Journal of Clinical EEG & Neuroscience, January, 2009
Brain Imaging in Substance Abusers
Editorial: Ronald I. Herning, Guest Editor
This special issue focuses on papers presented at the 2007 Joint ECNS-ISNIP Meeting in Montreal. While many outstanding papers in human electrophysiology and neuroimaging (EEG, ERP, MRI, fMRI, SPECT and PET) were presented at this meeting, the theme for the meeting was personality disorders and substance abuse. The papers presented in this issue center around this theme. These neuroimaging methods have been particularly useful in studying brain function in (1) individuals with premorbid psychiatric disorders (conduct disorder, ADHD) or comorbid Antisocial Personality Disorder (ASPD, affective disorders) psychiatric disorders related to substance abuse, (2) persons given acute doses of abused substances in the laboratory and (3) individuals during abstinence after prolonged substance abuse.
The first two papers touch on personality characteristics that predispose individuals to substance abuse. Drs. Knyazev and Slobodskoy-Plusnin present electrophysiology data on Behavioral Approach System (BAS) that has been shown to be one of the strong predictors of substance use. They suggest that BAS theory models craving, an important feature of substance abuse, better than Eysenck’s theory. Nonsubstance abusing individuals who responded differently on Carver and White’s Behavioral Inhibition System /BAS scales had differing electrophysiological responses to reward and punishment expectancy. Drs. Surmeli and Ertem demonstrate their success in treating individuals with ASPD with neurofeedback. Both rating scales and EEG measures showed improvement. ASPD has been linked to substance use disorders.¹
The next two papers investigate the acute effects of drugs on the brain. Dr. Knott’s group investigates the effects of nicotine on cognitive event-related potentials and performance in nonsmokers. Research on the effects of nicotine or tobacco smoking on cognition has shown that smokers when abstinent have impaired cognition and altered electrophysiology as compared to nonsmokers and smoking/nicotine improves these measures. Whether nicotine/smoking can improve cognitive brain potentials and performance in nonsmokers has not been carefully studied. The question is simply; does nicotine do more than reduce the effects of nicotine withdrawal? Their study with nicotine gum in nonsmokers suggests that nicotine does have cognitive enhancing effects. The paper by Lindlsey and associates reports an improved device for the delivery of smoked drugs such as tobacco and marijuana in MRI scanners. Their device does not interfere with drug effects produced by normal smoking. They report the smoking induced changes in the BOLD response to visual stimulation that were not affected by the “improved device, the act of smoking, air puffing, nicotine, or other components of cigarette smoke.” This contribution is important since the effects of natural smoking of tobacco and other abused drugs on brain function can now be carried out in the fMRI studies.
The final two studies look at the effects of heavy drug use on the brain. Squeglia, Jacobus, and Tapert review studies investigating heavy alcohol and marijuana use on adolescent brain development. They note that substance use resulted in abnormalities in brain processing, including poorer cognitive performance, poorer white matter quality, changes in brain volume, and abnormal neuronal activation patterns in adolescents with heavy substance abuse. The Copersino study finds adult cocaine abusers who used cocaine for on the average of eight years had EEG and blood flow velocity deficits during monitored abstinence. Both studies suggest that the imaging results indicate cognitive impairments. In addition; the Copersino study suggests the perfusion deficits may place the cocaine abusers at risk for cerebrovascular accidents.
While brain imaging methods have been useful in studying brain function of substance abusers, there are problems. Subjects in many elegant imaging studies were not well characterized. An incomplete drug and psychiatric history could result in erroneous results. For example, approximately 22% of adults in the United States are tobacco smokers,² while the rate of current tobacco smoking among cocaine users is about 85% .³ Thus, the studies of the brain function of cocaine abusers during abstinence have compared cocaine abusers who smoke tobacco with nonsmoking control subjects. Are the results due to differences between smokers and nonsmokers or to the prolonged effects of cocaine on the brain? To make matters worse, the cigarette smoking history of subjects in many of these studies is most often not presented. An experimental design that included four groups (cocaine abusers that smoked tobacco, cocaine abusers that do not smoke, control subjects that smoke and control subjects that do not smoke) would be preferred, but there are no such studies. While it is not the purpose of this commentary to review this literature, it is important to remind those engaged in neuroimaging studies to carefully consider and characterize their subjects and to use an appropriate experimental design. Elegant imaging techniques alone do not make good science.
Ronald I. Herning, PhD
1. Mariani JJ, Horey J, Bisaga A, Aharonovich E, Raby W, Cheng WY, Nunes E, Levin FR. Antisocial behavioral syndromes in cocaine and cannabis dependence. Am J Drug Alcohol Abuse 2008; 34: 405-414.
2. Wade H, Berrettini, CH, Lerman CE. Pharmacotherapy and pharmacogenetics of nicotine dependence. Am J Psychiatry 2005 162:1441-1451.
3. U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. National Survey on Drug Use and Health, 2005 [Computer file]. ICPSR04596v1. Research Triangle Park, NC: Research Triangle Institute [producer], 2006. Ann Arbor, MI: Interuniversity Consortium for Political and Social Research [distributor], 2006: 1116.