Akademik Veri Yönetim Sistemi
INTERNATIONAL JOURNAL OF NEUROSCIENCE, cilt.114, sa.3, ss.381-390, 2004 (SCI-Expanded)
Several previous studies have reported that cigarette smoking enhances performance of cognitive processing. These enhancements are generally attributed to the pharmacological effects of nicotine, while there is some debate whether the effects of smoking/nicotine are a result of recovery from abstinence. Evoked potentials (EPs) and event related potentials (ERPs) of the brain have been applied as an index of information processing in a wide variety of normal and cognitive impaired subjects. This study, was carried out on 20 health students (23 +/- 2.3 years old) from the medical faculty of 007 University. Study population. comprised ten chronic cigarette smokers consuming an average of 14 +/- 4.2 cigarettes per day, with a history of smoking for more than one year. Ten non-smokers served as control. Standard oddball paradigm was presented, and EEG activity was recorded at the F-z, C-z, P-z electrode sites. Twenty responses to target stimuli were averaged at each location. N1, P2, N2, and P300 components were evaluated in these recordings. Amplitudes were measured relative to prestimulus baseline, and peak latencies were defined as the time point of maximum amplitude. It was found that there were no significant differences between either N1, P2, N2, P300 amplitudes or peak latency values of cigarette smokers and non smokers. As a result, chronic cigarette smoking generally does not improve cognitive processing.