Medical Policy Manual
Topic: Neurofeedback
Date of Origin: July 1998
Section: Medicine
Approved Date: January 2014
Policy No: 65
Effective Date: April 1, 2014
IMPORTANT REMINDER
Medical Policies are developed to provide guidance for members and providers regarding coverage in
accordance with contract terms. Benefit determinations are based in all cases on the applicable contract
language. To the extent there may be any conflict between the Medical Policy and contract language, the
contract language takes precedence.
PLEASE NOTE: Contracts exclude from coverage, among other things, services or procedures that are
considered investigational or cosmetic. Providers may bill members for services or procedures that are
considered investigational or cosmetic. Providers are encouraged to inform members before rendering
such services that the members are likely to be financially responsible for the cost of these services.
DESCRIPTION[1]
Neurofeedback describes techniques of providing feedback about neuronal activity, as measured by
electroencephalogram (EEG) or functional magnetic resonance imaging (fMRI), in order to teach
patients to self-regulate brain activity. Also known as EEG biofeedback, neurofeedback may utilize
several techniques in an attempt to normalize unusual patterns of brain function. Neurofeedback may be
conceptualized as a type of biofeedback that uses EEG as a source of feedback data. Although related in
concept to biofeedback, neurofeedback differs in that the information fed back to the patient, i.e., EEG
tracings, is not physiologic in nature.
It is hypothesized that using the EEG as a measure of central nervous system (CNS) functioning can
help train patients to modify or control their brain function in the treatment of a variety of disorders.
MEDICAL POLICY CRITERIA
The use of neurofeedback as a treatment for any disorder is considered investigational.
SCIENTIFIC EVIDENCE[1]
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Behavioral (non-drug) treatments, including neurofeedback, result in both nonspecific and specific
therapeutic effects. Nonspecific effects, sometimes called placebo effects, occur as a result of therapist
contact, positive expectancies on the part of the patient and therapist, and other beneficial effects that
occur as a result of being a patient in a therapeutic environment. Specific effects are those that occur
only because of the active treatment, above any nonspecific effects that may be present.
In order to isolate the independent contribution of neurofeedback on health outcomes (specific effects)
and properly control for nonspecific treatment effects, well-designed clinical trials with the following
attributes are necessary:
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Randomization
Randomization helps to achieve equal distribution of individual differences by randomly assigning
patients to either neurofeedback or sham treatment groups. This promotes the equal distribution of
patient characteristics across the two study groups. Consequently, any observed differences in the
outcome may, with reasonable assuredness, be attributed to the treatment under investigation.
Sham control group
A comparable sham control group helps control for placebo effects as well as for the variable natural
history of the condition being treated.
Blinding
Blinding of study participants, caregivers, and investigators to the active or sham assignments helps
control for bias for or against the treatment. Blinding assures that placebo effects do not get
interpreted as true treatment effects.
Large study population
Small studies limit the ability to rule out chance as an explanation of study findings.
Adequate follow-up
Follow-up periods must be long enough to determine the durability of any treatment effects.
The focus of the evidence review for neurofeedback for all indications is on randomized controlled trials
(RCTs) with the attributes noted above.
Literature Appraisal
Relevant systematic reviews and key RCTs or controlled trials of neurofeedback are described below.
Attention Deficit Hyperactivity Disorder (ADHD)
Systematic Reviews and Meta-Analyses
•
In a June 2005 review/meta-analysis, Monastra and colleagues used criteria from the Association for
Applied Psychophysiology and Biofeedback (AAPB) and the International Society for Neuronal
Regulation (ISNR) to assess the clinical efficacy of neurofeedback for attention deficit/hyperactivity
disorder (ADHD).[2] The authors concluded that neurofeedback for ADHD was ranked at Level 3 or
"probably efficacious" on a scale of 1 to 5, 1 being not empirically supported and 5 being efficacious
and specific. The authors noted that benefits were reported in the 5 randomized group studies
(totaling 214 patients) included in their analysis; however, the ranking for neurofeedback for ADHD
was based on the need for further studies controlled for patient and therapist factors that could
unduly influence outcomes.
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•
In 2009, Arns and colleagues published a meta-analysis on the effects of neurofeedback on the
symptoms of hyperactivity, inattention, and impulsivity in children with a primary diagnosis of
ADHD.[3] Fifteen studies met criteria (either between-subject or within-subject design) and were
included in the analysis. Initial analysis indicated heterogeneity in study results, which typically
would preclude meta-analysis. For this paper, studies were removed from the analysis until
homogeneity was achieved. The adjusted analysis indicated similar effect sizes between
neurofeedback and stimulant medication, and the authors concluded that neurofeedback could be
considered “efficacious and specific” for ADHD. However, the analysis and conclusion were based
on nonrandomized studies in which patients chose their treatment, which could increase potential
selection bias. Four randomized controlled trials (RCTs) that utilized either a wait-list control or
active control group were included in the meta-analysis. One of the studies is a German language
report and another is an unpublished PhD thesis (total of 69 children); these have not been reviewed
for this policy. The other 2 RCTs included in the systematic review are described below.[4,5] Overall,
the literature included in this meta-analysis is characterized by small, poor quality studies with high
potential for bias. The findings of the meta-analysis are also limited by significant heterogeneity in
study results and exclusion of studies due to heterogeneity.
•
In 2013, Vollebregt and colleagues conducted a systematic review and RCT to assess EEGneurofeedback treatment on neurocognitive function in children with ADHD.[6,7] Both the blinded
RCT of 41 children (8-15 years) and the systematic review of additional studies found no significant
treatment effect on neurocognitive functioning. Authors note this may be due to the limited sample
size of available studies and other methodological limitations.
Randomized Controlled Trials (RCT)
•
The first of the RCTs mentioned above was a randomized study published in 2006 that examined
brain activity following neurofeedback in 15 children with ADHD.[4] The experimental subjects
learned to inhibit the amplitude of theta waves (4–7 Hz) and increase amplitude of beta waves (15–
18 Hz). Five children with ADHD were randomly assigned to a nontreatment control condition.
Functional magnetic resonance imaging revealed increased activation of the right anterior cingulate
cortex, an area related to selective attention that previously was shown to be altered in children with
ADHD. However, it could not be determined whether the change in brain function was related to the
specific neural training program (decreasing the amplitude of theta waves and increasing the
amplitude of beta waves) or to the additional attentional training received by the experimental group.
•
In the second RCT in the meta-analysis, to control for nonspecific effects (attention training) and
confounding variables (parental engagement), Gevensleben and colleagues compared neurofeedback
with a control intervention of participants in a computerized attention skills training.[5] All children
were drug-naïve or drug-free without concurring psychotherapy for at least 6 weeks before starting
training. The 2 training conditions were designed to be as similar as possible, using computer games,
positive reinforcement by a trainer, homework, and parental encouragement in using the
skills/strategies learned during training in real-life situations. Both groups participated in 2 blocks of
9 sessions (approximately 100 minutes per session plus a break), with 2–3 sessions per week, and
parents were informed that both treatments were expected to be beneficial but were not informed as
to which type of training their child had been assigned. A total of 102 children were randomly
assigned in a 3:2 ratio; 8 children were excluded due to need for medical treatment or
noncompliance with the study protocol by either the children or their parents, resulting in 59 children
in neurofeedback and 35 in attention training (92% follow-up). Slow cortical potentials (SCPs) and
theta/beta training were compared by starting with 1 type of training in the first block and then the
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other (counterbalanced order) in the second block. Investigator evaluations were performed by the
teachers, and thus, the teachers were not blinded to the treatment.
At the end of training/testing, there were no significant differences in parents’ attitude toward the 2
training conditions or in the perceived motivation of their children. Approximately 40% of the
parents either did not know which training their child had participated in or guessed the wrong
group. Both parents and teachers rated the neurofeedback group as more improved on the
hyperactivity subcomponent of a Strength and Disabilities Questionnaire (e.g., SDQ, 19% vs. 3%,
respectively, improved) and on a German ADHD scale (e.g., 26% vs. 9%, respectively, improved).
Thirty children in the neurofeedback group (52%) and 10 children in the attention training group
(29%) improved more than 25% in the German ADHD scale (odds ratio: 2.68), which was the
primary outcome measure. Other components of the SDQ, including emotional symptoms, conduct
problems, peer problems, and prosocial behavior, were not different between the 2 training
conditions. No significant differences were noted between the 2 neurofeedback training protocols.
Results of this randomized controlled study suggested that neurofeedback may have specific effects
on attention and hyperactivity beyond those achieved by attention training and parental involvement.
The authors concluded that future studies should further address the specificity of effects and how to
optimize the benefit of neurofeedback as a treatment module for ADHD.
•
Six-month follow-up from the Gevensleben et al RCT[5] described above was reported in 2010.[8] Of
the 94 children who completed treatment, 17 started medication during the follow-up interval, and
parents of 16 children did not return the questionnaires. Follow-up was obtained in 61 children
(65%) of the original per-protocol 102 children. Although the percentage of dropouts did not differ
between the 2 groups, dropouts tended to have higher scores on the German ADHD rating scale
(FBB-HKS), particularly in the control group. The difference in dropouts between the groups limits
the interpretation of the comparative data, as the scores in the 2 groups included in follow-up were
not similar at baseline (e.g., baseline FBB-HKS of 1.50 for the neurofeedback group and 1.37 for the
control group). The improvement observed in the neurofeedback group after treatment appeared to
be preserved at 6-month follow-up. For example, the inattention subscore of the FBB-HKS
improved from 2.02 to 1.51 after treatment and remained at 1.49 at 6-month follow-up (moderate
effect size of 0.73). The hyperactivity/impulsivity subscore improved from 1.10 to 0.79 after
treatment and remained at 0.76 at 6-month follow-up (small effect size of 0.35). The authors of this
European study noted that the treatment effects appear to be limited but considered neurofeedback to
be potentially effective as one component of a multimodal treatment approach.
•
Meisel and colleagues conducted a small study (n=23) comparing neurofeedback to pharmacological
treatment in children (7-14 years, 11 boys, 12 girls) with ADHD.[9] Patients either underwent 40
theta/beta sessions or received methylphenidate. Behavioral rating scores were gathered at baseline,
post-treatment, two and six months follow-up. Behavioral rating scale questionnaires were
completed by parents and teachers. No differences between groups were observed in ADHD
functional impairment or primary symptoms. Authors did report a significant improvement in
academic performance in the neurofeedback group over medication group; however, these results
should be interpreted with caution due to considerable methodological limitations of this study. It is
not clear the study sample size was sufficient enough to detect true differences between treatment
groups. In addition, treatment effects were evaluated by teachers and parents, which may have
introduced additional bias in the assessment of ADHD symptoms and functional impairment.
•
Three additional small RCTs found no significant difference between neurofeedback and either
attention skills training, placebo training, or biofeedback relaxation training.[10-12] Comparison with
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biofeedback relaxation training suggested that non-specific factors such as a structured learning
environment may contribute to the effects of neurofeedback.[11]
Nonrandomized Comparative Studies
Two studies were identified, comparing neurofeedback and methylphenidate (stimulant) therapy in
patients with attention deficit disorder.[13,14] In these nonrandomized studies, patients in both groups
reported improvements in various measures of attention; however, nonrandomized studies limit the
ability to reach scientific conclusions concerning the efficacy of neurofeedback in the treatment of
AD/HD due to the lack of design attributes described above.
Summary
There are a few small RCTs of neurofeedback for the treatment of ADHD, and systematic reviews of
these studies have also been conducted. The available studies have methodologic limitations, such as
small sample size, and the results are not consistent in showing improvements in health outcomes. One
difficulty with this area of research is isolating the effect of neurofeedback from non-specific effects of a
trial. Studies that attempted to use active controls suggested that at least part of the effect of
neurofeedback may be due to attention skills training, relaxation training, and/or other non-specific
effects. Larger sham-controlled studies are needed to evaluate whether neurofeedback (alone or in
combination with other treatments) has beneficial effects for children with ADHD.
Autism Spectrum Disorder (ASD)
Systematic Reviews
•
In 2013 Frye and colleagues conducted a systematic review on the treatment of seizures in
patients with autism spectrum disorder.[15] Studies were selected systematically from major
electronic databases and then reviewed by a panel of ASD treatment experts. Authors concluded
there was limited evidence to support the use of neurofeedback in patients with seizures
associated with ASD.
•
In a 2009 single-author systematic review of novel and emerging treatments for ASD,
neurofeedback received a grade C recommendation (Grade C recommendation: supported by 1
nonrandomized controlled trial).[16] The author reviewed literature in the PubMed and Google
Scholar databases for clinical trial reports on numerous biological (e.g., nutritional supplements,
special diets, medications) and nonbiological (e.g., neurofeedback, massage) treatments. Due to
the extensive amount of literature, a critical analysis of the quality of the studies was not
included. The study referenced for neurofeedback was a nonrandomized pilot study that included
12 children with ASD who received neurofeedback and an untreated control group of 12 children
who were matched by sex, age, and disorder severity.[17] The study found a greater reduction in
ASD symptoms based on the Autism Treatment Evaluation Checklists (A TEC) and parental
assessments in the group treated with neurofeedback compared with the control group. While
this trial is useful in informing hypothesis formation, it does not permit conclusions on efficacy
due to the lack of randomized treatment allocation, small patient population, lack of a sham
control group, and short-term followup period. Randomized sham controlled trials in larger
numbers of patients are required to validate these findings due to the possibility of nonspecific
effects (e.g., attention training) and confounding variables (e.g., parental engagement and
expectation).
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No randomized sham controlled trials on neurofeedback for ASD have been identified.
Cognitive Performance
One small (n=6) quasi-randomized, double-blind pilot study was identified that examined whether
increasing peak alpha frequency would improve cognitive performance in older adults (70–78 years of
age).[18] Control subjects were trained to increase alpha amplitude or shown playback of one of the
experimental subject’s sessions. Compared to controls, the experimental group showed improvements in
speed of processing for 2 of 3 cognitive tasks (Stroop, Go/No-Go) and executive function in 2 tasks
(Go/No-Go, n-back); other functional measures, such as memory, were decreased relative to controls.
Epilepsy
A 2009 meta-analysis by Tan and colleagues identified 63 studies on neurofeedback for treatment of
epilepsy.[19] Ten of the 63 studies met inclusion criteria; 9 of these studies included fewer than 10
subjects. The studies were published between 1974 and 2001 and utilized a pre-post design in patients
with epilepsy refractory to medical treatment; only one controlled study was included. The metaanalysis showed a small effect size for treatment (-0.233), with a likelihood of publication bias based on
funnel plot. Randomized placebo-controlled trials are needed to evaluate the effect of neurofeedback on
seizure frequency in patients with epilepsy.
Fibromyalgia
In 2010, Kayiran and colleagues reported a randomized single blind study of neurofeedback versus
escitalopram in 40 patients with fibromyalgia.[20] Patients in the neurofeedback group were instructed to
widen a river on a computer monitor which corresponded to increasing sensory motor activity and
decreasing theta activity. Patients received 5 sessions per week for 4 weeks. The control group received
escitalopram for 8 weeks. Outcome measures at baseline and at weeks 2, 4, 8, 16, and 24 included visual
analog scale (VAS) for pain, Hamilton and Beck Depression and Anxiety Inventory Scales,
Fibromyalgia Impact Questionnaire and Short Form-36. Mean amplitudes of electroencephalogram
(EEG) rhythms and the theta/sensory motor rhythms were also measured in the neurofeedback group. At
baseline, the control group scored higher on the Hamilton and Beck Anxiety Scales and the Hamilton
Depression Scale; all other baseline measures were similar between groups. Both groups showed
improvements over time, with significantly better results in the neurofeedback group. There were no
changes over time in mean amplitudes of EEG rhythms and essentially no change in the theta/sensory
motor rhythm ratio (reduced only at week 4). This study is limited by the difference in intensity of
treatment and contact with investigators between the neurofeedback and escitalopram groups. As
previously noted, sham controlled trials are needed when assessing the effect of neurofeedback on
subjective outcome measures.
Migraine Headaches
Walker reported quantitative EEG (QEEG) for the treatment of migraine headaches in a RCT of 46
patients.[21] Results were compared with 25 patients who chose not to do neurofeedback and continued
anti-migraine drug therapy. Since baseline QEEG assessment in all 71 patients showed a greater amount
of the high frequency beta band (21-30 Hz), the 5 neurofeedback sessions focused on increasing 10 Hz
activity and decreasing 21-30 Hz targeted individually to brain areas where high frequency beta was
abnormally increased. Patient diaries of headache frequency showed a reduction in migraines in a
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majority of patients in the QEEG group but not the drug therapy group. Fifty-four percent of the QEEG
group reported complete cessation of migraines over 1 year, with an additional 39% reporting a greater
than 50% reduction. In comparison, no patients in the drug therapy group reported a cessation of
headaches, and 8% had a reduction in headache frequency of greater than 50%. Limitations of this study
include the patient self-report of headache status through diary logs which may not be the most reliable
measure of symptom improvement. Randomized sham-controlled trials are needed to adequately
evaluate this treatment approach.
Obsessive-Compulsive Disorder (OCD)
In 2013, Koprivova et al. reported a double-blind randomized sham-controlled trial of independent
component neurofeedback in 20 patients with obsessive-compulsive disorder.[22] Independent
component neurofeedback is based on the individual diagnosis of pathological EEG sources and was
directed at down-training of abnormally high activity. All patients were hospitalized and participated in
a 6-week standard treatment program that included cognitive-behavioral therapy and 25 neurofeedback
or sham biofeedback sessions. The neurofeedback group showed greater reduction of compulsions
compared to the sham group (56% vs. 21%). However, clinical improvement was not associated with a
change in EEG. Larger, long-term RCTs are needed in order to assess the efficacy of neurofeedback
treatment on patients with OCD.
Primary Insomnia
In 2010, Cortoos et al. published a small (n=17) RCT on the effect of neurofeedback training or
biofeedback training (placebo control) on objective and subjective sleep in patients with primary
insomnia.[23] Of 158 subjects with sleep complaints who were interested in participating, 131 (89%)
were excluded due to study criteria or unwillingness to remain medication free during the study period.
Following polysomnograph (PSG) recorded sleep in the laboratory, all subjects received 20 sessions of
therapist-controlled telefeedback training at home over a period of 8 weeks. The neurofeedback group
was trained to increase the sensory-motor rhythm (12-15 Hz) and inhibit theta power (4-8 Hz) and high
beta power (20-30 Hz). The biofeedback group was trained to decrease electromyographic (EMG)
activity, which was equated with the reinforcement of relaxation (placebo control). Both treatments
reduced sleep latency by 40% to 45% (22 minutes at baseline) on post-treatment PSG, measured 2
weeks after the end of training. Neurofeedback training reduced wake after sleep onset (54% vs. 13%
decrease, respectively; however, no interaction was found on the two-way ANOVA) and increased total
sleep time (40 minutes vs. less than 5 minutes, respectively, p<0.05). This study is limited by the small
number of subjects, differences in sleep parameters at baseline, and short follow-up. Additional studies
are needed to evaluate this novel treatment approach.
Substance Abuse
A 2008 systematic review of neurofeedback as a treatment for substance abuse disorders described
difficulties in assessing the efficacy of this and other substance abuse treatments, including the lack of
clearly established outcome measures, differing effects of the various drugs, presence of comorbid
conditions, absence of a gold standard treatment, and use as an add-on to other behavioral treatment
regimens.[24] The authors concluded that alpha-theta training, when combined with an inpatient
rehabilitation program for alcohol dependency or stimulant abuse, would be classified as level 3 or
“probably efficacious.” This level is based on beneficial effects shown in multiple observational studies,
clinical studies, wait-list control studies, or within-subject or between-subject replication studies. The
authors also noted that few large-scale studies of neurofeedback in addictive disorders have been
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reported, and a shortcoming of the evidence for alpha-theta training is that it has not been shown to be
superior to sham treatment.
Tourette Syndrome
In 2011, the working group of the European Society for the Study of Tourette Syndrome conducted a
systematic review of behavioral and psychosocial interventions for Tourette syndrome and other tic
disorders.[25] There were no randomized or comparative trials on neurofeedback for Tourette syndrome;
the literature was limited to 2 case series.
Since the systematic review, no RCTs for neurofeedback for this indication have been published.
Other Conditions
Interest has been noted in the use of neurofeedback for the treatment of the following conditions:
•
•
•
•
•
•
•
Anxiety and panic disorders
Depression
Menopausal symptoms
Parkinson’s Disease
Posttraumatic stress disorder (PTSD)
Stress management and relaxation
Traumatic brain injury (TBI)
There are currently no RCTs, comparative trials, or systematic reviews published for these indications.
Clinical Practice Guidelines and Position Statements
There are currently no evidence-based clinical practice guidelines or position statements from U.S.
professional societies that recommend the use of neurofeedback for any indication.
American Academy of Pediatrics (AAP)
•
•
•
The AAP’s 2011 clinical practice guidelines on the diagnosis and treatment of ADHD did not
include neurofeedback in the treatment recommendations.[26] EEG biofeedback was included on
the list of areas for future research.
The AAP guidelines for adolescent depression and for closed head injury do not address
neurofeedback.[27]
In a 2013 statement on Neurofeedback, Hypnotherapy, and Guided Imagery, the AAP indicated
that, “The studies on the use of neurofeedback to date have been criticized for lacking the
appropriate controls or the random assignment of test subjects to the treatment or sham treatment
groups. It should also be pointed out that neurofeedback treatment is an expensive approach to
treating ADHD.”[28]
American Psychiatric Association (APA)
•
While the 2004 APA practice guideline for treatment of patient with acute or posttraumatic stress
disorder[29] was silent on neurofeedback, the 2009 updated review noted that “the utility and
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•
generalizability of conclusions from [current] studies are limited by methodological issues such
as lack of formalized diagnostic procedures, inclusion of non-PTSD patients, very high dropout
rates, unspecified handling of dropouts or missing data, and lack of blinding of assessors.”[30]
Neurofeedback was not included in APA practice guidelines on treatment of substance abuse[31],
major depression[32], obsessive-compulsive disorder (OCD)[33] or panic disorder[34].
American Academy of Child and Adolescent Psychiatry (AACAP)[35]
The current AACAP practice parameters do not include neurofeedback in the treatment
recommendations for any psychiatric condition.
International Society for Neurofeedback & Research (ISNR)[36,37]
The ISNR 2012 guideline is related to standards for practice but does not address specific treatments,
indications, or scientific evidence.
Summary
The scientific evidence does not permit conclusions concerning the effect of neurofeedback on health
outcomes for any condition. A number of questions regarding clinical efficacy remain to be answered
before applying neurofeedback techniques to patients with attention deficit hyperactivity disorder
(ADHD), autism spectrum disorder (ASD), cognitive performance, epilepsy, fibromyalgia, insomnia,
migraine headache, obsessive-compulsive disorder, substance abuse disorder or Tourette syndrome,. In
addition, there are no evidence-based clincial practice guidelines or clinical position statements from
U.S. professional societies that recommend the use of neurofeedback for any condition. Therefore,
neurofeedback is considered investigational for all indications.
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CROSS REFERENCES
11 - MED65
Biofeedback, Allied Health, Policy No. 32
CODES
NUMBER
DESCRIPTION
CPT
90875
Individual psychophysiological therapy incorporating biofeedback
training by any modality (face-to-face with the patient), with
psychotherapy (eg, insight oriented, behavior modifying or
supportive psychotherapy); approximately 20-30 minutes
90876
90901
HCPCS
45-50 minutes
Biofeedback training by any modality
No code
12 - MED65