A simple experiment is to record the EEG during active waking with eyes closed: as the eyes open, dramatic changes in the EEG patterns occur (called "alphablock"). More interactive recordings are beyond the scope of the present contribution, but can be found under ► event related potentials, which are the responses to specific stimuli, often sounds, recorded in the same manner as the EEG.
Life-style and habits also affect the EEG and must be taken into consideration. For example, long lasting changes are present in the EEG of cigarette smokers, particularly over parietal scalp regions (see Domino 2003 and ► Nicotine Dependence and its Treatment for relevant papers). Furthermore, consumption of ► caffeine and ► alcohol perturb the EEG (Gevins et al. 2002) and can bias study results. Gender, age, and mental health also affect the EEG and must be taken into consideration during the evaluation of drug effects in both healthy subjects and patient populations. When eliminating most of these confounding factors, the stability of spectrograms over time is satisfactory for the empirical detection of drug effects. EEG characteristics are strongly hereditary and as a consequence, intra-subject variability is low compared to inter-subject variability. Therefore, a crossover design where the same individual receives both the drug and a placebo treatment is recommended whenever possible; this also controls better for systematic fluctuations unrelated to the actual drug (see ► Randomized Controlled Trials).
The top panels in Fig. 6 illustrate time course of EEG-effects induced by two doses of a benzodiazepine, ► lor-azepam, and matching placebo. qEEG activity for beta-1 increased transiently followed by sustained elevations throughout the experimental day; alpha-1 was diminished
Electroencephalography. Fig. 6. Group data as part of a large project of qEEG for ten healthy volunteers, 1 or 2 mg doses. (a) Line-graphs (mean ±S.E.) for repeated measures of posterior alpha-1 EEG and the effects of two escalating (nontherapeutic) doses of lorazepam, a benzodiazepine drug having clearcut decreases for both treatments lasting about 4-5 h, with dose-dependency specially around 2 h postdose. Note the stability over time under placebo conditions. (b) same as in (a) but for frontal beta-1 EEG. (c) self rated alertness issued from VAS analog scales around the moment of significant EEG effects; only the 2 mg dose yielded a significance on the items interpreted as hypovigilance. (d) judgment of strength in drug effect (part of a separate project on metamemory) for the same two doses of lorazepam (adapted from Mintzer MZ, Griffiths RR (2005) Drugs, memory, and metamemory: a dose-effect study with lorazepam and scopolamine. Exp Clin Psychopharmacol 13:336-347).
for both doses from the first hour onwards, lasting >4 h, with a hint for dose dependency (see e.g., the 2 h). Comparative neuropharmacology of ► function of slow and fast alpha, issued from our unpublished multielectrode mapping of significant clonazepam modifications compared to placebo (Fig. 7 middle column, top p-values), or as single valued placebo-adjusted metric placebo (middle column, bottom). The decreased values cover almost the whole scalp. At the right, a similar statistical procedure shown increases for a single dose of donepezil which is more limited to the posterior scalp. Effects on other frequency bands are shown for the muscarinic acetylcholine receptor antagonist scopolamine (see ► Muscarinic Agonists and Antagonists). Scopolamine decreases slow and fast alpha (Fig. 8, top row) and has differential effects on e.g., the delta amplitude, which reaches enhanced levels in large precentral scalp regions (Fig. 8, bottom row). The decreasing alpha frequencies together with the increase in delta waves (► function of delta waves) show an increased sleep propensity, and are interpreted at the functional level as sedative "signature." Interestingly, ► benzodiazepine agonists (see also ► Benzodiazepines), anticholinergics, and first generation antihistamines (e.g., diphenhydramine, see ► Histaminic Agonists and Antagonists) yield similar EEG "signatures" and are all sedative. This suggests that their mechanisms of action converge onto similar vigilance-controlling substrates in the brain, despite the fact that their primary targets are different. A similar overlap has been found for drugs that cause increases in the beta frequency band: benzodiazepine anxiolytics, ► antidepressants, and ► barbiturates have similarities in their "signatures," most probably linked to GABAa receptor modulation. Such findings illustrate our increased understanding obtained by combining psychopharmacology and qEEG studies.
Electroencephalography. Fig. 7. Left column: descriptive qEEG topography for the alpha frequency band for a single subject without drug (bottom image with isocontours every 25p,V) and on clonazepam (top row, left panel). The crossover design allows subtraction (bottom, middle image) of EEG variables; finally inferential nonparametric testing of differences (mapping for groups) confirms drug-induced significant decreases. Topographic maps are constructed by interpolation for the values on 19 standard electrode positions+Oz and eight intermediate leads for active treatment. Example at the right mapping for a member of the class of acetylcholine esterase inhibitors, donepezil; a similar statistical procedure demonstrate that alpha frequency band increases in healthy volunteers (adapted from Boeijinga PH, Calvi-Gries F, Demazieres A, Luthringer R (2002) Planning of pharmacodynamic trials: specificities and possible solutions and interpretation of drug effects on EEG. Methods Find Exp Clin Pharmacol 24(suppl C):17-26).
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