Visual evoked potentials to flash and pattern reversal stimulation after administration of systemic or topical scopolamine

Abstract

It has previously been shown that 0.6 mg of scopolamine produces a delay in the flash visual evoked potential of young normal volunteers, while the pattern-reversal response does not change in latency. Recent work has shown that this drug differentially affects parvocellular and magnocellular systems. To investigate this effect, two studies were performed. In the first study, 0.4 mg of scopolamine was injected intramuscularly into 11 young, healthy male volunteers who had fasted overnight. The visual evoked potential was recorded to both binocular flash stimulation and monocular pattern-reversal stimulation by means of a checker-board consisting of 56' checks in a 28 degrees field. Responses were recorded before administration of the drug and then 1, 2, 4 and 6 hours after administration. The scopolamine produced a slowing of the flash P2 latency of approximately 6 ms (p < 0.05) two hours after drug administration. There was no effect on the latency of the flash N2 or pattern-reversal N75 or P100. There was an increase in amplitude of the flash N2-P2 component 6 hours after drug administration and an increase in the amplitude of the N75 and P100 2, 4 and 6 hours after the drug. Further subjects were investigated with the use of topical administration of 0.125% scopolamine applied monocularly. In all studies the other eye acted as a control. The subjects were again young healthy volunteers. The visual evoked potential was recorded to both flash and pattern-reversal stimulation with a checkerboard consisting of 60' checks counterphasing at 2 Hz within a 5 degrees field. Results suggest that systemic scopolamine affects the tectal pathway but has no peripheral effect.

Effects of flash mode and intensity on P2 component latency and amplitude

“…Patient groups whose dementia stems from etiologies other than AD generally do not show the selective P2 delay (Coburn et al, , 1993bDaniels et al, 1994). However, among AD patients, the delay increases over time in parallel with the severity of dementia symptoms Orwin et al, 1986;Parks et al, 1991), and among healthy participants, it can be produced de novo by cholinergic suppression (Bajalan et al, 1986;Harding et al, 1994;see Coburn et al, 1993a for additional examples). More importantly, the selective P2 delay has been reported to be pathognomonic for AD and several authors (Moore et al, 1995;Wright et al, 1984) have called for its evaluation as a diagnostic tool.…”

The Value of Quantitative Electroencephalography in Clinical Psychiatry: A Report by the Committee on Research of the American Neuropsychiatric Association

“…[160][161][162] However, among Alzheimer's disease patients the delay increases over time in parallel with the severity of dementia symptoms, 163,164,165 and among healthy subjects it can be produced de novo by cholinergic suppression. 162,166,167 (See Coburn et al 73 for additional examples). More importantly, the selective P2 delay has been reported to be pathognomonic for Alzheimer's disease and several authors 152,168 have called for its evaluation as a diagnostic tool.…”

The Virtual Tray of Objects Task as a novel method to electrophysiologically measure visuo-spatial recognition memory

“…However, there is also evidence that P100 deflections are sensitive to visual priming and to repetition effects i.e., a decrease in the perceptual response due to habituation to the stimulus (Huber et al, 2008). Interestingly, in humans, the administration of agonists or antagonists of cholinergic transmission in the brain has been shown to affect the latency and/or amplitude of visually evoked P100 components (Harding et al, 1994;Ray et al, 1991;Sitaram and Gillin, 1980). Moreover, in the rat, early potentials elicited during performance in object recognition tasks are linked to theta activity and their amplitude has been shown to be sensitive to the manipulation of cholinergic transmission in the brain (Sambeth et al, 2007).…”