Smoking-Induced Alterations in Brain Electrical Profiles: Normalization or Enhancement ?

Acute quantitative electroencephalographic effects of cigarette smoking were examined in 15 smokers within a repeated-measures design which assessed changes in power-spectral estimates following acute pre-treatment with placebo, a dose (20 mg) of mecamylamine, a dose (0.6 mg) of scopolamine and a combined dose of mecamylamine and scopolamine. Compared to sham smoking, the smoking of a single cigarette following placebo pre-treatment reduced absolute and relative power in slow (delta, theta) frequency bands, increased absolute and relative power in alpha and beta frequency bands and accelerated mean frequency. These smoking-induced power changes in slow- and fast-frequency bands were differentially affected by the separate and combined actions of the cholinergic antagonists with treatments involving mecamylamine tending to abolish smoking-induced slow-frequency absolute power reductions and fast-frequency relative power increments. Self-ratings of smoking-induced increases in alertness were altered by mecamylamine and combined treatments while sensory aspects of cigarette smoking were only altered with combined mecamylamine and scopolamine pre-treatment. The results are discussed with respect to brain-behaviour relationships and mechanisms maintaining the smoking habit.

Section: Discussionmentioning

confidence: 99%

The Cholinergic Basis of the Smoking-Induced EEG Activation Profile

Knott¹,

Harr²,

Ilivitsky³

et al. 1998

“…A relatively recent study suggests that the EEG blocking ability seen with acute haloperidol may exhibit tolerance, as the smoking-induced EEG activation profile was fully apparent in schizophrenic patients chronically treated with D 2 dopamine receptor antagonists [52]. Given the as yet unresolved debate as to whether the smoking-induced EEG response reflects a normalization or an absolute enhancement of cerebral arousal levels [53], these transmitter blockade studies may yield clearer results if they are pursued in non-smokers administered nicotine by routes other than smoke inhalation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Haloperidol Pretreatment on the Smoking-Induced EEG/Mood Activation Response Profile

Walker

Mahoney²,

Ilivitsky³

et al. 2001

This study examined the role of dopamine in modulating the CNS response to cigarette smoking. In a randomized, double-blind, repeated-measures design, quantitative electroencephalographic (EEG) changes and self-reports induced by the smoking of a single cigarette were assessed in 16 smokers following pretreatment with placebo and a dopamine antagonist, haloperidol (2 mg). Following placebo pretreatment, absolute (µV) and relative (%) amplitudes in slow-frequency bands (δ, Θ, α₁) were reduced and absolute and relative amplitudes in fast-frequency bands (α₂, β) were increased following cigarette smoking as compared to sham smoking. Haloperidol pretreatment inhibited the smoking-induced increase in absolute β frequency. Self-ratings indicated that cigarette smoking induced increases in alertness, contentedness and calmness but not euphoria, and reduced cigarette cravings as compared to the sham smoking conditions. Smoking-induced, α₂ increments were associated with increases in alertness and decreases in euphoria while β increments were associated with increased calmness. Smoking-related self-ratings of mood and cigarette acceptability were not altered by haloperidol, but subjects were less content overall in the haloperidol condition as compared to placebo. Discussion of these results focuses on transmitter systems and their relationship to neuro-electric and behavioural activities associated with the smoking habit.

“…Given the acute smoking effects on relative power and mean frequency indices together with the beta frequency differences existing be tween smokers and nonsmokers, study designs must make decisions as to whether to include smokers in subject sam ples and, when including smokers, they must make proce dural decisions with regard to smoking and smoking abstinence prior to EEG recording sessions. If, as recent evidence suggests, both acute smoking and smoking absti nence alter EEG characteristics of smokers relative to nonsmokers [67], future studies should, at a minimum, document the proportion of smokers and nonsmokers and their prerecording smoking state as routine sample de scriptors.…”

Section: Discussionmentioning

confidence: 99%

Assessing the Topographic EEG Changes Associated with Aging and Acute/Long-Term Effects of Smoking

Knott¹,

Harr²

1996

As neuroelectric research into the smoking/nicotine habit has focused exclusively on young and middle-aged adults, this electroencephalographic (EEG) study was conducted to determine whether a long-term smoking history alters the aging brain and/or whether the aging brain demonstrates an altered sensitivity to acute smoking/nicotine. Forty healthy adults, 20 young, aged 18-39 years, and 20 elderly, aged 64–81 years, volunteered for participation. Half of the young and elderly were nonsmokers with no previous smoking history and the remaining half of the young and elderly were current smokers with average smoking histories of 9.3 and 52.0 years, respectively. Smokers attended the laboratory for two randomized test sessions during which multisite EEG recordings were collected pre and post sham and cigarette smoking. Nonsmokers attended the laboratory for one nonsmoking EEG recording session. Spectral power indices showed aging to be associated with significant reductions in absolute delta and theta power and increases in relative beta power and faster mean total band frequency. Aging effects varied with recording region but not with smoker versus nonsmoker status. Smokers did exhibit a faster mean beta frequency. Acute cigarette smoking decreased absolute delta power in young smokers and increased relative alpha2, beta power and mean alpha frequency in both young and elderly smokers. Only the young smokers showed increase in mean theta and total frequency. The results are discussed in relation to cognition in normal and pathological aging.