Brain functional changes and duloxetine treatment response in fibromyalgia: a pilot study.
OBJECTIVE
Serotonin-norepinephrine reuptake inhibitor (SNRI) antidepressant medications may have efficacy in relieving pain associated with fibromyalgia syndrome (FMS), even in the absence of major depressive disorder (MDD). Current practice is to use a trial-and-error treatment strategy, often requiring 8-12 weeks to determine the effectiveness of a given pharmacological intervention. The ability to predict response to antidepressant medications would facilitate clinical management of FMS. Prior work in MDD has shown that the quantitative electroencephalographic (QEEG) cordance biomarker of brain functional changes early in the course of antidepressant treatment is related to later clinical response. We hypothesized that cordance might also predict response to antidepressant medications for symptoms of FMS.


METHODS
Twelve adults (9 females) meeting American College of Rheumatology criteria for FMS participated in a double-blind placebo-controlled treatment trial utilizing duloxetine 60 mg. QEEG cordance changes were examined over the first week of treatment. Primary clinical outcomes included change in average pain severity on the Brief Pain Inventory (BPI) and global improvement in pain on the Patient's Global Impressions of Improvement (PGI-I) scale at 12 weeks.


RESULTS
Changes in left frontal QEEG cordance after the first week of duloxetine treatment significantly predicted BPI pain improvement (regression coefficient = 2.9, R(2) = 0.93, P = 0.008) and PGI-I global improvement (regression coefficient = 0.94, R(2) = 0.81, P = 0.04).


CONCLUSIONS
This pilot study suggests that QEEG biomarkers may prove useful for predicting improvement in painful symptoms during SNRI treatment in FMS. Larger studies are needed to confirm this finding.
Hunter
Aimee M
AM
Laboratory of Brain, Behavior, and Pharmacology, Semel Institute for Neuroscience and Human Behavior at the University of California, Los Angeles, CA, USA.
Leuchter
Andrew F
AF
Cook
Ian A
IA
Abrams
Michelle
M
Siegman
Barbara E
BE
Furst
Daniel E
DE
Chappell
Amy S
AS
D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000328:Adult; D015415:Biomarkers / Q000032:analysis; D001921:Brain / Q000033:anatomy & histology / Q000187:drug effects* / Q000503:physiopathology; D002395:Catecholamines / Q000378:metabolism; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D000068736:Duloxetine Hydrochloride; D004569:Electroencephalography; D005071:Evoked Potentials / Q000187:drug effects* / Q000502:physiology; D005260:Female; D005356:Fibromyalgia / Q000188:drug therapy* / Q000503:physiopathology; D005625:Frontal Lobe / Q000033:anatomy & histology / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D017063:Outcome Assessment, Health Care; D010147:Pain Measurement; D017288:Pain Threshold / Q000187:drug effects / Q000502:physiology; D010865:Pilot Projects; D010919:Placebos; D011237:Predictive Value of Tests; D012680:Sensitivity and Specificity; D012701:Serotonin / Q000378:metabolism; D013876:Thiophenes / Q000494:pharmacology*; D016896:Treatment Outcome
D018759:Adrenergic Uptake Inhibitors; D015415:Biomarkers; D002395:Catecholamines; D010919:Placebos; D013876:Thiophenes; D012701:Serotonin; D000068736:Duloxetine Hydrochloride