High-Frequency Oscillation and Recovery Functions of Somatosensory Evoked Potentials in Human T-Cell Lymphotropic Virus Type 1–Associated Myelopathy

Objectives: Human T-cell lymphotropic virus type 1–associated myelopathy (HAM) involves not only spinal cord but also the cerebral cortex and the white matter in histopathological analysis. In addition, a previous study found that T2 hyperintensities on brain magnetic resonance imaging (MRI) in HAM patients were increased only in white matter. However, conventional neurophysiological examination of somatosensory pathway did not identify any abnormalities in the cerebral cortex or white matter. We evaluated the inhibitory function of the cerebral sensory cortex in HAM patients by analyzing high-frequency oscillations (HFOs) and somatosensory evoked potential recovery functions (SEP-Rs). Method: Eight HAM patients were enrolled in the present investigation. Twenty age-matched healthy subjects were enrolled (10 for HFOs, 10 for SEP-Rs). SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. HFOs were obtained by digitally filtering raw SEPs from 500 to 1000 Hz. We measured amplitudes of the N20 onset-peak (N20o-p), N20 peak-P25 peak (N20p-P25p), P25 peak-N33 peak (P25p-N33p), and the early (1st-2nd) and late (3rd-4th) HFOs. For recovery function study, paired-pulse stimuli at various interstimulus intervals (ISI; 20 200 ms) were given. Results: None of the SEP components, and neither early nor late HFOs, showed any significant differences between HAM patients and normal controls. In recovery function study, there were no significant differences in any of the components between the two groups, although the HAM group had a tendency to disinhibit in the recovery curve for N20o-p amplitudes (P=0.075). Conclusions: Normal early and late HFOs indicate that both basal ganglia and GABAergic inhibitory interneuron activity in the cortex are intact in HAM patients. The recovery function findings might indicate mild impairment of subcortical white matter in HAM patients because disinhibition of N20o-p and normal inhibition of the N20p-P25p pattern were previously observed in Binswanger’s disease. Our conclusions are: (1) HAM patients may demonstrate mild subcortical dysfunction as previously found on MRI. (2) Sensory cortical function is normal in HAM patients.