LEANDRO TAVARES LUCATO
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
LIM/44 - Laboratório de Ressonância Magnética em Neurorradiologia, Hospital das Clínicas, Faculdade de Medicina
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- Teaching NeuroImages: Lacunar stroke and polyarteritis nodosa Consider ADA2 deficiency (DADA2)(2019) GONCALVES, Tayrine da Silva; ALVES, Cesar Augusto Pinheiro Ferreira; PAZ, Jose Albino da; LUCATO, Leandro Tavares
- 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 deBackground 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.
- Neuroimaging in cerebral small vessel disease: Update and new concepts(2017) SHIBUYA, Mika; LEITE, Claudia da Costa; LUCATO, Leandro TavaresABSTRACT. In recent years, small vessel disease (SVD) has been recognized for its major impact on cognitive impairment in elderly people, where it is often difficult to separate its effects from those of neurodegenerative diseases individually. SVD is a systemic disease, probably related to diffuse endothelial dysfunction, which affects the perforating arterioles, capillaries and venules in the brain. Although often asymptomatic, it is responsible for almost half of all dementia cases and a significant proportion of stroke cases. Imaging features found on magnetic resonance include recent small subcortical infarctions, lacunes of presumed vascular origin, white matter hyperintensity of presumed vascular origin, prominent perivascular spaces and cerebral microbleeds. The recognition of these imaging findings as a spectrum of the same disease caused by endothelial dysfunction of small cerebral vessels can allow an overall analysis of the disease and thus the development of more effective preventive and therapeutic strategies.
- Reduced Diffusion in Neurocysticercosis: Circumstances of Appearance and Possible Natural History Implications(2013) SANTOS, G. T.; LEITE, C. C.; MACHADO, L. R.; MCKINNEY, A. M.; LUCATO, L. T.BACKGROUND AND PURPOSE: Few studies discuss DWI findings in patients with NCC, and their conclusions are variable and contradictory. The aim of our study was to describe DWI findings of a cohort of patients with NCC, emphasizing the frequency of reduced diffusion. MATERIALS AND METHODS: This retrospective study included 48 patients with NCC. Two neuroradiologists analyzed MR images regarding location, number, and stage of NCC lesions. On the basis of visual analysis, they defined, by consensus, the presence of high signal within NCC lesions on DWI and measured their ADC values when feasible. RESULTS: The total number of lesions was 342: parenchymal (263), subarachnoid (65), and intraventricular (14); 83 were DWI hyperintense. The first pattern was a small eccentric hyperintense dot/curvilinear structure on DWI (representing the scolex) noted in intraparenchymal lesions in vesicular (41 lesions, 29%) and colloidal vesicular (18 lesions, 19%) stages, in 14 (22%) subarachnoid lesions, and 2 (14%) intraventricular lesions; rADC calculations were hampered by the intrinsic small dimensions of this finding. The second pattern was the presence of total/subtotal DWI hyperintensity in intraparenchymal lesions, 5 in the colloidal vesicular stage (5%) and 1 in the granular nodular phase (3%). Two subarachnoid lesions also showed the same presentation; in this second pattern, reduced diffusion was present in different degrees, measured by rADC calculations. CONCLUSIONS: DWI may identify the scolex, increasing diagnostic confidence for NCC. Total/subtotal DWI hyperintensity, related to the stage of the lesion, though uncommon, allows including NCC as a consideration in the differential diagnosis of lesions with reduced diffusion and ring enhancement.
- Clinical and genetic characterization of leukoencephalopathies in adults(2017) LYNCH, David S.; PAIVA, Anderson Rodrigues Brandao de; ZHANG, Wei Jia; BUGIARDINI, Enrico; FREUA, Fernando; LUCATO, Leandro Tavares; MACEDO-SOUZA, Lucia Ines; LAKSHMANAN, Rahul; KINSELLA, Justin A.; MERWICK, Aine; ROSSOR, Alexander M.; BAJAJ, Nin; HERRON, Brian; MCMONAGLE, Paul; MORRISON, Patrick J.; HUGHES, Deborah; PITTMAN, Alan; LAURA, Matilde; REILLY, Mary M.; WARREN, Jason D.; MUMMERY, Catherine J.; SCHOTT, Jonathan M.; ADAMS, Matthew; FOX, Nick C.; MURPHY, Elaine; DAVAGNANAM, Indran; KOK, Fernando; CHATAWAY, Jeremy; HOULDEN, HenryLeukodystrophies and genetic leukoencephalopathies are a rare group of disorders leading to progressive degeneration of cerebral white matter. They are associated with a spectrum of clinical phenotypes dominated by dementia, psychiatric changes, movement disorders and upper motor neuron signs. Mutations in at least 60 genes can lead to leukoencephalopathy with often overlapping clinical and radiological presentations. For these reasons, patients with genetic leukoencephalopathies often endure a long diagnostic odyssey before receiving a definitive diagnosis or may receive no diagnosis at all. In this study, we used focused and whole exome sequencing to evaluate a cohort of undiagnosed adult patients referred to a specialist leukoencephalopathy service. In total, 100 patients were evaluated using focused exome sequencing of 6100 genes. We detected pathogenic or likely pathogenic variants in 26 cases. The most frequently mutated genes were NOTCH3, EIF2B5, AARS2 and CSF1R. We then carried out whole exome sequencing on the remaining negative cases including four family trios, but could not identify any further potentially disease-causing mutations, confirming the equivalence of focused and whole exome sequencing in the diagnosis of genetic leukoencephalopathies. Here we provide an overview of the clinical and genetic features of these disorders in adults.
- 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 deObjectives: 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).
conferenceObject ATYPICAL TERATOID RHABDOID TUMORS (ATRT): RESULTS FROM A SINGLE INSTITUTION IN BRAZIL - SAO PAULO UNIVERSITY(2022) BARRETO, Juliana Silveira; GOMEZ, Karen Nirit Melo; DUTRA, Alvaro Pimenta; AZAMBUJA, Alessandra Milani Prandini De; CRISTOFANI, Lilian Maria; SANDERS, Felipe Hada; PETITO, Carlo; BARALDI, Helena Espindola; WELTMAN, Eduardo; FERRACIOLLI, Suely Fazio; FRASSETTO, Fernando Pereira; LUCATO, Leandro Tavares; ROSEMBERG, Sergio; ODONE FILHO, Vicente- Drug-related demyelinating syndromes: understanding risk factors, pathophysiological mechanisms and magnetic resonance imaging findings(2021) RIMKUS, Carolina M.; SCHOEPS, Vinicius Andreoli; BOAVENTURA, Mateus; GODOY, Luis Filipe; APOSTOLOS-PEREIRA, Samira Luisa; CALICH, Ana Luisa; CALLEGARO, Dagoberto; LUCATO, Leandro Tavares; ROVIRA, Alex; SASTRE-GARRIGA, Jaume; LEITE, Claudia da CostaSome drugs and medications can precipitate immune system deregulations, which might be confused with recurrent demyelinating diseases, such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMO), exacerbations of an existing disease, neoplastic lesions or other conditions. In this narrative review we describe some of the most relevant drugs and medications associated with iatrogenic demyelination. The anthelminthic agent levamisole is a frequent cocaine adulterant and can precipitate an exacerbated immune response attacking the central nervous system (CNS). High-efficacy multiple sclerosis (MS) drugs might induce a selective CNS immunosuppression, making it susceptible for opportunistic infections that course with demye-lination, such as progressive multifocal leukoencephalopathy. Sometimes, the interruption of a high-efficacy drug to treat MS can induce a rapid CNS reentry of lymphocytes, exacerbating demyelinating processes and triggering rebound syndromes. Furthermore, selective cytokines inhibition, such as anti-TNF alpha agents, might induce an imbalance between cell death and proliferation inducing a paradoxical increase of CNS tumor necrosis factor (TNF), affecting the activity of lymphocytes, microglia and macrophages, triggering aberrant inflammation and demyelination. Immune checkpoint inhibitors are a new class of antineoplastic drugs that enhance the immune response against tumor cells by an upregulation of T-cell activity. However, this hyperactivation of the immune system might be associated with induction of unwanted autoimmune responses. In this paper we review the risk factors, the possible pathological mechanisms and the magnetic resonance imaging (MRI) findings of these drug-related demyelinating syndromes.
- Leukoencephalopathy resolution after atypical mycobacterial treatment: a case report(2015) OLIVEIRA, Marcos C. B.; SATO, Douglas Kazutoshi; SOARES-NETO, Herval R.; LUCATO, Leandro T.; CALLEGARO, Dagoberto; NITRINI, Ricardo; MEDEIROS, Raphael S. S.; MISU, Tatsuro; FUJIHARA, Kazuo; CASTRO, Luiz H.Background: Association of leukoencephalopathy and atypical mycobacteriosis has been rarely reported. We present a case that is relevant for its unusual presentation and because it may shed further light on the pathogenic mechanisms underlying reversible encephalopathies. Case report: We report the case of a Hispanic 64-year-old woman with cognitive decline and extensive leukoencephalopathy. Magnetic resonance imaging revealed white-matter lesions with increased water diffusivity, without blood-brain-barrier disruption. Brain biopsy showed tissue rarefaction with vacuolation, mild inflammation, few reactive astrocytes and decreased aquaporin water-channel expression in the lesions. Six months later, she was diagnosed with atypical mycobacterial pulmonary infection. Brain lesions resolved after antimycobacterial treatment. Conclusion: We hypothesize leukoencephalopathic changes and vasogenic edema were associated with decreased aquaporin expression. Further studies should clarify if reversible leukoencephalopathy has a causal relationship with decreased aquaporin expression and atypical mycobacterial infection, and mechanisms underlying leukoencephalopathy resolution after antimycobacterial treatment. This article may contribute to the understanding of pathogenic mechanisms underlying magnetic resonance imaging subcortical lesions and edema, which remain incompletely understood.
conferenceObject Clinical Course of LETM Associated with Neuroschistosomiasis(2013) APOSTOLOS-PEREIRA, Samira; MARCHIORI, Paulo; MACHADO, Luis; LIVRAMENTO, Jose; GOMES, Helio; LUCATO, Leandro; CALLEGARO, Dagoberto