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Middle latency and late components of event-related brain potential (ERPs) are closely related to perceptual and cognitive information processing, respectively. In a double-blind, placebo-controlled study, the acute effects of lorazepam (2 mg), haloperidol (3 mg), methylphenidate (20 mg) and citalopram (20 mg) on ERP latencies, amplitudes, topographies and tomographies were investigated in 20 healthy subjects of 23-34 years of age. After automatic artifact minimization and rejection, standard N1 and P2 and target N2 and P300 components were determined. The tranquilizer lorazepam prolonged P300 latency, which indicates an impairment of stimulus evaluation time. Low-resolution brain electromagnetic tomography (LORETA) revealed decreases in N1 and P300 source strength in those brain regions with relevant generators of these components, which reflects impairments of attentional and cognitive processing resources. The neuroleptic haloperidol decreased N1 and P300 source strength predominantly in those brain regions not involved in the generation of these components, suggesting a shift of resources. The psychostimulant methylphenidate increased P300 source strength in brain regions with major P3b generators, indicating increases in energetic resources associated with stimulus encoding. The antidepressant citalopram increased N1 and P3b source strength in multiple brain regions specifically in the left prefrontal cortex, a brain region in which reduced blood flow and metabolism was found in depressed patients.

In a double-blind, placebo-controlled, cross-over study, acute effects of suriclone--a cyclopyrrolone derivative--were investigated by means of topographic mapping of event-related potentials (ERPs). Fifteen normal volunteers, aged 22-35 years, received randomized, oral single doses of placebo, 0.1 mg, 0.2 mg and 0.4 mg suriclone and 1 mg alprazolam as a reference compound. ERPs were investigated in an auditory oddball paradigm before and 3 h after intake of each drug. In addition to 17 EEG leads, vertical and horizontal electro-oculograms (EOGs) were recorded. After EOG minimization and artifact identification, the peak latencies of the spatial average were determined by an automatic procedure. Compared to placebo, no significant effects of the low and middle doses of suriclone on N1 amplitude were observed; the highest dosage reduced N1 amplitude, as did 1 mg alprazolam to an even greater extent. While no consistent effects on P2 amplitude were observed after suriclone, alprazolam reduced P2 amplitude. P300 amplitude was reduced only after the highest dosage of suriclone, but much more so after alprazolam. P300 latency was not affected significantly by suriclone, but a marked prolongation of P300 latency was observed after 1 mg alprazolam. Concerning N1 and P2 effects, alprazolam, but not suriclone, may have an inhibitory influence on stimulus-induced cortical arousal. Concerning P300 effects, the used doses of suriclone were superior to 1 mg alprazolam, which seemed to have reduced cognitive information processing capacity and prolonged stimulus evaluation time. Self-rated well-being (adjective checklist) showed subtle beneficial effects after 0.1 mg and 0.2 mg, but marked sedative effects after both 0.4 mg suriclone and 1 mg alprazolam.

Venlafaxine is a novel non-tricyclic antidepressant, which preclinically has demonstrated serotonin, norepinephrine, and dopamine reuptake inhibiting effects. In this study acute effects of single oral doses of placebo, 12.5 mg, 25 mg, and 50 mg venlafaxine on event-related potentials (ERPs), eye blink rate and mood were studied in 16 healthy subjects. ERPs were investigated in an auditory odd-ball paradigm before as well as 3 h after each drug intake. In addition to 17 EEG leads, vertical and horizontal EOGs were recorded. After EOG minimization and visual artefact rejection the peak latencies of the spatial average were determined by an automatic procedure. The applied methods of data acquisition, artefact processing, objective component determination and statistical analysis were successful in describing acute effects of venlafaxine on ERPs in normals. N1 and P2 latencies were not affected. An increase in P2 amplitude in the relevant central and frontal regions was seen, reflecting some effect on automatic information processing. Stimulus evaluation time was not affected, as P300 latency remained unchanged. P300 amplitude was not affected at the relevant central and parietal region. Blink rate was not changed. By means of the adjective checklist a dose-dependent decrease of "extroversion" and "high spirits" and an increase of "introversion" was observed. Our findings suggest that venlafaxine affects human information processing less than would be expected from the more centrally inhibiting classical antidepressants.

Amantadine is generally used in the prophylaxis of infection with influenza A, in the treatment of Parkinson's disease and in the treatment of neuroleptic side effects. In this study acute effects of amantadine infusions on event-related potentials (ERP) were studied in 20 mildly demented patients diagnosed according to DSM-III-R criteria. Each patient was treated, in randomized order, with 0.2 g amantadine-sulfate in 500 ml NaCl and 500 ml NaCl placebo, i.v. over one hour with an interval of two weeks in-between. ERPs were investigated in an auditory odd-ball paradigm before as well as 5 hours after the infusion. In addition to 17 EEG records, vertical and horizontal EOGs were recorded. After EOG-minimization and visual artifact rejection the peak latencies of the spatial average were determined by an automatic procedure. There was no effect of amantadine on ERP latencies. N1 of the non-target showed a trend towards amplitude augmentation, P2 amplitude was reduced. As compared to placebo, P300 amplitude of targets was significantly augmented by 3.1 microV (30% of pre-treatment value), confirming the hypothesis that amantadine may influence the P 300 amplitude in the sense of an improved availability of cognitive processing resources.

In a double-blind placebo-controlled study, the effects of Actovegin on cognitive event-related potentials were studied in 18 age-associated memory impairment (AAMI) patients. Actovegin is a protein-free metabolically active hemoderivative improving oxygen and glucose utilization. Each patient was treated, in randomized order, for 2 weeks with 250 ml 20% Actovegin and 250 ml placebo daily with an interval of 3 weeks in between. Psychophysiological tests were carried out by means of the Viennese Psychophysiological Test System (VPTS) before as well as 5 h after the administration of one single infusion on day 1 (acute effect), before (subacute effect) as well as after one additional superimposed infusion on day 15 (superimposed effect). There was no effect on earlier stages of information processing measured by N1 and P2 component of nontarget ERP nor on ERP latencies. However, P300 amplitude increased after acute, subacute as well as superimposed infusion of Actovegin as compared to placebo, confirming the hypothesis that nootropic drugs may influence the P300 amplitude in the sense of an improved availability of cognitive processing resources. This increase of P300 amplitude (up to 4.8 microV), seen specifically in central and parietal regions, proved to be significant in a confirmatory test.