Alterações neurocognitivas em pacientes com mielopatia associada ao HTLV-1/Paraparesia Espástica tropical: doença primária ou secundária a outros fatores associados?
| Ano de defesa: | 2015 |
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| Autor(a) principal: | |
| Orientador(a): | |
| Banca de defesa: | |
| Tipo de documento: | Tese |
| Tipo de acesso: | Acesso aberto |
| Idioma: | por |
| Instituição de defesa: |
Universidade Federal de Minas Gerais
UFMG |
| Programa de Pós-Graduação: |
Não Informado pela instituição
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| Departamento: |
Não Informado pela instituição
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| País: |
Não Informado pela instituição
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| Palavras-chave em Português: | |
| Link de acesso: | http://hdl.handle.net/1843/BUBD-A2MGWP |
Resumo: | The HTLV (Human T cell lymphotropic virus) type 1 does not necessarily cause a pathological process in their carriers. Different factors between the virus and the patient will determine the disease if as an inflammatory or hematologic manifestation. While myelopathy associated with HTLV-1 (HAM/TSP) is the most common and wellknown neurological manifestation, few studies have examined the possibility of cognitive disorders in HTLV-1. Apparently, there are white matter lesions similar to HIV-infected patients, suggesting chronic perivascular involvement. The histological characteristic finding is a perivascular lymphocytic infiltrate in the central nervous system, suggesting vasculitis. The pathogenesis of HAM/TSP is not yet fully understood. The current understanding is that the infected T lymphocytes migrate to the central nervous system, interect with CD8 + T cells resulting in the production of cytokines such as TNF-, IL- 1 , IL-2 and IL-6 with consequent destruction of glial cells, fibroblast proliferation and lipohialinose of small arteries and veins. Understanding the diseases impact on cognition and immune disorders in central nervous system may help to determine the prognostic factors for the development of neurological damage associated with HTLV-1, and provides subsidies for future treatments that are not yet established. In endemic areas for HTLV-1, the differential diagnosis with other causes of myelopathy can be difficult, particularly if the patient has signs and symptoms of brain involvement, as seropositive for HTLV-1 can be detected in patients with other neurological diseases. In this study, we report a case of a patient diagnosed with Multiple Sclerosis and upon further investigation, was found to be HTLV-1 seropositive. We performed a cross-sectional study with 114 patients with HAM/TSP who underwent a comprehensive neuropsychological assessment through cognitive function tests (Mattis Dementia Rating Scale, Span of digits forward and backward, Trail Making Test A and B, Stroop Test, Verbal fluency tests included semantic and phonemic fluency, Auditory Learning Test Rey). We investigated the association between lowered cognitive function and clinical, epidemiological and sociodemographic, immunological, viral factors and findings on magnetic resonance imaging of the brain. Patients were stratified into three age groups and three education groups and neuropsychological tests were standardized so that was given a mean of zero and a standard deviation of 1 and 1,35 (z-scores). Participants with lower score less than or equal to 1 for your stratum of age and education were considered with lowered cognitive function. The chi-square (X2) and the t test were used for univariate analysis to association between variables. All independent variables with a significance level of 0.80 (p <0.20) were tested for the logistic regression and the level of statistical significance was set at p <0.05. We found 15 patients (13.1%) has lowered cognition function. In univariate and multivariate analysis, inflammatory factors - high levels of IgA, IgG, IL-6 and TNF- - lifestyle - tobacco - severity of the disease - use of wheelchair - and presence of brain white matter lesions and brain atrophy were associated with poor cognition. The results suggest that lowered cognitive function in patients with HAM / TSP appears to have a multifactorial association with persistent inflammation, disease severity, lifestyle and a real brain injury. There is also a possibility that disability is a factor by it self for poor cognition in these patients. Subpopulations of patients with HAM / TSP and these characteristics should receive special attention from a multidisciplinary professionals for investigation of cognitive function. In conclusion, we suggest that the brain lesions in HTLV- I infection may be secondary a worse severity of disease associated with persistent inflammation, which may hinder worse cognitive performance in the course of developing of the myelophaty |