Effect of the Heaviness of Smoking Index (HSI) and Duration of Smoking on Central Neural Processing Using Brainstem Auditory Evoked Responses (BAERs).

Abstract

Purpose of study The goal of this research was to find the correlation of nicotine dependence and duration of smoking with the status of central neuronal processing in chronic smokers. Our primary objective was to record brainstem auditory evoked responses (BAERs) in chronic smokers and further find their correlation to the Heaviness of Smoking Index (HSI) scores and years of non-abstained smoking of the subjects. We postulated that smoking leads to myelination abnormalities which in turn causes decreased impulse conduction velocity. Methods After obtaining informed consent, we conducted BAER on 60 male smokers who were further classified into groups based on their HSI scores (low, moderate, and high nicotine dependency) and 20 age-matched, non-smoking males. The obtained data was examined using the two-way ANOVA test and the Kruskal-Wallis test. Pearson's coefficient of correlationand the median (as a measure of central tendency) were calculated. Results We observed a non-significant negative correlation between wave I BAER latency and the degree of nicotine dependence. Wave II showed minimal correlation, whereas a positive correlation was seen in waves III, IV, and V. Interpeak latencies (IPL) I-III and III-V showed a non-significant positive correlation with the HSI score, whereas IPL I-V showed a significant positive correlation with the same. When correlated with the duration of smoking (years), the latencies (msec) of BAER waves I-V showed a pattern of progressively decreasing negative correlation, out of which waves I, II, and III were significantly affected. The IPL (msec) of waves I-III was non-significantly, yet positively, correlated, while the IPL of waves I-V and III-V showed a significant positive correlation to the duration of smoking. Conclusions The degree of nicotine dependence and duration of tobacco smoking progressively affected the latencies of BAER waves at the pontomedullary level of the brainstem. This indicates slower central neuronal processing at this level and an increased central transmission time, the extent of which is directly dependent on the extent of tobacco smoking. This is attributed to the myelination defects caused by direct and indirect effects of the toxic metabolites of tobacco smoke, chronic hypoxia, hypercapnia, and respiratory acidosis.