MARCELO DELBONI LEMOS
Índice h a partir de 2011
2
Projetos de Pesquisa
Unidades Organizacionais
LIM/44 - Laboratório de Ressonância Magnética em Neurorradiologia, Hospital das Clínicas, Faculdade de Medicina
2 resultados
Resultados de Busca
Agora exibindo 1 - 2 de 2
- Dissecting neuropathic from poststroke pain: the white matter within(2022) LEMOS, Marcelo Delboni; FAILLENOT, Isabelle; LUCATO, Leandro Tavares; TEIXEIRA, Manoel Jacobsen; BARBOSA, Luciana Mendonca; ALHO, Eduardo Joaquim Lopes; CONFORTO, Adriana Bastos; RODRIGUES, Antonia Lilian de Lima; GALHARDONI, Ricardo; SILVA, Valquiria Aparecida da; LISTIK, Clarice; ROSI, Jefferson; PEYRON, Roland; GARCIA-LARREA, Luis; ANDRADE, Daniel Ciampi dePoststroke 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.
- Dissecting central post-stroke pain: a controlled symptom-psychophysical characterization(2022) BARBOSA, Luciana Mendonca; SILVA, Valquiria Aparecida da; RODRIGUES, Antonia Lilian de Lima; FERNANDES, Diego Toledo Reis Mendes; OLIVEIRA, Rogerio Adas Ayres de; GALHARDONI, Ricardo; YENG, Lin Tchia; ROSI JUNIOR, Jefferson; CONFORTO, Adriana Bastos; LUCATO, Leandro Tavares; LEMOS, Marcelo Delboni; PEYRON, Roland; GARCIA-LARREA, Luis; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi deDissection 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.