Cerebral vasomotor reactivity in fibromyalgia patients and its relationship to central neuropathic pain.

Background - Cerebral vasomotor reactivity, defined as the cerebral vasculature response to hypoxia, is not wellunderstood in fibromyalgia (FM) patients. This study investigated the difference in the cerebrovascular reactivity (i.e., responsiveness to hypercapnia was evaluated by use of breath- holding index) to the breath-holding index (BHI) between patients with fibromyalgia and a group of normal controls. Methods - The study included 40 FM patients and 40 healthy subjects. Cerebrovascular reactivity was evaluated using the BHI, which is a nonaggressive, well-tolerated, real-time, reproducible screening method to study cerebral haemodynamics. Insonation depth and basal velocity were symmetrical and not significantly different between the two groups (p>0.05). All patients completed the Revised Fibromyalgia Impact Questionnaire (FIQR), Hospital Anxiety and Depression Scale (HADS), visual analogue scale (VAS), and the somatization subscale of the SCL-90-R symptom checklist. Results - The BHI ranged from 0.30 to 2.20 (mean 1.11±0.45) in the FM patients and 1.10 to 2.80 (mean 1.90±0.35) in the control group (p<0.001). Disease duration and right BHIaverage and left BHIaverage values exhibited a significant negative correlation (r=-0.877; p<0.001, r=-0.842; p<0.001, respectively). As pain and fatigue scores increased, the right BHIaverage and left BHIaverage values decreased (r=-0.431; p=0.005, r=-0.544; p<0.001, r=-0.341; p=0.031, r=-0.644; p<0.001, respectively). Conclusions - BHI values showed that cerebrovascular reactivity in FM patients decreased in comparison to healthy individuals. BHI decreased as disease duration and severity increased. Cerebrovascular reactivity decreased in FM patients, and this phenomenon should be accepted as an abnormality. Additionally, this outcome may have been the result of a mechanism responsible for central neuropathic pain.