Orbitofrontal Cortex - Orbitofrontal Cortex and Addiction

Orbitofrontal Cortex and Addiction

Involvement of OFC is often implicated in addictive behavior in addition to the nucleus accumbens and amygdala . The striato-thalamo-orbitofrontal circuit of the OFC has been implicated in the development of addictive behavior via dopaminergic activation of reward circuits as supported by brain imaging studies. The OFC has been associated with compulsive behavior and repetitive behavior, as well as with drive; in drug dependent individuals, disruption of the striato-thalamo- orbitofrontal circuit leads to compulsive behavior and increased motivation to take the drug.

Addicted individuals show deficits in orbitofrontal, striatal, and thalamic regions. Conscious and unconscious components are hypothesized to serve as mechanisms responsible for the maintenance of drug addiction: conscious mechanisms involve craving associated with loss of control and unconscious elements include anticipated conditioned responses to a drug and impulsivity.

Brain imaging studies show that during cocaine withdrawal, metabolism is increased in the OFC and that this is proportional to drug craving. In contrast, during protracted (up to 3–4 months) withdrawal cocaine abusers show reduced activity in the OFC compared to healthy controls.

Similarly, in alcoholics, during withdrawal there is decreased activity in the OFC (compared to the OFCs of healthy controls) but, in addition, detoxified alcoholics have significantly lower levels of benzodiazepine receptors in the OFC (compared with healthy controls). Hypoactivity in the OFC of alcoholics is also supported by blunted metabolism in the OFC to response to both serotonogenic and GABA- ergic agents.