Are the amplitudes of visual evoked potentials sensitive indices of hangover effects after repeated doses of benzodiazepines?

Abstract

Here we compared the efficacy of two electrophysiological techniques in detecting hangover effects after repeated administration (five days) of benzodiazepines. Twelve hours after the last ingestion, possible effects on evoked potentials (EPs) of the long- and short-acting benzodiazepines, flurazepam and lormetazepam, were compared here with those of placebo under a double-blind experimental condition. The EPs were recorded from occipital and parietal sites during an active discrimination of two amoeboid shapes and passive viewing of sine-wave grating patterns turned on and off. In the former task, the subject was requested to make a selective response with respect to whether the two shapes appeared the same or different and his reaction times were simultaneously recorded. Neither benzodiazepine influenced the latencies of any of the sensory and late EP components. Flurazepam's long-acting metabolite, N-desalkylflurazepam, reduced the amplitudes of all the EP components suggesting a somewhat general mode of action. This was not the case for lormetazepam. N-desalkylflurazepam reduced the amplitudes of the occipital visual evoked potentials (VEPs) to sine-wave gratings to a greater extent than the amplitudes of the late parietal EPs to amoeboid shapes. This effect did not show any particular preference for either of the subsystems processing pattern and movement information. The amplitudes of the late EP components, such as N200 and P300 waves recorded from parietal sites, were reduced considerably more after flurazepam administration than their counterparts recorded from the occiput. This observation points to the possible existence of at least two separate sources of the N200-P300 complex with different affinities to the N-desalkylflurazepam. The flurazepam-induced amplitude reduction observed for VEPs to gratings may reflect an attenuation in the detectability of both pattern and movement. The attenuation of the late EP amplitudes is possibly a function of several processes, one of which is conceivably the anxiolytic property of flurazepam which lowers the level of the activation state and this in turn is known to contribute to the amplitude size of the N200-P300 complex.