title: Descending Control of Nociceptive Processing in Knee Osteoarthritis Is Associated With Intracortical Disinhibition: An Exploratory Study.
abstract: Based on the hypothesis that an imbalance in excitatory and inhibitory input is a central mechanism of knee osteoarthritis chronic pain (KOACP), this exploratory study had the following aims: to compare whether the function of the descending inhibitory pain pathway is associated with the state of inhibition in the corticospinal system indexed by the motor-evoked potential (MEP) and the cortical salient period (CSP) in patients with severe osteoarthritis (OA) and healthy controls; and to determine if there is correlation between the measures of intracortical inhibition (CSP, MEP) with changes on the numerical pain scale (NPS [0-10]) in KOACP during a conditioned pain modulation (CPM)-task considering the effect of self-reported function assessed by the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and analgesic use.In a cross-sectional study, we included females (n = 21), with disability by pain or stiffness due to KOACP and healthy controls (n = 10), aged 19 to 75 years. The motor cortex excitability parameters (MEP and CSP) were assessed using the transcranial magnetic stimulation. We assessed the pain and disability by the WOMAC, and change on NPS (0-10) during CPM-task.A Multivariate analysis of covariance revealed that the adjusted mean (SD) on the MEP amplitude was 13.53% higher in the OA than in healthy subjects (1.33 [0.49] vs 1.15 [0.13]), respectively (P = 0.16). The adjusted mean (SD) on the CSP observed in OA patients was 23.43% lower than in healthy subjects (54.54 [16.10] vs 70.94 [22.87]), respectively (P = 0.01). The function of the descending pain modulatory system assessed by change on NPS (0-10) during a CPM-task was negatively correlated with the cortical excitability parameter indexed by the CSP (P = 0.001). Also, the CSP was negatively correlated with the pain and disability assessed by the WOMAC index.These findings support the hypothesis that the change in cortical plasticity in KOACP is associated with less intracortical inhibition, as measured by the CSP. These results show that the neural change in the motor cortex in KOACP is associated with pain and disability levels, and also with decreased activation of the endogenous pain-modulating system by a CPM-task.
authors.affiliation: From the Post-Graduate Program in Medical Sciences (UFRGS) (MDGLT, AD, APB, ILST, WC), School of Medicine, Universidade Federal do Rio Grande do Sul; Department of Surgery (WC), School of Medicine at UFRGS; Department of Pharmacology of Instituto de Ciencias Basicas da Saude at UFRGS (ILST); Post-Graduate Program in Biologic Sciences: Physiology, UFRGS (RV); Laboratory of Pain and Neuromodulation at Hospital de Clínicas de Porto Alegre (HCPA) (MDGLT, AD, APB, WC), Porto Alegre; Service of Pain and Palliative Care at HCPA (WC), Brazil; and Harvard Medical School, Department of Physical Medicine and Rehabilitation (FF), Boston, MA.
authors.forename: Maria da Graca L
authors.initials: MDGL
authors.lastname: Tarragó
authors.forename: Alícia
authors.initials: A
authors.lastname: Deitos
authors.forename: Aline Patrícia
authors.initials: AP
authors.lastname: Brietzke
authors.forename: Rafael
authors.initials: R
authors.lastname: Vercelino
authors.forename: Iraci L S
authors.initials: ILS
authors.lastname: Torres
authors.forename: Felipe
authors.initials: F
authors.lastname: Fregni
authors.forename: Wolnei
authors.initials: W
authors.lastname: Caumo
mesh_terms: D000368:Aged; D002540:Cerebral Cortex / Q000503:physiopathology*; D003430:Cross-Sectional Studies; D004185:Disability Evaluation; D004576:Electromyography; D019054:Evoked Potentials, Motor / Q000502:physiology; D005260:Female; D006801:Humans; D008875:Middle Aged; D009433:Neural Inhibition / Q000502:physiology*; D059225:Nociception / Q000502:physiology*; D020370:Osteoarthritis, Knee / Q000503:physiopathology*; D010147:Pain Measurement; D017288:Pain Threshold / Q000502:physiology; D011712:Pyramidal Tracts / Q000503:physiopathology*; D012016:Reference Values