Reward deficiency syndrome: a biogenetic model for the diagnosis and treatment of impulsive, addictive, and compulsive behaviors.

The dopaminergic system, and in particular the dopamine D2 receptor, has been implicated in reward mechanisms. The net effect of neurotransmitter interaction at the mesolimbic brain region induces "reward" when dopamine (DA) is released from the neuron at the nucleus accumbens and interacts with a dopamine D2 receptor. "The reward cascade" involves the release of serotonin, which in turn at the hypothalmus stimulates enkephalin, which in turn inhibits GABA at the substania nigra, which in turn fine tunes the amount of DA released at the nucleus accumbens or "reward site." It is well known that under normal conditions in the reward site DA works to maintain our normal drives. In fact, DA has become to be known as the "pleasure molecule" and/or the "antistress molecule." When DA is released into the synapse, it stimulates a number a DA receptors (D1-D5) which results in increased feelings of well-being and stress reduction. A consensus of the literature suggests that when there is a dysfunction in the brain reward cascade, which could be caused by certain genetic variants (polygenic), especially in the DA system causing a hypodopaminergic trait, the brain of that person requires a DA fix to feel good. This trait leads to multiple drug-seeking behavior. This is so because alcohol, cocaine, heroin, marijuana, nicotine, and glucose all cause activation and neuronal release of brain DA, which could heal the abnormal cravings. Certainly after ten years of study we could say with confidence that carriers of the DAD2 receptor A1 allele have compromised D2 receptors. Therefore lack of D2 receptors causes individuals to have a high risk for multiple addictive, impulsive and compulsive behavioral propensities, such as severe alcoholism, cocaine, heroin, marijuana and nicotine use, glucose bingeing, pathological gambling, sex addiction, ADHD, Tourette's Syndrome, autism, chronic violence, posttraumatic stress disorder, schizoid/avoidant cluster, conduct disorder and antisocial behavior. In order to explain the breakdown of the reward cascade due to both multiple genes and environmental stimuli (pleiotropism) and resultant aberrant behaviors, Blum united this hypodopaminergic trait under the rubric of a reward deficiency syndrome.

Electroencephalographic biofeedback of SMR and beta for treatment of attention deficit disorders in a clinical setting.

Six children were provided with long-term biofeedback and academic treatment for attention deficit disorders. Their symptoms were primarily specific learning disabilities, and, in some cases, there were varying degrees of hyperkinesis. The training consisted of two sessions per week for 10 to 27 months, with a gradual phase-out. Feedback was provided for either increasing 12- to 15-Hz SMR or 16- to 20-Hz beta activity. Inhibit circuits were employed for blocking the SMR or beta when either gross movement, excessive EMG, or theta (4-8 Hz) activity was present. Treatment also consisted of combining the biofeedback with academic training, including reading, arithmetic, and spatial tasks to improve their attention. All children increased SMR or beta and decreased slow EEG and EMG activity. Changes could be seen in their power spectra after training in terms of increased beta and decreased slow activity. All six children demonstrated considerable improvement in their schoolwork in terms of grades or achievement test scores. None of the children are currently on any medications for hyperkinetic behavior. The results indicate that EEG biofeedback training, if applied comprehensively, can be highly effective in helping to remediate children who are experiencing attention deficit disorders.