Joel F. Lubar

The Reward Deficiency Syndrome: A Biogenetic Model for the Diagnosis and Treatment of Impulsive, Addictive and Compulsive Behaviors

Abstract 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, Tourettes 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.

Quantitative analysis of EEG in boys with attention-deficit-hyperactivity disorder: Controlled study with clinical implications

Sixteen-channel topographic brain mapping of electroencephalograms of 25 right-handed males, 9-12 years of age, with attention-deficit-hyperactivity disorder revealed increased theta (4-7.75 Hz) and decreased beta 1 (12.75-21 Hz) when compared with 27 controls matched for age and grade level. The differences were greater when patients were tested for reading and drawing skills, but were decreased when they were at rest during visual fixation. Although the differences in patients with attention-deficit-hyperactivity disorder were generalized, increased theta was more prominent in frontal regions, while beta 1 was significantly decreased in temporal regions. Principal component analysis was used to combine the variables into 2 components which accounted for 82% of the total variance. A discriminant function analysis using these components was able to predict group membership for attention-deficit-hyperactivity disorder patients 80% of the time and 74% for controls. These findings support the use of topographic electroencephalography for further elucidation of the neurophysiology of attention-deficit-hyperactivity disorder.

Discourse on the development of EEG diagnostics and biofeedback for attention-deficit/hyperactivity disorders

This article presents a review of work that my colleagues and I have been doing during the past 15 years developing a rationale for the diagnosis of attention-deficit/hyperactivity disorder (ADHD) and treatment of ADHD employing EEG biofeedback techniques. The article first briefly reviews the history of research and theory for understanding ADHD and then deals with the development of EEG and event-related potential (ERP) assessment paradigms and treatment protocols for this disorder, including our work and that of others who have replicated our results. Illustrative material from our current research and child case studies is included. Suggestions for future experimental and clinical work in this area are presented and theoretical issues involving the understanding of the neurophysiological and neurological basis of ADHD are discussed.

Evaluation of the effectiveness of EEG neurofeedback training for ADHD in a clinical setting as measured by changes in T.O.V.A. scores, behavioral ratings, and WISC-R performance

A study with three component parts was performed to assess the effectiveness of neurofeedback treatment for Attention Deficit/Hyperactivity Disorder (ADHD). The subject pool consisted of 23 children and adolescents ranging in age from 8 to 19 years with a mean of 11.4 years who participated in a 2-to 3-month summer program of intensive neurofeedback training. Feedback was contingent on the production of 16–20 hertz (beta) activity in the absence of 4–8 hertz (theta) activity. Posttraining changes in EEG activity, T.O.V.A. performance, (ADDES) behavior ratings, and WISC-R performance were assessed. Part I indicated that subjects who successfully decreased theta activity showed significant improvement in T.O.V.A. performance; Part II revealed significant improvement in parent ratings following neurofeedback training; and Part III indicated significant increases in WISC-R scores following neurofeedback training. This study is significant in that it examines the effects of neurofeedback training on both objective and subjective measures under relatively controlled conditions. Our findings corroborate and extend previous research, indicating that neurofeedback training can be an appropriate and efficacious treatment for children with ADHD.

Assessing attention deficit hyperactivity disorder via quantitative electroencephalography : An initial validation study

Spectral analysis of the electrophysiological output at a single, midline prefrontal location (the vertex) was conducted in 482 individuals, ages 6-30 years old, to test the hypothesis that cortical slowing in the prefrontal region can serve as a basis for differentiating patients with attention deficit hyperactivity disorder (ADHD) from nonclinical control groups. Participants were classified into 3 groups (ADHD, inattentive; ADHD, combined; and control) on the basis of the results of a standardized clinical interview, behavioral rating scales, and a continuous performance test. Quantitative electroencephalographic (QEEG) findings indicated significant maturational effects in cortical arousal in the prefrontal cortex as well as evidence of cortical slowing in both ADHD groups, regardless of age or sex. Sensitivity of the QEEG-derived attentional index was 86%; specificity was 98%. These findings constituted a positive initial test of a QEEG-based neurometric test for use in the assessment of ADHD.

EEG and behavioral changes in a hyperkinetic child concurrent with training of the sensorimotor rhythm (SMR): a preliminary report.

Reduced seizure incidence coupled with voluntary motor inhibition accompanied conditioned increases in the sensorimotor rhythm(SMR), a 12–14 Hz rhythm appearing over rolandic cortex. Although SMR biofeedback training has been successfully applied to various forms of epilepsy in humans, its potential use in decreasing hyperactivity has been limited to a few cases in which a seizure history was also a significant feature. The present study represents a first attempt to explore the techniques applicability to the problem of hyperkinesis independent of the epilepsy issue. The results of several months of EEG biofeedback training in a hyperkinetic child tend to corroborate and extend previous findings. Feedback presentations for SMR were contingent on the production of 12–14-Hz activity in the absence of 4–7-Hz slow-wave activity. A substantial increase in SMR occurred with progressive SMR training and was associated with enhanced motor inhibition, as gauged by laboratory measures of muscular tone(chin EMG) and by a global behavioral assessment in the classroom. Opposite trends in motor inhibition occurred when the training procedure was reversed and feedback presentations were contingent on the production of 4–7 Hz in the absence of 12–14-Hz activity. Although the preliminary nature of these results is stressed, the subject population has recently been increased to establish the validity and generality of the findings and will include the use of SMR biofeedback training after medication has been withdrawn.

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.

EEG Neurofeedback: A Brief Overview and an Example of Peak Alpha Frequency Training for Cognitive Enhancement in the Elderly

Neurofeedback (NF) is an electroencephalographic (EEG) biofeedback technique for training individuals to alter their brain activity via operant conditioning. Research has shown that NF helps reduce symptoms of several neurological and psychiatric disorders, with ongoing research currently investigating applications to other disorders and to the enhancement of non-disordered cognition. The present article briefly reviews the fundamentals and current status of NF therapy and research and illustrates the basic approach with an interim report on a pilot study aimed at developing a new NF protocol for improving cognitive function in the elderly. EEG peak alpha frequency (PAF) has been shown to correlate positively with cognitive performance and to correlate negatively with age after childhood. The present pilot study used a double-blind controlled design to investigate whether training older individuals to increase PAF would result in improved cognitive performance. The results suggested that PAF NF improved cognitive processing speed and executive function, but that it had no clear effect on memory. In sum, the results suggest that the PAF NF protocol is a promising technique for improving selected cognitive functions.

Neocortical Dynamics: Implications for Understanding the Role of Neurofeedback and Related Techniques for the Enhancement of Attention

For nearly 25 years, EEG biofeedback (neurofeedback) has been utilized in research and clinical settings for the treatment and investigation of a number of disorders ranging from attention deficit hyperactivity disorder to seizure disorders as well as many other established and investigational applications. Until recently, mechanisms underlying the generation and origins of EEG have been poorly understood but now are beginning to become much more clarified. Now it is important to combine the information gathered on the genesis of EEG and neocortical dynamics with the findings from neurofeedback investigations. This will help us to develop models of how neurofeedback might operate in producing the changes in EEG and in clinical symptomatology. We know that the cortex operates in terms of resonant loops between neocortical columns of cells known as local, regional, and global resonances. These resonances determine the specific EEG frequencies and are often activated by groups of cells in the thalamus known as pacemakers. There are complex excitatory and inhibitory interactions within the cortex and between the cortex and the thalamus that allow these loops to operate and provide the basis for learning. Neurofeedback is a technique for modifying these resonant loops, and hence, modifying the neurophysiological and neurological basis for learning and for the management of a number of neurologically based disorders. This paper provides an introduction to understanding EEG and neocortical dynamics and how these concepts can be used to explain the results of neurofeedback training and other interventions particularly in the context of understanding attentive mechanisms and for the management of attention deficit/hyperactivity disorders.

Behavioral management of epileptic seizures following EEG biofeedback training of the sensorimotor rhythm

Eight severely epileptic patients, four males and four females, ranging in age from 10 to 29 years, were trained to increase 12–14 Hz EEG activity from the regions overlying the Rolandic area. This activity, the sensorimotor rhythm(SMR), has been hypothesized to be related to motor inhibitory processes(Sterman, 1974). The patients represented a crosssection of several different types of epilepsy, including grand mal, myoclonic, akinetic, focal, and psychomotor types. Three of them had varying degrees of mental retardation. SMR was detected by a combination of an analog filtering system and digital processing. Feedback, both auditory and/or visual, was provided whenever one-half second of 12–14-Hz activity was detected in the EEG. Patients were provided with additional feedback keyed by the output of a 4–7-Hz filter which indicated the presence of epileptiform spike activity, slow waves, or movement. Feedback for SMR was inhibited whenever slow-wave activity spikes or movement was also present. During the treatment period most of the patients showed varying degrees of improvement. Two of the patients who had been severely epileptic, having multiple seizures per week, have been seizure free for periods of up to 1 month. Other patients have developed the ability to block many of their seizures. Seizure intensity and duration have also decreased. Furthermore, the successful patients demonstrated an increase in the amount of SMR and an increase in amplitude of SMR during the training period. Spectral analyses for the EEGs were performed periodically. The effectiveness of SMR conditioning for the control of epileptic seizures is evaluated in terms of patient characteristics and type of seizures.