Serotonin Transporter mRNA Expression Is Reduced in the Peripheral Blood Mononuclear Cells of Subjects with Major Depression but Normal in Fibromyalgia.

BACKGROUND: Fibromyalgia (FM) and major depression disorder (MDD) frequently co-occur. Both disorders may share common serotonergic alterations, although there is less evidence of such alterations in FM. It is also unclear as to whether these alterations are persistent over time or transient. The objectives of this study were to (i) examine the changes in mRNA expression of serotonin transporter (SERT) on the surface of peripheral blood mononuclear cells (PBMCs) in FM, MDD, and the FM + MDD subjects compared to healthy controls, and to (ii) evaluate the effect of drug treatment on SERT expression. METHODS: PBMCs were isolated from FM, MDD, FM + MDD, and control subjects. SERT expression was analyzed at the mRNA level via quantitative real-time polymerase chain reaction. Statistical analyses were performed using analyses of variance and linear mixed-effects models. RESULTS: SERT mRNA expression was significantly reduced in MDD subjects compared to controls (p < 0.001), but not in FM nor in FM + MDD subjects. Although the drug treatments improved symptoms in FM, MDD, and FM + MDD subjects, they had no significant effect on SERT mRNA expression. CONCLUSIONS: These results corroborate the role of the SERT in the pathophysiology of MDD, but not in FM, and show that the decreased mRNA expression of SERT is a persistent, rather than transient, phenomenon.

Add-on treatment of quetiapine for fibromyalgia: a pilot, randomized, double-blind, placebo-controlled 12-week trial.

Recently, second-generation antipsychotic drugs have attracted interest in the treatment of chronic pain, including fibromyalgia (FM). Preliminary uncontrolled studies have shown that quetiapine treatment may be helpful for FM patients. In this trial, we sought to examine-for the first time-the efficacy and tolerability of quetiapine as a treatment for FM and its associated psychiatric symptoms. This was a 12-week double-blind, randomized, placebo-controlled trial of quetiapine XR as an add-on treatment for FM syndrome. Fifty-one female FM patients were randomized, and a flexible dosage of 50 to 300 mg/d was used. The primary outcome was the change from baseline to end point in the Fibromyalgia Impact Questionnaire total score. Secondary outcomes included mood symptoms, sleep disturbances, and tender points. Using a low dose (mean = 132.2 mg) of quetiapine, we observed significant benefits of drug treatment on sleep, uncertain effects on FM and mood symptoms, but no effects on pain, in a small group of polymedicated FM patients. Quetiapine was generally well tolerated.

Is the deficit in pain inhibition in fibromyalgia influenced by sleep impairments?

It has been proposed that a deficit in inhibitory conditioned pain modulation (ICPM) underlies the pathophysiology of fibromyalgia (FM), but there is high variability in ICPM efficacy in this syndrome that remains poorly understood. Based on emerging data showing that age, anxiety, depression and sleep can modulate ICPM efficacy, the main objective of this study was to determine the clinical correlates of experimentally-induced pain perception in FM. Fifty FM patients and 39 healthy controls (HC) were tested. Anxiety, depression, sleep and FM symptoms were measured with questionnaires or interview-type scales. Experimental pain testing consisted of two tonic heat pain stimulations separated by a 2-minute cold pressor test (CPT). Thermal pain thresholds and tolerance were higher in HC compared to FM patients. Pain ratings during the CPT were lower in HC relative to FM patients. ICPM efficacy was stronger in HC compared to FM patients. Finally, sleep quality was the only factor significantly related to ICPM efficacy. To our knowledge, this is the first study to report this association in FM. Future studies will need to replicate this finding, to determine whether impaired sleep is primary or secondary to deficient pain inhibition, and to characterize the neurobiological mechanisms underlying this association.