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A Position Paper on Neurofeedback for the Treatment of ADHD
Leslie Sherlin abc; Martijn Arns d; Joel Lubar e;Estate Sokhadze f
a Neurotopia, Inc., b Department of Mind-Body Medicine, Southwest College of Naturopathic Medicine
and Health Sciences, c Department of Psychology, University of Phoenix, d Brainclinics Diagnostics and
Department of Experimental Psychology, Utrecht University, e Department of Psychology, The
University of Tennessee, f Department of Psychiatry and Behavioral Sciences, University of Louisville,
Online publication date: 18 May 2010
To cite this Article Sherlin, Leslie , Arns, Martijn , Lubar, Joel andSokhadze, Estate(2010) 'A Position Paper on
Neurofeedback for the Treatment of ADHD', Journal of Neurotherapy, 14: 2, 66 — 78
To link to this Article: DOI: 10.1080/10874201003773880
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SCIENTIFIC FEATURES
A Position Paper on Neurofeedback
for the Treatment of ADHD
Leslie Sherlin, PhD
Martijn Arns, MSc
Joel Lubar, PhD
Estate Sokhadze, PhD
ABSTRACT. This position paper provides the current evidence supporting the use of
neurofeedback in the treatment of ADHD and recommendations on the implementation of
neurofeedback in clinical practice. The paper also provides basic information regarding the
diagnosis and psychophysiological etiology of ADHD. The paper does not focus on a specific
age range of a clinical population. Unless otherwise noted, we are referring to all subtypes of
ADHD (inattentive, hyperactive only, and combined). Conclusions and recommendation are
based on the most recent research; however, we also refer to relevant historical studies that
support our position on neurofeedback. The readers are strongly advised to research behavioral
diagnostic criteria and testing methods elsewhere. This paper is not intended as a comprehensive
educational tool for diagnosis or treatment of ADHD. Our purpose is to demonstrate the
rationale and to reference the necessary support for neurofeedback in order to be recognized
as a legitimate, scientific, and evidence-based intervention for the treatment of ADHD.
KEYWORDS. ADHD, efficacy rating, neurofeedback, position, treatment
Leslie Sherlin is affiliated with Neurotopia, Inc.; Department of Mind-Body Medicine, Southwest College of
Naturopathic Medicine and Health Sciences; and Department of Psychology, University of Phoenix.
Martijn Arns is affiliated with Brainclinics Diagnostics and Department of Experimental Psychology, Utrecht
University.
Joel Lubar is affiliated with the Department of Psychology, The University of Tennessee.
Estate Sokhadze is affiliated with the Department of Psychiatry and Behavioral Sciences, University of
Louisville.
Address correspondence to: Leslie Sherlin, PhD, Neurotopia, Inc., Los Angeles, CA 99049 (E-mail:
lesliesherlin@mac.com).
We acknowledge the support of the International Society for Neurofeedback and Research (ISNR) Board of
Directors in this endeavor. The ISNR adopted this paper as their official position paper for the use of neurofeed-
back for the treatment of ADHD on March 7, 2010. We also thank Robin Massey, MA Ed, for her help and
suggestions in editing the paper.
Journal of Neurotherapy, 14:66–78, 2010
Copyright #Taylor & Francis Group, LLC
ISSN: 1087-4208 print=1530-017X online
DOI: 10.1080/10874201003773880
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SUMMARY AND
RECOMMENDATIONS
This position paper provides basic infor-
mation regarding the diagnosis and psycho-
physiological etiology of attention-deficit=
hyperactivity disorder (ADHD) and the
evidence for treatment of ADHD to
include the modality of neurofeedback.
We have summarized the primary historical
research as well as the more recent investi-
gations in which neurofeedback has been
utilized in the ADHD population. Our
conclusions find that neurofeedback not
only is a suitable intervention for those
diagnosed with ADHD, but also may be
the preferred choice of interventions for
some individuals. Solid scientific evidence
and demonstrated clinical data, collected
from multiple studies across the world,
are the basis for our conclusions. The
following are our recommendations:
1. Neurofeedback is a safe and efficacious
treatment intervention for ADHD, meet-
ing the rating of Level 5: Efficacious and
Specific.
2. Neurofeedback in the treatment of
ADHD has been shown to have
long-term effects, lasting from 3 to 6
months. More research is required to
investigate the effects after 3 to 5 years
of treatment similar to the National
Institute of Mental Health Collaborative
Multisite Multimodal Treatment Study
of Children with ADHD (NIMH-MTA)
trial.
3. The effects of neurofeedback appear to
have similar effects to stimulant medi-
cation for inattention and impulsivity,
but more controlled and randomized
studies are required to further support
this observation.
4. Additional research is required to investi-
gate the working mechanism of neuro-
feedback.
5. Given that neurofeedback currently
requires multiple treatment sessions,
further research should be directed toward
improving neurofeedback treatment to
require fewer treatment sessions (e.g.,
LORETA neurofeedback, Independent
Component Analysis (ICA) neurofeed-
back, Z-score neurofeedback).
6. Neurofeedback is efficacious when
inattention and impulsivity are the main
problems. When the main complaint is
hyperactivity, medication is possibly a
better choice given the limited success
of neurofeedback in this domain. Con-
trolled and randomized studies are
required to further substantiate this
claim.
7. No differences in neurofeedback efficacy
have been found between medicated and
nonmedicated children; therefore, neuro-
feedback can be utilized in combination
with a medication regimen.
8. Licensed health care providers should
take necessary educational prerequisites
to understand the methods and proper
implementation of neurofeedback and
its appropriateness for the treatment of
ADHD.
9. When appropriately trained in the plan-
ning, implementation, and monitoring
of neurofeedback, the licensed health care
professional should consider including
neurofeedback as a potential modality
of treatment.
NEUROFEEDBACK FOR THE
TREATMENT OF ADHD
ADHD has become one of the most com-
mon neurodevelopmental and psychiatric
disorders of childhood (Rowland, Lesesne,
& Abramowitz, 2002). The general rate of
prevalence is reported between 3% and 10%
of school-age children (Erk, 1995). Cur-
rently, the disorder is primarily diagnosed
by referring to the criteria of the Diagnostic
and Statistical Manual of Mental Disorders
(4th ed., text rev. [DSM–IV–TR]; American
Psychiatric Association [APA], 2000) or the
International Statistical Classification of
Mental Disorders (World Health Organiza-
tion, 1992). ADHD is not only the most
common of the childhood psychiatric disor-
ders but also the best researched disorder
(Rowland et al., 2002). Depending on how
it is characterized and diagnosed, it is
estimated to affect as many as 3% to 7% of
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the school-age children (American Psychi-
atric Association, 2000). The APA has also
reported that the prevalence of adolescent
and adult ADHD is not well known.
According to the DSM–IV–TR (APA,
2000), the disorder presents itself in three
primary subtypes: combined type, predomi-
nantly inattentive, predominantly hyperactive-
impulsive type.
Neurofeedback is a type of operant con-
ditioning in which an individual modifies
the frequency, amplitude, or other character-
istic of his or her own EEG. As early as 1941,
Jasper and Shagass demonstrated that the
EEG alpha rhythm could be classically con-
ditioned. Furthermore, it has been demon-
strated that humans and animals can
control their EEG through feedback (S. S.
Fox & Rudell, 1968; Hetzler, Rosenfeld,
Birkel, & Antoinetti, 1977; Rosenfeld, Rudell,
& Fox, 1969; Sterman, 1996; Strehl et al.,
2006; Thatcher, 2000) and that the skill to
modulate EEG activity in the required direc-
tion is preserved over time (6 months: Leins
et al., 2007; 2 years: Gani, Birbaumer, &
Strehl, 2009). The application requires an
individual to have at least three electrodes
attached to the head, which records, ana-
lyzes, and gives near instantaneous feedback
based on the electrical activity of the brain;
thus giving us the term—neurofeedback.
Current Treatments and Future
Perspectives for ADHD Treatments
Recently, the 8-year follow up results
from an NIMH-sponsored trial on different
treatments for ADHD have been published;
the NIMH-MTA (Molina et al., 2009). This
study compared four different treatments
in 579 children. These participants were
randomly assigned to (a) systemic medi-
cation management, (b) multicomponent
behavior therapy, (c) a combination of (a)
and (b), and (d) usual community care. After
14 months, the first results initially showed
that the medication and combined groups
had the greatest improvements in ADHD
and ODD symptoms. Half of these effects
had dissipated 10 months after the treatment
was completed. More important, after an
8-years follow-up, there were no longer any
differences found between these four groups,
indicating that the initial treatment subject
randomization did not predict functioning
6 to 8 years later. This multicenter large-scale
study clearly demonstrates a lack of
long-term effects for stimulant medication,
multicomponent behavior therapy or
multimodal treatment (Molina et al., 2009).
Furthermore, general response rates to
stimulant medication in ADHD are
estimated to be between 70 and 90% (see
Hermens, Rowe, Gordon, & Williams,
2006, for an overview). These results clearly
show that at present there is no treatment
modality that has sufficient long-term effi-
cacy for children with ADHD and that there
is a need for new treatments with better
long-term outcomes. Given that the skills
and the treatment effects of neurofeedback
have the potential to last for longer than 6
months (Leins et al., 2007) or even more
than 2 years (Gani et al., 2009), this
makes neurofeedback a very interesting and
promising treatment for ADHD.
Neurofeedback is growing in popularity,
yet there is considerable controversy in using
it to treat some neurologically and psycho-
logically based disorders. However, neuro-
feedback is currently utilized in clinical
settings as an intervention to treat a number
of neurological and psychological impair-
ments. The published literature contains a
significant amount of support for the use of
neurofeedback techniques and the more
recent literature is most impressive; however,
it also has to be emphasized that neurofeed-
back is not a panacea and is at this moment
only a well-investigated treatment of ADHD
and epilepsy. In the following sections,
we briefly review the history of neurofeed-
back in the treatment of ADHD, critically
appraise its efficacy, and put this treatment
into perspective compared to other treat-
ment modalities.
HISTORICAL PERSPECTIVE OF
NEUROFEEDBACK IN ADHD
The growing number of individuals diag-
nosed with ADHD and the desire to avoid
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stimulant medication have brought increas-
ing attention to neurofeedback treatment in
recent years. Because standardized testing
has become an integral part of the edu-
cational system, ADHD is more apparent
and well documented. Despite the increasing
number of published studies, there is contro-
versy regarding the efficacy of neurofeed-
back for treating ADHD.
Lubar and Shouse were the first to publish
on the use of neurofeedback in ADHD in
1976. In their initial study they tested the
idea that neurofeedback training (Sensori-
motor Rhythm training [SMR] frequency
of 12–14 Hz), over the sensorimotor strip of
the brain, could be used to help children
with hyperkinesis. In this case study, the
child was rewarded to produce SMR
activity and at the same time inhibit theta
activity (4–7 Hz). During neurofeedback,
the child increased SMR by three times the
amount of the initial recording along with
a decreased classroom self-stimulation and
out-of-seat behavior. Simultaneously, the
child increased his sustained attention and
schoolwork. This study employed an ABA
design in which after this initial uptraining
of SMR (A) the procedure was reversed in
a blind fashion and the child was trained to
inhibit the SMR and to increase the theta
frequencies (B). After 35 sessions, the child
had regressed completely to baseline mea-
sures in both his EEG and school perform-
ance. To validate the initial procedure, the
child was trained again in the original proto-
col design with reinforcement for SMR and
no reinforcement for production of theta
(A). After 28 sessions of this protocol, the
child’s previous successes were regained.
Finally, the medication was removed to mea-
sure sustained attention and the improve-
ments were maintained (Lubar & Shouse,
1976). Follow-up after several years
demonstrated that the child continued to
do well without the readministration of the
medication (Lubar, 1991). Although this
study showed significant findings in a
controlled ABA design, its power is limited
because it is a case study.
In 1979, Shouse and Lubar replicated
the previous 1976 study with a hyper-
kinetic group (N¼4) of children. The same
experimental ABA design was used with
the addition of the gradual withdrawal of
Ritalin (Lubar & Shouse, 1976). This repli-
cation succeeded in that these children were
able to regulate their EEG by changing their
SMR levels (a doubling of SMR activity)
along with behavioral improvements. These
two initial studies inspired many subsequent
studies, which investigated neurofeedback as
a treatment for ADHD.
The first published controlled group study
was conducted by Linden et al., who utilized
a randomized design, comparing the effects
of neurofeedback to a waiting list control
group in 18 participants (Linden, Habib, &
Radojevic, 1996). In this study, participants
were required to increase beta and decrease
theta. The results reflected improvements in
measures of ADHD symptoms and IQ
measures.
Four studies compared neurofeedback
treatment with stimulant medication (Fuchs,
Birbaumer, Lutzenberger, Gruzelier, &
Kaiser, 2003; Monastra, Monastra, & George,
2002; Rossiter, 2004; Rossiter & La Vaque,
1995). These studies all used a variation
of theta=beta ratio neurofeedback protocols
at fronto-central locations and found that
this technique demonstrated significant
changes. Of interest, the effects of these
studies demonstrate similar treatment
responses between stimulant medication
and neurofeedback. In the Monastra et al.
(2002) study, all participants were medi-
cated; however, when the medication was
removed at the end of treatment, only the
participants who had completed neurofeed-
back were able to sustain their improve-
ments. The posttreatment quantitative
electroencephalography (QEEG) measure-
ments also showed a significant decrease in
cortical slowing of the individuals who had
completed the neurofeedback (Monastra
et al., 2002).
The Monastra et al. (2002) study differed
from the other three studies in that the
participants were preselected based on a
deviating theta=beta ratio. This most likely
resulted in selecting the ADHD children
who were to respond to theta=beta neuro-
feedback protocols. Furthermore, rando-
mized allocation to treatment groups was
Scientific Features 69
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not used in these four studies. Randomized
allocation has been shown to lead to an
overestimation of the clinical effects,
especially on hyperactivity, because clients
can select the treatment they prefer (Arns,
de Ridder, Strehl, Breteler, & Coenen,
2009). These are essential drawbacks in
all four studies; consequently, no firm
conclusions can be drawn on the compar-
ability between neurofeedback and the use
of medication in the treatment of ADHD.
Nonetheless, these studies suggest that
neurofeedback has potentially comparable
effects to medication, but further controlled
research is required to substantiate that
conclusion.
Le
´vesque, Beauregard, and Mensour
(2006) demonstrated in a randomized
controlled study not only improvements on
inattention and hyperactivity but also, above
all, a normalization of brain activity in the
anterior cingulate cortex measured with
functional magnetic resonance imaging
(fMRI) for the neurofeedback group only,
suggesting neurofeedback does normalize
underlying networks that have been shown
to deviate in children with ADHD.
Heinrich, Gevensleben, Freisleder, Moll,
and Rothenberger (2004) were the first to
report positive results after Slow Cortical
Potential (SCP) neurofeedback in the
treatment of ADHD. SCP neurofeedback
is different from the aforementioned
approaches in that changes in the polarity
of the EEG are rewarded (i.e., positivity vs.
negativity in the EEG) and a discrete reward
scheme is used in lieu of rewarding changes
in specific frequency bands. Intriguingly,
both the SCP neurofeedback and SMR
neurofeedback approaches have been suc-
cessfully used in treating epilepsy (for an
overview, also see Egner & Sterman, 2006),
and both are suggested to regulate cortical
excitability (Kleinnijenhuis, Arns, Spronk,
& Breteler, 2007). Several studies have com-
pared theta=beta training and SCP training
both within-subject and between-subjects,
and both neurofeedback approaches show
comparable effects on the different aspects
of ADHD such as inattention, hyperactivity,
and impulsivity (Arns, de Ridder, Strehl,
Breteler, & Coenen, 2009; Gevensleben,
Holl, Albrecht, Schlamp, et al., 2009; Leins
et al., 2007).
Strehl and colleagues (Leins et al., 2007;
Strehl et al., 2006) conducted a randomized
controlled prospective study in which clients
were randomized to either theta=beta neuro-
feedback or SCP neurofeedback. Both inter-
ventions showed similar efficacy in the
treatment of ADHD, which were sustained
over 6 months. Furthermore, the self-
regulation skills were also preserved at
follow-up.
Holtmann et al. (2009) conducted a study
with a randomized controlled design where
children were randomized either to theta=
beta neurofeedback protocol or to a control
group consisting of Captain’s Log training.
Thus both groups were exposed to an atten-
tion training program for the same amount
of time (neurofeedback or Captain’s Log),
thereby controlling for indirect attention
training. This study found a specific and
clinically relevant improvement of impulsiv-
ity on a Go-NoGo task for the neuro-
feedback group alone. An additional
observation worth noting is that in many
studies parent rating scales were utilized.
The rating scales improved for inattention,
hyperactivity, and impulsivity; however,
there was no significant interaction, suggest-
ing the effects were similar for both groups.
In 2009, one of the largest multisite rando-
mized controlled trials on neurofeedback in
ADHD was published by Gevensleben
(Gevensleben, Holl, Albrecht, Schlamp,
et al., 2009). This study incorporated data
from 94 participants and overcame many of
the criticism from the past while incorporat-
ing strong methodological aspects, such as
randomization, multicenter study, a large
sample size, and a credible sham control
consisting of attention training. Post-QEEG
data from this sample already showed that
the neurofeedback trained group—but not
the control group—showed reduced EEG
theta power (Gevensleben, Holl, Albrecht,
Vogel, et al., 2009), thereby demonstrating
the specificity of this intervention.
As suggested by Loo and Barkley (2005),
possible alternative explanations for the effi-
cacy of neurofeedback consist of the fact that
children who are exposed to neurofeedback
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spent more time with the therapist,
as compared to a control group. Another
explanation put forward by Loo and Barley
is that neurofeedback training, itself, could
be considered a form of cognitive-behavioral
training. These observations suggest that it
is not the actual training of EEG activity
per se, causing the treatment effects. The two
studies by Gevensleben et al. (Gevensleben,
Holl, Albrecht, Schlamp, et al., 2009;
Gevensleben, Holl, Albrecht, Vogel, et al.,
2009) and the Holtmann et al. (2009) study
controlled for both aspects. The (semiactive)
control groups that were employed can be
considered credible placebo control.
RATIONALE FOR NEUROFEEDBACK
IN ADHD
Psychophysiological Basis of Diagnosis
Cerebral blood flow and metabolism,
measured in fMRI, positron emission
tomography, and single-photon emission
computed tomography studies all support
the electrical and chemical signaling systems
that are the currency of information transfer
in the brain. In contrast, the EEG, a measure
of the electrical activity of the brain, may be
a more direct indicator of brain function.
Indeed, the EEG offers information that is
of greater temporal resolution but at the cost
of less spatial resolution. EEG research on
ADHD has been conducted at many levels
and suggests that EEG parameters can effec-
tively distinguish between children with
ADHD and normal controls. The EEG
reflects the electrical activity of large popula-
tions of synchronized neurons, mostly corti-
cal pyramidal neurons. Therefore, some
diseases can be more easily identified with
EEG than with functional imaging, especially
when the disease manifests into a form of
altered electrical brain activity, as in ADHD
(Van der Stelt, van der Molen, Gunning, &
Kok, 2001).
QEEG spectral analysis of the EEGs of
children with ADHD has frequently shown
increased levels of slow waves (predomi-
nantly theta) and decreased levels of relative
beta activity when compared to the EEGs
of normal controls (Barry, Clarke, &
Johnstone, 2003). In general, the abnormali-
ties seem to be more pronounced in children
with the combined type of ADHD than the
inattentive ADHD (Barry et al., 2003;
Chabot & Serfontein, 1996). A large-scale
multicenter study (Monastra et al., 1999) as
well as a meta-analysis (Boutros, Fraenkel,
& Feingold, 2005) have concluded that
excess theta is a robust biomarker for
ADHD. The literature is less consistent
about the decreased absolute beta in ADHD
(Callaway, Halliday, & Naylor, 1983;
Dykman, Ackerman, Oglesby, & Holcomb,
1982; Mann, Lubar, Zimmerman, Miller, &
Muenchen, 1992; Matsuura et al., 1993),
which was not found by several other studies
(Barry, Clarke, Johnstone, McCarthy, &
Selikowitz, 2009; Clarke, Barry, McCarthy, &
Selikowitz, 2001; Lazzaro et al., 1999;
Lazzaro et al., 1998) and was found to be
increased in one study (Kuperman, Johnson,
Arndt, Lindgren, & Wolraich, 1996).
These EEG deviations in ADHD have
been interpreted as a maturational lag
by some (Barry et al., 2003; Satterfield,
Cantwell, Saul, Lesser, & Podosin, 1973),
whereas others have interpreted the excess
theta to be reflective of a labile vigilance
regulation (Hegerl et al., 2008) or hypo-
arousal (Barry et al., 2009; Satterfield et al.,
1973) with the latter two models also
explaining why stimulant medication works
in the treatment of ADHD.
Several studies have also investigated the
differences in brain activity between respon-
ders and nonresponders to stimulant medi-
cation. Most of these studies have shown
that distinct neurophysiological groupings
within the behaviorally diagnosed subtypes
exist. Most studies have shown that
increased theta and=or theta=beta ratios are
related to a favorable treatment outcome,
and these do not relate to DSM subdiagnosis
(Arns, de Ridder, Strehl, Breteler, & Coenen,
2008; Clarke, Barry, McCarthy, & Selikowitz,
2002; Clarke, Barry, McCarthy, Selikowitz, &
Brown, 2002; Suffin & Emory, 1995) sug-
gesting that within behavioral homogenous
groups such as ADHD, neurophysiological
subgroups exist and respond differentially
to treatment.
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These investigations provide sufficient
evidence to conclude that not only is the
electrical activity of the brain reflective of
the condition of ADHD but dysregulation
contributes to the presence of the condition.
From this, it can be reasoned that operant
conditioning to decrease dysregulation and
alter electrical activity would not only be
possible but would stand as a treatment
option for the disorder.
STATUS OF NEUROFEEDBACK
FOR ADHD
Treatment of ADHD with neurofeedback
has gained promising empirical support in
recent years (Arns et al., 2009; D. J. Fox,
Tharp, & Fox, 2005; Lubar, 2003; Monastra
et al., 2002). In addition, neurofeedback
results in normalizations of neurophysiologi-
cal patterns with QEEG (Doehnert,
Brandeis, Straub, Steinhausen, & Drechsler,
2008; Gevensleben, Holl, Albrecht, Schlamp,
et al., 2009), event-related potential
(Heinrich et al., 2004; Holtmann et al.,
2009; Kropotov et al., 2005), and fMRI
(Levesque et al., 2006).
Historical Studies Suggesting Levels
of Efficacy
Anecdotal reports and case studies are
often the first steps to validating an inter-
vention. However, to be fully accepted as
empirical support they must pass rigorous
clinical trials (La Vaque et al., 2002). In
2002, according to the efficacy task force
criteria, established by the Association for
Applied Psychophysiology and Biofeedback
and the International Society for Neurofeed-
back and Research, neurofeedback applica-
tions based on the reviewed literature
achieved Level 3: Probably Efficacious (La
Vaque et al., 2002). The publication by
Monastra et al. (2002) and the reviewed
literature were catalysts for this recommen-
dation. In 2002 it was suggested that to
achieve ‘‘efficacious and specific levels,’’
studies should be conducted that will demon-
strate neurofeedback to be ‘‘statistically
superior to credible sham therapy, pill, or
alternative bona fide treatment in at least
two independent research settings’’ (La
Vaque et al., 2002).
Recent Studies Suggesting Levels
of Efficacy
In 2005 Monastra et al. critically reviewed
the literature and applied the APA guidelines
for rating clinical efficacy (see Table 1). It
was concluded that neurofeedback treatment
for ADHD could be considered as Level 3:
Probably Efficacious. However, in that same
year Loo and Barkley (2005) published a
review article in which they concluded that
‘‘the promise of EEG Biofeedback as a legit-
imate treatment cannot be fulfilled without
studies that are scientifically rigorous’’
(p. 73). The main concerns they raised were
the lack of well-controlled, randomized stu-
dies; the small group sizes; and the lack of
proof that the EEG feedback is solely
responsible for the clinical benefit and not
nonspecific factors such as the additional
time spent with a therapist or ‘‘cognitive
training.’’ In 2006, Holtmann and Stadtler
concluded that EEG biofeedback has gained
promising empirical support in recent years,
but there is still a strong need for more
empirically and methodologically sound
evaluation studies.
Since 2005, new research has been pub-
lished investigating the clinical efficacy of
neurofeedback for the treatment of ADHD.
A recently published meta-analysis on neu-
rofeedback in ADHD by Arns et al. (2009)
concluded that neurofeedback for ADHD
met Level 5: Efficacious and Specific and
that neurofeedback had large effect sizes
(large clinically relevant effect) on the
domains of impulsivity and inattention and
a medium (medium clinically relevant) effect
size on hyperactivity. The meta-analysis
included 15 studies and 1,194 clients with
ADHD, and of these six studies randomiza-
tion was used. Two randomized controlled
trials both published in 2009 were the key
studies on the basis of which the efficacy rat-
ing could be lifted to Level 5, the randomized
multicenter study from Gevensleben, Holl,
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Albrecht, Vogel, et al. (2009) and the rando-
mized study from Holtmann et al. (2009).
Both of these studies used sound methodolo-
gical designs, employed randomization, and
implemented semiactive control groups,
which can be considered a credible placebo
control. The study by Gevensleben, Holl,
Albrecht, Schlamp, et al. (2009) consisted
of a large sample size (N¼94). Therefore,
in line with the suggestion made by LaVaque
et al. (2002), neurofeedback was shown to be
superior to a credible placebo control, which
was demonstrated in two independent
research settings, thereby meeting Level 5.
Long-Term Effects
Several studies have investigated
long-term outcomes. In 2003 Lubar pub-
lished data on 52 cases, which were followed
for up to 10 years after neurofeedback treat-
ment in a single clinical setting. The data
involved a phone interview given by an inter-
viewer who was uninformed to the treat-
ment, using the Conner’s rating scale of 16
behavioral categories. Most participants
rated themselves as ‘‘very much improved
or more change.’’ Because the interview
was ‘‘blinded,’’ it was performed objectively
and had the advantage that the participants
interviewed were chosen randomly from a
group of more than 1,000 cases but repre-
sented those who had been out of treatment
the longest. Unfortunately, this was an
uncontrolled study with no control group,
thereby it cannot be ruled out that these
effects were simply because of maturation.
However, the following studies employed a
control group, and follow-up was performed
for both the experimental and control
groups. Heinrich et al. (2004) performed a
3-month follow-up for the SCP group and
found all measures improving further (Arns
et al., 2009). The study of Strehl and collea-
gues that measured scores in impulsivity,
inattention, and hyperactivity in a 6-month
follow-up were shown to improve even
further as compared to the end of treatment
(Leins et al., 2007). A 2-year follow-up for
this study showed that all improvements in
behavior and attention turned out to be
stable. Test results for attention and some
of the parents’ ratings once more improved
significantly (Gani et al., 2008). In addition,
EEG-self regulation skills turned out to be
still preserved, indicating that these children
were still able to regulate their brain activity
successfully. The 6-month follow-up data from
the large multicenter study by Gevensleben,
Holl, Albrecht, Schlamp, et al. (2009) are
currently being reviewed for publication,
but according to these data, ‘‘behavioral
improvements induced by NF training in
TABLE 1. Levels of efficacy (American Psychological Association).
Level 1 Not Empirically Supported Supported only through anecdotal evidence or
non-peer-reviewed case studies
Level 2 Possibly Efficacious Shown to have a significant impact in at least one
study, but the study lacked a randomized
assignment between controls
Level 3 Probably Efficacious Shown to produce positive effects in more than one
clinical, observational wait list or within-subject or
between-subject study
Level 4 Efficacious Shown to be more effective than a no-treatment or
placebo control group; the study must contain
valid and clearly specified outcome measures,
and it must be replicable by at least two
independent researchers demonstrating the same
degree of efficacy
Level 5 Efficacious and Specific Shown to be statistically superior to credible placebo
therapies or to actual treatments, and it must be
shown as such in two or more independent studies
Scientific Features 73
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children with ADHD were sustained at
6-month follow-up’’ (H. Heinrich, personal
communication, January 14, 2010).
Taken from the limited data available, it
can be concluded that the clinical effects of
neurofeedback remain stable and may
improve further over time. This is in contrast
to current treatments such as medication
management and multicomponent behavior
therapy as explained in the introduction,
based on the NIMH-MTA trial (Molina
et al., 2009). However, larger scale,
controlled studies with longer follow-up are
required to investigate this claim further.
Pre- and Post-QEEG Differences
It is often stated that studies fail to report
pre- and post-QEEG differences because the
EEG is the basis of treatment in neuro-
feedback (e.g., see Loo & Barkley, 2005).
However, this is not a credible reason to
criticize the clinical efficacy of neurofeed-
back or any other treatment. The primary
question is, ‘‘Does it work?’’ The secondary
question is, ‘‘How does it work?’’ Several
studies found a normalization of neurophy-
siological patterns with QEEG (Doehnert
et al., 2008; Gevensleben et al., 2009),
event-related potential (Heinrich et al.,
2004; Holtmann et al., 2009; Kropotov
et al., 2005), and fMRI (Levesque et al.,
2006). For rating clinical efficacy this is of
no concern, therefore we do not discuss this
issue further in this paper.
Neurofeedback versus Stimulant
Medication
As was shown in the overview of
neurofeedback studies, four studies directly
compared neurofeedback to stimulant medi-
cation in the treatment of ADHD. Although
the results of these four studies hint at
the fact that neurofeedback demonstrates
similar effects as compared to stimulant
medication, these studies suffer some metho-
dological issues making it impossible to draw
that conclusion, at present. Better controlled
studies (at least employing randomized
group assignments) are required to further
support that conclusion.
Recently, a meta-analysis was conducted
on two types of stimulant medication in
the treatment of ADHD by Faraone and
Buitelaar (2009). They compared the effects
of methylphenidate and amphetamines on
the domains of inattention and impulsivity=
hyperactivity. They found that ampheta-
mines are more efficacious in general as
compared to methylphenidate. Furthermore,
there was a significant publication bias for
methylphenidate studies, which means that
less efficacious studies on medication have
not been published. The effect size (ES) for
hyperactivity-impulsivity was 1.01 and the
ES for inattention was 0.84.
These data allow an indirect comparison
of the efficacy of neurofeedback and medi-
cation, as an ES is a standardized measure
that is obtained from a comparison of the
effects of multiple studies. Comparing these
data to the meta-analysis on neurofeedback
(Arns et al., 2009), it means that neurofeed-
back and methylphenidate have similar
effects on inattention (ES NF ¼0.81; ES
MPH ¼0.84) and for impulsivity=hyperac-
tivity, medication has a higher ES (ES
NF ¼0.4=0.69; ES MPH ¼1.01). The meta-
analysis on neurofeedback also concluded
that the effects on hyperactivity were most
susceptible to indirect treatment effects and
for controlled studies the ES was just signifi-
cant. Therefore, based on the current state of
research we conclude that neurofeedback is
best indicated when the main clinical pro-
blems are inattention and impulsivity. When
the main clinical problems are in the hyper-
activity domain, medication is most likely
a better treatment option. Lubar also pre-
viously suggested this in 1991:
Children with pure ADHD respond
extremely well to EEG biofeedback
training. Children with hyperkinesis,
especially if they are good responders
to stimulant medication, are also candi-
dates for biofeedback treatment, but
they may also require medication at
least during the initial part of the treat-
ment in order to obtain good control of
their disorder. (p. 205)
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CONCLUSIONS
One of the weaknesses within the neuro-
feedback studies is that they do not graph
learning curves, so there is minimal evidence
of day-to-day changes documented, in the
parameters being trained in the neurofeed-
back programs that are being used. It should
be noted that learning curves were presented
in the Lubar studies described, and addition-
ally, has been suggested by Lubar that in all
studies the trained parameters be graphed
over sessions to determine, if in fact, learning
has taken place. One of the primary criti-
cisms remains that there are many studies
that employ small sample sizes. However,
because of the publication of some very
recent and sound methodological rando-
mized controlled trials and a meta-analysis,
many potential confounding factors have
been addressed, and the clinical effects of
neurofeedback in the treatment of ADHD
can be regarded as clinically meaningful.
The two independent randomized controlled
trials, from Gevensleben, Holl, Albrecht,
Vogel, et al. (2009) and Holtmann et al.
(2009), have shown neurofeedback to be
superior to a (semiactive) control group.
The semiactive control group in these studies
can be regarded as a credible sham control
providing an equal level of cognitive training
and client-therapist interaction. Therefore, in
line with the guidelines for rating clinical
efficacy, it can be concluded that neuro-
feedback treatment for ADHD can be
considered Efficacious and Specific (Level 5).
The Monastra study (Monastra et al., 2002)
employed preselection of participants based
on deviating theta=beta ratios. This study
was also excluded from the meta-analysis
because it showed the highest ES for inatten-
tion (2.22) and hyperactivity (1.22) and there-
fore, most contributed to the heterogeneity of
variance, suggesting this study showed higher
efficacy due to preselection of deviating
theta=beta ratio (Arns et al., 2009). This large
study demonstrated that QEEG-based
preselection could potentially improve the
therapeutic outcome. Given that the three
investigated neurofeedback treatment proto-
cols (fronto-central theta=beta, central
SMR=theta, and slow cortical potentials) have
shown similar efficacy, we advise that
clinicians performing QEEG-based neuro-
feedback in the treatment of ADHD to utilize
these protocols based on QEEG findings
when determined appropriate to remain in
line with the evidence-based literature (Arns
et al., 2009).
These findings have led the current
authors to deem it necessary to provide an
updated position paper on neurofeedback
for the treatment of ADHD that is accepted
by the International Society for Neurofeed-
back and Research. Our conclusions are that
neurofeedback not only is a suitable inter-
vention for those diagnosed with ADHD
but also may be the preferred choice of inter-
ventions for some individuals. The conclu-
sions are based on solid scientific evidence
and demonstrated by clinical data collected
from multiple sites and studies across the
world. Therefore this position paper, in our
opinion, demonstrates the rationale and the
necessary support for neurofeedback to be
recognized, not only as legitimate and scien-
tific but also an evidence based intervention
for the treatment of ADHD.
The following is recommended:
1. Neurofeedback is a safe and efficacious
treatment intervention for ADHD meet-
ing the rating of Level 5: Efficacious
and Specific.
2. Neurofeedback in the treatment of
ADHD has been shown to have
long-term effects, lasting from 3 to 6
months. More research is required to
investigate the effects after 3 to 5 years
(of treatment?) similar to the NIMH-
MTA trial.
3. The effects of neurofeedback appear to
have similar effects to stimulant medi-
cation for inattention and impulsivity,
but more controlled and randomized
studies are required to further support
this observation.
4. Additional research is required to investi-
gate the working mechanism of neuro-
feedback.
5. Given that neurofeedback currently
requires multiple treatment sessions,
further research should be directed toward
improving neurofeedback treatment to
Scientific Features 75
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require fewer treatment sessions (e.g.,
LORETA neurofeedback, ICA neuro-
feedback, Z-score neurofeedback).
6. Neurofeedback is efficacious when inat-
tention and impulsivity are the main
problems. When the main complaint is
hyperactivity, medication is possibly a
better choice given the limited success of
neurofeedback in this domain. Controlled
and randomized studies are required to
further substantiate this claim.
7. No differences in neurofeedback efficacy
have been found between medicated and
nonmedicated children; therefore, neuro-
feedback can be utilized in combination
with a medication regimen.
8. Licensed health care providers should
take necessary educational prerequisites
to understand the methods and proper
implementation of neurofeedback and
its appropriateness for the treatment of
ADHD.
9. When appropriately trained in the plan-
ning, implementation, and monitoring
of neurofeedback, the licensed health
care professional should consider includ-
ing neurofeedback as a potential
modality of treatment.
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