Deep Brain Stimulation for Addiction?

deep brain stimulation

With the expanding knowledge of the neuronal circuits responsible for the behavioral disorders associated with addiction, though, DBS could become a future treatment option for patients suffering from addiction.

In people addicted to psychoactive substance it has been shown by Positron emission tomography studies that, when they take the psychoactive substance, dopamine is released in the nucleus accumbens, which causes “the high.”

They lack the decrease of the output neurons on this dopamine release. There is no brake on the “high” elicited by the drug and the subsequent dopamine release. This lack of inhibition causes activation of the reward system. The increased dopamine release is located in the nucleus accumbens. This reward circuit consists of dopaminergic neurons that project from the ventral tegmental area to the ventral striatum (including nucleus accumbens), the amygdala and septal nuclei, and prefrontal and cingulate cortices.

The feeling of well-being produced by activation of the reward system can be seen as positive reinforcement. Negative reinforcement involves escaping from or avoiding withdrawal symptoms, which occur after cessation of the substance use. In addicted individuals both positive and negative reinforcement involve disruption of the reward system by repeated administration of the substance.

Other brain regions involved in addiction are:

  • The amygdala. The amygdala couples the rewarding qualities of the substance and the environment in which the abuse takes place. This could explain why an environment with substance-
    associated stimuli causes the craving reported by addicted individuals
  • The prefrontal cortex and the anterior cingulate gyrus. Dysfunction of the dopaminergic transmission in these structures leads to impairment of inhibitory control and decision making. This may cause an inability to resist substance-abusing behavior in addicted individuals, even
    though they are explicitly aware of the negative consequences.

A recent review described the different psychosurgical procedures used for the treatment of addiction. Moreover this review also discusses the first reports on the treatment of substance-related addictive disorders by using Deep Brain Stimulation.

They found three cases in two publications. Two patients with Parkinson’s disease and Dopamine dysregulation syndrome.

Dopaminergic medications, share some of the stimulant properties of commonly abused drugs such as amphetamine and cocaine. These have the potential to be compulsively used by a small group of susceptible individuals with Parkinson’s disease, causing harmful social, psychological, and physical effects. Patients with this condition, termed “dopamine dysregulation syndrome”, meet clinical criteria for substance dependence and addiction. They frequently also show behavioural compulsions, such as compulsive gambling, eating and hyper-sexuality.

In both cases there was a good effect of deep brain stimulation on motor disability, but also on Dopamine Dysregulation Syndrome and related behavior characteristics. They both underwent bilateral subthalamic nucleus deep brain stimulation. The other case report was about a man with severe agoraphobia with panic attacks, secondary depressive disorder, and alcohol dependency. After bilateral deep brain stimulation of the nucleus accumbens the substance abuse disappeared. The nucleus accumbens is part of the “addictive circuit” in the brain.

Psychosurgery for the treatment of addiction has been done and published. Never in randomized controlled trials and the procedure is irreversible.

DBS is reversible and makes randomized placebo controlled trials for this indication feasible. Nevertheless, the evidence so far is circumstantial and limited

What do you think, should DBS be tried with addiction?

ResearchBlogging.org
Bianca M. L. Stelten, Lieke H. M. Noblesse, Linda Ackermans, Yasin Temel, Veerle Visser-Vandewalle (2008). The neurosurgical treatment of addiction Neurosurgical FOCUS, 25 (1) DOI: 10.3171/FOC/2008/25/7/E5