MARCELO DELBONI LEMOS

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LIM/44 - Laboratório de Ressonância Magnética em Neurorradiologia, Hospital das Clínicas, Faculdade de Medicina

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  • conferenceObject
    Brainstem syndrome and longitudinally extensive transverse myelitis (LETM) as first manifestation of Adult T-Cell Leukemia/Lymphoma (ATLL)
    (2017) GOMES, A. B. Ayroza Galvao Ribeiro; SOARES NETO, H.; LEMOS, M. Delboni; CALLEGARO, D.; PEREIRA, S. L. Apostolos
  • article 5 Citação(ões) na Scopus
    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 de
    Poststroke 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.
  • article 1 Citação(ões) na Scopus
    Site matters: Central neuropathic pain characteristics and somatosensory findings after brain and spinal cord lesions
    (2023) BARBOSA, Luciana Mendonca; VALERIO, Fernanda da; PEREIRA, Samira Luisa Apostolos; SILVA, Valquiria Aparecida da; RODRIGUES, Antonia Lilian de Lima; GALHARDONI, Ricardo; YENG, Lin Tchia; JR, Jefferson Rosi; CONFORTO, Adriana Bastos; LUCATO, Leandro Tavares; LEMOS, Marcelo Delboni; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi de
    Background: It is unknown if different etiologies or lesion topographies influence central neuropathic pain (CNP) clinical manifestation.Methods: We explored the symptom-somatosensory profile relationships in CNP patients with different types of lesions to the central nervous system to gain insight into CNP mechanisms. We compared the CNP profile through pain descriptors, standardized bedside examination, and quantitative sensory test in two different etiologies with segregated lesion locations: the brain, central poststroke pain (CPSP, n = 39), and the spinal cord central pain due to spinal cord injury (CPSCI, n = 40) in neuromyelitis optica.Results: Results are expressed as median (25th to 75th percentiles). CPSP presented higher evoked and paroxysmal pain scores compared to CPSCI (p < 0.001), and lower cold thermal limen (5.6? [0.0-12.9]) compared to CPSCI (20.0? [4.2-22.9]; p = 0.004). CPSCI also had higher mechanical pain thresholds (784.5 mN [255.0-1078.0]) compared to CPSP (235.2 mN [81.4-1078.0], p = 0.006) and higher mechanical detection threshold compared to control areas (2.7 [1.5-6.2] vs. 1.0 [1.0-3.3], p = 0.007). Evoked pain scores negatively correlated with mechanical pain thresholds (r = -0.38, p < 0.001) and wind-up ratio (r = -0.57, p < 0.001).Conclusions: CNP of different etiologies may present different pain descriptors and somatosensory profiles, which is likely due to injury site differences within the neuroaxis. This information may help better design phenotype mechanism correlations and impact trial designs for the main etiologies of CNP, namely stroke and spinal cord lesions. This study provides evidence that topography may influence pain symptoms and sensory profile. The findings suggest that CNP mechanisms might vary according to pain etiology or lesion topography, impacting future mechanism-based treatment choices.
  • bookPart
    Base do crânio
    (2017) GOMES, Regina Lúcia Elia; ZUPPANI, Henrique Bortot; LEMOS, Marcelo Delboni