LEANDRO TAVARES LUCATO

(Fonte: Lattes)
Índice h a partir de 2011
18
Projetos de Pesquisa
Unidades Organizacionais
Instituto de Radiologia, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/44 - Laboratório de Ressonância Magnética em Neurorradiologia, Hospital das Clínicas, Faculdade de Medicina

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  • article 16 Citação(ões) na Scopus
    Characterization of pain syndromes in patients with neuromyelitis optica
    (2020) VALERIO, Fernanda; APOSTOLOS-PEREIRA, Samira L.; SATO, Douglas Kazutoshi; CALLEGARO, Dagoberto; LUCATO, Leandro Tavares; BARBOZA, Victor Rosseto; SILVA, Valquiria A.; GALHARDONI, Ricardo; RODRIGUES, Antonia L. de Lima; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi de
    Background Pain is common and refractory in spinal cord injury (SCI). Currently, most studies evaluated pain in male-predominant traumatic-SCI. Also, concomitant secondary pain syndromes and its temporal evolution were seldom reported. Methods We aimed to prospectively describe the main and secondary pain and its associated factors in inflammatory-SCI evaluating neuromyelitis optica (NMO) patients. In-remission NMO patients underwent neurological, imaging and autoantibody evaluations. Questionnaires detailing main and secondary pains, functional state, mood, catastrophizing, quality of life (QoL) and ""non-motor symptoms"" were used at two time points. Results Pain was present in 53 (73.6%) of the 72 patients included. At-level neuropathic pain was the most common main pain syndrome, affecting 32 subjects (60.4% of those with pain). Over 70% (n = 38) of this cohort reported two pain syndromes. Those without pain were significantly younger (26.1 +/- 12.7 y.o. in those without pain and 40.1 +/- 12.5, 37.2 +/- 11.4 y.o. in those whose main pain was neuropathic and non-neuropathic, respectively,p = .001), and no differences in the inflammatory status were observed between groups. On follow-up, one-fifth (n = 11) had a different main pain syndrome from the first visit. Pain impacted QoL as much as disability and motor strength. Conclusion Pain is a prevalent and disabling non-motor symptom in NMO-SCI. Most patients experience more than one pain syndrome which can change in time even in the absence of clinical relapse. Age of the inflammatory-SCI was a major determinant of pain. Acknowledging temporal changes and multiplicity of pain syndromes in NMO-SCI may give insights into more precise designs of clinical trials and general management of pain in SCI. Significance In this longitudinal study with NMO-related SCI, pain affected almost three-quarters of patients with NMO. Over 70% have more than one pain syndrome and at-level neuropathic pain is the most common type of pain syndrome. Patients without pain were significantly younger but had the same burden of inflammatory lesions than those with pain. During follow-up, up to one fifth of patients presented with changes in the main pain syndromes, which can occur even in the absence of clinical activity of the inflammatory disease. In this cohort, Pain affected quality of life as much as disability or motor strength.
  • article 2 Citação(ões) na Scopus
    Corticomotor excitability is altered in central neuropathic pain compared with non-neuropathic pain or pain-free patients
    (2023) BARBOSA, Luciana Mendonca; VALERIO, Fernanda; SILVA, Valquiria Aparecida da; RODRIGUES, Antonia Lilian de Lima; GALHARDONI, Ricardo; YENG, Lin Tchia; JUNIR, Jefferson Rosi; CONFORTO, Adriana Bastos; LUCATO, Leandro Tavares; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi de
    Objectives: Central neuropathic pain (CNP) is associated with altered corticomotor excitability (CE), which can potentially provide insights into its mechanisms. The objective of this study is to describe the CE changes that are specifically related to CNP.Methods: We evaluated CNP associated with brain injury after stroke or spinal cord injury (SCI) due to neuromyelitis optica through a battery of CE measurements and comprehensive pain, neurological, functional, and quality of life assessments. CNP was compared to two groups of patients with the same disease: i. with non-neuropathic pain and ii. without chronic pain, matched by sex and lesion location.Results: We included 163 patients (stroke=93; SCI=70: 74 had CNP, 43 had non-neuropathic pain, and 46 were pain-free). Stroke patients with CNP had lower motor evoked potential (MEP) in both affected and unaffected hemispheres compared to non-neuropathic pain and no-pain patients. Patients with CNP had lower amplitudes of MEPs (366 mu V +/- 464 mu V) than non-neuro-pathic (478 +/- 489) and no-pain (765 mu V +/- 880 mu V) patients, p < 0.001. Short-interval intracorti-cal inhibition (SICI) was defective (less inhibited) in patients with CNP (2.6 +/- 11.6) compared to no-pain (0.80.7), p = 0.021. MEPs negatively correlated with mechanical and cold-induced allo-dynia. Furthermore, classifying patients' results according to normative data revealed that at least 75% of patients had abnormalities in some CE parameters and confirmed MEP findings based on group analyses.Discussion: CNP is associated with decreased MEPs and SICI compared to non-neuropathic pain and no-pain patients. Corticomotor excitability changes may be helpful as neurophysiological markers of the development and persistence of pain after CNS injury, as they are likely to pro-vide insights into global CE plasticity changes occurring after CNS lesions associated with CNP.(c) 2023 The Author(s).
  • article 73 Citação(ões) na Scopus
    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 de
    Objective 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.
  • article 1 Citação(ões) na Scopus
    Author response: Insular and anterior cingulate cortex deep stimulation for central neuropathic pain: Disassembling the percept of pain
    (2020) ANDRADE, Daniel Ciampi de; GALHARDONI, Ricardo; 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, 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.
  • article 25 Citação(ões) na Scopus
    Wilson's disease presenting as rapid eye movement sleep behavior disorder: a possible window to early treatment
    (2014) TRIBL, Gotthard G.; BOR-SENG-SHU, Edson; TRINDADE, Mateus C.; LUCATO, Leandro T.; TEIXEIRA, Manoel J.; BARBOSA, Egberto R.
    Objective: To describe characteristics of REM sleep behavior disorder in Wilson's disease. Method: Questionnaire-based interviews (patients and relatives), neurological examinations, two-week prospective dream-diary, video-polysomnography, transcranial sonography, MRI. Results: Four Wilson's disease cases with REM sleep behavior disorder were described; three had REM sleep behavior disorder as initial symptom. All showed mesencephalic tegmental/tectal sonographic hyperechogenicities and two presented ponto-mesencephalic tegmental MRI hyperintensities. Conclusion: This first description of REM sleep behavior disorder in Wilson's disease in literature documents REM sleep behavior disorder as a possible presenting symptom of Wilson's disease and adds further evidence to the parallelism of Parkinson's disease and Wilson's disease in phenotype and brainstem topography, which ought to be further studied. REM sleep behavior disorder has prognostic relevance for neurodegeneration in alpha-synucleinopathies. In Wilson's disease, usefulness of early diagnosis and treatment are already well established. REM sleep behavior disorder in Wilson's disease offers a possible theoretical model for potential early treatment in this extrapyramidal and brainstem paradigm syndrome, previewing the possibility of neuroprotective treatment for REM sleep behavior disorder in ""pre-clinical"" Parkinson's disease.
  • 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 24 Citação(ões) na Scopus
    Substantia nigra fractional anisotropy is not a diagnostic biomarker of Parkinson's disease: A diagnostic performance study and meta-analysis
    (2017) HIRATA, Fabiana C. C.; SATO, Joao R.; VIEIRA, Gilson; LUCATO, Leandro T.; LEITE, Claudia C.; BOR-SENG-SHU, Edson; PASTORELLO, Bruno F.; OTADUY, Maria C. G.; CHAIM, Khallil T.; CAMPANHOLO, Kenia R.; NOVAES, Natalia P.; MELO, Luciano Magalhaes; GONCALVES, Marcia R.; NASCIMENTO, Felipe Barjud Pereira do; TEIXEIRA, Manoel Jacobsen; BARBOSA, Egberto Reis; AMARO JR., Edson; CARDOSO, Ellison Fernando
    Objectives Our goal was to estimate the diagnostic accuracy of substantia nigra fractional anisotropy (SN-FA) for Parkinson's disease (PD) diagnosis in a sample similar to the clinical setting, including patients with essential tremor (ET) and healthy controls (HC). We also performed a systematic review and meta-analysis to estimate mean change in SN-FA induced by PD and its diagnostic accuracy. Methods Our sample consisted of 135 subjects: 72 PD, 21 ET and 42 HC. To address inter-scanner variability, two 3.0-T MRI scans were performed. MRI results of this sample were pooled into a meta-analysis that included 1,432 subjects (806 PD and 626 HC). A bivariate model was used to evaluate diagnostic accuracy measures. Results In our sample, we did not observe a significant effect of disease on SN-FA and it was uninformative for diagnosis. The results of the meta-analysis estimated a 0.03 decrease in mean SN-FA in PD relative to HC (CI: 0.01-0.05). However, the discriminatory capability of SN-FA to diagnose PD was low: pooled sensitivity and specificity were 72 % (CI: 68-75) and 63 % (CI: 58-70), respectively. There was high heterogeneity between studies (I-2 = 91.9%). Conclusions SN-FAcannot be used as an isolatedmeasure to diagnose PD.
  • 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.
  • article 11 Citação(ões) na Scopus
    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 de
    Dissection 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.
  • article 17 Citação(ões) na Scopus
    Dural-based lesions: is it a meningioma?
    (2021) YAMAKI, Vitor Nagai; GODOY, Luis Filipe de Souza; BANDEIRA, Gabriela Alencar; LUCATO, Leandro Tavares; LORDELO, Gustavo Correa; SOLLA, Davi Jorge Fontoura; NEVILLE, Iuri Santana; TEIXEIRA, Manoel Jacobsen; PAIVA, Wellingson Silva
    Purpose Meningiomas are the most common extra-axial intracranial neoplasms with typical radiological findings. In approximately 2% of cases, histopathological reports reveal different neoplasms or non-neoplastic lesions that can closely mimic meningiomas. We describe radiological features of meningioma mimics highlighting imaging red flags to consider a differential diagnosis. Methods A total of 348 lesions with radiological diagnosis of meningiomas which underwent to surgical treatment or biopsy between December of 2000 and September of 2014 were analyzed. We determined imaging features that are not a typical finding of meningiomas, suggesting other lesions. The following imaging characteristics were evaluated on CT and MRI: (a) bone erosion; (b) hyperintensity on T2WI; (c) hypointensity on T2WI; (d) bone destruction; (e) dural tail; (f) leptomeningeal involvement; (g) pattern of contrast enhancement; (h) dural displacement sign. Results We have a relatively high prevalence of meningioma mimics (7.2%). Dural-based lesions with homogeneous contrast enhancement (52%) are easily misdiagnosed as meningiomas. Most lesions mimic convexity (37.5%) or parafalcine (21.9%) meningiomas. We have determined five imaging red flags that can alert radiologists to consider meningioma mimics: (1) bone erosion (22.2%); (2) dural displacement sign (36%); (3) marked T2 hypointensity (32%); (4) marked T2 hyperintensity (12%); (5) absence of dural tail (48%). The most common mimic lesion in our series was hemangiopericytomas, followed by lymphomas and schwannomas. Conclusion The prevalence of meningioma mimics is not negligible. It is important to have awareness on main radiological findings suggestive of differential diagnosis due to a wide range of differentials which lead to different prognosis and treatment strategies.