Brainstem Auditory and Somatosensory Evoked Potential Study in Amphetamine Abusers

Abstract

Amphetamine is a potent sympathomimetic amine and has a strong stimulatory effect on the central nervous system (CNS). The CNS effects of amphetamine may include neuronal degeneration, axonal degeneration, disruptive effect on polyribosomes and neuronal protein synthesis, altered gene transcription (affect mRNA amounts), and alternations in several proteins (posttranscriptional effects) to induce tolerance. Only a few studies of evoked potentials of amphetamine abusers have been conducted. We developed a multimodal potential study of amphetamine abusers to evaluate the amphetamine effects on the human CNS. Nineteen amphetamine abusers were studied. They all had urine tests positive for amphetamine use within the previous 5 days. Seventeen healthy volunteers, adjusted for age and sex, were recruited for the control group. Brainstem auditory evoked potentials (BAEPs) and somatosensory evoked potentials (SEPs) from the median and the tibial nerves were obtained from these amphetamine abusers and healthy volunteers. The BAEPs of amphetamine abusers showed significantly prolonged peak latencies of waves I, III and V on the right side as well as wave III on the left side (p＜0.05). Interpeak latency (IPL) of I-III on the left side was also significantly prolonged (p ＜0.05). The median nerve SEPs study revealed a significant latency prolongation of bilateral waves N10, N13 and N20 (p＜0.05), but no significant prolongation in central conduction time (IPL). In the tibial nerve SEPs, the prolongation of conduction was demonstrated in bilateral waves N22 and P40 (p＜0.05). However, the central conduction time was not significantly prolonged as compared with healthy volunteers. This study reveals that amphetamine abuse had a significant effect on the peripheral nervous system (PNS), but only a small electrophysiological effect on the CNS (just one prolongation of central conduction time of BAEPs in amphetamine abusers). These strong electrophysiological PNS effects and very weak CNS effects of amphetamines may be due to the tolerance effect, timing of axonal degeneration, or racemic amphetamine isomers (the levo-isomer and the dextro-isomer) used. Other explanations such as the quantity of the amount of amphetamine inhaled may not be substantial, as well as the late recording of evoked potential.