Sleep disorders are frequently observed in chronic inflammatory diseases. Such disorders are believed to be an intrinsic component of the disease and not simply a consequence of the pain. Nonetheless, fatigue, pain, and muscle rigidity are associated to nonrestorative sleep (Nicassio, Moxham, Schuman, and Gevirtz 2002). What seems to take place is a vicious cycle in which pain and chronic fatigue leads to nonrestorative sleep, which in turn, worsens painful conditions.
Among the chronic inflammatory diseases, fibromyalgia, systemic lupus erythematosus, rheumatoid arthritis, and chronic fatigue syndrome are most frequently associated with impaired sleep (Lashley 2003). This is quite interesting, especially when the HPA axis is included in the equation. The association between HPA axis activity and immune functions is relevant to humans with illnesses including rheumatoid arthritis (Gutierrez, Garcia, Rodriguez, Mardonez, Jacobelli, and Rivero 1999), systemic lupus erythematosus (Gutierrez, Garcia, Rodriguez, Rivero, and Jacobelli 1998), fibromyalgia (Crofford et al. 1994), and chronic fatigue syndrome (Demitrack et al. 1991).
Chrousos and Gold (1992) have proposed the hypothesis that sustained stress system dysfunction, characterized by either hyper or hypoactivity of the HPA axis, play a role in various pathologic states, including a range of autoimmune/inflammatory, psychiatric, and endocrine diseases (Fig. 11.1). Although the concept of hyperactivity leading to sleep impairment (Kupfer 1995; Steiger 2002) is what comes more easily to min, it is necessary to acknowledge that, once again, glucocorticoids play a bimodal role on sleep regulation, insofar as insufficient cortisol production, as seen in Addison's disease, also results in sleep disruption, which is corrected by administration of hydrocortisone (Garcia-Borreguero et al.
2000; Lovas, Husebye, Holsten, and Bjorvatn 2003).
■ Atypical depression
■ Chronic fatigue syndrome
■ Rheumatoid mtlii itis
■ Melancholic depression
■ Anorexia nervosa
■ Memory problems
■ Immune suppr essioa
■ Reproductive problems
Figure 11.1. Theoretical model of the inverted U shaped curve, in which optimal levels of glucocorticoids are essential for the perfect organic functioning. Either hypo (left-hand side) or hyperactivity (right-hand side) of the hypothalamic-pituitary-adrenal axis will lead to unbalanced occupation of MR/GR corticosteroid receptors, likely resulting in many unfavorable conditions (based on Chrousos and Gold 1992).
Lupus patients often report to experience a poor sleep quality. Most of the studies which explore the relationship between lupus and sleep quality use questionnaires as a tool to assess sleep. Recent findings attribute the poor quality of sleep to associated features, such as depression, chronic use of corticoids, lack of physical activity (Costa et al. 2005), and painful condition (Gudbjornsson and Hetta 2001). In addition, a negative correlation between sleep quality and disease activity is observed (Tench, McCurdie, White, and D'Cruz 2000) so that intense production of cytokines and other inflammatory agents may exacerbate the already altered sleep pattern in these patients. The polysomnographic evaluation confirms the patients' complains of poor sleep quality, revealing low sleep efficiency, sleep fragmentation, breathing disorders, and periodic leg movements. The net result, and one of the major findings of the study, is the extreme daytime somnolence, pointing out to nighttime sleep impairment (Valencia-Flores et al. 1999).
In this regard, stress is also a major player in this relationship. Several studies have pointed out stress, either physical or psychological, as a triggering factor for the onset or worsening of lupus (Blumenfield 1978; Wallace 1987; Peralta-Ramirez, Jimenez-Alonso, Godoy-Garcia, and Perez-Garcia 2004). Besides anxiety and depression, lupus patients report that stress is related to aggravation of their physical and mental well-being (Wekking, Vingerhoets, van Dam, Nossent, and Swaak 1991; Da Costa et al., 1999).
In a recent study, Palma, Gabriel, Colugnati, and Tufik (2006) showed that sleep deprivation triggered an early onset of disease manifestation in an animal model of systemic erythematosus lupus (first generation of the New Zealand Black x New Zealand White breeding), without altering either the course or severity of the disease. Interestingly, sleep deprivation induced a potent secretion of corticosterone in these animals, but contrary to a strain that does not develop lupus, whose corticosterone levels returned to basal on the week following sleep deprivation, hormone levels in these animals never returned back to basal throughout the mice entire life span (unpublished data).
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