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EEG Biofeedback training for hyperactivity, attention deficit disorder, specific learning disabilities, and other disorders




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From EEG Spectrum, Inc., 16100 Ventura Blvd., Suite 10, Encino,
CA 91436  (818) 788-2083   email: EEGSpectrm@aol.com
---------------------------------------------------------------
EEG BIOFEEDBACK TRAINING FOR HYPERACTIVITY, ATTENTION DEFICIT
DISORDER, SPECIFIC LEARNING DISABILITIES, AND OTHER DISORDERS
                                   
    by Siegfried Othmer, Ph.D., and Susan F. Othmer
                          March, 1989


                   INTRODUCTION AND SUMMARY

     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 meagre. 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 find ings 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 (12-15Hz) 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 chemi cally 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 observ able 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 intermedi ate EEG frequencies
(in the range of 8-25 Hz) with inhibition of lower frequencies
(3-8Hz), 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).

     CONTROLLED STUDIES OF EEG BIOFEEDBACK TRAINING FOR EPILEPSY

     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 12-15Hz 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 nonspe cific 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 medi cally 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-contigent 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 enhance ment 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 signifi cant 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 incor porates 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.

     THE 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 12-14Hz, and inhibition of excessive 4-7Hz. The contingen
cies 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 substan tial 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 inappro priate 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 15-18Hz 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 4-8Hz 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 Metropo litan
Achievement Test scores as compared to controls.

          ONGOING CLINICAL WORK WITH EEG BIOFEEDBACK

     The protocol discussed above, namely reinforcement of
12-15Hz (SMR) or of the beta spectral band (15-20Hz), with
simultaneous inhibition of low frequency, typically 4-7Hz, 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 (12-15Hz), with apparently equivalent results. Also,
reinforce ment 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
(15-18Hz) 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 behav ioral problems (conduct disorder). In some
clinical settings, the experimental protocol has shifted to the
exclusive training of the 15-18Hz 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 overem phasize 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, 1984).

     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 func tion 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 discer nible 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.

               A 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 rela tively 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
(>20Hz) 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 behav ioral 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 accom plished 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 desynchron ized EEG activity,
one governed by a stochastic, random process. When a given mecha
nism 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 (15-18Hz), 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 reme diation 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.

                       REFERENCES

     References are in alphabetical order by first author, and in
chronological order within listings for first author.

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
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REFERENCE TEXTS

Basmajian,  John  V.,  Biofeedback, Principles and Practice for
Clinicians, Williams and Wilkins, Baltimore (1989).

Fischer-Williams, M., Nigl, A. J.,  and  Sovine, D. L.,  A
Textbook of Biological Feedback, Human Sciences Press, New York
(1981).

Giannitrapani, D. and L. Murri, eds., The EEG of Mental
Activities, Karger, Basel (1988).

Kilch,  L.G., McComas, A.J., Osselton, J.W., and Upton, A.R.M.,
Clinical Encephalography, Butterworths, London (1981).

Levin, H. S., Eisenberg, H. M.,  and Benton, A. L.,  Mild Head
Injury, Oxford University Press, London (1989).

Lubar, Joel F., and Deering, William M., Behavioral Approaches to
Neurology, Academic Press, New York (1981).


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