More than half of rheumatoid arthritis (RA) patients complain of sleep disturbance and this cardinal complaint is associated with fatigue, pain, and depressed mood in patients with this chronic inflammatory disorder. Despite the frequency of this complaint, there is limited effort to evaluate sleep or the psychobiological mechanisms that account for disordered sleep in RA patients. Given evidence that abnormal increases in the expression of proinflammatory cytokines play a key role in the progression of RA, we hypothesize that the cytokine network is one physiological system that is associated with sleep disturbance in RA patients. Proinflammatory cytokines signal the central nervous system and are associated with an integrated syndrome of behavioral changes described as """"""""sickness behaviors"""""""" that include changes in sleep, energy, and pain sensitivity. Preliminary studies suggest that disturbances of sleep are associated with increased symptoms of pain, fatigue, and depressed mood in rheumatic patients. Moreover, sleep loss is coincident with alterations in sympathetic tone, which is thought to contribute to increases of pro- inflammatory cytokine activity.
The specific aims of this study are to: 1) determine the nature and severity of disordered sleep RA patients vs. controls; 2) evaluate the effects of sleep, sleep loss, and recovery sleep on symptoms of pain, fatigue, and mood and on measures of sympathovagal balance and proinflammatory cytokine activity in RA patients and controls; 3) examine the contribution of cytokines on sleep by administering a TNF antagonist vs. placebo to probe the action of proinflammatory cytokines on sleep in RA patients. Examination of sleep and its consequences for autonomic functioning and proinflammatory cytokine activity within the framework of an observational and experimental research design will have implications for understanding the psycho-biological mechanisms that link sleep and the clinical manifestations of RA. Results from this study will guide the development of interventions that target disordered sleep with potential effects on disability in RA. ? ?
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