Aging, Smoking and Hemispheric EEG Asymmetry

Abstract

As previous research has shown central nicotinic receptors to (a) be asymmetrical, (b) decline with age, and (c) be more abundant in smokers, quantified EEG indices of hemispheric asymmetry were employed to assess whether smoker/non-smoker status affected the aging brain and whether the aging brain demonstrated an altered response to acute smoking/nicotine. Forty healthy volunteers participated, including 20 young (18–39 years) and 20 elderly (64–81 years) adults. Half of the subjects in each age category were lifelong non-smokers and half were cigarette smokers with average smoking histories of 9.3 and 52.0 years for young and elderly respectively. Inter-hemispheric theta and alpha asymmetry indices illustrated greater left hemisphere power (relative to right) in elderly adults, while the reverse trend was seen in young adults. Smokers and non-smokers both showed similar aging trends but differed with respect to their presence in frontal and posterior regions. Intra-hemispheric asymmetry indices, particularly with alpha activity, illustrated a reduced anterior-posterior gradient of power distribution in the elderly. Acute smoking increased slow (delta) and fast (beta) inter-hemispheric indices but only in elderly smokers. Smoking also altered the intra-hemispheric balance of slow wave activity in both age groups of smokers. The results are discussed in relation to normal and pathological aging.

Effects of quitting smoking on EEG activation and attention last for more than 31 days and are more severe with stress, dependence, DRD2 A1 allele, and depressive traits

“…The EEG slowing resulting from quitting also were greater during high-stress than during low-stress conditions in the present study. The situationdependent effects of abstinence on EEG asymmetry replicate and extend previous findings (e.g., Gilbert, 1996;Gilbert et al, , 1997aGilbert et al, , 1999bKnott & Harr, 1997). The effects of abstinence also influenced EEG asymmetry in a manner that depended on interaction of stress with eyes open vs. closed status and personality trait factors (DRD2, trait depression, and FTND nicotine dependence).…”

Effects of nicotine on brain responses to emotional pictures

“…Finally, greater amplitudes at frontocentral sites than at posterior sites are observed for both PN (Näätä nen, 1982;Smolnik, Pietrowsky, Fehm, & Born, 1998) and N300 (Warren & McDonough, 1999). We also predicted hemispheric asymmetries in the effects of nicotine based on evidence that both nicotine (Gilbert et al, 2004;Knott & Harr, 1997;Pritchard, 1991) and emotional states (Coan & Allen, 2003) are associated with hemispheric asymmetries in electrocortical activity. Whereas emotionrelated asymmetries have been observed most often at frontal sites, posterior asymmetries also have been observed frequently.…”

Effects of nicotine and caffeine, separately and in combination, on EEG topography, mood, heart rate, cortisol, and vigilance

“…that neurotransmitters and associated agonist drugs have situation-and CNS state-dependent functions. The present find- ing of lateralized and localized effects and interactions of caffeine and nicotine are also consistent with previous findings of nicotine on EEG~e.g., Knott & Harr, 1997;Pritchard, 1991! and caffeine on lateralized perceptual effects Barraclough & Beech, 1995!, as well as with evidence of relatively greater densities of dopamine and acetylcholine in the LH and greater densities of serotonin and norepinephrine in the RH~reviewed by Wittling, 1995!.…”

“…Better characterization of how smokingdelivered nicotine influences EEG activation during caffeineinduced states is important given that smokers report being more likely to smoke when drinking coffee and find smoking while drinking coffee especially enjoyable~Swanson, Lee, & Hopp, 1994!. The limited work in this area suggests that caffeine may produce a somewhat different pattern of electrocortical activation than nicotine~Cohen et al, 1994;Knott, 1990;Newman, Stein, Trettau, Coppola, & Uhde, 1992;Pritchard et al, 1995!. Repeated observations of situation-and personality-dependent lateralized, localized, and arousal-state-dependent effects of nicotine on EEG activation~Gilbert, 1987; Gilbert, Estes, et al, 1997;Gilbert et al, in press;Gilbert, Meliska, Welser, & Estes, 1994;Gilbert, Robinson, Chamberlin, & Spielberger, 1989;Knott & Harr, 1997;Pritchard, 1991;Pritchard et al, 1995! are contrasted with a general lack of caffeine studies that have assessed more than a few lateralized sites~Cohen Hasenfratz & Bättig, 1992!.…”