Magnetic resonance imaging studies of cigarette smoking

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA.
Handbook of experimental pharmacology 02/2009; 192(192):113-43. DOI: 10.1007/978-3-540-69248-5_5
Source: PubMed


This chapter reviews studies that have applied magnetic resonance imaging (MRI) toward a better understanding of the neurobiological correlates and consequences of cigarette smoking and nicotine dependence. The findings demonstrate that smokers differ from nonsmokers in regional brain structure and neurochemistry, as well as in activation in response to smoking-related stimuli and during the execution of cognitive tasks. We also review functional neuroimaging studies on the effects of nicotine administration on brain activity, both at rest and during the execution of cognitive tasks, independent of issues related to nicotine withdrawal and craving. Although chronic cigarette smoking is associated with poor cognitive performance, acute nicotine administration appears to enhance cognitive performance and increase neural efficiency in smokers.

51 Reads
  • Source
    • "It is now apparent that cigarette smoking-related morbidity extends well beyond cardiovascular disease, chronic obstructive pulmonary diseases, and various cancers, and includes neurobiological and neurocognitive abnormalities, some of which are progressive over time, and are not directly attributable to the foregoing biomedical conditions (Azizian et al., 2009; Durazzo et al., 2010; Sharma and Brody, 2009; Swan and Lessov-Schlaggar, 2007). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Cigarette smoking in adults is associated with abnormalities in brain neurobiology. Smoking-induced central nervous system oxidative stress (OxS) is a potential mechanism associated with these abnormalities. The goal of this study was to compare cognitively-normal elders on cerebrospinal fluid (CSF) levels of F2-isoprostane biomarkers of OxS. Methods Elders with a lifetime history of smoking (smokers; n = 50; 75 ± 5 years of age; 34 ± 28 pack-years; approximately 12% were actively smoking at the time of study) were compared to never-smokers (n = 61; 76 ± 6 years of age) on CSF iPF2α-III and 8,12, iso-iPF2α-VI F2-isoprostanes levels. F2-isoprostanes levels were quantitated with HPLC-atmospheric pressure chemical ionization-tandem mass spectrometry. Associations between F2-isoprostanes levels, hippocampal volumes, and cigarette exposure measures were also evaluated. Results Smokers showed higher iPF2α-III level than never-smokers. An age x smoking status interaction was observed for 8,12, iso-iPF2α-VI, where smokers demonstrate a significantly greater concentration with increasing age than non-smokers. In smokers only, higher 8,12, iso-iPF2α-VI concentration was associated with smaller hippocampal volume, and greater iPF2α-III level was related to greater pack years. Conclusions This is the first study to demonstrate that a history of cigarette smoking in cognitively-normal elders was associated with significantly elevated CSF F2-isoprostane levels and greater age-related increases in F2-isoprostane levels, and that higher F2-isoprostane levels in smokers were related to smaller hippocampal volume. These findings provide additional novel evidence that a history of chronic smoking during adulthood is associated with adverse effects on the human brain that are potentially persistent even with extended smoking cessation.
    Drug and Alcohol Dependence 09/2014; 142. DOI:10.1016/j.drugalcdep.2014.06.030 · 3.42 Impact Factor
  • Source
    • "Active-smokers showed significantly higher cortical F 4 -neuroprostane level, a measure of free radical-mediated lipid peroxidation in neurons. Thus, the persistently elevated level of OxS imposed by chronic cigarette smoking may serve as a primary mechanism contributing to the hippocampal volume deficits observed in this study, as well as the other neurobiological and neurocognitive abnormalities observed in clinical and non-clinical cohorts of chronic smokers across the lifespan (for review, see Azizian et al., 2009; Durazzo et al., 2010). See (Durazzo et al., 2010) for a more detailed discussion on OxS and other potential mechanisms contributing to neurobiological and neurocognitive dysfunction in chronic smokers. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Previous cross-sectional MRI studies with healthy, young-to-middle-aged adults reported no significant differences between smokers and non-smokers on total hippocampal volume. However, these studies did not specifically test for greater age-related volume loss in the total hippocampus or hippocampal subregions in smokers, and did they did not examine relationships between hippocampal and subfield volumes and episodic learning and memory performance. Healthy, young-to-middle-aged (45±12 years of age) smokers (n=39) and non-smokers (n=43) were compared on total hippocampal and subfield volumes derived from high-resolution 4Tesla MRI, emphasizing testing for greater age-related volume losses in smokers. Associations between hippocampal volumes and measures of episodic learning and memory were examined. Smokers showed significantly smaller volumes, as well as greater volume loss with increasing age than non-smokers in the bilateral total hippocampus and multiple subfields. In smokers, greater pack-years were associated with smaller volumes of the total hippocampus, presubiculum, and subiculum. In the entire cohort, performance on measures of learning and memory was related to larger total hippocampal and several subfield volumes, predominately in the left hemisphere. Chronic cigarette smoking in this young-to-middle aged cohort was associated with smaller total hippocampal and subfield volumes, which were exacerbated by advancing age. Findings also indicated an adverse smoking dose/duration response (i.e., pack-years) with total hippocampal and select subfield volumes. These hippocampal volume abnormalities in smokers may be related to the deficiencies in episodic learning and memory in young-to-middle-aged smokers reported in previous studies.
    Drug and alcohol dependence 09/2013; 133(2). DOI:10.1016/j.drugalcdep.2013.08.020 · 3.42 Impact Factor
  • Source
    • ", USA e-mail: effects on the brain (Azizian et al. 2009). Smaller gray matter volumes have been observed in frontal, temporal, and occipital lobes in smokers than in nonsmokers (Brody et al. 2004; Gallinat et al. 2006), as has an inverse relationship between cortical volume and exposure to smoking (Brody et al. 2004; Kühn et al. 2010). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Diffusion tensor imaging has been used before in testing associations between cigarette smoking and white matter integrity, with inconsistent results. Published reports indicate higher fractional anisotropy (FA, a measure of linear water diffusion) in some brain regions and lower FA in others in adult smokers compared to nonsmokers. Adolescent smokers exhibited elevated FA at several brain regions and a positive correlation of FA in the genu corpus callosum with exposure to smoking (pack-years). To help resolve prior discrepancies, we studied adults, sampling multiple brain regions, and testing for relationships to clinical features of nicotine dependence and exposure to smoking. Brain MRI scans (1.5 T) were acquired, and FA and apparent diffusion coefficient (ADC, a measure of random diffusion) were assayed in corpus callosum and prefrontal white matter, corona radiata, internal capsule, cingulum bundle, and hippocampal perforant fibers in 18 smokers (33.7 ± 7.9 years of age) and 18 age- and gender-matched nonsmokers. ADC showed no group difference, but smokers had higher (4.3-21.1%) FA than nonsmokers. The differences were significant in right prefrontal white matter, cingulum, and genu corpus callosum. FA in several regions was negatively correlated with nicotine dependence or cigarettes/day. Combined with earlier findings, these results suggest a model of changing trajectories whereby FA is higher with tobacco exposure during adolescence and declines with continued smoking in adulthood. This notion is supported by the observation that, at multiple sampling sites, participants who had started smoking earlier in life had higher FA than those who had started later.
    Psychopharmacology 01/2012; 221(2):285-95. DOI:10.1007/s00213-011-2621-9 · 3.88 Impact Factor
Show more