" EEG Training for ADHD and Learning Disorders", Othmer, S & Othmer, S.F.

EEG Biofeedback Training for Hyperactivity,
Attention Deficit Disorder, Specific Learning Disabilities,
and Other Disorders
Siegfried Othmer, Ph.D., and Susan F. Othmer
March, 1989
Page 1 of 5

INTRODUCTION
The technique of EEG biofeedback has been investigated by researchers for nearly 20 years. It is still relatively uncommon because its usage has been restricted largely to drug-refractory cases of epilepsy. It has also been investigated for use with minor neurological conditions such as hyperactivity , attention deficit disorder, and specific learning disabilities. Finally, its clinical application has broadened to include other conditions such as endogenous depression, sleep disorders, and the motor, sensory, cognitive and psychosocial dysfunctions attributable to minor closed head injury. In the latter applications, research backup is still meager. The clinical application of the technique is now outpacing the capability of research to provide the statistical underpinnings, on the one hand, and to evaluate testable models on the other.
EARLY RESEARCH BASIS of the EEG BIOFEEDBACK TECHNIQUE
Numerous research studies have confirmed the identification of a 12-14 Hz rhythm in the EEG of a number of species, observed over the Rolandic (sensorimotor) cortex. This rhythm is associated with inhibition of motor activity (Chase and Harper, 1971; Howe and Sterman, 1972; Sterman, 1977). It was labeled SensoriMotor Rhythm (SMR) for its location at the sensorimotor cortex. The rhythm has also been identified in humans. An increase in SMR in the EEG of cats by operant conditioning was subsequently demonstrated (Sterman and Wyrwicka, 1967; Wyrwicka and Sterman, 1968). Similar findings were observed in primates. One effect of such training in cats and in humans was to increase the incidence and duration of Rolandic sleep spindles, which occur in the identical spectral band (12-15 Hz) as the waking SMR, and in the same location. This is accompanied by more sustained periods of quiet sleep in both normal subjects and insomniacs (Sterman, Howe, and MacDonald, 1970).
It was also noted that paraplegics and quadraplegics exhibited larger than normal amounts of the sleep spindles, and reduced amounts of low frequency (4-7 Hz) EEG activity. Concomitantly, victims of spinal cord injury exhibit a relative dearth of epileptic behavior. Moreover, cats with cervical dorsal column transsections exhibited a heightened threshold for drug induced seizures. Finally, a case was observed in which an epileptic subject suffered a high cervical cord compression, and his clinical and EEG seizure activity subsequently disappeared (Sterman and Shouse, 1982). These findings suggested a correlation on the one hand between the quality of sleep and epilepsy (Sterman, 1976a) and on the other a fundamental relation between the relative incidence of SMR rhythm and that of seizures with a motor symptomatology. Reduction in 4-7 Hz power has also been demonstrated in monkeys during sleep, after administration of four anticonvulsant drugs. This suggests that excessive low frequency amplitude is indicative of insufficient cortical control, and is a concomitant of susceptibility to seizure onset; moreover, it can be impacted by the medication.
Following on such hypotheses, it was found as early as 1969 that after training for enhanced SMR rhythm in cats the threshold for seizure onset was increased for chemically induced seizures (Fairchild, 1974, Sterman, 1976b). Subsequently, EEG feedback training in poorly controlled epileptics yielded numerous reports of seizure reduction. In 1972, Sterman and Friar published a study of seizure reduction achieved in one person using SMR augmentation training only. There were, in addition, favorable personality changes as well: "Initially she was a quiet and unobtrusive person. She became more confident, outgoing, and interested in her appearance as time went on. She reported that she went to sleep faster, had a more refreshing sleep, and woke up faster in the morning." (Sterman, 1972). Sterman, MacDonald, and Stone achieved an average 66% reduction in seizure incidence in four epileptics using SMR enhancement training in combination with inhibition of excessive slow-wave activity in the 6-9 Hz regime (Sterman, 1974).
Finley, Smith, and Etherton achieved a factor of ten reduction in seizure incidence in a 13-year-old epileptic with an initial seizure rate of eight per hour. These results were achieved with SMR enhancement training in the 11-13 Hz range over some 6 months. There was a concomitant reduction in number of epileptiform discharges observable in the EEG (Finley, 1975). In a followup study after one year of SMR training, seizure incidence had decreased to one per 3 hours (Finley, 1976). Seifert and Lubar achieved significant seizure reduction for 5 of 6 subjects with three months of SMR training, although no significant change in SMR EEG amplitude was demonstrated. Excessive 4-7 Hz amplitudes were inhibited. Subjects were uncontrolled with near-toxic levels of anticonvulsants (Seifert, 1975). Lubar and Bahler used the same protocol with eight severely epileptic patients, and achieved seizure reduction with seven. Two were seizure-free for as long as a month after training. Others acquired the ability to block seizures. Severity and duration of seizures also decreased (Lubar, 1976).
The above studies and other similar ones were reviewed by Sterman (1982). The common elements were that they typically combined positive reinforcement of intermediate EEG frequencies (in the range of 8-25 Hz) with inhibition of lower frequencies (3-8 Hz), but differed in many aspects, such as electrode placement and reward criteria. Taking all the studies together indiscriminately, some 70% of subjects showed seizure reduction with the various experimental protocols.
Recently, Tozzo et al compared EEG biofeedback with relaxation training. Five of 6 drug-refractory epileptics were found to be able to reduce seizure incidence and severity with SMR augmentation training combined with theta (i.e., 4-7 Hz) inhibition. Two subjects benefited in seizure rate from relaxation training (Tozzo, 1988).

In order to establish the validity of the EEG biofeedback training technique, controlled studies were needed. For the case of operant conditioning, such controlled studies consist of ABAB studies, in which the contingency for reward is periodically reversed. Nonspecific effects of the training are ascertained by the use of non-contingent reward, using "yoked controls", where the feedback signal to the patient is derived, unbeknownst to him, from another patient.
Cabral and Scott used EEG biofeedback and relaxation in a crossover design with three cases of drug resistant epilepsy. Both biofeedback and relaxation improved patients' control of their seizures, and the benefit was maintained during the followup period (Cabral, 1976). Wyler, Lockard, and Ward showed that enhancement of EEG activity above 14 Hz, and suppression of activity below 10 Hz also was effective in seizure reduction. A contingency reversal design was used. Synchronization of the EEG worsened seizure incidence; desynchronization of the EEG improved it. Two patients showed improved incidence; two showed improved severity. A fifth was a control with EMG biofeedback alone, and showed no change (Wyler, 1976). An ABAB single-blind study of the effect of EEG biofeedback training on seizure incidence was performed by Sterman and MacDonald (1978). Two frequency bands were employed for enhancement: 12-15 Hz, the SMR band; and 18-23 Hz, in the beta band, associated with EEG activation, focus and arousal. Reduction in seizure incidence was reported for 6 of 8 patients, and amounted to 44-100%, with an average reduction of 74%. When 12-15 Hz was used for reward, and the contingency subsequently reversed, seizure incidence once again increased as expected. However, with the use of 18-23 Hz, the seizure incidence did not change significantly after contingency reversal. (This is not entirely unexpected. Once EEG regulation is effected, the tolerance to epileptogenic EEG activity appears to be permanently enhanced, and not easily reversed.) The experiment was single-blind in that the subject was unaware of the sense of the contingency.
The possibility that the beneficial effect of EEG biofeedback training is nonspecific was ruled out with studies using noncontingent or random rewards. Several studies obtained the consistent result that noncontingent reward was ineffective in seizure reduction. Wyler's and Finley's studies were the first to include such pseudo-conditioning and control periods (Wyler, 1976; Finley, 1976). Such sham training was also provided for in a more exhaustive, double-blind study (neither the experimenter nor the patient was aware of the contingency of reward) undertaken by Lubar, et al. in 1981. Eight medically intractable epileptics were subjected to a lengthy experimental paradigm which included a four-month baseline for recording of seizures, a two-month period of non-contingent reward, a four-month EEG training phase, a reversal phase, a second training phase, another four-month pseudotraining phase, and followup. During the training phase, patients were given one of three contingencies: suppression of 3-8 Hz activity, enhancement of 12-15 Hz, or simultaneous suppression of 3-8 Hz and enhancement of 11-19 Hz activity, the latter to achieve normalization of the EEG.
Five of 8 patients exhibited seizure reduction with respect to baseline, the reduction being 35% for the entire group. The training to reduce 3-8 Hz amplitude was the most effective. Reversal training to enhance 3-8 Hz was likewise effective in increasing seizure incidence, so much so that the training had to be interrupted for two patients who deteriorated rapidly with that training. The fact that facilitation of abnormal EEG patterns can exacerbate seizures provides additional verification of efficacy of the training. Restoration of the appropriate contingency restored the previous gains. Those who trained for EEG normalization did not show deterioration during the reversal phase. EEG studies performed during the training as well as during sleep confirmed a decrease in abnormal low-frequency patterns, as well as increase in mid-frequency activity (12-15 Hz and 16-19 Hz), even when that was not specifically trained for (Whitsett, 1982). Hence, relaxation effects or other nonspecific effects do not appear to explain the results obtained.
These conclusions were recently again confirmed in a controlled study of 24 drug-refractory epileptics, in which impacts of the training on motor, cognitive, and psychosocial function were investigated (Lantz and Sterman, 1988). An overall 61% reduction in seizure incidence was achieved with training, with a range of 0-100%. Cognitive and motor function improved only in that population which achieved significant seizure reduction with training. Psychosocial performance improvements, on the other hand, appeared to be uncorrelated with training history according to some tests, and to be significantly correlated according to others.
The controlled studies just referred to serve to establish that specific benefits in terms of seizure management are achievable with EEG biofeedback training which incorporates the elements of 1) suppression of excessive low-frequency activity, in the 3-8 Hz band; 2) enhancement of activity in the 12-15 Hz or 11-19 Hz bands. These results are not explainable in terms of non-specific factors related to participation in these studies.
Effectiveness of EEG Biofeedback in the Treatment of Hyperactivity, Attention Deficit Disorder, and Learning Disabilities
The utilization of EEG biofeedback in the treatment of hyperactivity was initially an incidental corollary to the study of epilepsy. It was observed that symptoms of hyperactivity subsided during training for seizure reduction with epilepsy (Lubar and Bahler, 1976a). This was not entirely surprising, since hyperactivity may also be regarded in terms of insufficient motor inhibition, and since the EEG observables are similar in general to interictal epileptiform activity: a relative abundance of low-frequency activity (beyond age-appropriate norms), and a relative dearth of intermediate frequency activity (SMR and beta).
The first systematic study of EEG biofeedback effectiveness with hyperactivity in the absence of seizure history was reported by Lubar and Shouse (1976b). An ABAB study, it employed reward for 12-14 Hz, and inhibition of excessive 4-7 Hz. The contingencies were periodically reversed. The subject was able to acquire the SMR task, increasing the fraction of time that SMR was produced above threshold. A number of behaviors associated with the hyperactivity were monitored, and significant changes, in line with expectations, were observed for 8 of 13 behavior categories. The EEG training was shown to be more effective than the use of stimulant medication (methylphenidate, or Ritalin (R)) alone.
A more comprehensive study of hyperkinesis and EEG biofeedback is that of Shouse and Lubar, (1979). A test of stimulant drug withdrawal was included in this work. 3 of 4 subjects showed contingent increases in SMR which were correlated with class room motor inactivity. Combining SMR training with drug treatment resulted in substantial improvements in tested behaviors that exceeded the effects of drugs alone, "and were sustained with SMR training after medication was withdrawn". One subject failed to acquire the SMR task. There was a correlation of pre-training SMR levels with inappropriate motor behavior, as well as with the susceptibility to training.
The undesirable behaviors monitored in the study were disruptive motor activities such as self-stimulation, object play, out-of-seat, self-talk, opposition, and non-interaction. Desirable behaviors were increased attention span and cooperation. Social behaviors evaluated were self-initiated approaches to peers or teachers, and sustained interactions with them. In the three responding individuals, percent of time with SMR increased from 5-35%, 13-25%, and 10-32%, respectively. Desirable behaviors increased from 7-40 events per day, 12-40, and 12-28, respectively; whereas undesirable behaviors decreased from 50-12, 30-12, and 38-12, respectively. The study suggested that the SMR may have both diagnostic and prognostic value in hyperkinesis remediation, with particular regard to motor rather than attentional deficits.
Finally, a clinical study by Lubar and Lubar (1984) extends the technique to attentional deficits and learning disabilities. The appropriateness of doing so is based, among other considerations, on the observation that more than 60% of the cases of learning disability exhibit EEG abnormalities (Muehl, Knott, and Benton, 1965). The experimental protocol was complemented with training in the 15-18 Hz region associated with EEG activation in general, and with arousal and focus. Changes in the EEG were documented with power spectral density measurements, which were compared with those of normal subjects. The EEG biofeedback was also accompanied by academic training. Acquisition of the desired EEG characteristics was observed in all 6 subjects under study. Significant improvements in academic performance were also documented for all of the subjects. A recent review of EEG biofeedback applied to hyperkinesis and learning disabilities may be found in Lubar, (1989). The fact that hyperkinesis and attention deficit disorder is conventionally treated with stimulant medication is evidence that we are dealing with insufficient arousal. This tends to support the enhancement of 15-18 Hz EEG activity as a strategy for activating the arousal and focus mechanisms affecting the sensorimotor cortex, as well as other cortical and subcortical areas of the brain.
One remaining question with the study is that of separating out the effects of the EEG biofeedback from those of the academic augmentation. It was observed that "five of the 6 children were receiving such academic training prior to the onset of the EEG biofeedback training, with no significant improvement over several years." Hence, the beneficial effects are ascribed primarily to the EEG biofeedback. This conclusion is buttressed by the objective changes observed in the EEG, which are appropriate to the training protocol.
A large fraction of specific learning disabilities (as distinct from obvious attentional problems or hyperactivity) also appear to find their basis in minor neurological deficits. By using a large number of indicators, some 95% of learning disabled children could be correctly identified strictly on the basis of the EEG (Lubar, 1989). Using as few as 8 variables, predictability was already above 75%. The best predictor was excessive 4-8 Hz activity in the frontal-temporal locations. Enhancement of beta activity was found to be successful in most of a group of 37 children evaluated over a period of two years. The children showed a significant improvement in Metropolitan Achievement Test scores as compared to controls.
Ongoing Clinical Work with EEG Biofeedback
The protocol discussed above, namely reinforcement of 12-15 Hz (SMR) or of the beta spectral band (15-20 Hz), with simultaneous inhibition of low frequency, typically 4-7 Hz, has been used extensively in clinical settings. For research purposes, experimental methodology in a clinical setting suffers from the fact that controlled studies are not generally possible with paying patients. In particular, it is not professional to subject such patients to contingency reversals or non-contingent feedback, or to some other test of placebo or non-specific effects. On the other hand, the data are numerous, and hence gain a certain credibility from the sheer weight of evidence. These continuing clinical evaluations are summarized briefly in the following, to the extent that we are aware of them.
Epilepsy
The technique has been used extensively over the years for drug refractory and other cases of epilepsy. Some users have adopted the strategy of reinforcing beta (e.g. 15-18 Hz) instead of SMR (12-15 Hz), with apparently equivalent results. Also, reinforcement strategies have been changed to enhance the rate of task acquisition. Reduction or elimination of anticonvulsant medication has been possible in numerous cases. The acquisition of the new EEG pattern also appears to be permanent in many cases, although some patients will return for refresher sessions on a bi-monthly basis.
The technique has also shown itself to be helpful for other consequences of epilepsy, such as the emotional, social and cognitive deficits. With respect to psychosocial aspects, results were mixed in the recent Lantz and Sterman study. We may speculate that the SMR-enhancement protocol may be more effective with a motor symptomatology, and that psychosocial performance can be expected to improve in cases where there is limbic system involvement. In the latter case, the enhancement of low beta (15-18 Hz) may be a preferable training goal.
Hyperactivity and Attention Deficit Disorder
Clinical experience in the treatment of hyperactivity and attention deficit disorder, as well as specific learning disabilities, extends to about 2000 children. Residual type (adult) attention deficit disorder has been successfully treated as well. As in the case of epilepsy, training has been done preferentially with the most challenging cases, namely those which are not adequately managed with medication, and those presenting behavioral problems (conduct disorder). In some clinical settings, the experimental protocol has shifted to the exclusive training of the 15-18 Hz spectral band, to the exclusion of the SMR. The symptoms of hyperactivity subside readily in either case, although a rigorous comparative study would be of interest. The success of this strategy tends to imply that inadequate arousal and poor desynchronization of the cortex may underlie both the attentional and the motor deficits. (On the other hand, perhaps one should not overemphasize the distinction, since typical filters will not exhibit high rejection of the neighboring band.) Whereas some degree of treatment success is reasonably predictable for these conditions, training may extend to 50 or more sessions. A significant effect of beta enhancement training (concurrent with theta suppression) on conduct disorder has been observed by several practitioners.
Variations of the "standard" paradigm of training to enhance 12-15 Hz or 15-18 Hz amplitudes with simultaneous inhibition of excess 4-7 Hz have also been reported by other clinical workers. Tansey trained to augment SMR with audio feedback to the patient. He also employed a midline placement for the electrode, rather than over sensorimotor cortex. In an early reported study, both EMG and EEG biofeedback were evaluated with one patient. EMG biofeedback was used successfully to reduce motoric activity level to below that previously achieved with Ritalin. Further, ADD was no longer diagnosable after the EMG training. Subsequent SMR enhancement training effected remediation of the developmental reading disorder, and the child's ocular instability (Tansey, 1983).
Learning Disabilities and Dyslexia
EEG biofeedback has now been evaluated in realistic settings in two separate studies: first, that of the Lubars in Tennessee schools (already referred to), and second, a study by J. Carter and H. Russell in Texas schools (See Lubar, 1989). In the former, training was carried out by resource teachers or school psychologists. In the Texas study, indications were that left hemisphere beta enhancement led to improvements in verbal IQ, as measured by the WISC-R, whereas beta enhancement of the right hemisphere led to improvement in the performance measures of the WISC.
Tansey has also evaluated the training for specific learning disabilities, i.e. those apparently unrelated to attentional deficits. In those cases (4) in which the verbal and performance IQ (WISC-R) differed by more than 15 points, EEG training effected an improvement by no less than 60% in the lower of the two scores. This demonstrated 1) that midline placement is effective in training either hemisphere, and 2) that the training effects preferential remediation of deficits (Tansey, 1985).
In a recent study (Tansey, 1990), 24 learning disabled children were given EEG training and evaluated with the WISC-R. Here the training paradigm included inhibition of excessive 7 Hz amplitudes via verbal cues. Eleven of the subjects had been diagnosed neurologically impaired, eleven were judged perceptually impaired, and two were diagnosed with ADD. Training sessions were conducted weekly for 30 minutes. The average number of training sessions was 28. The average increase in verbal IQ was found to be 16 points, in performance IQ 19 points, and in full scale IQ, 19 points. When either verbal or performance was in deficit with respect to the other by more than 12 points, the improvement in IQ scores for the area in deficit was twice that of the other.
The available evidence suggests that the EEG biofeedback technique has an impact on certain specific learning disabilities, while others remain relatively unaffected. Some cases of dyslexia, for example, respond readily to training, while others remain resistant. The large variety of brain lesions which could be responsible for these specific deficits may account for this variability in response to training. The evidence is tantalizing, and demanding of more rigorous study. The use of the technique for learning disabilities constitutes perhaps its most widespread application at the present time. However, much of this work has not been published.
Sleep Disorders
There is a close connection of the entire history of EEG biofeedback for control of epilepsy with the study of sleep disorders. The identification of the SMR rhythm with sleep spindles has already been referred to. It was also noted that enhancing the SMR rhythm by means of biofeedback training resulted in more normal, peaceful sleep in individuals referred for treatment of seizure disorders and those referred for other conditions such as primary unipolar depression. In clinical studies, the effectiveness of SMR and low-beta training for treatment of insomnia has been demonstrated.
Treatment for hyperactivity in young children will often lead to the early report that sleep walking, night terrors, bedwetting, bruxism (teeth grinding), and sleep-talking or walking have stopped. Treatment for depression will often lead to the report that quality of sleep is improved.
Minor Traumatic Brain Injury
The EEG biofeedback technique appears to be quite effective in recovering function in cases of minor brain injury, particularly in those cases where the organic damage is relatively minor and diffuse (e.g. ischemia or anoxia), and may not even be discernible by conventional imaging techniques. Examples of brain injury where the EEG training has been effective include concussion, whiplash, central nervous system infection, chemical CNS injury, stroke, and cerebral palsy. Clinical experience now extends to more than 500 cases of closed head injury.
The chronic effects of concussion appear to be subject to remediation by EEG training. These include headaches, dizziness, fatigue, poor concentration and memory, irritability, mood swings, insomnia, poor hearing and vision, slurred speech, anxiety and depression. It will not have escaped notice that a number of the other conditions discussed, such as epilepsy and hyperactivity, may be caused by minor closed head injury as well. The prominence of birth trauma in the medical histories of children referred for hyperactivity, ADD, and learning disabilities renders it only too likely that these conditions are frequently attributable to this mechanism of brain injury. (This is not to deny the manifest contribution of heredity.) Hence, the story of EEG biofeedback is to a large extent the story of minor brain injury in its inclusive sense.
Discussion of Possible Mechanisms
The EEG training technique discussed above appears to be effective over quite a range of conditions which are traceable to the existence of anomalous EEGs. In the case of hyperactivity, the observable anomaly generally consists of excessive low-frequency activity with insufficient beta activity, related to arousal. In the case of epilepsy, interictal activity is likewise characterized by enhanced low frequency activity (in addition to subclinical spike-and-wave or other epileptiform phenomena). In the case of endogenous depression, the EEG shows abnormally low amplitude overall, in particular low beta activity. In all cases, the changes effected in the EEG are such as to make the EEG more normal. In general, the changes appear to be permanent, once learning has been consolidated. Severe cases may benefit from periodic booster sessions.
The normal adult EEG in the awake and focused state is characterized by relatively low amplitude activity, with the statistical characteristics of noise. The spectral density is roughly monotonically declining with frequency. The result of training is to approach this ideal characteristic. This occurs regardless of the initial EEG characteristic. For example, if the intermediate frequency amplitude is high initially, it will come down toward normal levels, even though the training is reinforcing in that frequency band. This paradoxical result is ascribed to the existence of mid-frequency components of the adverse low-frequency EEG characteristics one wishes to suppress, as well as to the existence of excess high frequency activity (>20 Hz) in many EEGs. When the excessive low frequency components are trained out, the higher frequency components are reduced also. Training also effects elimination over time of the excess high frequency activity. For these reasons, we cannot use an increase in mid-frequency EEG amplitude as a measure of treatment success in all cases. One needs to use more comprehensive criteria for normalcy of the EEG. In practice, the more appropriate observables are the behavioral ones. Behavioral change is often noted well before changes are unambiguously registered within the EEG. The converse may also occur: dramatic changes in the EEG may be noted, with significant behavioral change noted only later. A tight correlation between what is observed behaviorally and what is seen in the EEG is probably not in prospect.
The observation that EEG training effects changes in the EEG toward more normal values, regardless of the starting point, buttresses the hypothesis that the training effects improved cortical regulation. A further observation is that the training appears to have little observable effect on a person characterized by a normal EEG. This suggests that we are not producing a particular brain state (creative or otherwise), but rather are restoring conditions of normalcy when these are absent. Cortical regulation is accomplished by activation of the brain stem and thalamic activating system, and inhibitory feedback circuits involving both nonspecific and specific thalamic nuclei. Hence, we are in all likelihood effecting change subcortically. This also helps to account for the fact that the effects of training are non-local. That is, training one hemisphere may also train the other, and the effect of training on emotional factors indicates an impact on the limbic system as well. Whereas it appears to be true that training at the sensorimotor cortex impacts on the entire brain, the converse is not true. That is, what goes on in the rest of the brain is not necessarily discernible at the sensorimotor cortex. This may account for the absence of tight coupling between what is observed behaviorally and what is seen in the EEG.
The effectiveness of training in the 15-18 Hz spectral band, as well as the 12-15 Hz spectral band, suggests that a more general mechanism than motor inhibition is involved. One may associate coherent activity such as alpha spindles and sleep spindles with self-generative mechanisms within the thalamus or reticular formation, since these spindles occur preferentially when external stimuli are excluded (closed-eyes, or sleep, respectively). By contrast, a state of focused attention which is optimally receptive to sensory inputs (which are random in phase) is likely to be characterized by desynchronized EEG activity, one governed by a stochastic, random process. When a given mechanism is shifted from coherence to incoherence, the observed spectral content shifts to higher frequency, and reduces in amplitude. Conversely, if a given cortical process is entrained to function at a lower frequency (12-15 Hz), it may do so by augmenting inhibitory functions. By using the higher frequency band (15-18 Hz), one may still be training the same mechanism, but one may be training it toward more appropriate activation, rather than specifically enhancing inhibitory processes. This is consistent with the subjective experiences reported with SMR and beta training, which are distinctly different.
Summary and Conclusion
The EEG biofeedback technique appears to be quite successful in effecting remediation in hyperactivity, attention deficit disorder, specific learning disabilities, drug-resistant and other cases of epilepsy, in sleep disorders, and in cases of closed head injury. The effects of training appear to be permanent in most cases.
The unifying criterion underlying the conditions treated appears to be that they exhibit anomalous EEG properties. In a large fraction of the cases, these anomalous EEG properties are traceable to identifiable injury to the brain in the patient's life history, including fetal drug exposure and birth trauma. Detailed family histories commonly indicate a genetic vulnerability or predisposition as well. At least partial normalization of the EEG is a demonstrated consequence of the biofeedback training in most cases. The clinical studies have considerably outdistanced the research to date, and clearly justify further research in order to put these findings on a sound basis, as well as to refine the technique and permit the determination of mechanisms. The generality of the technique suggests that we are dealing with a very fundamental mechanism of cortical regulation affecting areas of the brain beyond the sensorimotor cortex where training takes place.
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