Abstract

PurposeTo assess the efficacy of pregabalin by showing differences in the neuronal activities of fibromyalgia (FM) patients before and after longitudinal treatment using functional magnetic resonance imaging (fMRI).Materials and MethodsIn total, 21 female patients with FM and 11 age- and gender-matched healthy controls participated. FM patients underwent fMRI at baseline and following pharmacological therapy with pregabalin to diminish their pain. Pressure-pain stimuli were delivered on the subject’s thumbnail bed during fMRI scans. Brain activation regions in fMRI were evaluated for longitudinal changes using a paired t-test. Changes in clinical features were also assessed with the Fibromyalgia Impact Questionnaire (FIQ), Brief Fatigue Inventory (BFI), Beck Depression Inventory (BDI), Widespread Pain Index (WPI), Symptom Severity Scale Score (SSS), and State-Trait Anxiety Inventory (STAI).ResultsClinical scores were reduced significantly following therapy with five of the six clinical tests (FIQ, BFI, BDI, WPI, SSS; p < 0.05). Brain activation post-treatment was significantly lower than that pre-treatment in 13 regions of the brain (p < 0.001).ConclusionsOur findings confirm that pregabalin influences aspects of the whole pain matrix, using fMRI, inducing longitudinal changes in neuronal activity during the pain state, and that it reduces pain and other core symptoms of FM. This method could be applied to other longitudinal clinical trials of pharmacological treatments for FM.

Highlights

  • Fibromyalgia (FM) is characterized by chronic widespread musculoskeletal pain and allodynia [1]

  • While the corresponding clinical scores of healthy control group were 10.97±7.65, 0.82±0.85, 0.18±0.6, 0.82±1.47, 43.64±7.90 and 42.91±8.14. Clinical scores of both groups were significantly different in terms of Fibromyalgia Impact Questionnaire (FIQ), Brief Fatigue Inventory (BFI), Beck Depression Inventory (BDI), Widespread Pain Index (WPI), and Severity Scale Score (SSS)

  • These results support the hypothesis that FM is caused by alterations in neuronal pain processing and that pregabalin restricts the release of neurotransmitters in the pain-processing path

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Summary

Introduction

Fibromyalgia (FM) is characterized by chronic widespread musculoskeletal pain and allodynia [1]. Et al [3] reported that comparable levels of subjectively reported painful stimulation resulted in similar patterns of brain activation in both FM patients and healthy controls, whereas, for similar intensities of pressure pain, there was no common activation region but greater effects in specific pain-processing regions.

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