• Pain · Apr 2022

    Dissecting neuropathic from poststroke pain: the white matter within.

    • Marcelo Delboni Lemos, Isabelle Faillenot, Tavares LucatoLeandroL0000-0001-9181-5245Department of Radiology, LIM-44, University of São Paulo, São Paulo, Brazil., Jacobsen TeixeiraManoelMPain Center, Department of Neurology, LIM-62, University of São Paulo, São Paulo, Brazil., Mendonça BarbosaLucianaL0000-0002-5239-5935Pain Center, Department of Neurology, LIM-62, University of São Paulo, São Paulo, Brazil., Joaquim Lopes AlhoEduardoE0000-0002-8774-3485Pain Center, Department of Neurology, LIM-62, University of São Paulo, São Paulo, Brazil., Bastos ConfortoAdrianaA0000-0001-7869-3490Department of Neurology, LIM-62, University of São Paulo, São Paulo, Brazil., Lilian de Lima RodriguesAntoniaAPain Center, Department of Neurology, LIM-62, University of São Paulo, São Paulo, Brazil., Ricardo Galhardoni, Valquíria Aparecida da Silva, Clarice Listik, Jefferson Rosi, Roland Peyron, Luis Garcia-Larrea, and Daniel Ciampi de Andrade.
    • Department of Radiology, LIM-44, University of São Paulo, São Paulo, Brazil.
    • Pain. 2022 Apr 1; 163 (4): 765-778.

    AbstractPoststroke pain (PSP) is a heterogeneous term encompassing both central neuropathic (ie, central poststroke pain [CPSP]) and nonneuropathic poststroke pain (CNNP) syndromes. Central poststroke pain is classically related to damage in the lateral brainstem, posterior thalamus, and parietoinsular areas, whereas the role of white matter connecting these structures is frequently ignored. In addition, the relationship between stroke topography and CNNP is not completely understood. In this study, we address these issues comparing stroke location in a CPSP group of 35 patients with 2 control groups: 27 patients with CNNP and 27 patients with stroke without pain. Brain MRI images were analyzed by 2 complementary approaches: an exploratory analysis using voxel-wise lesion symptom mapping, to detect significant voxels damaged in CPSP across the whole brain, and a hypothesis-driven, region of interest-based analysis, to replicate previously reported sites involved in CPSP. Odds ratio maps were also calculated to demonstrate the risk for CPSP in each damaged voxel. Our exploratory analysis showed that, besides known thalamic and parietoinsular areas, significant voxels carrying a high risk for CPSP were located in the white matter encompassing thalamoinsular connections (one-tailed threshold Z > 3.96, corrected P value <0.05, odds ratio = 39.7). These results show that the interruption of thalamocortical white matter connections is an important component of CPSP, which is in contrast with findings from nonneuropathic PSP and from strokes without pain. These data can aid in the selection of patients at risk to develop CPSP who could be candidates to pre-emptive or therapeutic interventions.Copyright © 2021 International Association for the Study of Pain.

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