizophrenia, possibly related to an autoimmune diathesis (Pearce 2001; Rothermundt et al. 2001). Elevated levels of cytokines and their receptors, including IL-2, sIL-2, and IL-6, have been reported in the blood and CSF of patients with schizophrenia, and a high level of CSF IL-2 has been found to predict subsequent schizophrenic relapse (Rothermundt et al. 2001). In a related fashion, consideration has been given to the role of viral infection early in development (Pearce 2001), based on seasonal birth patterns that have been reliably replicated in large epidemiological studies of patients with schizophrenia. These findings are consistent with in utero infections of relevant brain structures, including the hippocampus, during critical periods of development (especially during the second trimester) (Pearce

2001). Moreover, cross-reactivity between brain antigens and antigens of infectious agents may contribute not only to schizophrenia but also to the neurological and psychiatric complications associated with streptococcal infection (i.e., pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections [PANDAS]) (Snider and Swedo 2000).

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