ANTONIA LILIAN DE LIMA RODRIGUES
Projetos de Pesquisa
Unidades Organizacionais
LIM/62 - Laboratório de Fisiopatologia Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
4 resultados
Resultados de Busca
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- Pregabalin for the Prevention of Oxaliplatin-Induced Painful Neuropathy: A Randomized, Double-Blind Trial(2017) ANDRADE, Daniel Ciampi De; TEIXEIRA, Manoel Jacobsen; GALHARDONI, Ricardo; FERREIRA, Karine S. L.; MILENO, Paula Braz; SCISCI, Nathalia; ZANDONAI, Alexandra; TEIXEIRA, William G. J.; SARAGIOTTO, Daniel F.; SILVA, Valquiria; RAICHER, Irina; CURY, Rubens Gisbert; MACARENCO, Ricardo; HEISE, Carlos Otto; BROTTO, Mario Wilson Iervolino; MELLO, Alberto Andrade De; MEGALE, Marcelo Zini; DOURADO, Luiz Henrique Curti; BAHIA, Luciana Mendes; RODRIGUES, Antonia Lilian; PARRAVANO, Daniella; FUKUSHIMA, Julia Tizue; LEFAUCHEUR, Jean-Pascal; BOUHASSIRA, Didier; SOBROZA, Evandro; RIECHELMANN, Rachel P.; HOFF, Paulo M.; SILVA, Fernanda Valerio Da; CHILE, Thais; DALE, Camila S.; NEBULONI, Daniela; SENNA, Luiz; BRENTANI, Helena; PAGANO, Rosana L.; SOUZA, Angela M. DeBackground. Patients with colorectal cancer (CRC) receiving oxaliplatin (OXA) develop acute and chronic painful oxaliplatin-induced peripheral neuropathy (OXAIPN). Acute and chronic OXA-related neuropathies have different pathophysiological bases, but both lead to a common phenomenon: central sensitization (CS) of nociceptive neuronal networks, leading to increased sensitivity (hyperlgesia, allodynia) in the somatosensory system, the common ground of chronic neuropathic pain. Because CS is related to increased risk of painful OXAIPN, we hypothesized that preemptive use of the anti-hyperalgesic drug pregabaline (known to decrease CS) during OXA infusions would decrease the incidence of chronic OXAIPN. Methods. Pain-free, chemotherapy-naive CRC patients receiving at least one cycle of modified-FLOX [5-FU(500 mg/m(2)) 1 leucovorin(20 mg/m(2))/week for] 6 weeks+oxaliplatin(85 mg/m2) at weeks 1-3-5 every 8 weeks] were randomized (1:1) into the study. Patients received either pregabalin or placebo for 3 days before and 3 days after each OXA infusion and were followed for up to 6 months. Clinical assessments were performed at baseline, at the end of chemotherapy, and after the follow-up period. The main outcome was average pain at the last visit assessed by the visual analogic scale (0-10) item of the Brief Pain Inventory (BPI). Secondary endpoints were presence of neuropathic pain according to the Douleur Neuropathique-4 (DN-4), pain dimensions (short-form McGill Pain Questionnaire [MPQ]), Neuropathic Pain Symptom Inventory (NPSI), and changes in nerve conduction studies (NCS) and side effect profile. Results. One hundred ninety-nine patients (57.0 +/- 10.7 years old, 98 female, 101 male) were randomized. Data from 56 patients were not included in the analyses (as they did not receive at least one full cycle of modified FLOX). Data from 78 patients in the pregabalin group and 65 patients in the placebo group were retained for analyses. At the last visit, pain intensity in the pregabalin group was 1.03 (95% confidence interval [CI] 50.79-1.26), and 0.85 (95% CI50.64-1.06) in the placebo group, which did not reach significance. Scores from the BPI, MPQ, DN-4, NPSI, and NCS and side-effect profiles and incidence of death did not differ between groups. Quality of life (QoL) score did not differ between groups (placebo = 576.9 +/- 23.1, pregabalin group 79.4 +/- 20.6). Mood scores were not significantly different between groups (placebo 9.7 [8.1-11.2]; pregabalin 6.8 [5.6-8.0]). Conclusion. The preemptive use of pregabalin during OXA infusions was safe, but did not decrease the incidence of chronic pain related to OXAIPN.
- Insular and anterior cingulate cortex deep stimulation for central neuropathic pain Disassembling the percept of pain(2019) GALHARDONI, Ricardo Geront; SILVA, Valquiria Aparecida da; GARCIA-LARREA, Luis; DALE, Camila; BAPTISTA, Abrahao F.; BARBOSA, Luciana Mendonca; MENEZES, Luciana Mendes Bahia; SIQUEIRA, Silvia R. D. T. de; VALERIO, Fernanda; ROSI JR., Jefferson; RODRIGUES, Antonia Lilian de Lima; FERNANDES, Diego Toledo Reis Mendes; SELINGARDI, Priscila Mara Lorencini; MARCOLIN, Marco Antonio; DURAN, Fabio Luis de Souza; ONO, Carla Rachel; LUCATO, Leandro Tavares; FERNANDES, Ana Mercia B. L.; SILVA, Fabio E. F. da; YENG, Lin T.; BRUNONI, Andre R.; BUCHPIGUEL, Carlos A.; TEIXEIRA, Manoel J.; ANDRADE, Daniel Ciampi deObjective To compare the analgesic effects of stimulation of the anterior cingulate cortex (ACC) or the posterior superior insula (PSI) against sham deep (d) repetitive (r) transcranial magnetic stimulation (TMS) in patients with central neuropathic pain (CNP) after stroke or spinal cord injury in a randomized, double-blinded, sham-controlled, 3-arm parallel study. Methods Participants were randomly allocated into the active PSI-rTMS, ACC-rTMS, sham-PSI-rTMS, or sham-ACC-rTMS arms. Stimulations were performed for 12 weeks, and a comprehensive clinical and pain assessment, psychophysics, and cortical excitability measurements were performed at baseline and during treatment. The main outcome of the study was pain intensity (numeric rating scale [NRS]) after the last stimulation session. Results Ninety-eight patients (age 55.02 +/- 12.13 years) completed the study. NRS score was not significantly different between groups at the end of the study. Active rTMS treatments had no significant effects on pain interference with daily activities, pain dimensions, neuropathic pain symptoms, mood, medication use, cortical excitability measurements, or quality of life. Heat pain threshold was significantly increased after treatment in the PSI-dTMS group from baseline (1.58, 95% confidence interval [CI] 0.09-3.06]) compared to sham-dTMS (-1.02, 95% CI -2.10 to 0.04, p = 0.014), and ACC-dTMS caused a significant decrease in anxiety scores (-2.96, 95% CI -4.1 to -1.7]) compared to sham-dTMS (-0.78, 95% CI -1.9 to 0.3; p = 0.018). Conclusions ACC- and PSI-dTMS were not different from sham-dTMS for pain relief in CNP despite a significant antinociceptive effect after insular stimulation and anxiolytic effects of ACC-dTMS. These results showed that the different dimensions of pain can be modulated in humans noninvasively by directly stimulating deeper SNC cortical structures without necessarily affecting clinical pain per se.
- 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.