Abstract:SUMMARYThe chronic effects of smoking on regional cerebral blood flow (CBF), and on serum lipids and lipoprotein levels in neurologically normal subjects, were studied. CBF was studied by the 133-Xenon inhalation method and gray matter flow was calculated following the method of Obrist et al. One hundred and eleven subjects, who had no abnormalities in neurological examinations nor in CT scans, were divided into two groups: smokers (37) and non-smokers (74). Those who had a smoking index (Number of cigarettes/… Show more
“…Similarly, smokers who smoke ad lib prior to SPECT scanning (including the morning of the scan) have decreased global brain activity compared to former smokers and non-smokers (Rourke et al, 1997). These findings are generally supported by studies using transcranial Doppler ultrasound or the Xe 133 inhalation method to measure responses to smoking, with some (Cruickshank et al, 1989;Kubota et al, 1983Kubota et al, , 1987Rogers et al, 1983), but not all (Kodaira et al, 1993;Terborg et al, 2002), studies showing diminished cerebral blood flow.…”
Section: Brain Activity Responses To Nicotine/cigarette Administrationmentioning
While most cigarette smokers endorse a desire to quit smoking, only about 14% to 49% will achieve abstinence after 6 months or more of treatment. A greater understanding of the effects of smoking on brain function may (in conjunction with other lines of research) result in improved pharmacological (and behavioral) interventions. Many research groups have examined the effects of acute and chronic nicotine/cigarette exposure on brain activity using functional imaging; the purpose of this paper is to synthesize findings from such studies and present a coherent model of brain function in smokers. Responses to acute administration of nicotine/smoking include: a reduction in global brain activity; activation of the prefrontal cortex, thalamus, and visual system; activation of the thalamus and visual cortex during visual cognitive tasks; and increased dopamine (DA) concentration in the ventral striatum/nucleus accumbens. Responses to chronic nicotine/cigarette exposure include decreased monoamine oxidase (MAO) A and B activity in the basal ganglia and a reduction in α 4 β 2 nicotinic acetylcholine receptor (nAChR) availability in the thalamus and putamen. Taken together, these findings indicate that smoking enhances neurotransmission through cortico-basal ganglia-thalamic circuits either by direct stimulation of nAChRs, indirect stimulation via DA release or MAO inhibition, or a combination of these factors. Activation of this circuitry may be responsible for the effects of smoking seen in tobacco dependent subjects, such as improvements in attentional performance, mood, anxiety, and irritability.
“…Similarly, smokers who smoke ad lib prior to SPECT scanning (including the morning of the scan) have decreased global brain activity compared to former smokers and non-smokers (Rourke et al, 1997). These findings are generally supported by studies using transcranial Doppler ultrasound or the Xe 133 inhalation method to measure responses to smoking, with some (Cruickshank et al, 1989;Kubota et al, 1983Kubota et al, , 1987Rogers et al, 1983), but not all (Kodaira et al, 1993;Terborg et al, 2002), studies showing diminished cerebral blood flow.…”
Section: Brain Activity Responses To Nicotine/cigarette Administrationmentioning
While most cigarette smokers endorse a desire to quit smoking, only about 14% to 49% will achieve abstinence after 6 months or more of treatment. A greater understanding of the effects of smoking on brain function may (in conjunction with other lines of research) result in improved pharmacological (and behavioral) interventions. Many research groups have examined the effects of acute and chronic nicotine/cigarette exposure on brain activity using functional imaging; the purpose of this paper is to synthesize findings from such studies and present a coherent model of brain function in smokers. Responses to acute administration of nicotine/smoking include: a reduction in global brain activity; activation of the prefrontal cortex, thalamus, and visual system; activation of the thalamus and visual cortex during visual cognitive tasks; and increased dopamine (DA) concentration in the ventral striatum/nucleus accumbens. Responses to chronic nicotine/cigarette exposure include decreased monoamine oxidase (MAO) A and B activity in the basal ganglia and a reduction in α 4 β 2 nicotinic acetylcholine receptor (nAChR) availability in the thalamus and putamen. Taken together, these findings indicate that smoking enhances neurotransmission through cortico-basal ganglia-thalamic circuits either by direct stimulation of nAChRs, indirect stimulation via DA release or MAO inhibition, or a combination of these factors. Activation of this circuitry may be responsible for the effects of smoking seen in tobacco dependent subjects, such as improvements in attentional performance, mood, anxiety, and irritability.
“…Candidate covariates were selected based on literature review of variables impacting CBF as well as exploratory analyses. Specifically, previous studies have identified relationships between CBF and age (Kubota et al, 1983;Naritomi et al, 1979), gender (Gur et al, 1982), and intima-media thickness (Claus et al, 1996;Nobili et al, 1993). Systolic and diastolic blood pressure, body mass index (BMI), and smoking status were also examined as potential covariates.…”
A substantial epidemiological literature now supports the existence of a J-or U-shaped association between alcohol consumption and a broad range cardiovascular health outcomes including stroke. Although it is well documented that alcoholics exhibit both global and regional cerebral hypoperfusion in the sober state, little is known regarding the effects of a broader range of alcohol consumption on cerebral blood flow (CBF). The present study employed positron emission tomography with H 2 15 O to assess quantitative global and regional CBF in 86 participants (51 men and 35 women; mean age 60.1) as a function of self-reported weekly alcohol consumption (none, <1, 1 to <7, 7 to <15, and >15 drinks per week). Analyses controlling for age, gender, and vascular health (carotid intima-media thickness) revealed that, relative to the weighted population mean, global CBF was greater in the lightest alcohol consumption group (<1 per week) and lower in the heaviest (>15 per week). Effects did not vary across regions of interest. This report is the first to describe an inverted J-shaped relationship between alcohol consumption and CBF in the absence of stroke.
“…Chronic smoking decreases basal cerebral blood flow (Kubota et al, 1983) and increases hematocrit (Isaka et al, 1993), which increases the blood oxygenation level-dependent (BOLD) contrast (Levin et al, 2001). As the fMRI signal in this study is based on BOLD contrasts, group differences in the coupling between neural function and associated increases in cerebral blood could introduce a potential confound for interpretation of BOLD signal change (Jacobsen et al, 2002).…”
Smoking is usually initiated in adolescence, and is the leading preventable cause of death in the United States. Little is known, however, about the links between smoking and neurobiological function in adolescent smokers. This study aimed to probe prefrontal cortical function in late adolescent smokers, using a response inhibition task, and to assess possible relationships between inhibition-related brain activity, clinical features of smoking behavior, and exposure to cigarette smoking. Participants in this study were otherwise healthy late adolescent smokers (15-21 years of age; n ¼ 25), who reported daily smoking for at least the 6 months before testing, and age-and education-matched nonsmokers (16-21 years of age; n ¼ 25), who each reported smoking fewer than five cigarettes in their lifetimes. The subjects performed the Stop-signal Task, while undergoing functional magnetic resonance imaging. There were no significant group differences in prefrontal cortical activity during response inhibition, but the Heaviness of Smoking Index, a measure of smoking behavior and dependence, was negatively related to neural function in cortical regions of the smokers. These findings suggest that smoking can modulate prefrontal cortical function. Given the late development of the prefrontal cortex, which continues through adolescence, it is possible that smoking may influence the trajectory of brain development during this critical developmental period.
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