of Attention Deficit Hyperactivity Disorder with Neurotherapy
for reprints should be addressed to John K. Nash, Ph.D., Behavioral
Medicine Associates, Inc., 3300 Edinborough Way, Suite 110, Edina, MN
his website: www.qeeg.com
©2000 VOL. 31 NO. 1
John K. Nash
Attention Deficit Hyperactivity Disorder EEG Biofeedback
Neurofeedback Neurotherapy Quantitative EEG
increasing number of clinicians use operant conditioning of electroencephalographic
activity (termed neurotherapy, neurofeedback, or EEG biofeedback) as
a method of helping children and adults with Attention Deficit Hyperactivity
Disorder (ADHD) learn improved control of their, attention and activity
levels. The present review examines 1) the nature of ADHD, 2) the scientific
and public health rationale for the use of neurotherapy, 3) the nature
of the neurotherapy process and 4) the published outcome studies on
EEG and behavioral change following neurotherapy.
NATURE OF ADHD
is a psychiatric disorder characterized by clinically significant levels
of symptoms of either inattentiveness, hype ractivity/impulsivity or
both. Persons with this pattern are easily bored, distractible, disorganized,
often stimulation-seeking and impulsive. Epidemiological studies have
estimated 6 to 9% of our children have ADHD.',2 Children with ADHD show
lowered vigilance, sustained attention, impulse inhibition, executive
functions such as organization and complex problem solving and verbal
learning and memory." These deficits persist into adolescence and
ADHD traits show significant heritability' strongly suggesting this
pattern is a genetic predisposition. It is likely that societal factors,
including economic and physical adversity, dissolution of traditional
family and group/tribal structures contribute to the pathological expression
of the ADHD phenotype as well as other childhood mental disorders.'
One might suspect our desire for standardized, rather regimented educational
processes (prescribed sequences of study, timed learning periods, sitting
for long periods of time) might also play a role in the pathological
expression of ADHD traits.'
RATIONALE FOR NEUROTHERAPY Public Health Concerns
the effectiveness of psychostimulants in the treatment of ADHD is well
documented, medications fail to produce the desired improvement in behavior
in a significant percentage of patients, as high as 30-40%.'° Further,
gains from pharmacotherapy are "state dependent," i.e., are
often lost when the medication wears off or is discontinued. While short-term
side effects are considered minimal according to Barkley," some
mixture of appetite loss, weight loss, slowed growth, tics, headaches
and stomach aches may appear in 20-50% of patients" and may lead
to discontinuation of treatment. Although considered a rare problem,
in some cases adolescents or even their parents may abuse the stimulants,
selling their medications on the street or "snorting" higher
doses of them personally. 12,11 A study of a sample of 161 school children
who had taken Ritalin for 5 years showed 16% reported being asked to
give, sell or trade their medication." Comorbid anxiety, occurring
in as many as 30% of ADHD youths, may limit the success of stimulant
therapy. These limitations have led to the rapid adoption in clinical
practice of alternative and adjunctive medications despite the current
lack of controlled research on safety and efficacy." So while medications
carry considerable benefits for ADHD patients, there are also considerable
shortcomings and risks.
Despite research indicating a relatively low rate of sideeffects and
the apparent short-term safety of these medications, many parents have
safety concerns. Psychostimulants elevate heart rate and systolic blood
pressure; the response is variable between individuals and is dose dependent."
This may be a concern in patients with elevated risk for hypertension
and heart disease. No longterm study has evaluated potential effects
on the cardiovascular system or on the brain. One early CT scan study
documented apparent cortical atrophy in a group of 25 young adult males
with a history of ADHD and psychostimulant medication use." Although
this study could not directly relate the atrophy to psychostimulant
use, the authors noted there may be a relationship. This somewhat alarming
finding has never been followed up with contemporary imaging techniques.
Newly identified unmedicated adult patients with ADHD should be compared
to adults with a history of medical psychostimulant use as children.
The recent NIH Consensus Conference on ADHD'8 pointed out the longest
follow-up with methylphenidate is 14 months, and this did not involve
As the psychosocial difficulties associated with ADHD have been noticed,
and as the only partial success of medical management has become apparent,
there has been increasing interest in the possibility that persons with
attentional, hyperactivity and impulse control difficulties can learn
to regulate their central nervous systems with neurotherapy and thereby
ameliorate symptoms of ADHD. It would be highly desirable if neurotherapy
produced long-lasting improvements in CNS function with concomitant
improvements in behavior, without side effects. Ideally, medication
might be used as a safe, immediate short-term aid, with trained self-regulation
of the attention, impulsivity and hyperactivity developing in the longer
term. The idea of neurotherapy is not to "cure" ADHD, but
to afford the individual with the ADHD trait a means of learning to
counterbalance his or her genetic tendencies with learned skill.
RATIONALE FOR NEUROTHERAPY
1971 Satterfield and Dawson" suggested underarousal of frontal
cortex might explain ADHD symptoms. Niedermeyer and Naidu2° have
recently discussed this "lazy frontal brain" ADHD hypothesis
further. Niedermeyer presents a detailed, integrative review of frontal
lobe function that shows neuroanatomical possibilities for the variety
of behavioral manifestations seen in ADHD.2' Lowered average arousal
levels, poor connectivity and perhaps structural differences in the
brain regions that subserve the deployment and persistence of attention,
planning, the examination and regulation of impulses - the ability to
notice impulses and "think better of it"-would create most
of the ADHD pattern.
As long ago as 1938 Jasper, Solomon and Bradley22 showed evidence that
a behaviorally divergent group of youngsters had EEG "slowing."
Recent literature in quantitative electroencephalography (QEEG), single
photon emission computed tomography (SPELT) and positron emission tomography
(PET) lend further support to the relative underarousal hypothesis.
EEG signal coupled with normative databases and discriminant functions
has permitted the development of a "neurometric" approach
to the examination of EEG in psychiatric populations .23 In a comprehensive
review of this literature Hughes and John" discuss the range of
over 500 QEEG articles published just in the last decade relating specific
pattems of abnormality to particu
lar diagnoses. This literature documents reliable EEG differences between
ADHD and non-ADHD children and shows QEEG discriminant analysis to be
sensitive and specific to subtypes of ADHD, ADHD versus normals and
ADHD versus specific developmental learning disorders (SDLD) individuals.
Elevated frontal theta activity and diminished beta activity in the
resting EEG have been documented in children with ADHD. Mann et al.,25
studying matched groups of 25 9-12 year old boys with and without ADHD
(inattentive type) documented increases of theta during tasks that suggests
children with ADHD actually become less activated when presented with
cognitive challenge. Discriminant analysis of QEEG variables correctly
classified 74% of controls and 80% of ADHD participants. Matsuura et
al .2e have also reported this frontal theta/alpha excess with alpha
slowing. Lazzaro et al .2' have reported similar QEEG results in 26
nonmedicated adolescents with ADHD diagnoses versus 26 matched controls
showing elevated absolute frontal theta and diminished relative posterior
beta in the participants with ADHD.
Chabot and Serfontein" compared the QEEGs of 407 children with
ADHD diagnoses with 310 normal children. QEEG discriminated between
the groups with 93.7% sensitivity and 88% specificity. ADHD children
showed increased theta absolute and relative power, particularly in
frontal regions. Marked interhemispheric frontal and parietal hypercoherence,
posterior asymmetries and frontaloccipital as well as central-parietal
hypocoherence also distinguished ADHD from normal children's QEEG. These
findings were consistent with deviations from normal development as
opposed to maturational delay, i.e., these were not patterns that would
be normal at an earlier time in life. Two distinct neurophysiological
ADHD subtypes, one showing elevated theta/alpha, the other also showing
elevated theta/alpha but also slowing of the alpha mean frequency, were
seen, suggesting the "underarousal" hypothesis may not be
adequate to describe the complexity of the subtypes of ADHD.
Chabot et al.2e went on to show that QEEG discriminant functions classified
learning disabled, ADHD and normal children with high sensitivity and
specificity. The same paper showed QEEG discriminates between methylphenidate
versus dextroamphetamine responders. This is clinically important, since
results showed that if initial diagnosis had included QEEG, 27 cases
of adverse medication response could have been prevented. Suffin and
Emory" showed that patients with frontal theta excess responded
well to methylphenidate whether their diagnosis was attentional or affective
disorder. Patients with elevated alpha responded well to Prozac. An
earlier study by Simeon et a1." showed ADHD children with elevated
alpha responded well to bupropion. These findings have led Chabot and
others to call for routine use of QEEG in diagnosing ADHD.
PET Corroboration of Frontal Abnormalities in ADHD
and Carmichael,31 using high resolution SPECT imaging showed regions
of prefrontal hypometabolism in 87% of a group of medication-free children
and adolescents with ADHD, compared with 5% of youths with other diagnoses.
Lou et al" have also reported prefrontal hypoperfusion in SPECT
studies on children with ADHD and SDLD. Seig et al." reported SPECT
findings on 10 ADHD patients, with less uptake on left frontal and left
parietal compared to controls. The PET studies of Zametkin et al."
have been widely cited as evidence for hypometabolism of frontal cortex
in ADHD patients. This population showed worsening of the hypometabolism
during a cognitive task, paralleling both the SPECT findings of Amen
and Carmichael" and the QEEG findings of Lubar," who describes
increased theta during rest and even greater abnormality during cognitive
The findings described above emphasize the importance of moving toward
objective neurophysiological diagnoses for psychiatric disorders. Given
the present lack of objective measures to make differential diagnoses
of ADHD, it appears time to integrate this powerful tool into standard
CONDITIONING OF THE EEG
public health concerns and QEEG studies outlined above form a strong
scientific rationale for neurotherapy. The QEEG abnormalities seen in
ADHD are common, appear in most identified patients, and are not subtle
when the proper technology is used to observe them.
As documented in the previous section, ADHD is often marked on the average
by elevations of slow wave theta and/or alpha activity over frontal
or in parietal regions (the latter more prevalent in inattentive ADHD).
When the spontaneous EEG is observed, however, it is clear that there
are moments when abnormal appearing EEG records "clear up."
When these moments occur the person appears focused on the task. When
asked "What are you doing?" a patient will usually respond
"Nothing. I'm just concentrating." Patients will often note
a clearing of the mind, reduction in distracting thoughts, or less "cognitive
noise" as one of my patients puts it. These moments of improved
EEG can be considered "operants of alertness."
Operant conditioning of the EEG is called EEG biofeedback, neurofeedback
or neurotherapy. Neurotherapy helps the person learn to recognize the
small shifts in state they go through during the course of the session,
as well as during the course of their day. Patients gradually begin
to notice and influence their ambient state of alertness. Neurotherapy
is a' fine-grained" form of cognitive behavior modification in
which improvements in cortical function are operationalized as changes
in the EEG.
Neurotherapy involves presentation of auditory and/or visual signals
that are proportional to the relevant EEG measure (e.g., amplitude,
correlation, symmetry, etc.) A tone may come on when theta amplitude
drops below a pre-set threshold; a second tone may come on when sensorimotor
rhythm (SMR) or beta amplitudes rise above a given value with the goal
of decreasing theta and increasing SMR or beta. A wide range of feedback
presentations is currently in use, some of them quite creative. Computer
displays exist in which various "games" can be played, e.g.,
Pac-Man advances when certain parameters are met, an airplane flies
to the top of the screen and an American flag lights up when parameters
are met, etc. The specific values of the parameters are determined individually,
such that reinforcement (tones on, airplane up) occurs 60 - 80% of the
time. Training is usually done twice weekly for 20 - 40 sessions.
Control must be obtained over muscle tension artifact, since tense muscles
can produce artifactual "beta" activity. Many people equate
a certain amount of tension with "paying attention" and frown,
lift their eyebrows or clench their jaws when trying to concentrate.
A quiet body and alert mind is the explicit target state.
Cognitive tasks, including reading, listening, visual attentional tasks
are used concurrently with auditory neurofeedback to promote generalization.
The aim is to promote improved self-monitoring of the onset of ADHD
behaviors and improved conscious self-regulation of the internal state
at such moments. Like any operant conditioning program, neurotherapy
requires generalization and establishing a reinforcing environment to
support small, progressive changes in behavior. Parents and teachers
should be trained in basic behavior modification methods. With neurotherapy
small gains usually begin to be apparent after approximately 10 sessions.
It is critical that parents and teachers be prepared to meet small improvements
Sessions must occur regularly, typically twice weekly, although some
summer programs will train daily. If the family cannot comply with this,
putting off treatment for a better time should be considered. If there
is major family conflict, illness, tragedy, or a hostile relationship
between divorced custodial parents or criminal conduct, these issues
should be dealt with before a course of neurotherapy is considered.
Further, although there are no studies that report untoward side-effects
from neurotherapy, patients should be screened for psychotic disorders.
Mental retardation, severe depression or bipolar illness, or severe
conduct/oppositional defiant disorder may prevent successful therapy.
Occasionally patients report headaches, but this is likely due to tensing
up during training and disappears rapidly when muscles are relaxed.
Tiredness after the initial sessions may occur, presumably due to the
intensity of the "workout." On the other hand, many patients
will feel more alert and more awake after neurotherapy sessions. Lubar"
has published a detailed account of the procedures involved in neurotherapy
Studies of the Treatment of ADHD with Neurotherapy The 1970s and 1980s
use of EEG operant conditioning to treat ADHD developed out of the work
of M.B. Sterman and colleagues with epileptic patients"" in
the 1970s and the early literature showing slow wave excess in ADHD.
Sterman demonstrated reduction in epileptiform background activity following
treatment that successfully reduced seizure frequency. This healthier
background EEG persisted even during sleep. This observation suggests
neurotherapy produces increased cortical stability.
The first case study of applying Sterman's methods to ADHD was by Lubar
and Shouse39 who reported EEG and behavioral improvement in an 8 year
11 month old "hyperkinetic" child following application of
neurofeedback. Lubar and Shouse rewarded increases in SMR and lower
theta amplitude. Two independent observers documented reduced oppositional
behavior and increased cooperation in the classroom. Self stimulation,
object play and out-ofseat behavior decreased and attentive and school
work behaviors increased. All of these changes were reversed over a
4 week period when increases in theta and decreases in SMR were reinforced.
Finally, return to SMR enhancement and theta decrease resulted in a
second and apparently long lasting improvement in the child's behavior.
Medication was permanently discontinued by the end of treatment, and
follow-up several years later revealed the child continued to function
well with no medication.
The Lubar and Shouse39 study was in the classic style of applied behavior
analysis using an ABA reversal design. The importance of this design
must be highlighted, since there have been criticisms directed at the
studies of neurotherapy for lack of large double blind, placebo controlled
designs, which have high internal validity, but are uncommon in the
scientific study of behavior modification and often lack external validity.
The ABA reversal design with subject as his or her own control has been
an acceptable method in the scientific investigation of behavior for
Further studies involving more children were undertaken by Shouse and
Lubar using the same blind, ABA design with SMR enhancement, theta suppression.°°°'
Lubar noted a decrease in hyperactivity with reduced theta and increased
SMR, with less of an effect on attentiveness. Again, the effects were
reversible, showing statistically significant changes dependent on the
stage of the design.
These early studies could be criticized largely for limited generalizability
due to small sample size. Follow-ups that are reported indicate sustained
improvements in social and academic behavior for substantial periods
of time after
treatment, something that cannot be said for psychostimulants. The finding
of apparent academic improvement is most interesting given the general
lack of any such effect from psychostimulants.
Lubar and Luba02 published a group of six case studies that used a combination
of reinforcement of lowered theta and increased SMR along with reinforcement
of elevated beta amplitudes. Feedback was shut off during moments of
elevated theta activity, EMG activity or gross motor movements. Reading,
arithmetic and spatial tasks were conducted concurrent with the feedback.
Training was conducted twice weekly for 10 to 27 weeks. No reversal
of conditions was done, as these were clinical cases. The children were
described as having a variety of learning, hyperactivity and attentional
difficulties. Letter grades improved and were sustained. The Metropolitan
Achievement Test, Peabody, Stanford Achievement Test and California
Achievement Test were administered preand post-treatment and systematic
improvements were seen. EEG changes were noted in all children (decreases
in theta, increases in SMR or beta). This methodology has become the
basis for the most common clinical practice style today. This study
demonstrates a clinically useful procedure that produces consistent
results and likely promotes generalization to real world situations.
In the same era as the initial Lubar studies a private practice psychologist,
Michael Tansey, Ph.D., published his first report on improvements in
ADHD following neurotherapy using a narrow band of EEG centered on 14
Hz.^3 His patient was diagnosed "perceptually impaired" and
hyperactive and had been on Ritalin since age 7. The boy was in a special
education class for fourth grade, which he had failed and was scheduled
to repeat fourth grade. Tansey used 3 initial EMG training sessions
followed by amplitude and frequency modulated auditory feedback to increase
14 Hz (SMR band). Tansey and Bruner" indicate Ritalin was stopped
by the pediatrician who no longer saw him as hyperactive prior to the
onset of EEG treatment, but after the three EMG sessions. The family
moved and placed the boy in a normal fourth grade class because of the
improvement in reading comprehension and behavior seen over the summer.
Evidence of remediation was the boy's grades, which were 3 As, 3 Bs
and 4 Cs the first quarter, improving to 4 As, 5 Bs and 1 C by the end
of the third quarter. A 10 year follow-up on this boy showed he had
successfully completed high school, was attending college and had remained
A single case study like this naturally raises many questions of causality.
Nonetheless, one has something of a time-series design, with 3 years
of special education producing failing results and a sudden, post-treatment
turn of events. The stability of the reported improvement is encouraging.
The studies of this era were carefully reviewed by Joel Lubar in 1991.'5
The 1990s - Contemporary Studies
Swartwood, Swartwood and Timmerman" reported a series of studies
further defining the QEEG and auditory event-related potential (AEP)
characteristics of ADHD, methylphenidate effects and the efficacy of
neurotherapy. The AEP and methylphenidate literatures are complex and
beyond the scope of the present review." Briefly, these authors
found no significant effects of Ritalin on theta/beta ratios. Lubar
et al.^1 also reported habituation of P2 ERP amplitude in AND children
that may correspond to the degradation of their performance on continuous
performance tasks. Of most interest to the present review is the fourth
study in this report. Seventeen children diagnosed with ADD/HD were
given 30 to 45 sessions of neurofeedback training to decrease theta
and increase beta activity. Two groups emerged: 11 were successful in
either lowering theta percentage or power or increasing beta percentage;
6 were unable to produce these changes in their EEGs. As a result, the
11 successful learners showed reduced theta/beta ratios, compared with
the unsuccessful learners whose theta/beta ratios did not change over
their baseline recordings. Interestingly, the lowered theta/beta ratios
appeared over a wide range of scalp locations, not just in the region
from which the feedback had been derived, suggesting global activation
of the EEG can occur as a result of neurofeedback at a single placement.
Unfortunately, teacher or parent report data for this study group (successful
learner versus unsuccessful learner) were not presented.
Lubar, Swartwood, Swartwood and O'Donnell" presented data on 19
participants in an intensive summer neurofeedback training program.
Patients were given daily 1 hour training sessions for 8 - 10 weeks,
with the goal of accomplishing 40 training sessions during the summer
months. Neurofeedback was given during two 5-minute onscreen periods,
followed by a 5-minute reading and 5minute listening periods during
which auditory feedback was given simultaneous with the cognitive task.
A key methodological point future researchers should pay attention to
is that all neurofeedback therapists had bachelors or master's degrees
in health care or education and at least 1 year experience providing
neurotherapy for ADHD.
Outcome measures were theta amplitude, TOVA continuous performance test,
WISC-R and Attention Deficit Disorder Evaluation Scale (ADDES). Twelve
of the 19 patients showed significant lowering of theta across sessions.
These 12 showed improvement on an average of three TOVA scales, while
the group that showed no lowering of theta improved on an average of
1.5 TOVA scales. Pre-postADDES showed significant improvement (p<.001)
for inattention, hyperactivity and impulsivity for all patients. The
criticism that such improvements are merely the result of parents reporting
improvement simply because of the length and intensity of treatment
is not intuitive. One might
expect that parents who saw no improvement after substantial investment
of time and money might well be expected to have quite the opposite
reaction if there were not substantial changes.
WISC-R tests were administered post-treatment by an independent neuropsychologist
for 10 children who had WISC-R data from approximately 2 years prior
to treatment. All children in this group showed reductions in theta
activity during the course of their neurotherapy. Significant improvements
(p<005) in Verbal, Performance and Full Scale IQ were found. Mean
Verbal IQ increased from 113.3 to 122, Performance from 109.6 to 116.1
and Full Scale from 112.4 to 122.1.
The objective reduction in theta amplitude in about two thirds of the
cases suggests neuromodulation was taking place. The fact that patients
who did not show theta or beta change still apparently improved behaviorally
may be accounted for by changes in the cortical EEG that were not measured,
e.g., coherence (known to be abnormal in ADHD), or by subcortical change
that cannot be observed by scalp-recorded EEG. Further, TOVA data are
known to be stable on retest and if anything, second TOVAs may produce
lower scores due to boredom," so the TOVA data is supportive of
a treatment effect. The improvement in Wechsler IQ scores is consistent
with a globally more activated, less "lazy," brain.
Alhambra et al.^9 reported on the results of 20 sessions of neurofeedback
on TOVA and QEEG measures in a case series. Questionnaires were also
sent to patients who received at least 30 sessions of training. Decreased
theta and increases in beta or SMR were reinforced. Feedback was provided
by a Pac-Man style display, where meeting threshold criteria on the
relevant EEG measures caused Pac-Man to advance. Sessions were 30-45
minutes long. Of 43 surveys sent, there were 36 responses, 26 for males
and 10 for females. Of the 36 respondents, 31 (86%) showed "some
overall improvement" from the treatment. Improvement was judged
"significant" in 30 of these. Three respondents noted no improvement
and 2 were uncertain.
Rossiter and LaVaquel° compared 23 patients who received EEG biofeedback
as part of their treatment for AND with 23 age matched controls drawn
from a pool of patients in the author's practice who were treated with
psychostimulants and did not receive neurotherapy (MED group). This
is an important comparison, since for general acceptance neurotherapy
must be shown to have at least equivalent effects to those of the stimulants,
with some additional advantages such as a long-lasting effect after
treatment and no negative side effects. Five of the EEG group were taking
psychostimulants before and during the course of the treatment. All
participants discontinued medication 2 days prior to pre- and post-testing
consisting of EEG measures and the TOVA. Behavior Assessment Scales
for Children (mothers' ratings) were obtained for the EEG group, pre-
and post-treatment. Pre-test intelligence testing was obtained. Analysis
revealed the groups to be well matched, with no significant differences
between group in age, gender distribution, intelligence, frequency of
ADHD vs "undifferentiated" ADD, frequency of secondary/tertiary
diagnoses, or LD/EBD placements. The groups did not differ on baseline
TOVA measures. More of the EEG (N=17) than the MED group (N=10) had
been treated with psychostimulants previously.
The EEG training protocols were varied depending on age, symptoms, baseline
results and responses of the patient to the treatment. Generally, 4-8
Hz theta was trained down in children through adolescents, while 12-15
Hz SMR and/or 16-20 Hz beta was trained up in adolescents and adults.
Twenty sessions of EEG training were completed prior to re-testing.
Post-treatment TOVA scores indicated highly significant improvement
for both the EEG and medication groups on all scales. The BASC scales
also demonstrated highly significant improvements on all scales.
The medication group improved significantly and the size and significance
of the changes were not significantly different from the EEG group.
Members of the EEG group were re-tested without medication; the MED
group was retested during the optimum "window" 1.5-2.5 hours
after taking their medication. The study demonstrated good experimental
control of a wide range of potential confounding variables. Comparison
of the gains made by the two groups was limited to the TOVA test results,
which are machine-generated and less likely than rating scales or other
tests to be subject to observer bias. If patients showed improvement
after 20 sessions, another 20 sessions were recommended to consolidate
and "overlearn" the skills. This procedure has become a common
practice model in neurotherapy.
Linden, Habib and Radojevic5' have reported the results of a waiting
list control study of the effects of neurotherapy. Eighteen children
were randomly assigned to either the experimental group or a waiting
list control condition. No patient received any medication or other
psychotherapy during the study. Forty twice-weekly 45-minute sessions
were given to the experimental group across 6 months. Participants received
10 minutes of visual and auditory feedback in a videogame-like format,
10 minutes of auditory feedback during reading and 10 minutes of auditory
and visual feedback while listening to age appropriate material being
read to them. Reductions in 4-8 Hz theta and increases in 16-20 Hz beta
were reinforced. Recording was from a bipolar montage at Cz/Pz. The
treatment group showed a significant IQ increase (mean 101.1 increased
to 110.4, p=.02 relative to controls 99.1 to 100.0, n.s.) on the K-Bit
IQ Composite. The treatment group also showed reduced inattentive behaviors
pre- to post (p=.04), but the groups did not differ on aggressive/defiant
This study supports Lubar's 1995 study" that documents an apparent
IQ increase following neurofeedback treatment, consistent with a generally
improved cortical functioning.
Another single case study with similar IQ results was reported by Tansey.12
One would like to have seen prepost-treatment data for a continuous
performance task in the Linden study in order to compare these results
with previous studies.
Rossiter" reports essential normalization on the TOVA test following
30 sessions of home-based, patient-directed training in six patients.
Patients received 10 clinic sessions during which they or their parents
were trained to run the Lexicor POD-2 software. Feedback was aimed at
increasing 15-18 Hz beta or 12-15 Hz sensorimotor rhythm and reducing
amplitudes of delta, theta and 22-30 Hz beta.
Boyd and Campbell" reported improvements on WISC-III Digit Span
and TOVA Inattention and Hyperactivity scales in five of six students.
The students received SMR training during twenty 30-minute training
sessions conducted in a school environment. Operational problems in
either a home or school environment may prove daunting: training, time
commitment, equipment issues can arise. Nonetheless, out-of-clinic training
is an interesting possibility.
Further research should address several issues: the potential importance
of basing training protocols on deviations from normative databases,
the relevance of abnormal QEEGs during tasks, and the mechanisms of
action of neurotherapy. Appropriate controls might be designed by random
assignment of children/families desiring neurotherapy to an initial
20 sessions of neurotherapy or an initial 20 sessions of twice weekly
cognitive therapy and family therapy, in a cross-over design. A blind
"placebo" controlled study could easily be designed, for example,
by attaching an EMG electrode to the shoulder region of all patients
and feeding back the EMG signal instead of the EEG signal to the controls
unknown to the neurotherapist or the patient. Ethical questions arise
from false-feedback designs, due to the commitment required from the
children and their families and the potential for discouragement. Ideally,
participants in a study would be off medication entirely for the course
of the study. Pre-post IQ, QEEG, auditory and visual CPT, and parent/teacher
ratings should be obtained. Follow-up of a year or more would be very
public health concerns exist regarding our current level of success
in treating ADHD. Medication management is very helpful in 60-70% of
patients. Side effects, lack of compliance and the fact that stimulant
medications cannot be given late in the day limit the benefits largely
to school hours. While stimulants improve behavior and attention, less
of an effect has been noted on academic and social performance. Continuing
concerns exist about long-term safety, and studies on long-term cardiovascular
and neurophysiological effects have not been carried out. Neurotherapy
for ADHD offers an effective alternate for patients whose treatment
is limited by side effects, poor medication response and in cases in
which the patients and/or their parents refuse to consider medications.
Studies indicate clinical improvement is largely related to measurable
improvements in the EEG signature, evidenced by declining theta/beta
ratios over frontal/central cortex and/or reduced theta/alpha band amplitudes.
author wishes to thank Joel Lubar, Ph.D., and Norman Moore, M.D., for
their kind assistance and input on the development of this article.
1. Shahar R. Childhood hyperactivity. J Child Psychol 15.
Psychiat1991; 32: 155-191.
2. Taylor E, Sandberg S, Thorley C, Giles S (eds). The
Epidemiology of Childhood Hyperactivity. New York: Oxford 16.
University Press; 1991.
3. Barkley RA, Grodzinsky G, Du Paul GJ. Frontal lobe functions
in attention deficit disorder with and without hyperactivity. J
Abnorm Child Psychol 1992; 20: 163-188. 17.
4. Pennington BF, Ozonoff S. Executive functions and developmental psychopathology.
J Child Psychol Psychiatry 1996; 37: 51-87.
5. Seidman LJ, Biederman J, Weber W, Hatch M, Faraone SV. Neuropsychological
function in adults with attention-deficit hyperactivity disorder. Biol
Psychiatry 1998; 44: 260-268.
6. Seidman LJ, Biederman J, Faraone SV, Weber W, Ouellette C. Toward
defining a neuropsychology of ADHD: performance of children and adolescents
from a large clinically referred sample. J Consult Clin Psychol 1997;
7. Faraone SV, Biederman J. Is attention deficit hyperactivity disorder
familial? Harvard Rev Psychiat 1994; 1:271-287.
8. Biederman J, Milberger S, Faraone S, et al. Family-environment risk
factors for ADHD: A test of Rutter's indicators of adversity. Arch Gen
Psychiat 1995; 49: 464-470.
9. Hartman T. Beyond ADD: Hunting for Reasons in the Past
and Present. Grass Valley, CA: Underwood Books; 1996. 23.
10. Barkley RA. Attention deficit hyperactivity disorder: a hand
book for diagnosis and treatment. New York: Guilford Press; 24.
11. Goldstein S, Goldstein M. Managing attention disorders in
children: a guide for practitioners. New York: John Wiley & 25.
12. Jaffe SL. Intranasal abuse of prescribed methylphenidate by
an alcohol and drug abusing adolescent with ADHD. J Am
Acad Child Adolesc Psychitatry 1991; 30: 773-775. 26.
13. Goldman LS, Genel M, Bezman RJ, Slanetz PJ. Diagnosis
and treatment of attention-deficiVhyperactivity disorder in chil
dren and adolescents. Council on Scientific Affairs, American
Medical Association. JAMA 1998; 279:1100-1107. 27.
14. Musser CJ, Ahmann PA, Theye FW, Mudt P, Broste SK,
Mueller-Rizner N. Stimulant use and the potential for abuse
in Wisconsin as reported by school administrators and longi 28.
tudinally followed children. J Dev Behav Pediatr 1998;
18. Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder.
National Institutes of Health Consensus Development Conference Statement,
November 16-18, 1998.
19. Satterfield JH, Dawson ME. Electrodermal correlates of hyperactivity
in children. Psychophysiology 1971; 8:191-197.
20. Niedermeyer E, Naidu SB. Attention-deficit hyperactivity disorder
(ADHD) and frontal-motor cortex disconnection. Clin Electroencephalogr
1997; 28: 130-136.
21. Neidermeyer E. Frontal lobe functions and dysfunctions. Clin Electroencephalogr
1998; 29: 79-90.
22. Jasper HH, Solomon P, Bradley C. Electroencephalographic analysis
of behavior problems in children. Am J Psychiatry 1938; 95: 641-658.
Garland EJ. Pharmacotherapy of adolsecent attention deficit hyperactivity
disorder: challenges, choices and caveats. J Psychopharmacol 1998; 12:
Volkow ND, Wang GJ, Gatley SJ, et al. Temporal relationships between
the pharmacokinetics of methylphenidate in the human brain and its behavioral
and cardiovascular effects. Psychopharmacology 1996; 123: 23-33.
Nasrallah HA, Loney J, Olson SC, McCalley-Whitters M,
Kramer J, Jacoby CG. Cortical atrophy in young adults with a history
of hyperactivity in childhood. Psychiatric Res 1986: 17: 241-246.
John ER, Prichep, LS, Friedman J, Easton P. Neurometrics: computer-assisted
differential diagnosis of brain dysfunctions. Science 1988; 239: 162-169.
Hughes JR, John ER. Conventional and quantitative electroencephalography
in psychiatry. J Clin Neuropsychiatry Clin Neurosci 1999; 11: 190-208.
Mann CA, Lubar JF, Zimmerman AW. Quantitative analysis of EEG in boys
with attention deficit-hyperactivity disorder: controlled study with
clinical applications. Pediatr Neurol 1992; 8: 30-36.
Matsuura M, Okubo Y, Toru M, et al. A cross-national study of children
with emotional and behavioral problems: a WHO collaborative study in
the Western Pacific region. Biol Psychiatry 1993; 34: 59-65.
Lazarro I, Gordon E, Whitmont S, et al. Quantified EEG activity in adolescent
attention deficit hyperactivity disorder. Clin Electroencephalogr 1998;
Chabot RJ, Serfontein G. Quantitative electroencephalographic profiles
of children with attention deficit disorder. Biol Psychiatry 1996; 40:
02000 VOL. 31 NO. 1
29. Chabot RJ, Merkin H, Wood LM, Davenport TL, Serfontein G. Sensitivity
and specificity of QEEG in children with attention deficit or specific
developmental learning disorders. Clin Electroencephalogr 1996; 27:
30. Suffin SC, Emory WH. Neurometric subgroups in attentional and affective
disorders and their association with pharmacotherapeutic outcome. Clin
Electroencephalogr 1995; 25:1-8.
31. Simeon JG, Ferguson HB, Fleet JVW. Bupropion effects in attention
deficit and conduct disorders. Can J Psychiatry 1986 31: 581-585.
32. Amen DG, Carmichael BD. High resolution brain SPECT imaging in ADHD.
Ann Clin Psychiatry 1997; 9: 81-86.
33. Lou HC, Henriksen L., Bruhn P. Focal cerebral hypoperfusion in children
with dysphasia and/or attention deficit disorder. Arch Neurol 1984;
34. Sieg KG, Gaffney GR, Preston DF, Helling JA. SPECT brain imaging
abnormalities in attention deficit hyperactivity disorder. Clin Nucl
Med 1995; 20: 55-60.
35. Zametkin AJ, Nordahl TE, Gross M, et al. Cerebral glucose metabolism
in adults with hyperactivity of childhood onset. New Eng J Med 1990;
36. Lubar JF. Neurofeedback for the management of attention
deficit/hyperactivity disorders. In: Schwarz MS. (ed).
Biofeedback: a Practitioner's Guide. New York: Guilford;
37. Sterman MB, Macdonald LR. Effects of central cortical EEG
feedback training on incidence of poorly controlled seizures.
Epilepsia 1978; 19: 207-222. 50.
38. Sterman MB, Friar L. Suppression of seizures in an epileptic
following senosrimotor EEG feedback training. Electroen
cephalogr Clin Neurophysiol 1972; 33: 89-95. 51.
39. Lubar JF, Shouse MN. Use of biofeedback in the treatment of
seizure disorders and hyperactivity. Adv Clin Child Psychol
40. Shouse MN, Lubar JF. Physiological bases of hyperkinesis 52.
treated with methylphenidate. Pediatrics; 1978: 343-351.
41. Shouse MN, Lubar JF. Sensorimotor rhythm (SMR) operant conditioning
and methylphenidate in the treatment of hyperkinesis. Biofeedback Self
Regul 1979; 4: 299-311.
42. Lubar JO, Lubar JF. Electroencephalographic biofeedback of SMR and
beta for treatment of attention deficit disorders in a clinical setting.
Biofeedback Self Regul 1984; 9: 1-23.
43. Tansey MA, Bruner RL. EMG and EEG biofeedback training in the treatment
of a 10-year old hyperactive boy with a developmental reading disorder.
Biofeedback Self Regul 1983; 8: 25-37.
44. Tansey MA. Ten-year stability of EEG biofeedback results for a hyperactive
boy who failed fourth grade perceptually impaired class. Biofeedback
Self Regul 1993; 18: 33-44.
45. Lubar JF. Discourse on the development of EEG diagnostics and biofeedback
for attention-deficit/hyperactivity disorders. Biofeedback Self Regul
1991; 16: 201-225.
46. Lubar JF, Swartwood MO, Swartwood JN, Timmerman DL. Quantitative
EEG and auditory event-related potentials in the evaluation of attention-deficit/hyperactivity
disorder: effects of methylphenidate and implications for neurofeedback
training. J Psychoed Assess ADHD Special 1995; 143-160.
47. Greenberg L. An objectrive measure of methylphenidate response:
clinical use of the MCA. Psychopharm Bull 1987; 23: 279-282.
48. Lubar JFSwartwood MO, Swartwood JN, O'Donnell PH,
. Evaluation of the effectiveness of EEG neurofeedback training for
ADHD in a clinical setting as measured by changes in TOYA. scores, behavioral
ratings, and WISC-R performance. Biofeedback Self Regul 1995; 20: 83-99.
Alhambra MA, Fowler TPP, Alhambra AA. EEG biofeedback: a new treatment
option for ADD/ADHD. J Neurotherapy 1995; 1(2): 39-43.
Rossiter TR, LaVaque TJ. A comparison of EEG biofeedback and psychostimulants
in treating attention deficit/hyperactivity disorders. J Neurotherapy
1995; 1: 48-59.
Linden M, Habib T, Radojevic V. A controlled study of EEG biofeedback
effects on cognitive and behavioral measures with attention-deficit
disorder and learning disabled children. Biofeedback Self Regul 1996;
Tansey M. Wechsler (WISC-R) changes following treatment of learning
disabilities via EEG biofeedback training in a pri
vate practice setting. Austral J Psychol 1991; 43: 147-153.
53. Rossiter TR. Patient-directed neurofeedback for ADHD. J Neurotherapy
54. Boyd WD, Campbell SE. EEG biofeedback in the schools: the use of
EEG biofeedback to treat AND in a school setting. J Neurotherapy 1998;