Journal of Attention Disorders
© The Author(s) 2018
Article reuse guidelines:
This is now Thibault, Veissière, Olson, and Raz’s (2018)
eighth publication making the same argument based on the
consistent finding of no separation on any outcome measure
when comparing so-called “genuine” neurofeedback (NFB)
and sham feedback in sham-controlled trials (e.g., Thibault
& Raz, 2017). The authors therefore assert that NFB oper-
ates as a placebo, all be it a powerful one, with effects com-
monly equivalent to optimized versions of established
ADHD treatments (e.g., Pigott, 2017). In their current
effort, the authors provide guidance how clinicians can ethi-
cally prescribe NFB “as a form of neurosuggestion therapy”
(Thibault et al., 2018, p. 2). Our Guest Editorial decon-
structs these sham-controlled studies demonstrating the fal-
lacies of the authors’ argument. We also examine the
evidence supporting neurosuggestion as a therapeutic inter-
vention as well as that supporting NFB’s specificity, sus-
tainability, and effectiveness when compared with stimulant
medication (SM). Finally, we question why prescribe NFB
as a placebo when with proper training clinicians can pro-
vide operant conditioning of the electroencephalogram
(EEG) with proven sustained effects.
Learning Methodology Matters
Table 1 summarizes the methodology and findings from six
sham-controlled trials treating ADHD. Although each study
acknowledged NFB is based on operant learning, their
methodology violated established learning science by using
either automated or manually adjusted EEG reward thresh-
olds to maintain an “about 80%” level of reward across ses-
sions and subjects. This procedure is contrary to basic
learning principles. First, operant conditioning targets a
response followed by a stimulus-event to make the desired
response occur more or less frequently and then plots the
target response’s occurrence over time to document whether
or not learning has occurred. In these studies, the target
response was not consistently calculated, monitored, plot-
ted, and presented to NFB subjects. Therefore, it is not
known what response (if any) was conditioned. Second, the
studies do not reference the effects of practice in the experi-
mental process. Subjects in both groups engaged in the
same set of behaviors during sessions (e.g., maintaining
stillness and focus, reducing muscle and eye-movement
artifacts, relaxation, posture, and breathing). If subjects did
790802JADXXX10.1177/1087054718790802Journal of Attention DisordersPigott et al.
1NeuroThrive, LLC, Lutherville, MD, USA
2Private Practice, Juno Beach, FL, USA
3Knoxville Neurofeedback Group, TN, USA
H. Edmund Pigott, Private Practice, 430 N. Lyra Circle, Juno Beach,
FL 33408, USA.
The Fallacy of Sham-Controlled
Neurofeedback Trials: A Reply to
Thibault and Colleagues (2018)
H. Edmund Pigott1,2, Rex Cannon3, and Mark Trullinger1
Background: Sham-controlled neurofeedback (NFB) trials consistently find no separation on ADHD outcome measures
leading many to conclude that NFB’s beneficial effects are due to placebo. Method: We deconstruct the NFB training
methodology and findings of six sham-controlled trials that assessed for evidence of learning. Results: All six studies found
no evidence NFB subjects learned to self-modulate the targeted electroencephalogram (EEG). Careful analyses revealed
these studies’ training methodologies were antithetical to the established science of operant conditioning thereby preventing
subjects from learning to self-modulate. These findings are in marked contrast to NFB studies whose methodology mirror
the best practices of operant conditioning. Conclusion: The premise that NFB’s beneficial effects are due to placebo
phenomenon is unproven as these studies compared two forms of false-feedback, not operant conditioning of the EEG.
Because these studies are highly cited and considered the gold standard in scientific rigor, a reappraisal of the evidence is
urgently needed. (J. of Att. Dis. XXXX; XX(X) XX-XX)
operant conditioning, neurofeedback, sham-controlled trials, placebo
2 Journal of Attention Disorders 00(0)
Table 1. Sham-Controlled NFB Studies.
Study citation NFB training methodology Key findings
van Os, Bocker, and
“Feedback thresholds were
automatically and dynamically
adjusted every 30 s to keep power
80% of time above or below
threshold (depending on whether
feedback consisted of up or down
training)” (p. 51).
1. Study terminated when there was no trend of an NFB
effect in the interim analysis.
2. Found “NFB treatment did not seem to affect EEG”
3. Found “most participants thought they were in the
sham group. For the treatment group, 10 out of
14 (71%) participants thought they received sham
feedback. 10 out of 12 participants in the sham group
thought they were in the sham group” (p. 51).
Lansbergen, van Dongen-
“Reward threshold levels were
automatically adjusted every 30
s so that the child was rewarded
about 80% of the time (i.e., received
positive feedback)” (p. 279).
1. Found “analyses revealed significant improvements of
ADHD symptoms over time, but changes were similar
for both Groups” (p. 275).
2. Found “75% of children and their parent(s) in the
active neurofeedback group and 50% of children and
their parent(s) in the placebo feedback group thought
they received placebo feedback” (p. 275).
3. Based on these pilot results, the authors changed their
NFB training methodology to have trainers adjust
“manually the feedback parameters” for new subjects
Arnold etal. (2013)
“Reinforcement was provided for
EEG theta–beta power ratio below
a threshold that was set minute-
to-minute by fuzzy logic based on
the immediately preceding EEG” (p.
412). Auto-thresholding ensured
subjects played videogames with
full-control approximately 80% of
1. Both groups showed significant improvement in ADHD
symptoms but there was no NFB specific effect.
2. In a subsequent publication (Collaborative
Neurofeedback Group, 2013), authors report, “the
sham group (as well as active group) showed no
obvious EEG changes in a simple pre–post measure of
theta/beta ratio” (p. 5).
Willemse, and Buitelaar
Vollebregt, van Dongen-
Willemse, and Buitelaar
This is a continuation of Lansbergen
etal. (2011). For newly enrolled
subjects (n = 27) “reward threshold
levels were manually adjusted so
that the child was rewarded about
80% of the time (ie, received positive
feedback), consequently the amount
of reward remained at about the
same level across sessions and
across groups” (p. 823).
1. Authors combined subjects from Lansbergen etal.
(n = 14) with 27 new subjects who had “trainers”
manually readjust thresholds to maintain the same
“about 80%” level of reward.
2. Found “while total ADHD symptoms improved
over time for both groups, there was no significant
treatment effect” (p. 821).
3. Although authors report that “guessing assignment was
no better than chance level” (p. 821), in a subsequent
article (Vollebregt etal., 2014b), the authors note,
“most participants of NFB placebo-controlled
RCTs conducted until now seem to experience the
treatment as a placebo condition” (p. 2).
Vollebregt, van Dongen-
Same subjects/method as van Dongen-
Boomsma etal. (2013).
1. Found “no significant treatment effect on any of the
neurocognitive variables” (p. 460).
2. Pre–post EEG data were reported for only 10 of the
22 NFB subjects. Found more evidence of negative
shaping of the EEG away from the reward targets than
“Reward thresholds were
automatically adjusted every 15 s to
provide positive feedback about 80%
of the time” (p. 677).
1. Found “self-reported ADHD symptoms decreased
substantially for all treatment groups between
pretreatment and the end of 6 month follow-up,
independent of treatment condition” (p. 673).
2. Found “no significant effect of time or treatment-
by-time interaction was observed” (p. 678) for the
targeted EEG confirming there was no evidence NFB
subjects learned to self-modulate.
Note. NFB = neurofeedback; EEG = electroencephalogram; RCT = randomized controlled trials.
Pigott et al. 3
not engage in these practiced behaviors, their EEG data
were riddled with artifact and worthless. Third, operant
conditioning of the EEG requires that these core concepts
are strictly adhered to demonstrating the operant behavior
has been learned and such documentation of learning should
occur before examining outcome measures of interest
In these studies, every reset of the EEG reward thresh-
old delivered operant consequences to subjects’ brains
antithetical to the goal of training. As Pigott and colleagues
if the targeted EEG was strengthening, reinforcement was
withdrawn and reset down to 80% thereby punishing participants
for learning to self-modulate. Conversely, if the targeted EEG
was decreasing, participants were reinforced up to 80% thereby
rewarding them for decreasing its strength. (p. 897)
At every reset of the reward threshold, NFB subjects there-
fore were either rewarded for not learning to self-modulate
the targeted EEG or administered a Type 2 punishment for
the beginnings of success.
Given their flawed methodology, it is not surprising that
all six studies found:
No evidence NFB subjects learned to self-modulate
the targeted EEG;
No separation between NFB and sham feedback on
any outcome measure; and
When assessed, the vast majority (71% to 75%) of
NFB subjects thought they received sham-feed-
back—correctly determining the NFB they received
was often false.
Intriguingly, four of the studies also found significant
improvement in both groups, leading Thibault and col-
leagues among many others to argue that these beneficial
effects are due to placebo phenomena versus any specific
effects from NFB. Two points in response below:
First, flawed methodology prevented NFB subjects from
learning to self-modulate the targeted EEG and therefore no
specific effects should be expected since each study com-
pared two forms of false-feedback. Second, both groups
participated in an active intervention. Ninaus and colleagues
(2013) found multiple cortical regions of the brain are acti-
vated when blinded subjects were told to focus and try to
control randomly moving bars during five 20-s rounds. In
contrast, no such changes occurred when subjects were
instructed to merely watch the moving bars. Subjects in
sham-controlled trials are commonly instructed to sit still,
focus, and use their brains to increase positive feedback.
Similar cortical regions therefore likely underwent a vigor-
ous workout during subjects’ 30+ sessions sitting still and
trying to control that which was uncontrollable. This is
hardly a “placebo” intervention as traditionally understood
and likely only had positive effects because subjects were
deceived into believing they had a 50% chance of receiving
accurate EEG feedback. Transparency eliminated the brain
activation found by Ninaus et al. as it likely would in all
Thibault and colleagues’ (2018) claim that NFB is a pla-
cebo is not supported by the referenced data. Their refer-
enced studies compared two forms of false-feedback—not
operant conditioning of the EEG. NFB has a 75+ year his-
tory of scientific inquiry documenting operant conditioning
of the EEG in cats (e.g., Wyrwicka & Sterman, 1968), pri-
mates (e.g., Schafer & Moore, 2011), and people (e.g.,
Jasper & Shagass, 1941), including a 40-year history of
research treating ADHD children (Lubar & Shouse, 1976;
Shouse & Lubar, 1979). The authors though dismiss this
extensive research history asserting that “Following the
results from recent double-blind studies, we can now add
EEG-nf for ADHD to this list of placebo therapies that mas-
querade under other biomedical labels” (p. 2). In contrast, it
is our assessment that it is these double-blind studies them-
selves that are the masquerade since they did not compare
operant conditioning of the EEG with a sham-control but
rather two forms of false-feedback.
Bad Science Begets More Bad Science
In their introductions, each of these sham-controlled studies
states something similar to “neurofeedback is based on the
assumption that deviant brain activity patterns can be vol-
untarily modulated by operant learning strategies”
(Schönenberg et al., 2017a, p. 674) and yet then used a
methodology antithetical to operant learning. When we
challenged Schönenberg and colleagues to either “acknowl-
edge that their neurofeedback methodology violates the
very essence of operant conditioning or explain the errors in
our analysis” (Pigott et al., 2017, p. 897), these authors
stated that they used a “previously established protocol”
(Schönenberg et al., 2017b, p. 897) and then made addi-
tional points unrelated to our analysis.
This is the problem. Bad science begets more bad sci-
ence until it is corrected. Each of these studies cited one or
more of their predecessors and appears more focused on
single/double/triple blinding and empirical rigor than
ensuring competence in administering the independent
variable, in this case operant conditioning of the EEG. True
scientific rigor demands a higher level of adherence to
learning principles when evaluating treatments based on
Unfortunately, the impact factors of the journals publish-
ing these six studies ranged from 2.5 to 11.6 placing them in
the mid-to-top tier of behavioral health journals. These
studies therefore have had a nefarious impact on the scien-
tific literature as they are highly cited in research and review
4 Journal of Attention Disorders 00(0)
articles, meta-analyses, editorials, and authoritative practice
guidelines (e.g., AACAP, 2011) as well as by insurance
companies when denying coverage since these studies are
presumed to demonstrate that NFB has no specific effects
when rigorously evaluated and therefore does not meet evi-
dence-based treatment standards. This contaminated scien-
tific literature has harmed the public by limiting access to a
treatment with a long history of using operant conditioning
to improve lives by teaching children and adults how to
self-modulate targeted neuronal activity.
Neurosuggestion, Specificity, and
Thibault and colleagues (2018) argue it is the efficacy of
suggestion and the placebo effect that drives behavioral
change from NFB—nothing specific to NFB itself—and if
transparent, clinicians can ethically prescribe NFB as a pla-
cebo treatment “with an eye for amplifying the psychoso-
cial mechanisms of suggestion rather than grasping at the
elusive neural signatures many practitioners speciously
assign as the cause of ADHD” (p. 709). To buttress their
argument, the authors cite an unpublished, uncontrolled,
open-label feasibility study they presented at a hypnosis
conference (Veissière, Olson, & Raz, 2017). In this study,
the authors used a decommissioned magnetic resonance
imaging (MRI) machine as a prop with nine ADHD chil-
dren. They told the children it was an inactive “brain
machine” and the authors would “use it as a suggestion” to
“help their brain heal itself.” While in the MRI, the authors
“gave the children positive verbal suggestions to promote
relaxation, focus, and confidence.” They report that in fol-
low-up interviews, parents of two children “reported near
complete remission of symptoms, and six reported improve-
ments in areas such as confidence, self-control, and social
skills” (p. 709) The authors then claim that “In essence, this
study provided neurofeedback-like treatment, but instead of
focusing on a specific physiological mechanism, we empha-
sized suggestion-based healing” (Thibault et al., 2018, p.
708, 709). Four points in response below:
First, besides the inherent potential for multiple biases in
an unpublished, uncontrolled, open-label hypnosis study,
we have no evidence of functional deficits or improvements
in ADHD symptoms using standardized measures for such
deficits in the children themselves. Instead, just post-treat-
ment “qualitative” interviews conducted by the authors
with the children’s parents of domains unrelated to ADHD’s
core symptoms (e.g., “confidence, self-control, and social
skills”). Furthermore, we have no data indicating the diag-
noses were correct. One would assume an accurate differen-
tial diagnosis was conducted at some point in these
children’s evaluation procedures; however, this is not clear
given the lack of information available. Finally, this is a
hypnosis feasibility study using an MRI machine as a prop,
not “neurofeedback-like treatment.” It is hard to see how
this study provides anything more than anecdotal support
for a new experimental treatment.
Second, Thibault and colleagues ignore the evidence
suggestive of NFB’s specificity and effectiveness in treat-
ing the “neural signatures” of ADHD. For example, in
their double-blinded within-subject reversal design stud-
ies, Lubar and Shouse (Lubar & Shouse, 1976; Shouse &
Lubar, 1979) demonstrated both (a) the functional rela-
tionship between the sensory motor rhythm (SMR) and
manifestation of hyperkinetic behaviors and (b) that
through real-time SMR feedback paired with operant con-
ditioning, ADHD children could learn to self-regulate
SMR with the resulting improvements or worsening in
their hyperkinetic behaviors based on whether they were
reinforced to increase or decrease SMR. In their clinical
utility of EEG article, Loo and Barkley (2005) state, “To
demonstrate that EEG changes are responsible for treat-
ment effects, reporting of actual EEG changes and correla-
tion with treatment outcome must be shown” (p. 72). Four
studies have met this challenge by correlating the extent of
NFB subjects’ learning to self-modulate the targeted EEG
with treatment outcome and found that those subjects
demonstrating the greatest learning experience the most
improvement on ADHD outcome measures (Drechsler
et al., 2007; Gevensleben et al., 2009; Janssen et al., 2016;
Lubar, Swartwood, Swartwood, & O’Donnell, 1995).
These findings provide further evidence that enhancing
EEG self-regulation is the mechanism of change from
NFB treatment versus “neurosuggestion” or other placebo
effects. Furthermore, two randomized controlled trials
(RCT) have compared electromyographic (EMG) biofeed-
back with NFB to control for both nonspecific effects and
the effects of self-regulation training (Bakhshayesh,
Hansch, Wyschkon, Rezai, & Esser, 2011; Strehl et al.,
2017). Both of these studies found that subjects learned to
self-modulate the targeted physiological mechanism
(either EMG or EEG) with NFB demonstrating significant
superiority over EMG in reducing ADHD symptoms and
this despite the fact that EMG subjects demonstrated more
pronounced learning to self-regulate. Finally, in one RCT
SM combined with NFB was found superior in multiple
outcome domains at the end of treatment and 6-month
follow-up to SM combined with attention training that
used the identical instructions and game sequences as
NFB except that the feedback was not based on subjects’
EEG thereby suggesting a specific effect for NFB as an
augmentation to SM (Li, Yang, Zhuo, & Wang, 2013). Lia
and colleagues also found that the combined SM/NFB
subjects used significantly lower doses of SM during fol-
low-up and reported fewer adverse side effects.
Third, the authors fail to acknowledge that in eight head-
to-head comparisons with SM (see Table 2), NFB resulted in
essentially equivalent improvement in treating ADHD’s
Pigott et al. 5
Table 2. Studies Comparing NFB With SM in Treating ADHD’s Core Symptoms.
Study Subjects/design Key findings
Rossiter and La Vaque (1995) 46 ADHD children and adults matched by age (M = 12.8 years), IQ,
gender, and ADHD subtype to receive either 20 NFB sessions
based on standardized EEG protocols (n = 23) or SM (n = 23)
based on patient or parent preference. Outcome measure was
1. Both the NFB and SM groups improved (p < .05) on
measures of inattention, impulsivity, information processing,
and variability, but did not differ (p > .3) on TOVA change
2. The authors concluded, “The EEG biofeedback program
is an effective alternative to stimulants and may be the
treatment of choice when medication is ineffective, has side
effects, or compliance is a problem” (p. 48).
Lutzenberger, Gruzelier, and
34 ADHD children ages 8 to 12 years were assigned based on
parental preference to NFB (n = 22) or SM (n = 12). NFB
consisted of 30 60-min sessions with sessions administered 3
times per week. The NFB protocol was either theta/beta or SMR
training dependent the child’s subtype of ADHD. The doses for
the SM group were adjusted during study based on need and
ranged between 10 and 60 mg/day. Outcome measures were the
TOVA, Attention Endurance Test, and parent- and teacher-rated
1. Both groups showed significant improvement in each of the
outcome measures with no significant differences between
2. The authors concluded, “These findings suggest that
neurofeedback was efficient in improving some of the
behavioral concomitants of ADHD in children whose
parents favored a nonpharmacological treatment” (p. 1).
Rossiter (2004) 62 ADHD children and adults ages 7-55 were matched to NFB
(n = 31) or SM (n = 31) based on patient or parent preference.
Patients were matched by (in order) age, sum of 4 baseline TOVA
scores, IQ, gender, and ADHD subtype. The SM patients were
titrated based on TOVA results and maintained on the dose that
maximized TOVA scores. The NFB patients received either 40
sessions in office or 60 at home over 3 to 3.5 months based on
standard protocols. Outcome measures were the TOVA for both
groups and for the NFB group only the BASC and BADDS.
1. Both the NFB and SM groups had similar significant
improvements in attention, impulsivity, and processing
speed on the TOVA with no significant differences between
2. The NFB group demonstrated statistically and clinically
significant improvement on behavioral measures (BASC,
ES = 1.16, and BADDS, ES = 1.59).
3. The author concluded that “confidence interval and
nonequivalence null hypothesis testing confirmed that
the neurofeedback program produced patient outcomes
equivalent to those obtained with stimulant drugs”
Duric, Assmus, Gundersen, and
130 ADHD children and adolescents, ages 6 to 18 years, were
randomly assigned to receive either (a) NFB, (b) SM, or (c)
combined NFB/SM. After randomization, 39 dropped out (36
immediately after randomization), 13 from the NFB group, 15
from the SM group, 11 from the combined group resulting in 91
completing the study; NFB (n = 30), SM (n = 31), and combined
(n = 30). The NFB group received 30 40-minute theta/beta
sessions 3 times per week for 10 weeks. Outcome measures
were the Inattention and Hyperactivity subscales of the parent-
1. The parents reported highly significant effects of the
treatments in reducing the core symptoms of ADHD, but
no significant differences between the treatment groups
2. Although not significant, the NFB group showed twice
the level of pre–post change in attention compared with
the other two treatments (3.1 vs. 1.1 and 1.5 for the
means) and NFB’s effect size was larger than the other
two treatments on both the Inattention and Hyperactivity
subscales and total score measures.
3. The authors concluded, “NFB produced a significant
improvement in the core symptoms of ADHD, which was
equivalent to the effects produced by methylphenidate,
based on parental reports. This supports the use of NFB
as an alternative therapy for children and adolescents with
ADHD” (p. 1).
Meisel, Servera, Garcia-Banda,
Cardo, and Moreno (2013)
23 ADHD children, ages 7 to 14 years, were randomly assigned
to receive either 40 theta/beta NFB (n = 12) or SM (n = 11).
Outcome measures were behavioral rating scales completed by
fathers, mothers, and teachers (ADHD RS-IV and ODDRS-IV) at
baseline and post-treatment as well as 2- and 6-month follow-up
of academic performance.
1. In both groups, there were similar significant reductions in
ADHD functional impairment as rated by parents and in
primary ADHD symptoms by parents and teachers.
2. Significant academic performance improvements were only
detected in the NFB group.
3. NFB gains were maintained in both the 2- and 6-month
4. The authors concluded, “Our findings provide new evidence
for the efficacy of Neurofeedback, and contribute to enlarge
the range of non-pharmacological ADHD intervention
choices” (p. 12).
Ogrim and Hestad (2013) 32 ADHD children, ages 7 to 16 years, were randomly assigned
to receive either 30 sessions of QEEG-guided NFB (n = 16) or
SM (n = 16). The 30 NFB sessions took place over 6 to 9 months.
Outcome measures were parent and teacher Conners’ Rating
Scales, BRIEF, CPT, QEEG and ERP.
1. SM was superior to NFB with a large effect size on the
Conners’ Rating Scales and confirmed by other outcome
2. The QEEG spectral power in the theta and beta bands did
not change in either group.
3. In ERP, the P3 no-go component increased significantly in
eight of 12 SM responder patients, but did not increase in
nonresponders or the NF group.
3. The authors concluded, “Our study supports effects for
stimulants, but not for NFB. Effects of NFB may require
thorough patient selection, frequent training sessions, a
system for excluding nonresponders, and active transfer
training” (p. 448).
6 Journal of Attention Disorders 00(0)
Table 2. (continued)
Study Subjects/design Key findings
Kiejna, Kalinowski, and
115 ADHD children, ages 6 to 14 years, meeting similar criteria
regarding the nature of ADHD were assigned to receive either
20 NFB sessions (n = 85) or MPH adjusted to their age (n =
30). Outcome measure was a structured interview of ADHD
symptoms based on DSM-IV criteria.
1. Both treatments significantly reduced (p < .01) the
number of attention deficit, hyperactivity and impulsiveness
symptoms in subgroups with attention deficit prevalence
and mixed type ADHD.
2. There were only four children with hyperactivity and
impulsiveness prevalence and none in the MPH group so a
comparison between treatments could not be made for this
subtype of ADHD.
3. The authors concluded, “The NF method proved similarly
effective to methylphenidate in reducing the number
of symptoms in two types of ADHD: ADHD with the
prevalence of attention deficit and in mixed type ADHD”
Gelade et al. (2016)
Gelade et al. (2017)
(6-month follow-up findings)
112 ADHD children, ages 7 to 13 years, were randomly assigned to
receive either 30 sessions of theta/beta NFB (n = 39), 30 sessions
of moderate to vigorous PA (n = 37), or optimally titrated
SM (n = 36) over the course of 10 weeks. Optimal SM was
determined via the same procedures as the MTA (i.e., double-
blind placebo-controlled titration in which subjects received in
random order 1-week each of 5 mg, 10 mg, 15 mg, and 20 mg
SM along with 1-week of placebo). At the end of each week,
parents and teachers completed rating scales of inattention and
hyperactivity-impulsivity along with a side effects questionnaire.
This information was used to determine optimal SM dosing for
4 weeks prior to administering the post treatment outcome
measures. There was no similar involvement of parents and
teachers in NFB and PA treatments. Outcome measures were
parent and teacher ratings on the SDQ and SWAN.
1. All three treatments evidenced significant improvement on
the parent-rated SDQ and SWAN Hyperactivity/Impulsivity
scales (p < .001).
2. SM was superior to NFB and PA on the parent-rated
SWAN Inattention scale (p < .001) and on all teacher-rated
scales (p < .001).
3. Gelade et al. (2016) concluded, “optimally titrated
methylphenidate is superior to neurofeedback and physical
activity in decreasing ADHD symptoms in children with
ADHD” (p. 1)
4. At 6-month follow-up, Gelade et al. (2017) reported,
“Interestingly, teacher reports showed less inattention and
hyperactivity/impulsivity at follow-up for NFB than PA
(p = .004–.010), even after controlling for medication use
(p = .013–.036). Our findings indicate that the superior
results previously found for parent reports and
neurocognitive outcome measures obtained with MPH
compared to NFB and PA post intervention became smaller
or non-significant at follow-up. Teacher reports suggested
superior effects of NFB over PA” (p. 1).
COMMENT: As the authors note, they followed a similar
strategy as the MTA Cooperative study to determine
optimal SM dosing. As Pigott’s (2017) analysis of the MTA
study demonstrates, making parents and teachers integral
to delivering SM and BT treatments biased the use of their
ratings when compared to outcomes of treatments they were
not involved with. Similarly in this study, it was the parent and
teacher ratings that both identified the optimal SM dose and
their subsequent ratings were then compared with parent/
teacher ratings of NFB and PA subjects even though there is
strong evidence that using parent/teacher ratings biases the
report of outcomes favoring those treatments the parents and
teachers were most involved in delivering.
This is consistent with Gelade et al.’s (2017) 6-month results
that showed “outcome measures obtained with MPH
compared to NFB and PA post intervention became smaller
or non-significant at follow-up” as parents and teachers were
“less proximal” in their follow-up assessments to their prior
role of providing these assessments weekly for 5 weeks to
determine optimal SM dosing.
Pardo, Camacho-Vara de
Rey, Meneres-Sancho, and
Servera (2015); Moreno-
Camacho-Vara de Rey, and
59 ADHD children, ages 7 to 14 years, were randomly assigned to
receive either 40 sessions of theta/beta NFB that was tailored
based on learning curves (n = 21), BT that combined parent and
teacher training along with 15 individualized cognitive therapy
sessions for the child (n = 19) and protocol-driven pharmacology
(PH; n = 19). Outcomes measures were parent and teacher
ADHD RS-IV ratings, parent ADDES ratings, and IVA/CPT.
1. All three treatments evidenced a significant impact in
reducing ADHD symptoms based on parent and teacher
ratings as well as on IVA measures of attention and
2. While the authors concluded that “From a global perspective,
BT had the most extensive results, but PH had the greatest
capacity to improve overall attention. NF was able to
improve both control response and inattention” (Moreno-
García et al., 2017, p. 1), Pigott (2017) documents how this
conclusion for BT was based on the biased ratings of parents
and teachers who were integral to delivering the package of
BT treatments, but not the NFB and PH treatments.
3. Furthermore, as reported by Moreno-García et al. (2015),
“Treatment differences observed in attentional variables in
post-treatment are not maintained in follow-up phase” (p.
222) thereby indicating that the report that “PH had the
greatest capacity to improve overall attention” was not
maintained in the follow-up IVA/CPT assessment.
Pigott et al. 7
Study Subjects/design Key findings
Li, Yang, Zhuo, and Wang
(NFB/SM combination RCT)
40 ADHD children, ages 7 to 16, were randomly assigned to
combined NFB and SM or SM combined with attention training
that used the identical instructions and game sequences as NFB
except the feedback was not based on subjects’ EEG. Subjects
were assessed using multiple parameters at baseline, after 20
treatment sessions, after 40 treatment sessions, and at 6-month
1. The study found that “compared to the control group,
patients in the combination NFB/SM group had reduced
ADHD symptoms and improved in related behavioural and
brain function” (p. 1).
2. The combined SM/NFB subjects used significantly lower
doses of SM during 6-month follow-up and reported fewer
adverse side effects.
3. The authors concluded, “The combination of EEG
feedback and methylphenidate treatment is more effective
than methylphenidate alone. The combined therapy is
especially suitable for children and adolescents with ADHD
who insufficiently respond to single drug treatment or
experience drug side effects” (p. 1).
Note. IQ = intelligence quotient; NFB = neurofeedback; EEG = electroencephalogram; SM = stimulant medication; TOVA = Test of Variables of Attention; SMR =
sensory motor rhythm; CBRS = Conners’ Behavior Rating Scale; BASC = Behavior Assessment System for Children; BADDS = Brown Attention Deficit Disorder Scales;
ES = effect size; CMADBD-P = Clinician’s Manual for the Assessment of Disruptive Behavior Disorders–Rating Scale for Parents; ADHD-RS-IV = ADHD Rating Scale-IV;
ODDRS-IV = Oppositional defiant disorder rating scale based on DSM-IV; BRIEF = Behavior Rating Inventory for Executive Function; CPT = Continuous Performance Test;
DSM = Diagnostic and statistical manual of mental disorders; PA = physical activity; SDQ = Strength and Difficulty Questionnaire; SWAN = Strengths and Weaknesses of
ADHD symptoms and Normal Behavior Scale; MPH = methylphenidate; BT = behavior therapy; ADDES = Attention Deficit Disorder Evaluation Scale; IVA = Integrated
Visual and Auditory; CPT = Continuous Performance Task; RCT = randomized controlled trials; QEEG = quantitative EEG; ERP = evoked response potential; MTA =
multimodal treatment study of children with ADHD; PH = pharmacology.
Table 2. (continued)
core symptoms (Duric, Assmus, Gundersen, & Elegen,
2012; Flisiak-Antonijczuk, Adamowska, Chładzińska-
Kiejna, Kalinowski, & Adamowski, 2015; Fuchs, Birbaumer,
Lutzenberger, Gruzelier, & Kaiser, 2003; Gelade et al., 2017;
Meisel, Servera, Garcia-Banda, Cardo, & Moreno, 2013;
Moreno-García, Meneres-Sancho, Camacho-Vara de Rey, &
Servera, 2017; Rossiter, 2004; Rossiter & La Vaque, 1995).
These eight studies comprised 581 subjects and in only one
head-to-head comparison (n = 32) has SM been found supe-
rior to NFB (Ogrim & Hestad, 2013). These comparative
effectiveness studies provide strong evidence that NFB is an
evidence-based treatment for ADHD.
Fourth, Thibault and colleagues fail to acknowledge the
extensive evidence from NFB studies whose training meth-
odology mirror the best practices of operant conditioning.
These studies consistently find NFB subjects learn to self-
modulate the targeted EEG, this learning is associated with
improvements on a wide variety of ADHD outcome mea-
sures of interest, and both are sustained at follow-up (e.g.,
Leins et al., 2007; Strehl et al., 2017; Strehl et al., 2006)
even up to 2 years later (Gani, Birbaumer, & Strehl, 2008).
These findings demonstrating the sustained ability to self-
modulate the targeted EEG during follow-up with ongoing
symptomatic improvement are unlike anything in the pla-
cebo literature. Findings further buttressed by Doren et al.’s
(2018) recent meta-analysis documenting the sustained
effects on ADHD outcomes for NFB subjects in RCTs.
The NFB Field Shares the Blame
Although NFB’s origins are based in the science of learn-
ing, the field has been negligent at ensuring that clinicians,
researchers, and device manufactures adhere to this science.
Examples include the following:
Monitoring within-session learning curves is not
standard practice for NFB clinicians, and in fact it is
our observation that most clinicians do not assess for
evidence of learning.
The vast majority of NFB studies do not assess for
evidence of learning even though this is the pre-
sumed mechanism of change. It is only recently that
this is required for publication in the industry-spon-
sored journal NeuroRegulation when authors claim
to provide operant conditioning of the EEG.
Virtually all device manufacturers include an auto-
thresholding option despite Sherlin and colleagues
(2011) clarion call that such systems violate learning
science and “could effectively train in the opposite
direction and result in an increase in aberrant and
negative (EEG) behaviors” (p. 299). Unfortunately,
this option is used by many, if not most, clinicians,
particularly those who oversee multiple “NFB” ses-
sions at a time.
As with any form of operant conditioning, there are
learners and nonlearners. The same is true with NFB and it
is learners who experience the most improvement on ADHD
outcome measures. Given this fact, it is an indictment of the
field that there are no studies comparing strategies to iden-
tify those practices that best promote subjects’ learning to
self-modulate the targeted EEG. Consequently, there is no
empirical guidance to determine which operant training
methodologies are most effective in maximizing learning—
and this in a field with a 75+ year history of basic and
Finally, the NFB field and its detractors continue to con-
duct research that violates behavioral principles, and both
sides cite such substandard research when it supports their
8 Journal of Attention Disorders 00(0)
viewpoint. This practice must stop. Evidence of learning
trumps all, and if there is no evidence of learning, operant
conditioning of the EEG did not occur.
There is plenty of blame to go around, yet if the field is to
evolve and progress, we must demand training methodolo-
gies that follow learning principles and proof that learning
occurred from all who claim to perform NFB. Hence, our
critique of Thibault and colleagues, and the sham-controlled
studies on which their argument is based, is also a plea to
NFB researchers and clinicians to demonstrate that their
methods are consistent with the best practices in behavioral
learning. If both sides can agree to this rigor, it will promote
clarity and consistency in the NFB literature that is not pres-
ent today and provide guidance to necessary steps for
advancing it forward.
Most importantly, we hope our Guest Editorial conveys
the truth that learning methodology matters. With this
caveat, we strongly recommend operant conditioning of
the EEG for the treatment of ADHD, either as a standalone
treatment or augmentation to other evidence-based treat-
ments. As for prescribing “neurosuggestion therapy” for
the treatment of ADHD, more research is required since its
underlying premise is unproven and evidentiary base
Declaration of Conflicting Interests
The author(s) declared the following potential conflicts of interest
with respect to the research, authorship, and/or publication of this
article: H.E.P. is board certified in neurofeedback and has con-
sulted for Amen Clinics, Brain Resources, CNS Response, and the
International Society of Neurofeedback and Research. He is also
on the scientific advisory board of Narbis, a neurofeedback tech-
nology company. R.C. is board certified in neurofeedback and
Editor-in-Chief of the journal NeuroRegulation. M.T. is board cer-
tified in neurofeedback.
The author(s) disclosed receipt of the following financial support
for the research, authorship, and/or publication of this article: The
International Society of Neurofeedback and Research, Biofeedback
Certification International Alliance, and Association of Applied
Psychophysiology and Biofeedback contributed equally to the
open access publication fees with our deep gratitude.
American Academy of Child and Adolescent Psychiatry, (2011).
ADHD: Clinical practice guideline for the diagnosis, evalu-
ation, and treatment of attention-deficit/hyperactivity disor-
der in children and adolescents. Pediatrics, 128, 2011-2654.
Arnold, L. E., Lofthouse, N., Hersch, S., Pan, X., Hurt, E., Bates,
B., . . . Grantier, C. (2013). EEG neurofeedback for ADHD:
Double-blind sham-controlled randomized pilot feasibility
trial. Journal of Attention Disorders, 17, 410-419.
Bakhshayesh, A. R., Hansch, S., Wyschkon, A., Rezai, M. J., &
Esser, G. (2011). Neurofeedback in ADHD: A single-blind
randomized controlled trial. European Child & Adolescent
Psychiatry, 20, 481-491.
Cannon, R. (2015). Editorial perspective: Defining neurofeedback
and its functional processes. Neuroregulation, 2, 60-69.
Collaborative Neurofeedback Group. (2013). A proposed multi-
site double-blind randomized clinical trial of neurofeedback
for ADHD: Need, rationale, and strategy. Journal of Attention
Disorders, 17, 420-436. doi:10.1177/1087054713482580
Doren, J. V., Arns, M., Heinrich, H., Vollebregt, M. A., Strehl,
U., & Loo, S. K. (2018). Sustained effects of neurofeedback
in ADHD: A systematic review and meta-analysis. European
Child & Adolescent Psychiatry. Advance online publication.
Drechsler, R., Straub, M., Doehnert, M., Heinrich, H., Steinhausen,
H., & Brandeis, D. C. (2007). Controlled evaluation of a neu-
rofeedback training of slow cortical potentials in children
with attention deficit/hyperactivity disorder. Behavioral and
Brain Functions, 3, 35.
Duric, N. S., Assmus, J., Gundersen, D. I., & Elegen, I. B. (2012).
Neurofeedback for the treatment of children and adolescents
with ADHD: A randomized and controlled clinical trial
using parental reports. BMC Psychiatry, 12, Article 107.
Flisiak-Antonijczuk, H., Adamowska, S., Chładzińska-Kiejna,
S., Kalinowski, R., & Adamowski, T. (2015). Treatment of
ADHD: Comparison of EEG-biofeedback and methylpheni-
date. Archives of Psychiatry and Psychotherapy, 4, 31-38.
Fuchs, T., Birbaumer, N., Lutzenberger, W., Gruzelier, J. H.,
& Kaiser, J. (2003). Neurofeedback treatment for atten-
tion-deficit/hyperactivity disorder in children: A compari-
son with methylphenidate. Applied Psychophysiology and
Biofeedback, 28, 1-12.
Gani, C., Birbaumer, N., & Strehl, U. (2008). Long term effects after
feedback of slow cortical potentials and of theta-beta-ampli-
tudes in children with attention-deficit/hyperactivity disorder
(ADHD). International Journal of Bioelectromagnetism, 10,
Gelade, K., Janssen, T. W., Bink, M., Mourik, R., Maras, A., &
Oosterlaan, J. (2016). Behavioural effects of neurofeedback
compared to stimulants and physical activity in attention defi-
cit/hyperactivity disorder. Journal of Clinical Psychiatry, 77,
Gelade, K., Janssen, T. W., Bink, M., Twisk, J. W., Mourik, R.,
Maras, A., & Oosterlaan, J. (2017). A 6-month follow-up of an
RCT on behavioral and neurocognitive effects of neurofeed-
back in children with ADHD. European Child & Adolescent
Psychiatry, 27, 581-593. doi:10.1007/s00787-017-1072-1
Gevensleben, H., Holl, B., Albrecht, B., Schlamp, D., Kratz,
O., Studer, P., . . .Heinrich, H. (2009). Distinct EEG effects
related to neurofeedback training in children with ADHD:
A randomized controlled trial. International Journal of
Psychophysiology, 74, 149-157.
Janssen, T. W., Bink, M., Geladé, K., Mourik, R., Maras, A.,
& Oosterlaan, J. (2016). A randomized controlled trial
into the effects of neurofeedback, methylphenidate, and
Pigott et al. 9
physical activity on EEG power spectra in children with
ADHD. Journal of Child Psychology and Psychiatry, 57,
Jasper, H., & Shagass, C. (1941). Conscious time judgments related
to conditioned time intervals and voluntary control of the alpha
rhythm. Journal of Experimental Psychology, 28, 503-508.
Lansbergen, M. M., van Dongen-Boomsma, M., Buitelaar, J. K., &
Slaats-Willemse, D. (2011). ADHD and EEG-neurofeedback:
A double-blind randomized placebo-controlled feasibility
study. Journal of Neural Transmission, 118, 275-284.
Leins, U., Goth, G., Hinterberger, T., Klinger, C., Rumpf, N., &
Strehl, U. (2007). Neurofeedback for children with ADHD:
A comparison of SCP and Theta/Beta protocols. Applied
Psychophysiology and Biofeedback, 32, 73-88.
Li, L., Yang, L., Zhuo, C., & Wang, Y. (2013). A randomised con-
trolled trial of combined EEG feedback and methylphenidate
therapy for the treatment of ADHD. Swiss Medical Weekly,
143, w13838. doi:10.4414/smw.2013.13838
Logemann, H. N. A., Lansbergen, M. M., van Os, T. W. D. P.,
Bocker, K. B. E., & Kenemans, J. L. (2010). The effective-
ness of EEG-feedback on attention, impulsivity and EEG: A
sham feedback controlled study. Neuroscience Letters, 479,
Loo, S., & Barkley, R. A. (2005). Clinical utility of EEG in atten-
tion deficit hyperactivity disorder. Applied Neuropsychology,
Lubar, J. F., & Shouse, M. N. (1976). EEG & behavioral changes
in a hyperkinetic child concurrent with training of the sen-
sorimotor rhythm (SMR): A preliminary report. Biofeedback
and Self-Regulation, 3, 293-306.
Lubar, J. F., Swartwood, M. O., Swartwood, J. N., & O’Donnell,
P. (1995). Evaluation of the effectiveness of EEG neurofeed-
back training for ADHD in a clinical setting as measured by
changes in T.O.V.A. scores, behavioral ratings, and WISC-R
performance. Biofeedback and Self-Regulation, 20, 83-99.
Meisel, V., Servera, M., Garcia-Banda, G., Cardo, E., & Moreno,
I. (2013). Neurofeedback and standard pharmacological inter-
vention in ADHD: A randomized controlled trial with six-
month follow-up. Biological Psychology, 94, 12-21.
Moreno-García, I., Delgado-Pardo, G., Camacho-Vara de Rey, C.,
Meneres-Sancho, S., & Servera, M. (2015). Neurofeedback,
pharmacological treatment and behavioral therapy in hyper-
activity: Multilevel analysis of treatment effects on electroen-
cephalography. International Journal of Clinical and Health
Psychology, 15, 217-225.
Moreno-García, I., Meneres-Sancho, S., Camacho-Vara de Rey,
C., & Servera, M. (2017). A randomized controlled trial
to examine the posttreatment efficacy of neurofeedback,
behavior therapy, and pharmacology on ADHD measures.
Journal of Attention Disorders. Advance online publication.
Ninaus, M., Kober, S. E., Witte, M., Koschutnig, K., Stangl, M.,
Neuper, C., & Wood, G. (2013). Neural substrates of cogni-
tive control under the belief of getting neurofeedback train-
ing. Frontiers in Human Neuroscience, 7, 914.
Ogrim, G., & Hestad, K. A. (2013). Effects of neurofeedback versus
stimulant medication in attention-deficit/hyperactivity disorder:
A randomized pilot study. Journal of Child and Adolescent
Psychopharmacology, 23, 448-457.
Pigott, H. E. (2017). Reply to Moreno-García et al.: Using par-
ents and teachers Integral to delivering behavior therapy
as raters likely biased the report of outcomes. Journal
of Attention Disorders. Advance online publication.
Pigott, H. E., Trullinger, M., Harbin, H., Cammack, J., Harbin, F.,
& Cannon, R. (2017). Confusion regarding operant condition-
ing of the EEG. The Lancet Psychiatry, 4, 897-898.
Rossiter, T. (2004). The effectiveness of neurofeedback and stim-
ulant drugs in treating AD/HD: Part II. Replication. Applied
Psychophysiological and Biofeedback, 29, 233-243.
Rossiter, T. R., & La Vaque, T. J. (1995). A comparison of EEG
biofeedback and psychostimulants in treating attention deficit
hyperactivity disorders. Journal of Neurotherapy, 1, 48-59.
Schafer, R. J., & Moore, T. (2011). Selective attention from vol-
untary control of neurons in prefrontal cortex. Science, 332,
Schönenberg, M., Wiedemann, E., Schneidt, A., Scheeff, J.,
Logemann, A., Keune, P. M., & Hautzinger, M. (2017b).
Authors’ reply. The Lancet Psychiatry, 4, 897-898.
Schönenberg, M., Wiedemann, E., Schneidt, A., Scheeff, J.,
Logemann, A., Keune, P. M., & Hautzinger, M. (2017a).
Neurofeedback, sham neurofeedback, and cognitive-behav-
ioural group therapy in adults with attention-deficit hyper-
activity disorder: A triple-blind, randomised, controlled trial.
The Lancet Psychiatry, 4, 673-684.
Sherlin, L. H., Arns, M., Lubar, J., Heinrich, H., Kerson, C., Strehl,
U., & Sterman, M. B. (2011). Neurofeedback and basic learn-
ing theory: Implications for research and practice. Journal of
Neurotherapy, 15, 292-304.
Shouse, M. N., & Lubar, J. F. (1979). Operant conditioning of
EEG rhythms and ritalin in the treatment of hyperkinesis.
Biofeedback and Self-Regulation, 4, 299-312.
Strehl, U., Aggensteiner, P., Wachtlin, D., Brandeis, D., Albrecht,
B., Arana, M., . . . Holtmann, M. (2017). Neurofeedback of
slow cortical potentials in children with attention-deficit/
hyperactivity disorder: A multicenter randomized trial con-
trolling for unspecific effects. Frontiers Human Neuroscience,
Strehl, U., Leins, U., Goth, G., Klinger, C., Hinterberger, T., &
Birhaumer, N. (2006). Self- regulation of slow cortical poten-
tials: A new treatment for children with attention-deficit/
hyperactivity disorder. Pediatrics, 118, 1530-1540.
Thibault, R. T., & Raz, A. (2017). The psychology of neuro-
feedback: A clinical intervention even if applied placebo.
American Psychologist, 72, 679-688.
Thibault, R. T., Veissière, S., Olson, J. A., & Raz, A. (2018).
Treating ADHD with suggestion: Neurofeedback and placebo
therapeutics. Journal of Attention Disorders, 22, 707-711.
van Dongen-Boomsma, M., Vollebregt, M. A., Slaats-Willemse,
D., & Buitelaar, J. K. (2013). A randomized placebo-con-
trolled trial of electroencephalographic (EEG) neurofeed-
back in children with attention-deficit/hyperactivity disorder.
Journal of Clinical Psychiatry, 74, 821-827.
10 Journal of Attention Disorders 00(0)
Veissière, S., Olson, J. A., & Raz, A. (2017, October).
Neurosuggestion improves self-regulation in neurodevelop-
mental disorders: A feasibility study. Presented at the 68th
Annual Meeting of the Society for Clinical and Experimental
Hypnosis, Chicago, IL.
Vollebregt, M. A., van Dongen-Boomsma, M., Buitelaar, J. K.,
& Slaats-Willemse, D. (2014a). Does EEG-neurofeedback
improve neurocognitive functioning in children with atten-
tion-deficit/hyperactivity disorder? A systematic review and a
double-blind placebo-controlled study. The Journal of Child
Psychology and Psychiatry, and Allied Disciplines, 55, 460-472.
Vollebregt, M. A., van Dongen-Boomsma, M., Slaats-Willemse,
D., & Buitelaar, J. K. (2014b). What future research should
bring to help resolving the debate about the efficacy of EEG-
neurofeedback in children with ADHD. Frontiers in Human
Neuroscience, 8, 321. doi:10.3389/fnhum.2014.00321
Wyrwicka, W., & Sterman, M. B. (1968). Instrumental condition-
ing of sensorimotor cortex EEG spindles in the waking cat.
Physiology & Behavior, 3, 703-707.
H. Edmund Pigott is a licensed psychologist trained as a scien-
tist-practitioner. He enjoys deconstructing and documenting errors
in published research.
Rex Cannon is a neuroscientist and an accomplished author,
researcher, and Editor-in-Chief for Neuroregulation. He is a
staunch supporter of non-pharmaceutical, evidence-based prac-
tices to aid individuals to improve performance. He currently
directs science and operations for Knoxville Neurofeedback
Group and the development of treatment models for Intrauterine
Drug Exposure (IUDE) and addictions.
Mark Trullinger is a PhD Candidate in the International
Psychology Department of The Chicago School of Professional
Psychology, Washington, D.C. He studies the barriers to the
acceptance of innovative medical devices and technologies in
mental healthcare. He is a Registered Psychology Associate in
Maryland and the Managing Director of NeuroThrive, LLC.