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.

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%.

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.

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.

Reduction of epileptic seizures through EEG biofeedback training.

Biofeedback training of the sensorimotor rhythm (SMR) was carried out in three male and three female adolescent epileptics and in two normal controls. The patients represented a cross-section of epilepsies including grand mal, myoclonic, afocal and psychomotor types. Three of the cases were mentally retarded. 12-14 Hz (SMR) activity was detected by a combination of sharp analog filtering and digital processing. The patients were provided with feedback whenever they produced 0.5 sec of 12-14 Hz activity of a specified amplitude. Additional feedback was provided for epileptiform activity slow waves or movement. Furthermore, feedback for SMR production was inhibited by digital logic circuitry when movement, slow waves or spikes were present. Seizure reduction was obtained in five of the six epileptics. Several patients showed increased percentage of SMR when feedback was provided and varying degrees of normalization in their EEG as demonstrated by fast Fourier, crossed power spectral density and coherence analyses.

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.

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.

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.

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.

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.

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 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).