Potencial evocado miogênico vestibular por estimulação galvânica e potenciais evocados auditivos de longa latência na mielopatia associada ao HTLV-1

Abstract

Introduction: Human T-cell lymphotropic virus type 1 (HTLV-1) causes inflammatory damage in the spinal cord and brain. The aims of this study were to evaluate the spinal cord motor function using vestibular evoked myogenic potential with galvanic stimulation (GVEMP) and to evaluate the cognition using neuropsychological tests and long latency auditory evoked potentials (P300, N200, P160 and N100) in individuals infected with HTLV- 1 in different phases of progression of HTLV-1-associated myelopathy/ tropical spastic paraparesis (HAM/TSP). Methods: We conducted a cross-sectional and comparative study. The postural evaluation was performed in 122 subjects, 45 not-infected (control) and 77 infected with HTLV-1: 26 asymptomatic, 26 with possible HAM/TSP and 25 with HAM/TSP, according to neurological evaluation. VEMP was generated by 2mA/400ms binaural galvanic vestibular stimulation (GVS). The G-VEMP was recorded from gastrocnemius muscles. The G-VEMP studied parameters were the short-latency (SL) and the medium-latency (ML) components of the VEMP wave. The cognition was evaluated in 113subjects, 40 controls and 73 infected with HTLV-1 (27 asymptomatic, 26 with possible HAM/TSP and 20 with HAM/TSP). The variables of interest were the scores of neuropsychological tests, latency and amplitude of long latency auditory evoked potentials. Results: The groups were similar in gender, age, height, and education. Abaout G-VEMP, the components SL and ML were delayed in HTLV-1 groups compared to controls (p<0.001). Based on neurological examination as the gold standard, ROC curve showed area under the curve of 0.83 (p<0.001) for SL and 0.86 (p<0.001) for ML to detect of spinal cord injury. Sensibility and specificity were, respectively, 76% and 86% for SL and 79% and 85% forML. G-VEMP showed progressive vestibulospinal deficit related to HTLV-1-neurological disease, ranging from SL delayed latency in the asymptomatic carriers, SL and ML delayed latency in the possible-HAM/TSP group to absence of EMG wave in the HAM/TSP group.Regarding cognition, the groups did not differ in processing speed, general intelligence (p>0.05). Compared to controls, possible HAM/TSP and HAM/TSP groups presented a worse performance to execute the Rey Auditory Verbal Learning Test (RAVLT), attesting a worse verbal memory (p<0.001). HTLV-1-asymptomatic carrier, possible HAM/TSP and HAM/TSP groups presented a worse performance to execute Nine Hole Peg Test (NINE HOLE), attesting worse motor skills and attention (p<0.001). HTLV-1-asymptomatic carrier, possible HAM/TSP and HAM/TSP groups presented delay in P300 latency (p<0.001) and onlyHAM/TSP group delayed N200 latency (p<0.001). RAVL worse performance correlated with delay in N200 and P300 latency; longer time to execute NINE HOLE correlated with delay in P300 and N200 latencies. The study showed cognitive impairment of HTLV-1-seropositiveindividuals in different phases of neurologic disease characterized by deficits in verbal memory, learning, attention, auditory discrimination, and motor skills. P300 and NINE HOLE identified subclinical alterations related to cortical function in HTLV-1-infected individuals with HAM/TSP and also with apparently asymptomatic infection. Conclusion: The G-VEMP and P300 identified subclinical alterations related respectively tomedullar and cortical function in individuals infected with HTLV -1 that were considered to be asymptomatic. Possibly, these individuals have a higher risk of developing HAM/TSP as compared to HTLV-1-infected individuals with normal neurocognitive and electrophysiological assessment.