" EEG Training for ADHD and Learning Disorders", Othmer, S & Othmer, S.F.
Training for Hyperactivity,
Attention Deficit Disorder, Specific Learning Disabilities,
and Other Disorders
Siegfried Othmer, Ph.D., and Susan F. Othmer
Page 1 of 5
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
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
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
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
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.
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
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
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.
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
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.
Cabral, R.J., and Scott, D.F. (1976).
The Effects of Desensitization Techniques, Biofeedback and Relaxation
on Intractable Epilepsy: Follow-up Study.
J. Neurol. Neurosurg. Psychiatry, 39, 504-507.
Chase, M.H., and Harper, R.M. (1971).
Somatomotor and visceromotor correlates of operantly conditioned
12-14 c/sec sensorimotor cortical activity. Electronencephalogr.
Clinical Neurophysiology, 31, 85-92.
Ellertsen, B., and Klove, H. (1976).
Clinical application of biofeedback training in epilepsy.
Scandinavian Journal of Behavior Therapy, 5, 133-144.
Fairchild, M.D., and Sterman, M.B. (1974).
Unilateral Sensory-Motor-Rhythm (SMR) Training in Cats: A Basis
for Testing Neurophysiological and Behavioral Effects of Monomethylhydrazine
Report to the Aerospace Medical Research Laboratory, AMRL-TR-73-123.
Finley, W.W., Smith, H.A., and Etherton, M.D. (1975).
Reduction of seizures and normalization of the EEG in a severe epileptic
following sensorimotor biofeedback training: Preliminary study.
Biol. Psychology, 2, 189-203.
Finley, W.W. (1976).
Effects of Sham Feedback Following Successful SMR Training in an
Epileptic: A Follow-Up Study.
Biofeedback and Self-Regulation, 1, 227-235.
Howe, R.C., and Sterman, M.B. (1972).
Cortical-subcortical EEG correlates of suppressed motor behavior
during sleep and waking in the cat.
J. Electroencephalography and Clinical Neurophysiology, 32, 681-695.
Lantz, DeLee, and Sterman, M.B. (1988).
Neuropsychological Assessment of Subjects with Uncontrolled Epilepsy:
Effects of EEG feedback Training.
Epilepsia, 29(2), 163-171.
Lubar, J.F., and Bahler, W.W. (1976a).
Behavioral management of epileptic seizures following biofeedback
training of the sensorimotor rhythm.
Biofeedback and Self-Regulation, 1, 77-104.
Lubar, J.F., and Shouse, M.N. (1976b).
EEG and behavioral changes in a hyperactive child concurrent training
of the sensorimotor rhythm (SMR).
A preliminary report. Biofeedback and Self-Regulation, 1, 293-306.
Lubar, J.F., Shabsin, H.S., Natelson, S.E., Holder, G.S., Whitsett,
S.F., Pamplin, W.E., and Krulikowski, D.I. (1981).
EEG Operant Conditioning in Intractable Epileptics.
Arch. Neurol., 38, 700-704.
Lubar, J. O., and Lubar, J.F. (1984).
Electroencephalographic biofeedback of SMR and beta for treatment
of attention deficit disorders in a clinical setting.
Biofeedback and Self-Regulation, 9(1), 1-23.
Lubar, J.O. (1989).
Electroencephalographic Biofeedback and Neurologic Applications.
In Basmajian, J.V. (Ed.), Biofeedback, Principles and Practice for
Clinicians. Williams and Wilkins, Baltimore.
Muehl, S., Knott, J.R., and Benton, A.L. (1965)
EEG abnormality and psychological test performance in reading disability.
Cortex, 1, 434-439.
Peniston, E. G., and Kulkosky, P.J. (1989).
Alpha-Theta Training and Beta-endorphin Levels in Alcoholics.
Alcoholism: Clin. and Exper. Research, 13, 271.
Seifert, A.R., and Lubar, J.F. (1975).
Reduction in epileptic seizures through EEG biofeedback training.
Biol. Psych., 3, 157-184.
Shouse, M.N., and Lubar, J.F. (1979).
Operant conditioning of EEG rhythms and Ritalin in the treatment
Biofeedback and Self-Regulation, 4(4), 301-312.
Sterman, M.B. & Wyrwicka, W.A. (1967).
EEG correlates of sleep: Evidence for separate forebrain substrates.
Brain Research, 6, 143-163.
Sterman, M.B., Howe, R.C., and MacDonald, L.R. (1970).
Facilitation of spindle-burst sleep by conditioning of electroencephalographic
activity while awake.
Science, 167, 1146-1148.
Sterman, M.B. and Friar, L. (1972).
Suppression of seizures in an epileptic following sensorimotor EEG
Electroencephalogr. Clinical Neurophysiology, 33, 89-95.
Sterman, M.B., MacDonald, L.R., and Stone, R.K. (1974).
Biofeedback training of the sensorimotor EEG rhythm in man: Effect
Epilepsia, 15, 395-416.
Sterman, M.B. (1976a).
Effects of Sensorimotor EEG Feedback Training on Sleep and Clinical
Manifestations of Epilepsy.
In Beatty, J. and Legewie, H. (Eds.), Biofeedback and Behavior,
Plenum Press, New York; pp. 167-200.
Sterman, M.B. (1976b).
Effects of brain surgery and EEG operant conditioning on seizure
latency following MMH intoxication in the cat.
Experimental Neurology, 50, 757-765.
Sterman, M.B. (1977).
Sensorimotor EEG operant conditioning and experimental and clinical
Pavlovian J. Biological Science, 12(2), 65-92.
Sterman, M.B., and MacDonald, L.R. (1978).
Effects of central cortical EEG feedback training on seizure incidence
in poorly controlled epileptics.
Epilepsia, 19, 207-222.
Sterman, M.B., and Shouse, M.N. (1982).
Sensorimotor Mechanisms Underlying a Possible Common Pathology in
Epilepsy and Associated Sleep Disturbances.
In Sleep and Epilepsy, Chapter 3, Academic Press.
Sterman, M.B. (1982).
EEG Biofeedback in the treatment of epilepsy: an overview circa
In White, L. & Tursky, B. (Eds.), Clinical Biofeedback: Efficacy
and Mechanisms. The Guilford Press, New York.
Tansey, M.A., Bruner, R.L. (1983).
EMG and EEG Biofeedback Training in the Treatment of a 10-year-old
Hyperactive Boy with a Developmental Reading Disorder.
Biofeedback and Self-Regulation, 8, 25-37.
Tansey, M.A. (1985).
Brainwave Signatures. An index reflective of the brain's functional
neuroanatomy: Further findings on the effect of EEG sensorimotor
rhythm feedback training on the neurologic precursors of learning
Int. J. Psychophysiology, 4, 91-97.
Tansey, M.A. (1986).
A simple and a complex tic (Giles de la Tourette's syndrome): Their
response to EEG sensorimotor rhythm biofeedback training.
Int. J. Psychophysiology, 4, 91-97.
Tansey, M.A. Righting the Rhythms of Reason (1990).
EEG Biofeedback Training as a Therapeutic Modality in a Clinical
Medical Psychotherapy, 3, 57-68.
Tozzo, C.A., Elfner, L.F., and May, Jr., J.G. (1988).
EEG biofeedback and relaxation training in the control of epileptic
Int. J. of Psychophysiology, 6, 185-194.
Whittsett, S.F., Lubar, J.F., and Holder, G.S. (1982).
A double-blind investigation of the relationship between seizure
activity and sleep following EEG biofeedback training.
Biofeedback and Self-Regulation, 7, 193-207.
Wyler, A.R., Lockard, J.S., and Ward, A.A. (1976).
Conditioned EEG Desynchronization and Seizure Occurrence in Patients.
Electroencephalography and Clinical Neurophysiology, 41, 501-512.
Wyrwicka, W. and Sterman, M.B. (1968).
Instrumental conditioning of sensorimotor cortex EEG spindles in
the waking cat.
Physiol. Behavior, 3, 703-707.