Cocaine Addicts Display A Thinner Cortex Which May Reflect Drug Use And A Pre-Existing Disposition To Drug Abuse

Main Category: Alcohol / Addiction / Illegal Drugs
Also Included In: Neurology / Neuroscience
Article Date: 09 Oct 2008 - 5:00 PDT

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New research findings suggest that structural abnormalities in the brains of cocaine addicts are related in part to drug use and in part to a predisposition toward addiction. The research, published by Cell Press in the October 9th issue of the journal Neuron, maps the topography of the addicted brain and provides new insight into the effect of cocaine on neural systems mediating cognition and motivation.

"Human studies have shown differences in how addicts make judgments and decisions, but it is not well understood how these differences relate to alterations in the structure of the brains of addicts. Claims have been made that cocaine, potentially in connection with alcohol or other drugs, may be toxic to brain cells. We sought evidence supporting a hypothesis that brain thickness is reduced in some brain regions in addicts, is related to altered decision-making and cognition, and might to some limited degree, be connected to their exposure to cocaine," explains senior study author Dr. Hans Breiter from Massachusetts General Hospital.

Dr. Breiter and colleagues found that brain regions involved with regulation of attention and reward, specifically the dorsolateral prefrontal cortex (DLPFC) and insular cortices, were significantly thinner in cocaine addicts when compared with matched controls. Behavioral tests revealed that the thinner cortex was associated with restrictions in preference-based judgment and decision-making, and with less accurate effortful attention. A general reduction in the level of preference and in the range of decisions reflecting these preferences can be considered an example of a fundamental feature of addiction - the loss of interest in many things outside of drug use.

Some cortical thickness differences were associated with years of drug use, but the researchers also observed differences in the symmetry of DLPFC thickness between control subjects and cocaine addicts that suggested predisposition to drug abuse. "In human and animal studies, differences in the structure of the right and left sides of the brain are important for many behaviors, and when these normal differences in brain structure are altered, there may be a genetic basis for the change. We found an altered right/left relationship in a part of the frontal cortex that was also associated with altered judgment and decision-making in addicts. We further found that the overall brain thickness in the cocaine addicts was more uniform across the brain, which is quite different from what is observed in non-drug users. These differences did not correlate with any drug use measure. Together, this set of findings point to predisposing factors being a potential contributing factor to the addiction," explains Dr. Breiter.

In total, these observations provide evidence that cortical thickness abnormalities associated with cocaine addiction may be a reflection of both drug use and a preexisting inclination to drug abuse. "A fundamental component of addiction may involve adaptations and/or developmental predispositions involving brain regions necessary for judgment and decision-making regarding complex rewards and attention towards goal-objects. Addiction thus may represent a complex phenotype with multiple effects necessary for compulsive drug use, and the resulting restriction in the range of behaviors they show," concludes Dr. Breiter.

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Article adapted by Medical News Today from original press release.
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The researchers include Nikos Makris, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Gregory P. Gasic, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; David N. Kennedy, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Steven M. Hodge, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Jonathan R. Kaiser, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Myung Joo Lee, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Byoung Woo Kim, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Anne J. Blood, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; A. Eden Evins, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA Larry J. Seidman, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA, Massachusetts Mental Health Center Public Psychiatry Division of Beth Israel Deaconess Medical Center and HMS, Boston, MA; Dan V. Iosifescu, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Sang Lee, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Claudia Baxter, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Roy H. Perlis, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Jordan W. Smoller, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; Maurizio Fava, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA; and Hans C. Breiter, Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), Boston, MA.

Source: Cathleen Genova
Cell Press