Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSPBARBOSA, Luciana MendoncaSILVA, Valquiria Aparecida daRODRIGUES, Antonia Lilian de LimaFERNANDES, Diego Toledo Reis MendesOLIVEIRA, Rogerio Adas Ayres deGALHARDONI, RicardoYENG, Lin TchiaROSI JUNIOR, JeffersonCONFORTO, Adriana BastosLUCATO, Leandro TavaresLEMOS, Marcelo DelboniPEYRON, RolandGARCIA-LARREA, LuisTEIXEIRA, Manoel JacobsenANDRADE, Daniel Ciampi de2022-06-202022-06-202022BRAIN COMMUNICATIONS, v.4, n.3, article ID fcac090, 16p, 2022https://observatorio.fm.usp.br/handle/OPI/47151Dissection of distinct post-stroke pain syndromes evidenced that the neuropathic pain inventory, the presence of cold thermal deficit and the finding of allodynia on bedside examination, explained 77% of the occurrence of neuropathic central post-stroke pain, a new finding that has clear diagnostic potential. Central post-stroke pain affects up to 12% of stroke survivors and is notoriously refractory to treatment. However, stroke patients often suffer from other types of pain of non-neuropathic nature (musculoskeletal, inflammatory, complex regional) and no head-to-head comparison of their respective clinical and somatosensory profiles has been performed so far. We compared 39 patients with definite central neuropathic post-stroke pain with two matched control groups: 32 patients with exclusively non-neuropathic pain developed after stroke and 31 stroke patients not complaining of pain. Patients underwent deep phenotyping via a comprehensive assessment including clinical exam, questionnaires and quantitative sensory testing to dissect central post-stroke pain from chronic pain in general and stroke. While central post-stroke pain was mostly located in the face and limbs, non-neuropathic pain was predominantly axial and located in neck, shoulders and knees (P < 0.05). Neuropathic Pain Symptom Inventory clusters burning (82.1%, n = 32, P < 0.001), tingling (66.7%, n = 26, P < 0.001) and evoked by cold (64.1%, n = 25, P < 0.001) occurred more frequently in central post-stroke pain. Hyperpathia, thermal and mechanical allodynia also occurred more commonly in this group (P < 0.001), which also presented higher levels of deafferentation (P < 0.012) with more asymmetric cold and warm detection thresholds compared with controls. In particular, cold hypoesthesia (considered when the threshold of the affected side was <41% of the contralateral threshold) odds ratio (OR) was 12 (95% CI: 3.8-41.6) for neuropathic pain. Additionally, cold detection threshold/warm detection threshold ratio correlated with the presence of neuropathic pain (rho = -0.4, P < 0.001). Correlations were found between specific neuropathic pain symptom clusters and quantitative sensory testing: paroxysmal pain with cold (rho = -0.4; P = 0.008) and heat pain thresholds (rho = 0.5; P = 0.003), burning pain with mechanical detection (rho = -0.4; P = 0.015) and mechanical pain thresholds (rho = -0.4, P < 0.013), evoked pain with mechanical pain threshold (rho = -0.3; P = 0.047). Logistic regression showed that the combination of cold hypoesthesia on quantitative sensory testing, the Neuropathic Pain Symptom Inventory, and the allodynia intensity on bedside examination explained 77% of the occurrence of neuropathic pain. These findings provide insights into the clinical-psychophysics relationships in central post-stroke pain and may assist more precise distinction of neuropathic from non-neuropathic post-stroke pain in clinical practice and in future trials.engopenAccesscentral post-stroke painpost-stroke painneuropathic pain phenotypingcentral neuropathic painquantitative sensory testingperipheral neuropathic painpost-stroke paintranscranial magnetic stimulationdeep brain-stimulationquality-of-lifelong-term painsensory abnormalitiesdouble-blindmultiple-sclerosisa-deltaarticleCopyright OXFORD UNIV PRESS10.1093/braincomms/fcac090Biochemistry & Molecular BiologyChemistry, Multidisciplinary2632-1297