The development of a quantitative electroencephalographic scanning process for attention deficit-hyperactivity disorder: reliability and validity studies.

The development of a quantitative electroencephalographic (QEEG)-based procedure for use in the assessment of attention deficit-hyperactivity disorder (ADHD) was examined through a series of studies investigating test reliability and validation issues. This process, involving a spectral analysis of the electrophysiological power output from a single, midline, central location (the vertex), was conducted in 469 participants, 6 to 20 years of age, classified as ADHD, inattentive type; ADHD, combined type; or control. The results indicated that the QEEG scanning procedure was reliable (r = .96), was consistent with the Attention Deficit Disorders Evaluation Scale (S. B. McCarney, 1995) and the Test of Variables of Attention (L. M. Greenberg, 1994; chi-square, p < .01), and differentiated participants with ADHD from a nonclinical control group (p < .001). The sensitivity of the QEEG-derived attentional index was 90%; the specificity was 94%.

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.

Methylphenidate effects on global and complex measures of EEG.

Methylphenidate (MPH) effects on global and complex measures of electroencephalography were examined in boys with attention-deficit-hyperactivity disorder between the ages of 9 and 11 years. Electroencephalogram (EEG) data were collected separately from the administration of a continuous performance task and were evaluated for changes in overall frequency, coherence, phase, and asymmetry and against a referential database. MPH did not produce a clear change in EEG frequency measures compared with the task condition, although it did induce regional changes in the EEG and produced an improvement in task performance. In comparison against the referential database, MPH appeared to lessen the impact of abnormalities in EEG coherence, EEG phase, and EEG asymmetry on performance measures.

Limitations of the American Academy of Neurology and American Clinical Neurophysiology Society paper on QEEG.

The AAN/ACNS report is misleadingly negative regarding the current status of quantitative EEG and tends to discourage its development and use with other related clinical problems. There have been many excellent studies showing that QEEG can be useful for the evaluation and understanding of mild traumatic brain injury, learning disabilities, attention deficit disorders, alcoholism, depression, and other types of substance abuse. In fact, Hughes and John recently provided in this Journal an extensive and detailed review of the use of QEEG in psychiatric disorders. The bias of the AAN/ACNS report is also evident when contrasted to the outstanding review of the clinical utility of QEEG by the American Medical EEG Association, which clearly articulates the opposite points in many cases and concludes that QEEG has reached maturity. At present, the most one can say is that there are legitimate scientific debate and differences of opinion concerning the utility of QEEG, as there are in many other areas of medicine. The AAN/ACNS article should not be considered the definitive opinion. Too many implications for health care are at stake. The debate and research may continue without withholding valuable help from the public. We hope that revised guidelines will be drafted in such a way as to encourage the development of quantitative EEG and brain mapping rather than discourage future research support and use of QEEG with patients. Furthermore, we strongly feel that this technology should be available to, and be explored and used by, nonphysicians who are properly trained and certified.

Effects of 20-min audio-visual stimulation (AVS) at dominant alpha frequency and twice dominant alpha frequency on the cortical EEG.

The effects of audio-visual stimulation at the dominant alpha frequency and twice dominant alpha frequency on the EEG were investigated. An eyes-closed baseline EEG determined each subject's dominant alpha frequency. Subjects were stimulated at their dominant alpha frequency and at twice dominant alpha frequency for 20 min on two occasions. A 30-min post-session eyes-closed EEG was recorded after each session. Power data were analyzed for 19 locations in six bandpasses using repeated-measures ANOVAs and appropriate post-hoc tests. Alpha stimulation significantly increased power over baseline levels in the delta 1, delta 2, theta, beta 1 and beta 2, with significant effects remaining 30 min later in beta 1. Twice alpha stimulation significantly increased theta, beta 1 and beta 2 power over baseline levels, with significant effects remaining 30 min later in theta, alpha, beta 1 and beta 2.

Electroencephalographic biofeedback methodology and the management of epilepsy.

Currently considerable research is being directed toward developing methodologies for controlling internal processes. An applied branch of the basic field of psychophysiology, known as biofeedback, has developed to fulfill clinical needs related to such control. Current scientific and popular literature abounds with numerous examples of how biofeedback is being used. For example, germinal studies by Kamiya (1962), and later work by Lynch and Paskewitz (1971), Beatty (1973), as well as many others have shown that the EEG alpha rhythm (8 to 13 Hz) recorded from occipital regions of the human brain can be behaviorally manipulated when feedback or reward is provided for changing the density of this activity. Other researchers have provided evidence that theta activity (4 to 7 Hz) and the beta activity (greater than 14 Hz) can also be controlled by humans and analogs of this activity have been conditioned in animals as well (Green, Green and Walters, 1971). In addition to the work that has been carried out with the EEG, researchers such as Engle and Bleecker (1973) have indicated that it might be possible to control cardiac arrhythmias through biofeedback. Studies by Elder et al. (1973) have provided some hope that blood pressure in humans might also be conditioned. Also, considerable effort has been directed to the control of responses from single muscles with particular applied emphasis in neuromuscular rehabilitation, control of muscle tension for tension headaches and the management of migraine headaches through vasomotor conditioning (Brudny et al., 1974; Basmajian, 1963, 1971; Sargent et al., 1973).

Methylphenidate effects on EEG, behavior, and performance in boys with ADHD.

The psychophysiologic and behavioral effects of methylphenidate were assessed in boys with attention deficit hyperactivity disorder between the ages of 9 and 11 years. The effects of methylphenidate on the EEG during baseline and cognitive tasks were evaluated using spectral analysis. Both subjective (rating scales) and objective (continuous performance) measures were administered and analyzed in conjunction with the electrophysiologic data. Although methylphenidate induced regional changes in the EEG under certain task-specific conditions, it had no global effects. Behavioral and performance measures improved with methylphenidate.

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.

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.

Differences in semantic event-related potentials in learning-disabled, normal, and gifted children.

Cortical event-related potentials (ERP) were recorded over FZ, CZ, and PZ scalp sites in 15 learning-disabled (LD), 14 gifted (G), and 13 normal control (N) children of ages 8-12. The common stimulus consisted of nouns presented 80 percent of the time; the target stimulus of animal names presented 20 per cent of the time. ERPs were averaged over subjects from 180 msec pre-stimulus to 900 msec post-stimulus. Principal components analysis was used to determine if there were amplitude differences at different post-stimulus latencies as a function of condition. Differences in ERP's between groups (LD, gifted, and controls), scalp locations, and common versus target stimuli were analyzed by ANOVAs. P3, Late, P2, and N1 components represented by four factors were identified. Significant differences between G and LD and the N and LD groups were found target stimulus at all central locations for the P3 component. Differences were found centrally between G and LD, G and N, and N and LD groups for the P2 component centrally. Other differences were found for the N1 and late components. These differences could be interpreted as a deficit in either attentional mechanisms or information processing for the LD group.

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.

EEG correlates of hypnotic susceptibility based upon fast Fourier power spectral analysis.

The purpose of the present study was to determine if there were differences between high and low hypnotic susceptible subjects based upon fast Fourier power spectral analysis of the EEG recorded both before and during hypnotic tasks from frontal-temporal and occipital-parietal locations. Significant differences were obtained based upon EEG recording electrode location, EEG frequency within six different frequency domains, and hypnotic tasks. However, no main effect differences were obtained based upon hypnotic susceptibility. In contrast to some evoked potential studies in which a few differences have been obtained based on hypnotic susceptibility the lack of any EEG differences in this study even when positive and negative hallucination tasks were employed may have implications for the role of the neocortex in mediating hypnotic phenomena.

Spectral analysis of the central nervous system effects of the relaxation response elicited by autogenic training.

This study examined the effects of the relaxation response, elicited by autogenic training, on central nervous system (CNS) activity. We used computerized spectral analysis of EEG activity as a dependent measure. After baseline EEG data were obtained for all subjects, the experimental group practiced standard autogenic exercises for 15 experimental sessions with home practice. The control subjects received the same number of sessions under identical conditions, except that they listened to a pleasant radio show without home practice. Subjects were then posttested to assess the acute and chronic effects of autogenic training and the relaxation response on CNS activity. The results indicated significant acute effects differences between groups; the experimental group showed greater increases in theta and greater decreases in alpha percent total power. The results suggest that the relaxation response elicited by autogenic training produces significant acute changes in EEG activity and a characteristic spectral pattern; the results also suggest that focusing attention on a repetitive, internal stimulus is a key element in Benson's relaxation response model.

Basal forebrain infusion of HC-3 in rats: maze learning deficits and neuropathology.

Ten adult male Sprague-Dawley rats were infused with hemicholinium (HC-3) using mini-osmotic pumps over a 14 day period through bilateral, chronically implanted cannulae in the nucleus basalis magnocellularis (nbm). Ten matched controls were infused in the same fashion with saline. HC-3 rats receiving implants demonstrated a significant deficit in maze-learning ability compared with individual and group performances before receiving the implants. In saline rats there was no significant difference in maze-learning ability before and after receiving implants. The HC-3 group receiving implants demonstrated a significant deficit in maze-learning ability compared with the saline control group. Serial sections through nbm from control and HC-3 rats indicated that all cannulae were located within infusion range of nbm. In HC-3 subjects, cholinergic cell bodies were destroyed with concurrent degeneration of terminal fields in cortex. Except for cannula insertion damage, the cholinergic neurotransmitter system appeared unharmed in controls. Stains for neuritic plaques and neurofibrillary damage were negative in both groups. The memory deficit in experimental subjects supported by the demonstrated destruction of nbm cholinergic neurons suggests that HC-3 may be useful in the development of an animal model for Alzheimer's Disease.

Auditory elicitation of the P300 event-related evoked potential in the rat.

Auditory stimuli were used to elicit a P300 event-related evoked potential (ERP) in rat. Test conditions were comparable to those for eliciting ERP's in humans. A train of background tones with a randomly inserted target tone at a ten to one ratio were presented individually to ten unrestrained subjects in a baseline, a novel, and a trained condition. In the novel condition EEG's were averaged from subjects hearing both background and target stimuli for the first time. In the trained condition, subjects were previously trained using footshock in a shuttle box to discriminate the target tone. A statistical comparison of an ERP peak elicited at approximately 300 msec in both the novel and target condition compared with the baseline demonstrated the presence of the P300 in the rat.

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.

A double-blind investigation of the relationship between seizure activity and the sleep EEG following EEG biofeedback training.

The sleep EEGs of eight medically refractory epileptic patients were examined as part of a double-blind, ABA crossover study designed to determine the effectiveness of EEG biofeedback for the control of seizures. The patients were initially reinforced for one of three EEG criteria recorded from electrodes placed over sensorimotor cortex: (a) suppression of 3- to 7-Hz activity, (b) enhancement of 12- to 15-Hz activity, or (c) simultaneous suppression of 3- to 7-Hz and enhancement of 11- to 19-Hz activity. Reinforcement contingencies were reversed during the second or B phase, and then reinstated in their original form during the final A' phase. All-night polysomnographic recordings were obtained at the end of each conditioning phase and were subjected to both visual and computer-based power spectral analyses. Four of the patients showed changes in their nocturnal paroxysmal activity that were either partially or totally consistent with the ABA' contingencies of the study. The spectral data proved difficult to interpret, though two trends emerged from the analyses. Decreases in nocturnal 4- to 7-Hz activity were correlated with decreases in seizure activity, and increases in 8- to 11-Hz activity were correlated with decreases in seizure activity. These findings were shown to strengthen the hypothesis that EEG biofeedback may produce changes in the sleep EEG that are related to seizure incidence.

EEG operant conditioning in intractable epileptics.

Eight epileptic patients with mixed seizures refractory to medical control participated in a double-blind crossover study to determine the effectiveness of operant conditioning of the EEG as an anticonvulsant procedure. Baseline levels of seizures were recorded for four months prior to the beginning of treatment. Participants then received false (noncontingent) feedback for two months followed by an ABA-patterned training program lasting a total of ten months. Subjects were assigned to three treatment groups based on different schedules of EEG feedback. They were first trained (A1 phase) either to suppress slow activity (3 to 8 Hz), to enhance 12- to 15-Hz activity, or to simultaneously suppress 3- to 8-Hz and enhance 11- to 19-Hz activity. This was followed by a B phase, in which patients were trained to enhance slow activity (3 to 8 Hz). In the final phase (A2), the initial training contingencies were reinstated. Neuropsychological tests were performed before and after training, and changes in EEG activity as determined by Fast Fourier spectral analyses were analyzed. Five of eight patients experienced a decrease in their mean monthly seizure rate at the completion of feedback training as compared with their initial baseline level.