TY - JOUR
T1 - Corticomotor excitability is altered in central neuropathic pain compared with non-neuropathic pain or pain-free patients
AU - Barbosa, Luciana Mendonça
AU - Valerio, Fernanda
AU - da Silva, Valquíria Aparecida
AU - Rodrigues, Antônia Lilian de Lima
AU - Galhardoni, Ricardo
AU - Yeng, Lin Tchia
AU - Junior, Jefferson Rosi
AU - Conforto, Adriana Bastos
AU - Lucato, Leandro Tavares
AU - Teixeira, Manoel Jacobsen
AU - de Andrade, Daniel Ciampi
PY - 2023/6/1
Y1 - 2023/6/1
N2 - Objectives: Central neuropathic pain (CNP) is associated with altered corticomotor excitability (CE), which can potentially provide insights into its mechanisms. The objective of this study is to describe the CE changes that are specifically related to CNP. Methods: We evaluated CNP associated with brain injury after stroke or spinal cord injury (SCI) due to neuromyelitis optica through a battery of CE measurements and comprehensive pain, neurological, functional, and quality of life assessments. CNP was compared to two groups of patients with the same disease: i. with non-neuropathic pain and ii. without chronic pain, matched by sex and lesion location. Results: We included 163 patients (stroke=93; SCI=70: 74 had CNP, 43 had non-neuropathic pain, and 46 were pain-free). Stroke patients with CNP had lower motor evoked potential (MEP) in both affected and unaffected hemispheres compared to non- neuropathic pain and no-pain patients. Patients with CNP had lower amplitudes of MEPs (366 μV ±464 μV) than non-neuropathic (478 ±489) and no-pain (765 μV ± 880 μV) patients, p < 0.001. Short-interval intracortical inhibition (SICI) was defective (less inhibited) in patients with CNP (2.6±11.6) compared to no-pain (0.8±0.7), p = 0.021. MEPs negatively correlated with mechanical and cold-induced allodynia. Furthermore, classifying patients' results according to normative data revealed that at least 75% of patients had abnormalities in some CE parameters and confirmed MEP findings based on group analyses. Discussion: CNP is associated with decreased MEPs and SICI compared to non-neuropathic pain and no-pain patients. Corticomotor excitability changes may be helpful as neurophysiological markers of the development and persistence of pain after CNS injury, as they are likely to provide insights into global CE plasticity changes occurring after CNS lesions associated with CNP.
AB - Objectives: Central neuropathic pain (CNP) is associated with altered corticomotor excitability (CE), which can potentially provide insights into its mechanisms. The objective of this study is to describe the CE changes that are specifically related to CNP. Methods: We evaluated CNP associated with brain injury after stroke or spinal cord injury (SCI) due to neuromyelitis optica through a battery of CE measurements and comprehensive pain, neurological, functional, and quality of life assessments. CNP was compared to two groups of patients with the same disease: i. with non-neuropathic pain and ii. without chronic pain, matched by sex and lesion location. Results: We included 163 patients (stroke=93; SCI=70: 74 had CNP, 43 had non-neuropathic pain, and 46 were pain-free). Stroke patients with CNP had lower motor evoked potential (MEP) in both affected and unaffected hemispheres compared to non- neuropathic pain and no-pain patients. Patients with CNP had lower amplitudes of MEPs (366 μV ±464 μV) than non-neuropathic (478 ±489) and no-pain (765 μV ± 880 μV) patients, p < 0.001. Short-interval intracortical inhibition (SICI) was defective (less inhibited) in patients with CNP (2.6±11.6) compared to no-pain (0.8±0.7), p = 0.021. MEPs negatively correlated with mechanical and cold-induced allodynia. Furthermore, classifying patients' results according to normative data revealed that at least 75% of patients had abnormalities in some CE parameters and confirmed MEP findings based on group analyses. Discussion: CNP is associated with decreased MEPs and SICI compared to non-neuropathic pain and no-pain patients. Corticomotor excitability changes may be helpful as neurophysiological markers of the development and persistence of pain after CNS injury, as they are likely to provide insights into global CE plasticity changes occurring after CNS lesions associated with CNP.
KW - Central pain
KW - Central post-stroke pain
KW - Chronic pain
KW - Cortical excitability
KW - Motor evoked potentials
KW - Neuropathic pain
KW - Spinal cord injury
KW - Transcranial magnetic stimulation
UR - http://www.scopus.com/inward/record.url?scp=85148764427&partnerID=8YFLogxK
U2 - 10.1016/j.neucli.2023.102845
DO - 10.1016/j.neucli.2023.102845
M3 - Journal article
SN - 0987-7053
VL - 53
JO - Neurophysiologie Clinique
JF - Neurophysiologie Clinique
IS - 3
M1 - 102845
ER -