Disruptive compensatory mechanisms in fibromyalgia syndrome and their association with pharmacological agents.

Autor: Silva FMQ; Neuromodulation Center, Center for Clinical Research Learning, Spaulding Rehabilitation Hospital, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA., Pacheco-Barrios K; Neuromodulation Center, Center for Clinical Research Learning, Spaulding Rehabilitation Hospital, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.; Vicerrectorado de Investigación, Unidad de Investigación para la Generación y Síntesis de Evidencias en Salud, Universidad San Ignacio de Loyola, Lima, 15024, Peru., Fregni F; Neuromodulation Center, Center for Clinical Research Learning, Spaulding Rehabilitation Hospital, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. fregni.felipe@mgh.harvard.edu.
Jazyk: angličtina
Zdroj: Experimental brain research [Exp Brain Res] 2024 Dec; Vol. 242 (12), pp. 2701-2714. Date of Electronic Publication: 2024 Oct 05.
DOI: 10.1007/s00221-024-06924-6
Abstrakt: Fibromyalgia syndrome (FMS) is a chronic disorder characterized commonly by widespread musculoskeletal pain and fatigue, predominantly affecting women, with its complexity often leading to underdiagnosis and complicating treatment effectiveness. Transcranial magnetic stimulation (TMS) metrics are potential markers to optimize FMS treatments; however, evidence is limited. Our study aimed to explore the relationship between cortical excitability and inhibition, assessed through TMS markers, and clinical characteristics in patients with FMS. This presented cross-sectional study employed baseline data from a clinical trial with 108 FMS patients, mostly female (88.8%), and mean age of 47.3 years old (SD = 12.06). Our analysis showed that decreased short-intracortical inhibition (SICI) was associated with gabapentinoids use, nicotine history, and increased fatigue levels, suggesting its connection with compensatory mechanisms for non-painful FMS features. Increased motor intracortical facilitation (ICF) was linked with greater pain severity and shorter FMS duration, implying its relationship with a reorganization of sensorimotor pathways due to chronic pain. Additionally, higher resting motor threshold (rMT) was associated with less effective pain modulation (lower conditioned pain modulation [CPM]), indicating a disruption of pain compensatory mechanism. Given the role of SICI in indexing homeostatic brain mechanisms and its association with fatigue, a hallmark characteristic of FMS-induced behavioral changes, these results suggest that FMS likely has a deleterious effect on brain inhibitory function, thus providing a potential novel insight for FMS mechanisms. In addition, it seems that this compensatory mechanism's disruption is enhanced by pharmacological agents such as gabapentioids and nicotine.
Competing Interests: Declarations Ethics approval and consent to participate This study obeys the Declaration of Helsinki and was approved by the Institutional Review Board (IRB) of Partners Healthcare at Mass General Brigham under the protocol approval number 2017P002524. Informed consent was obtained from all participants. Consent for publication All authors give their consent for this study to be published in Experimental Brain Research journal. Competing interests All authors disclose no potential conflicts of interest.
(© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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