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Transcript
Optum
Behavioral Clinical Policy
NEUROFEEDBACK/BIOFEEDBACK FOR BEHAVIORAL AND
SUBSTANCE USE DISORDERS
Policy Number: BH727NFB_012017
Table of Contents
Page
INSTRUCTIONS FOR USE .......................................... 1
BENEFIT CONSIDERATIONS ...................................... 1
COVERAGE RATIONALE ............................................. 2
DEFINITIONS .......................................................... 2
DESCRIPTION OF SERVICES ...................................... 3
CLINICAL EVIDENCE ................................................. 3
U.S. FOOD AND DRUG ADMINISTRATION ................... 10
CENTERS FOR MEDICARE AND MEDICAID SERVICES ... 11
APPLICABLE CODES ................................................ 11
REFERENCES .......................................................... 11
ADDITIONAL RESOURCES ........................................ 13
HISTORY/REVISION INFORMATION ........................... 13
Effective Date: January, 2017
Related Clinical Policies & Guidelines:
•
Neurodevelopmental Disorders
•
Complementary and Alternative Medicine (CAM)
INSTRUCTIONS FOR USE
This Behavioral Clinical Policy provides assistance in interpreting and administering behavioral health benefit plans
that are managed by Optum and U.S. Behavioral Health Plan, California (doing business as OptumHealth Behavioral
Solutions of California (“Optum-CA”)). When deciding coverage, the member-specific benefit plan document must be
referenced. The terms of the member-specific benefit plan document [e.g., Certificate of Coverage (COC), Schedule of
Benefits (SOB), and/or Summary Plan Description (SPD)] may differ greatly from the standard benefit plan upon
which this Behavioral Clinical Policy is based. In the event of a conflict, the member’s specific benefit plan document
supersedes this Behavioral Clinical Policy.
All reviewers must first identify member eligibility, the member-specific benefit plan coverage, and any federal or
state regulatory requirements that supersede the COC/SPD prior to using this Behavioral Clinical Policy. Other Policies
and Coverage Determination Guidelines may apply. Optum reserves the right, in its sole discretion, to modify its
Policies and Guidelines as necessary.
This Behavioral Clinical Policy is provided for informational purposes. It does not constitute medical advice.
Optum may also use tools developed by third parties that are intended to be used in connection with the independent
professional medical judgment of a qualified health care provider and do not constitute the practice of medicine or
medical advice.
BENEFIT CONSIDERATIONS
Before using this policy, please check the member-specific benefit plan document and any federal or state
mandates, if applicable.
Pre-Service Notification
Admissions to an inpatient, residential treatment center, intensive outpatient, or a partial hospital/day treatment
program require pre-service notification. Notification of a scheduled admission must occur at least five (5) business
days before admission. Notification of an unscheduled admission (including emergency admissions) should occur as
soon as is reasonably possible. Benefits may be reduced if Optum is not notified of an admission to these levels of
care. Check the member’s specific benefit plan document for the applicable penalty and provision of a grace period
before applying a penalty for failure to notify Optum as required.
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Additional Information
The lack of a specific exclusion for a service does not necessarily mean that the service is covered. For example,
depending on the specific plan requirements, services that are inconsistent with Level of Care Guidelines and/or
prevailing medical standards and clinical guidelines may be excluded. Please refer to the member’s benefit document
for specific plan requirements.
Essential Health Benefits for Individual and Small Group
For plan years beginning on or after January 1, 2014, the Affordable Care Act of 2010 (ACA) requires fully insured
non-grandfathered individual and small group plans (inside and outside of Exchanges) to provide coverage for ten
categories of Essential Health Benefits (“EHBs”). Large group plans (both self-funded and fully insured), and small
group ASO plans, are not subject to the requirement to offer coverage for EHBs. However, if such plans choose to
provide coverage for benefits which are deemed EHBs, the ACA requires all dollar limits on those benefits to be
removed on all Grandfathered and Non-Grandfathered plans. The determination of which benefits constitute EHBs is
made on a state by state basis. As such, when using this policy, it is important to refer to the member-specific benefit
document to determine benefit coverage.
COVERAGE RATIONALE
Neurofeedback/biofeedback (with or without EEG guidance) is unproven for the treatment of individuals
with behavioral and substance use disorders, including attention-deficit/hyperactivity disorder (ADHD),
depression, anxiety, obsessive-compulsive disorder, posttraumatic stress disorder, alcohol/drug abuse, and autism
spectrum disorder.
The reviewed evidence, including randomized controlled trials and systematic reviews, does not clearly demonstrate a
treatment effect of neurofeedback/biofeedback on symptoms of ADHD. Many of these reviewed studies contained a
number of significant limitations. Additionally, there is a lack of well-designed clinical trials with sufficient sample sizes
demonstrating the effectiveness of neurofeedback/biofeedback in the treatment of other behavioral and substance use
disorders.
The requested service or procedure must be reviewed against the language in the member's benefit document. When
the requested service or procedure is limited or excluded from the member’s benefit document, or is otherwise
defined differently, it is the terms of the member's benefit document that prevails.
Per the specific requirements of the plan, health care services or supplies may not be covered when inconsistent with
Level of Care Guidelines and/or evidence-based clinical guidelines.
All services must be provided by or under the direction of a properly qualified behavioral health provider.
DEFINITIONS
Diagnostic and Statistical Manual of Mental Disorders (DSM): A manual produced by the American Psychiatric
Association which provides the diagnostic criteria for mental health and substance-related disorders and other
problems that may be the focus of clinical attention. Unless otherwise noted, the current edition of the DSM applies.
Proven Services: Services or technologies that, after a review of the evidence, demonstrate they can be safely and
effectively administered to a defined patient population, under a set of specific conditions that are clearly identified. A
service found to be proven does not necessarily indicate that the service is covered. The member’s specific benefit
plan must be referenced to determine coverage, limitations, and exclusions.
Scientific Evidence: The results of controlled clinical trials or other studies published in peer-reviewed, medical
literature generally recognized by the relevant medical specialty community.
Unproven Services: Services including medications that are not consistent with prevailing medical research that has
determined the services to not be effective for treatment of the condition and/or not to have the beneficial effect on
behavioral health outcomes due to insufficient and inadequate clinical evidence from well-conducted randomized
controlled trials or cohort studies in the prevailing published peer-reviewed literature. Unproven services and all
services related to unproven services are typically excluded. The fact that an unproven service, treatment, device, or
pharmacological regimen is the only available treatment for a particular condition will not result in benefits if the
procedure is considered to be unproven in the treatment of that particular condition.
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DESCRIPTION OF SERVICES
Neurofeedback/biofeedback therapy teaches individuals to alter EEG patterns or other physiological processes through
real-time visual, auditory or other feedback and learning. As the individual’s EEG pattern or other physiological
process improves or is learned through the feedback, symptoms of ADHD or other behavioral disorders are expected
to improve.
In some instances, neurofeedback and quantitative electroencephalography (qEEG) are used in combination. When
this occurs, the individual’s EEG pattern is analyzed by qEEG, and an individualized feedback protocol is defined for
the individual based on the reported findings.
CLINICAL EVIDENCE
Summary of Clinical Evidence
The reviewed evidence does not clearly demonstrate a treatment effect of neurofeedback/biofeedback on symptoms of
attention-deficit/hyperactivity disorder (ADHD). Some of the reviewed studies compared the effectiveness of
neurofeedback/biofeedback to stimulant medications, such as methylphenidate. In these studies,
neurofeedback/biofeedback and medications were typically found to have similar efficacy, with no significant
differences found between groups in terms of outcome. A more recent randomized controlled trial (Jannsen, et al
2016a) found the effects of stimulant medication to be greater than neurofeedback. A series of recent studies by Bink
et al (2014, 2015, 2016) found no additional value of neurofeedback over treatment as usual. Other studies have
compared the effects of neurofeedback to those of placebo-neurofeedback, with some of them finding a greater effect
for neurofeedback and others (e.g., van Dongen-Boomsma, et al, 2012; Vollebregt, et al 2014) finding no significant
difference between the two groups. Studies of long-term follow-up are limited. Steiner, et al (2014b) found greater
sustained gains at 6-months post-treatment with neurofeedback compared to cognitive training and control conditions.
Bink, et al (2016) found both treatment as usual and neurofeedback groups had improved after a one-year period.
A number of limitations among the reviewed studies limit conclusions regarding the effectiveness of
neurofeedback/biofeedback for the treatment of ADHD. Many of the earlier trials that were reviewed permitted open
treatment choice and had small sample sizes. Other studies reported difficulties isolating the effects of neurofeedback
in participants who were also taking stimulant medications at the time of study.
A number of professional societies have issued statements and proposed treatment guidelines for ADHD. Many of
them agree that a current lack of efficacy in larger, well-controlled and methodologically sound trials prevent
neurofeedback/biofeedback from being considered a front-line treatment for ADHD.
The reviewed evidence indicates that there is a lack of well-designed clinical trials with sufficient sample sizes
demonstrating the effectiveness of neurofeedback/biofeedback in the treatment of other behavioral and substance use
disorders, such as depression, anxiety, obsessive compulsive disorder, posttraumatic stress disorder, alcohol/drug
abuse, and autism spectrum disorder.
Clinical Trials: ADHD
A meta-analysis conducted by Cortese and colleagues (2016) examined the effects of neurofeedback on ADHD
symptoms and neuropsychological deficits in randomized controlled trials (RCTs) made up of children and adolescents
with ADHD. The authors found and included a total of 13 RCTs, totaling 520 participants with ADHD in all. Included
studies had a neurofeedback training component, and participants were required to be between 3 and 18 years of
age. Control conditions allowed included “treatment as usual”, “wait list”, “active”, or “placebo/sham”. Trials where
medication was part of normal clinical provision in either the control or active arm were permitted. Outcome measures
included ADHD symptoms and neuropsychological laboratory-based measures. There was a small-to-moderate effect
found on inattention, impulsivity/hyperactivity and total ADHD symptoms when proximal assessments were the
outcome. However, the effects dropped to non-statistically significant levels for total ADHD and inattention symptoms
in sensitivity analyses considering only trials with active/sham controls. When “probably blinded” outcomes were
included in the analysis, effect size for outcomes dropped further, and none were significant. The authors concluded
that the evidence from RCTs currently fails to support neurofeedback as an effective treatment for ADHD.
Janssen and colleagues (2016) conducted a randomized controlled trial to compare the effects of neurofeedback (NF),
methylphenidate (MPH), and physical activity (PA) in children with DSM-IV-diagnosed ADHD. The study used a
multicenter three way parallel group RCT design, enrolling a total of 112 children, all between the ages of 7 and 13.
Participants in the NF training group completed 30 sessions of theta/beta training over a period of 10 weeks. Those
enrolled in the MPH group were titrated using a double-blind placebo controlled procedure for 6 weeks, followed by a
stable dose for 4 weeks. The PA group served as a semi-active control group, and was matched in frequency and
duration to the other groups. Event-related potential (ERP) measures (N2; P3) were available for a total of 81 children
at both pre- and post-intervention (NF = 32; MPH = 25; PA = 24). Results found that the MPH group showed a
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specific increase in P3 amplitude (demonstrating improved response inhibition) when compared to the NF and PA
groups. The authors note that their finding of stimulants being the lone treatment to demonstrate significant
improvement in response inhibition was in line with recent doubts on efficacy and specificity of NF as a treatment for
ADHD.
Bink and colleagues (2016) conducted a one-year follow-up of neurofeedback (NFB) treatment in adolescents with
ADHD, compared with treatment as usual (TAU). Using the study population and parameters described in Bink, et al
(2014), a total of 60 adolescents (41 receiving NFB+TAU and 19 receiving TAU only) were followed-up with after one
year. Attrition analysis showed that participants who dropped out from the study did not differ from the completers in
terms of characteristics or behavioral measures. The authors found that after the one year period, self-reported
inattention levels had decreased, and neurocognitive task performance became faster, regardless of treatment group.
The authors caution their use of post hoc analyses and that by splitting up the treatment groups, the relatively small
subgroups led to a subsequent decrease in power. They note that further research, comparing neurofeedback and
stimulant medication is essential to determine whether neurofeedback can be a long-term alternative for stimulant
medication.
Using the same study population and parameters as Bink, et al (2014), Bink and colleagues (2015) investigated the
additional value of neurofeedback on behavior over treatment as usual (TAU) among adolescents with ADHD and
comorbid disorders. For this study, primary behavioral outcome measures, assessed both before and after the
intervention, included the ADHD-rating scale, the Youth Self Report, and the Child Behavior Checklist. For all of the
outcome measures, behavioral problems, mainly inattention, were found to decrease equally for both groups with
medium to large effect sizes. The authors concluded that the combination of neurofeedback combined with treatment
as usual was not more effective than treatment as usual only on the outcome measures. Reported adverse effects
were found to be similar for both groups.
Bink and colleagues (2014) conducted a multicenter parallel randomized controlled trial study to study the additional
influence of neurofeedback over treatment as usual (TAU) on neurocognitive functioning for adolescents with ADHD. A
total of 71 male adolescents were randomized to receive either a combination of TAU and neurofeedback (n = 45) or
TAU only (n = 26). In the TAU only group, participants received treatment as prescribed by the main therapist of the
participating center. Interventions for TAU included cognitive behavioral therapy, systemic therapy, and/or supportive
counseling. Stimulant medication was also used, including immediate release methylphenidate, sustained release
methylphenidate, and dexamphetamine. Participants had a mean age of 16 years; age grouping was stratified (12-15;
16-20; 21-24) and randomization was generated via computer. Patients receiving neurofeedback as a component of
the intervention received an average of 37 sessions over a period of 25 weeks. Primary outcomes included
neurocognitive performance parameters, including the D2 Test of Attention, the Digit Span backward, and the Stroop
Color-Word Test. Primary outcomes were assessed before and after intervention. After intervention completion, the
authors found that attention and motor speed outcomes improved with medium to large effect sizes. However, no
additional value for neurofeedback over TAU was observed by the authors.
In a randomized, controlled investigation of adults without a clinical diagnosis, Studer and colleagues (2014)
examined whether theta/beta and SCP training would have an effect on motor system excitability, compared to a
control group. Of the initial 59 participants enrolled, a final sample of 55 adults (aged 19-31) completed the study.
The participants were randomly assigned to one of three groups: theta/beta frequency band training (T/B; n=19),
training of SCPs (SCP; n=19), or control training (CON; n=17). The two neurofeedback trainings (T/B and SCP)
consisted of 20 sessions at 50 minutes each, conducted as 10 double sessions taking place twice per week. Control
training (six sessions of 20 minutes each taking place twice per week) was only designed to parallel the transfer tasks
included in the neurofeedback trainings. Pre- and post-training assessments (Attention Network Test; EEG)
encompassed performance and event-related potential measures during an attention task, and motor system
excitability was assessed by transcranial magnetic stimulation. Results found that some neurofeedback protocolspecific effects (increased response speed, reduced attentional resource allocation during target processing) were
obtained; however, due to the limited sample size, medium effects did not reach a level of significance. Self-regulation
skills were not sufficiently learned during theta/beta and SCP training, which the authors considered a limitation. The
authors note that future studies including larger sample sizes are needed to evaluate the protocol-specific effects on
attention and motor system excitability.
As a follow-up to Steiner, et al (2014a), Steiner and colleagues (2014b) next evaluated sustained improvement from
the intervention at 6-month follow-up. Parent response rates were 90%. At six months post-intervention, the
neurofeedback participants maintained significant gains on Conners 3-P (Inattention; Executive Functioning;
Hyperactivity/Impulsivity), and BRIEF subscales, including the Global Executive Composite. These remained
significantly greater than gains found among children in the cognitive training and control conditions. At the 6-month
follow-up, neurofeedback participants also maintained the same stimulant medication dosage, while the cognitive
training and control conditions showed statistically and clinically significant increases.
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Steiner and colleagues (2014a) conducted a randomized control trial to evaluate the efficacy of 2 computer attention
training systems administered in school for children with ADHD. The trial took place in 19 public elementary schools.
All children were in either second or fourth grade and were randomized to 40 sessions of neurofeedback (n = 34) or
cognitive training (n = 34), or to a control (n = 36) condition that received computer attention training treatment the
following school year. Change was assessed from pre-post intervention on parent reports (Conners 3-P; BRIEF);
teacher reports (SKAMP; Conners 3-T), and systematic classroom observations (BOSS). The neurofeedback
intervention trained the child to increase beta waves and suppress theta waves. The cognitive training intervention
included an array of cognitive exercises. There were no statistical differences between randomization conditions at
baseline or between participants who completed or did not complete the intervention. Results found that children in
the neurofeedback group showed significant improvement compared with those in the control condition on many
indices. Children who received cognitive training showed no improvement compared to the control condition. Children
in the neurofeedback condition showed significant improvements compared to those in the cognitive training condition
on Conners 3-P Executive Functioning, all BRIEF summary indices, SKAMP Attention, and Conners 3-T Inattention
subscales. Stimulant medication dosage in methylphenidate equivalencies significantly increased for children in the
cognitive training and control conditions, but not for those in the neurofeedback condition. Limitations noted by the
authors include that both children and parents were aware of the child’s intervention condition, and that projected
sample size based on the power analysis was not achieved.
A randomized, placebo-controlled trial conducted by van Dongen-Boomsma and colleagues (2012) assessed the
efficacy and safety of EEG neurofeedback in children with ADHD. This was a follow-up to the pilot study conducted by
Lansbergen, et al (2011). Children were assigned in a double-blind manner to either EEG-neurofeedback or placeboneurofeedback, with treatments given twice per week for a total of 30 sessions. Psychostimulants or atomoxetine
were permitted. The primary endpoint was efficacy, measured as differences in total severity of inattentive and
hyperactive/impulsive symptoms according to the ADHD-RS. The CGI-I was also administered in a final interview. In
total, 63 children and their parents were eligible; of these, 22 were excluded, leaving a total of 41 children (mean age
of 10.6) to participate in the study. A total of 22 children were allocated to the EEG-neurofeedback group, with 19
allocated to the placebo-neurofeedback group. All children completed training. Results found that ADHD symptoms
decreased over time in both groups. Similar results were observed when inattentive and hyperactive/impulsive scores
were analyzed separately. Teacher-rated ADHD symptoms decreased significantly over time, without a difference
between groups. On the CGI-I scale, 18% of children in the EEG-neurofeedback group were rated as “much
improved”, with 41% in the EEG-neurofeedback and 42% in the placebo-neurofeedback group rated as “minimally
improved”; differences between the groups were not significant. Total adverse events decreased significantly over
time, and similarly in the two groups. Post-hoc analyses did not reveal any significant treatment effect for any
outcome. Based on the results, the authors concluded that EEG-neurofeedback was not superior to placeboneurofeedback in improving symptoms in children with ADHD.
A randomized, controlled trial with two- and six-month follow-up conducted by Meisel and colleagues (2012)
evaluated the efficacy of neurofeedback compared to standard pharmacological intervention in the treatment of 27
children (aged 7-14) with ADHD. The final sample consisted of 23 children, with 11 receiving standard
pharmacological intervention (methylphenidate) and 12 completing 40 sessions of neurofeedback (two sessions per
week, at 35 minutes each). During the two months of treatment, four participants were excluded from the study (two
from each group). The efficacy between the two treatments was based on teacher and parent reports (ADHD RS-IV;
ODDRS-IV; academic performance; WFIRS-P) with two- and six-month follow-up. There were no significant
differences between the groups according to sex, age, IQ, and ADHD subtype; however, differences were found
between the groups on academic performance in math and reading, with the pharmacological group showing
significantly higher scores. In the post-assessment, the pharmacological group had significantly lower levels of
inattention according to teachers, and better scores in math. At two-month follow-up, ADHD-RS inattention and math
scores were significantly better for the pharmacological group. At six-month follow-up, no significant differences were
found between the two groups in inattention, hyperactivity, or functional impairment. The authors conclude that,
taking into consideration large and medium effects sizes throughout the different behavioral evaluations,
neurofeedback and medication effects were comparable. However, the authors caution that the sample was limited,
and not all neurofeedback participants remained medication-free at six-month follow-up, making it unfeasible to
conclude that neurofeedback and medication are equivalent treatments for ADHD.
A controlled, randomized clinical study of children and adolescents with ADHD conducted by Duric and colleagues
(2012) evaluated the effects of neurofeedback on the core symptoms of ADHD. Of an initial subject pool of 275
children and adolescents ranging in age from 6-18 years, 91 participated in 30 sessions of intensive neurofeedback.
The participants were randomized into three groups, with 30 in the neurofeedback group, 31 in a control group given
methylphenidate, and 30 in a group receiving both neurofeedback and methylphenidate. ADHD core symptoms were
reported by parents using the parent form of the Clinician’s Manual for Assessment. Neurofeedback was conducted
three times a week, with each treatment lasting 30 minutes. Subjects receiving methylphenidate had it administered
twice per day at a recommended dose of 1 mg/kg. No significant differences in demographic factors or ADHD core
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symptoms were noted between groups at baseline. Results found that parents reported significant effects for all three
treatment groups, while no significant differences between the treatment groups were observed.
A double-blind, randomized, placebo-controlled feasibility (pilot) study conducted by Lansbergen and colleagues
(2011) explored the initial efficacy of individualized EEG-neurofeedback training in children with ADHD. A total of 14
children (aged 8-15 years) with ADHD were randomly allocated to either 30 sessions of EEG-neurofeedback (n = 8) or
placebo feedback (n = 6). After recruitment, screening, and baseline assessments, EEG-neurofeedback training or
placebo feedback training started for a period of 4-5 months. After, 6, 10, 20, and 30 training sessions, DSM-IV TR
ADHD criteria were evaluated in a telephone interview with parents. In a final interview by the investigator with the
parents, general clinical improvement was assessed. Five of 8 children in the EEG-neurofeedback group and 4 of 6
children in the placebo group were medicated with psychostimulants; none of the children changed type or dose of
medication during participation. All children completed the training sessions and attended all study visits. Blinded
analysis demonstrated clinical improvement over time (reduced ADHD DSM-IV symptoms rated by investigator), but
did not reveal significant differences between the groups. The authors suggest that the findings may indicate that
behavioral improvements after individualized EEG-neurofeedback training may not be caused by the ability to selfregulate brain activity, but rather by unspecific effects such as invested time and attention, therapist interaction, or
expectancy. Given the small sample size, the authors note that it is preliminary to conclude that individualized EEGneurofeedback training is not effective in improving ADHD symptoms.
In a randomized, double-blind, crossover, placebo-controlled study, deBeus and Kaiser (2011) studied whether
participants in a neurofeedback (NF) intervention who learned to change their EEG would improve in functioning
compared to a placebo condition. Children with primary ADHD and co-occurring diagnoses were permitted, as well as
those using only stimulant medication. Functioning was measured with Conners’ parent and teacher ratings of DSM-IV
ADHD symptoms, and participant’s performance on the IVA CPT. Participants served as their own controls. Fifty-six
subjects were randomized into the study, with three children not completing the first 20 sessions. Upon completion of
a baseline assessment, participants were randomized to receive either neurofeedback or placebo conditions. Each
group participated in their assigned procedure for 10 weeks, with sessions occurring at an average rate of twice per
week. After a one-week washout period, the participants were crossed over to receive the other condition. Fortyseven children completed the NF intervention and 45 completed the placebo condition; 42 children completed both
conditions. Because there were distinct differences in results between those who responded to neurofeedback training
and those who did not, only those who showed response were included in the authors’ analysis. The findings
demonstrated significant positive treatment effects for teacher rating scales and IVA quotients for successful
neurofeedback learners. Parental ratings improved regardless of whether a child was a learner or a placebo
participant. The authors point out several limitations: the use of a crossover design; allowing children to be medicated
during neurofeedback training; not using EEG profiling to guide neurofeedback protocol choices; and not enough
neurofeedback sessions.
In a single-blind, randomized controlled trial, Bakhshayesh and colleagues (2011) compared the effects of two
matched biofeedback training variants on the primary symptoms of ADHD. The first variant was EEG neurofeedback
(NF) aimed at theta/beta ratio reduction. The second variant was EMG biofeedback (BF) aimed at forehead muscle
relaxation. A total of 35 children with ADHD, aged 6-14 years old, were randomly assigned to either the NF group (n
= 18) or the BF group (n = 17). No significant differences were identified between groups on demographic,
psychological, and clinical variables prior to treatment. Children currently taking stimulant medication were not
excluded, but parents were asked to keep medication levels constant throughout the training period. There were no
pre-testing differences between both groups concerning medication. Treatment for both groups consisted of 30 thirty
minute sessions held 2-3 times per week. A psychotherapist met with parents twice per month for a total of 4
sessions. Pre- and post-treatment assessment consisted of a structured standardized clinical interview, parent and
teacher questionnaires about ADHD-related behaviors (German ADHD Rating Scale), a paper-and-pencil attention test
(bp/d2), non-verbal intelligence tests (CPM/SPM), continuous performance tests (CPT), and standardized behavioral
observations in the classroom. Results found that training reduced theta/beta ratios and EMG levels in both groups.
Parents reported significant reductions in primary ADHD symptoms, and inattention improvements in the NF group
were higher compared to the BF group. NF training also improved attention and reaction times on the psychometric
measures. Regarding hyperactivity and impulsivity symptoms, the results implied that non-specific factors, such as
behavioral contingencies, self-efficacy, structured learning environment, and feed-forward processes, may also
contribute to the positive behavioral effects induced by neurofeedback training.
Gevensleben and colleagues (2010) conducted a six-month follow-up of treatment effects from Gevensleben, et al
2009. Of the children with complete data from the previous study, follow-up information was analyzed in 61 children
on a per-protocol basis. Of these children who followed-up, 38 were from the neurofeedback group and 23 were from
the control group (computerized attention skills training). For the primary outcome measure (FBB-HKS), statistics
revealed that neurofeedback training effects were still superior to control training at 6-month follow-up (medium
effect size of 0.71 from pre-training to follow-up). Reductions of inattention and hyperactivity/impulsivity at follow-up
(compared to pre-training) were 25-30% in the neurofeedback group compared to 10-15% in the control group. The
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authors note the large number of dropouts, and also the non-blind design, which could not rule out the contribution of
unspecific effects to the behavioral effects, and that the low responder rate and the portion of children starting a
medication argue against neurofeedback as a stand-alone intervention for children with ADHD. They emphasize a
need for further research to determine optimal neurofeedback protocol and adequate number of treatment sessions.
In a multisite, randomized controlled study, Gevensleben and colleagues (2009) evaluated the clinical efficacy of
neurofeedback in children with ADHD. A total of 102 children with ADHD, aged 8 to 12 years, participated. Subjects
were randomly assigned to either neurofeedback or computerized attention skills training, with no significant pretraining differences in demographic, psychological, or clinical variables. Both trainings consisted of two blocks of 18
sessions, with each block lasting 3-4 weeks. Treatment of both groups entailed computer-game-like tasks that
demanded attention, development of strategies for focusing one’s attention, and practicing of acquired strategies at
home and school. Exercises were documented by keeping a log and homework was kept identical in quantity and
quality between the groups. Neurofeedback treatment consisted of one block of theta/beta training, and one block of
slow cortical potential (SCP) training. The attention skills training was based on learning software that exercised visual
and auditory perception, vigilance, sustained attention, and reactivity. Pre-training, intermediate, and post-training
assessment encompassed several behavior rating scales (e.g., the German ADHD rating scale, FBB-HKS), completed
by parents and teachers. For parent and teacher ratings, improvements in the neurofeedback group were superior to
those of the control group. For the primary outcome measure (parent-rated FBB-HKS total score), the effect size was
.60. The authors note that owing to various restrictions of the training setting, it may not be appropriate to indirectly
compare the efficacy of neurofeedback based on the results of this RCT with other treatment approaches, such as
long-acting medications with similar effect sizes. The authors also point to a need for further studies to replicate these
findings, control for factors not covered in this study, further isolate specific effects of neurofeedback, and address
how to optimize neurofeedback training.
An open-label study by Monastra, et al (2002) examined the effects of EEG biofeedback and Ritalin on the primary
symptoms of ADHD and neuropsychological and electrophysiological measures, while controlling for other commonly
provided types of clinical interventions. A total of 100 children, ages 6-19 and their parents participated in the study.
Based on parental preference, patients with ADHD participated in a 1-year comprehensive program including
medication management, parent counseling and school consultation. All participants were prescribed a 5 mg dose,
t.i.d. for 1 week of Ritalin, and this was continually adjusted based on Test of Variables of Attention (TOVA) score. All
parents participated in a 10-session parenting class, followed by consultation on an as-needed basis. Fifty-one
children also completed EEG biofeedback, consisting of individual weekly sessions lasting 30-40 minutes. The groups
were comparable on domains of intelligence, age, gender, and parental education. One year after the intake
evaluation, patients were evaluated using the Attention Deficit Disorders Evaluation Scale (ADDES: home and school),
the TOVA, and a QEEG Scan. Observations were first recorded while participants were still being treated with Ritalin. A
second post-treatment assessment was conducted after a 1-week period in which no stimulant therapy was provided.
Significant improvement was noted on the TOVA and the ADDES when participants were tested while using Ritalin.
Only those who had received EEG biofeedback sustained these gains when tested without Ritalin. The results of the
QEEG-Scan revealed significant reduction in cortical slowing only in those patients who had received EEG biofeedback.
The authors conclude that the findings of this study are supportive of multimodal treatment models that include
parent counseling and EEG biofeedback, in addition to stimulant therapy. They comment that long-term follow-up
studies examining the relationship between EEG biofeedback and stimulant dosing patterns are required.
Systematic Reviews/Meta-Analyses: ADHD
A systematic review and double-blind placebo-controlled study conducted by Vollebregt and colleagues (2014)
determined if EEG-neurofeedback improves neurocognitive functioning in children with ADHD. First, 10 randomized
controlled trials, including a range of different sample sizes and control conditions, were examined. The neurofeedback
protocol, as well as the duration, frequency, and number of sessions varied between studies. Three of the ten studies
reported significant improvement on at least one neurocognitive variable for the neurofeedback condition superior to
the control condition. The authors concluded that these studies had many methodological limitations and the majority
failed to show positive neurocognitive effects of neurofeedback. Next, the authors conducted a double-blind, placebocontrolled treatment trial for children aged 8-15 with ADHD. Forty-one children were randomly allocated to EEGneurofeedback (n = 22) or placebo-neurofeedback (n = 19) for 30 sessions, twice a week. Results from the trial found
no significant treatment effect on any neurocognitive variables (sustained attention dots task, visuospatial
sequencing, digit span WISC-III, Rey Auditory-Verbal Learning Test, instrumental learning task, time production task,
time reproduction task). The authors conclude that the study was unable to establish positive treatment effects on
neurocognitive functioning after EEG-neurofeedback when compared to placebo-neurofeedback.
A systematic review of pharmacological and psychosocial treatments for adolescents with ADHD was conducted by
Sibley and colleagues (2014). This review included three studies (two controlled trials and one open trial) that
evaluated two classes of cognitive enhancement training: neurofeedback or EEG biofeedback, and working memory
training. The authors note that all reviewed studies employed methodologically sound multi-informant assessment
strategies, but no studies examined intervention effects on impairment. Available symptom effect sizes for the
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cognitive enhancement training interventions suggested that overall, these treatments did not produce significant
gains.
A meta-analytic review of nonpharmacological treatments for ADHD was conducted by Hodgson and colleagues
(2014). Included in the 14 selected studies was neurofeedback therapy (3 studies). The authors found that two
interventions most commonly resulted in improvement in the treatment groups across a range of different outcomes
measures: neurofeedback and behavior modification. Improvement was observed in attention, self-control, and
performance on the Digit Span test for neurofeedback treatment. One major limitation noted was a focus on studies
comparing treatment and control groups while excluding all studies using within-subjects designs. While minimizing
the influence of placebo effects, this reduced the total number of studies. The authors conclude that this meta-analytic
study provides initial evidence that nonpharmacological treatments, such as neurofeedback, have potential in the
treatment of children with ADHD and that more and better outcome research is necessary.
A systematic review and meta-analysis of 54 studies conducted by Sonuga-Barke and colleagues (2013) determined
the efficacy of various dietary and psychological ADHD treatments. Included among the psychological treatments was
neurofeedback. The outcome measure was pre- to post-treatment change in total ADHD symptom severity measured
at the first post-treatment assessment. Results from ADHD-specific symptom scales were used where available. Of the
eight neurofeedback trials with data for most assessments, four reported “probably blinded” assessments. Significant
treatment effects were seen for most assessments. These were substantially reduced and fell short of statistical
significance for the “probably blinded” assessments. Sensitivity analysis to test for medication effects was not possible
because of the small number of no-medication trials. The authors conclude that based on these results, the value of
psychological approaches that directly target neuropsychological processes should be further investigated. Also noted
is that evidence of efficacy from blinded assessments is required before behavioral interventions such as
neurofeedback are likely to be supported as ADHD treatments.
Moriyama and colleagues (2012) reviewed literature on the effectiveness and specificity of neurofeedback for the
treatment of ADHD. The authors found 3 systematics reviews on the use of neurofeedback for ADHD, and 6
randomized controlled trials not been included in these reviews. The authors note that the available studies point to a
possible efficacy and specificity of neurofeedback for the treatment of ADHD, but additional large, randomized
controlled studies using blind assessment procedures are needed to clarify this issue. Very few studies were found to
compute response ratio to neurofeedback, and since sample sizes are small for the majority of the included studies,
most do not investigate possible predictors of response. No safety issues emerged with neurofeedback, with studies
having low dropout rates and no discontinuation due to side effects. Very few of the studies examined long-term
effects of neurofeedback, but the few studies that did found promising results. The authors note that while
neurofeedback has been efficacious in the majority of trials conducted so far, there is not enough data to support the
use of neurofeedback as a monotherapy for ADHD. The great majority of studies tested neurofeedback as an
adjunctive treatment. The authors conclude that although some data suggest possible efficacy and specificity of
neurofeedback for the treatment of ADHD, considerable work is still needed to determine the contribution of specific in
comparison to nonspecific components, when and how to use neurofeedback in routine clinical practice, and how to
implement neurofeedback standards covering the fidelity of the EEG and artifact control methodology.
Arns, et al (2009) conducted a meta-analysis to investigate the effects of neurofeedback and stimulant medication on
the core symptoms of ADHD. All included subjects had a primary diagnosis of ADHD and study designs could be
controlled, prospective, or retrospective in nature. All neurofeedback was provided in a standardized manner, and no
more than two treatment protocols (SCP; theta/beta) were used. Standardized pre- and post-assessment means and
standard deviations (SDs) were available for at least 1 of the following domains: hyperactivity, inattentiveness, or CPT
commission errors. If there was not sufficient information available, the study was excluded. Fifteen studies met all
criteria and were included in the meta-analysis. Two separate effect sizes were calculated - for the controlled
between-subject design studies (n = 10), the effect size of the neurofeedback group as compared to the control group
was calculated. Effect size was also calculated and plotted for all ADHD children treated with neurofeedback from both
the controlled and within-subject designs. For all controlled studies, there were a total of 476 subjects, and for the
pre/post-design studies there were a total of 718 subjects. Drop-out rates were reported in 5 studies, and around
10%. Six studies employed randomized allocation of subjects, and 3 studies compared neurofeedback with stimulant
medication. Results found that both the prospective controlled studies and those studies employing a pre- and postdesign found large effect sizes for neurofeedback (compared to control) on impulsivity and inattention, and a medium
effect size for hyperactivity. No differences were found between neurofeedback studies in medicated vs. unmedicated
subjects. None of the studies comparing neurofeedback with stimulant medication used random assignment;
participants were allowed to self-select the treatment of their preference. As a result, it is noted that more studies
using randomization and larger sample sizes are needed to investigate further how neurofeedback compares to
stimulants in the treatment of ADHD. The authors also note that further research on the impact of medication on
neurofeedback is needed. Long-term effects could not be addressed in the meta-analysis, though several studies did
report follow-up results showing that the clinical effects of neurofeedback were stable.
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Clinical Trials: Other Behavioral Disorders
Koprivova and colleagues (2013) assessed the effect of neurofeedback (NFB) on EEG and clinical symptoms in
patients with obsessive-compulsive disorder (OCD). A randomized, double-blind, parallel design of 20 inpatients with
OCD was conducted, with patients undergoing 25 sessions of NFB (n = 10) or sham feedback (SFB; n = 10). All
patients were either drug free (n = 5) or medicated with SSRIs (n = 15). All participants first completed a 6-week
standard treatment program that included cognitive-behavioral therapy; patients then completed 25 thirty-minute
sessions of NFB or SFB. Resting-state EEG was recorded before and after treatment to assess post-treatment
changes, relationships with clinical symptoms, and treatment response. Results found that patients receiving NFB
showed a higher percentage of improvement on compulsion scores when compared to patients receiving SFB, and that
NFB led to a small and non-significant EEG change in the direction of training. Other clinical outcome measures did not
differ between the NFB and SFB groups. The authors note that further research is necessary to elucidate the
relationship between EEG patterns and their role in treatment responsiveness in patients with OCD.
Kouijzer and colleagues (2013) conducted a randomized controlled trial to evaluate the effects of EEG-biofeedback in
autism spectrum disorder (ASD). The randomized pretest-posttest control group design included a blinded active
comparator and six month follow-up. A total of 38 participants were randomly assigned to either EEG-biofeedback (n
= 13), skin conductance (SC)-biofeedback (n = 12), or wait list group (n = 13). Assessments were conducted at pretreatment, post-treatment, and after 6 months, and included parent ratings of ASD symptoms, executive function
tasks, and 19-channel EEG recordings. Both EEG- and SC-biofeedback treatment included 40 individual sessions
provided twice a week at the participant’s school. Four participants in the EEG group and five in the SC group did not
complete the entirety of the 40 sessions. Results found that 54% of the EEG group participants (n = 7) significantly
reduced delta and/or theta power and were identified as EEG-regulators. However, in these individuals, no statistically
significant reductions of ASD symptoms were observed, though they did show improvement in cognitive flexibility
when compared to participants who regulated SC. The authors conclude that the results are inconclusive with respect
to the clinical application of EEG-biofeedback in children and adolescents with ASD.
Knox and colleagues (2011) evaluated the effects of a game-based biofeedback intervention on symptoms of anxiety
and depression among a pediatric sample. A total of 24 individuals (aged 9-17 years) reporting symptoms of anxiety
or diagnosed with an anxiety disorder completed the study, with 12 individuals participating in a biofeedback
intervention and 12 assigned to a wait list comparison group. The eight-session biofeedback intervention used
computer-based gaming technology to teach and practice relaxation, and also incorporated psychoeducation,
identification of triggers and signs of anxiety, and in vivo practice. Symptoms were measured by tools including the
Multidimensional Anxiety Scale for Children (MASC), the State-Trait Anxiety Inventory for Children (STAIC) and the
Children’s Depression Inventory (CDI). Results found the intervention group to have reduced anxiety and depression
scores on the outcome measures, with the largest effect size found on the depression scale. The authors conclude
that, despite the promise of these results, more research is needed to examine whether these outcomes can be
replicated in children and youths with anxiety and depression. The authors additionally note that the study contained
a small sample size, a non-random assignment to groups, and an unknown contribution of each component of
treatment intervention (e.g., psychoeducation, biofeedback) to the outcomes.
Lande and colleagues (2010) conducted a pilot study to investigate the potential effectiveness of heart rate variability
biofeedback as a complementary treatment for posttraumatic stress disorder (PTSD). Active duty service members
deployed to an area of combat operations were alternately assigned to a treatment as usual (TAU) control group (n =
17) or a group consisting of TAU with the addition of biofeedback (n = 22). Outcomes were measures using the
posttraumatic stress disorder checklist (PCL)-Military version and the Zung Self-Rating Depression Scale, administered
before treatment and at the conclusion of three weeks of biofeedback therapy. Results found that biofeedback did not
produce a measurable improvement in either PTSD or depression scores, though subjective satisfaction with
biofeedback was found among many of the participants. The authors conclude that the study’s exploratory design can
be strengthened by future research, and that a more empirical study, using strict random sampling techniques and a
sham biofeedback unit could improve the potential generalizability of results.
Systematic Reviews/Meta-Analyses: Other Behavioral Disorders
Bergemann and colleagues (2016) conducted a meta-analysis of studies investigating the efficacy of EEG
neurofeedback in the treatment of psychiatric disorders. A total of 30 studies were included (n = 1171) and evaluated
neurofeedback for ADHD, autism, obsessive-compulsive disorder, generalized anxiety disorder and depression. The
majority of studies included a passive-semi-active control group, with only three placebo-controlled trials identified.
Twenty-one of the thirty studies used randomization procedures. The authors’ analysis found small to medium effect
sizes for treating the symptoms of ADHD, with varying results for its effect on other diagnoses. The authors conclude
that a lack of methodologically sound studies prevents evidence-based conclusions on the efficacy of EEG
neurofeedback in the treatment of various psychiatric disorders. They recommend that future studies are carefully
planned and executed, including power calculations to establish required sample sizes, randomization, blinding and
adequate control conditions, to assess whether neurofeedback is a viable treatment option in the field of psychiatry.
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Schoenberg and David (2014) conducted a systematic review to explore the current therapeutic use of biofeedback for
a range of psychiatric disorders, including addictions, anxiety disorders, autism spectrum disorders, depressive
disorders, dissociative disorders, personality disorders, and psychoses. A total of 63 articles were included in the
review. EEG biofeedback was used in 32% of the reviewed studies; with 29% incorporating electromyographic (EMG),
16% heart rate variability (HRV) and/or sole respiration, 6% heart rate, 5% electrodermal (EDA) and 3% thermal
biofeedback methodologies. Anxiety disorders were the most commonly treated among the reviewed studies (68%).
Mean biofeedback session duration was 27.4 minutes and an average of 15.6 sessions in length. A total of 29 studies
(46%) reported no medication use, and 25 (40%) reported patients already receiving medication before and during
the biofeedback intervention. Non-randomized studies were included if specified categories relating to study design
and methodology were fulfilled. In articles where patients were randomly allocated to experimental conditions, the
randomization procedure was rarely described. The review found 81% of articles to report some level of clinical
amelioration related to biofeedback exposure, and 65% to a statistically significant level of symptom reduction.
However, the review highlights a lack of standardization amongst biofeedback studies for psychiatric disorders, and
methods/results sections were inconsistent in structure and lacking empirical detail, resulting in the exclusion of
several studies from the review. The authors note that Level 1 (“not empirically supported”) studies were not included
in the review because of exclusion criteria, potentially skewing the overall evaluation of biofeedback treatments used
in psychiatric domains. The authors conclude that further development of standardized controlled methodological
protocols tailored for specific disorders and guidelines to generate comprehensive reports may contribute towards
establishing the value of biofeedback interventions within mainstream psychiatry.
Holtmann and colleagues (2011) reviewed 15 studies on the effectiveness of neurofeedback as a method of treatment
on the core symptoms of autism spectrum disorder (ASD). The review found that the existing evidence does not
support the use of neurofeedback in the treatment of ASD. The authors hypothesized that those studies with
outcomes in favor of neurofeedback may be showing an improvement in comorbid attention-deficit/hyperactivity
disorder symptoms, rather than a true improvement in core ASD symptoms. The authors conclude that a number of
methodological limitations will need to be addressed in future studies on neurofeedback in the treatment of ASD.
Professional Societies
American Academy of Pediatrics (AAP): In the AAP’s Clinical Practice Guideline for the Diagnosis, Evaluation, and
Treatment of ADHD in Children and Adolescents (2011), the section titled “Areas for Future Research” includes “study
of medications and other therapies used clinically but not approved by the FDA for ADHD, such as
electroencephalographic biofeedback.”
The appendix to the AAP’s Clinical Practice Guidelines for the Treatment of ADHD in Children and Adolescents (2011)
states that alternative therapies for treatment of ADHD…include “large doses of vitamins, essential fatty acids, and
other dietary alterations; chelation; and electroencephalographic (EEG) biofeedback”. The appendix notes that there is
“insufficient evidence to determine whether these therapies lead to changes in core symptoms of ADHD or function,
and for many of them, there is limited information about their safety. For these reasons, these therapies cannot be
recommended”.
AAP guidance material titled “ADHD, What Every Parent Needs to Know” (2011) states that studies on the use of
neurofeedback to date have been criticized for lacking appropriate controls or random assignment of test subjects to
the treatment/sham treatment groups.
Institute for Clinical Systems Improvement (ICSI): Guidance material from the ICSI (Dobie, et al 2012) states
that neurofeedback has been demonstrated in one randomized, controlled clinical trial to be significantly better than a
computerized attention skills training control and that ADHD symptoms were moderately improved. Long-term
benefits have not been definitively proven. The cost and time involved in treatment need to be taken into account.
Neurofeedback for ADHD lacks sufficient research support. Treatment response rates have not reached the level
shown with psychostimulant medications; therefore neurofeedback cannot be recommended as an alternative to
medication use in ADHD.
U.S. FOOD AND DRUG ADMINISTRATION
Neurofeedback/biofeedback equipment registered with the FDA is considered a medical device. At this time,
neurofeedback has been approved by the FDA for purposes of relaxation therapy.
The FDA has granted qEEG a Class II exemption. qEEG analysis involves comparison of the patient’s EEG to a
reference population. The norms used for comparison are FDA-registered, and include cross-validation statistics and
peer reviewed publications.
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CENTERS FOR MEDICARE AND MEDICAID SERVICES
A National Coverage Determination (NCD) is available for biofeedback therapy. Biofeedback therapy is covered under
Medicare only when it is reasonable and necessary for the individual patient for muscle re-education of specific muscle
groups or for treating pathological muscle abnormalities of spasticity, incapacitating muscle spasm, or weakness, and
more conventional treatments (heat, cold, massage, exercise, support) have not been successful. This therapy is not
covered for treatment of ordinary muscle tension states or for psychosomatic conditions.
APPLICABLE CODES
The following list(s) of procedure and/or diagnosis codes is provided for reference purposes only and may not be all
inclusive. Listing of a code in this policy does not imply that the service described by the code is a covered or noncovered health service. Benefit coverage for health services is determined by the member-specific benefit plan
document and applicable laws that may require coverage for a specific service. The inclusion of a code does not imply
any right to reimbursement or guarantee claim payment. Other Policies and Coverage Determination Guidelines may
apply.
CPT Code
90901
90875
90876
Description
Biofeedback training by any modality
Individual psychophysiological therapy incorporating biofeedback training by any modality (face-toface with the patient), with psychotherapy (e.g., insight oriented, behavior modifying or supportive
psychotherapy); 30 minutes
Individual psychophysiological therapy incorporating biofeedback training by any modality (face-toface with the patient), with psychotherapy (e.g., insight oriented, behavior modifying or supportive
psychotherapy); 45 minutes
CPT® is a registered trademark of the American Medical Association
REFERENCES
1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA:
American Psychiatric Publishing; 2013.
2. American Academy of Pediatrics. ADHD: Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of
Attention-Deficit/Hyperactivity Disorder in Children and Adolescents. Pediatrics 2011; 128(5): 1007-1022.
3. Arns, M, de Ridder S, Strehl U, et al. Efficacy of neurofeedback treatment in ADHD: The effects on inattention,
impulsivity and hyperactivity: A meta-analysis. Clinical EEG and Neuroscience 2009; 40(3): 180-189.
4. Bakhshayesh AR, Hansch S, Wyschkon A, et al. Neurofeedback in ADHD: A single-blind randomized controlled trial.
Eur Child Adolesc Psychiatry 2011; 20(9): 481-491.
5. Begemann MJ, Florisse EJ, van Lutterveld R, Kooyman M, & Sommer IE. Efficacy of EEG neurofeedback in
psychiatry: A comprehensive overview and meta-analysis. Translational Brain Rhythmicity 2016; 1(1): 19-29.
6. Bink M, Bongers IL, Popma A, Jannsen TW, & van Nieuwenhuizen C. 1-year follow-up of neurofeedback treatment
in adolescents with attention-deficit hyperactivity disorder: Randomized controlled trial. British Journal of
Psychiatry Open 2016; 2(2): 107-115.
7. Bink M, van Nieuwenhuizen C, Popma A, Bongers IL, & van Boxtel GJ. Behavioral effects of neurofeedback in
adolescents with ADHD: A randomized controlled trial. European Child & Adolescent Psychiatry 2015; 24(9):
1035-1048.
8. Bink M, van Nieuwenhuizen C, Popma A, Bongers IL, & van Boxtel GJ. Neurocognitive effects of neurofeedback in
adolescents with ADHD: A randomized controlled trial. Journal of Clinical Psychiatry 2014; 75(5): 535-542.
9. Centers for Medicare & Medicaid Services. National Coverage Determination (NCD) for Biofeedback Therapy (30.1).
Retrieved from: https://www.cms.gov/medicare-coverage-database/details/ncddetails.aspx?NCDId=41&ncdver=1&bc=AAAAgAAAAAAAAA%3d%3d&
10. Cortese S, Ferrin M, Brandeis D, Holtmann M, Aggensteiner P, Daley D, . . .Sonuga-Barke EJ. Neurofeedback for
attention-deficit/hyperactivity disorder: Meta-analysis of clinical and neuropsychological outcomes from
randomized controlled trials. Journal of the American Academy of Child and Adolescent Psychiatry 2016;
55(6):444-455.
11. deBeus RJ, & Kaiser DA. Neurofeedback with children with attention deficit hyperactivity disorder: A randomized
double-blind placebo-controlled study. Neurofeedback and Neuromodulation Techniques and Applications 2011:
127-152. London, England: Academic Press.
Neurofeedback/Biofeedback for Behavioral and Substance Use Disorders
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12. Dobie C, Donald WB, Hanson M, Heim C, Huxsahl J, Karasov R, Kippes C, Neumann A, Spinner P, Staples T,
Steiner L. Institute for Clinical Systems Improvement. Diagnosis and Management of Attention Deficit
Hyperactivity Disorder in Primary Care for School-Age Children and Adolescents. Updated March 2012.
13. Duric NS, Assmus J, Gundersen DI, & Elgen IB. Neurofeedback for the treatment of children and adolescents with
ADHD: A randomized and controlled clinical trial using parental reports. BMC Psychiatry 2012; 12: 107. doi:
10.1186/1471-244X-12-107.
14. Gevensleben H, Holl B, Albrecht B, et al. Neurofeedback training in children with ADHD: 6-month follow-up of a
randomized controlled trial. European Child & Adolescent Psychiatry 2010; 19: 715-724.
15. Gevensleben H, Holl B, Albrecht B, et al. Is neurofeedback an efficacious treatment for ADHD? A randomized
controlled clinical trial. The Journal of Child Psychology and Psychiatry 2009; 50(7): 780-789.
16. Hodgson K, Hutchinson AD, & Denson L. Nonpharmacological treatments for ADHD: A meta-analytic review.
Journal of Attention Disorders 2014; 18(4): 275-282.
17. Holtmann M, Steiner S, Hohmann S, Poustka L, Banaschewski T, & Bolte S. Neurofeedback in autism spectrum
disorders. Developmental Medicine & Child Neurology 2011; 53: 986-993
18. Janssen TW, Bink M, Gelade K, van Mourik R, Maras A, & Oosterlaan J. A randomized controlled trial investigating
the effects of neurofeedback, methylphenidate, and physical activity on event-related potentials in children with
attention-deficit/hyperactivity disorder. Journal of Child and Adolescent Psychopharmacology 2016; 26(4): 344353.
19. Knox M, Lentini J, Cummings TS, McGrady A, Whearty K, & Sancrant L. Game-based biofeedback for pediatric
anxiety and depression. Mental Health in Family Medicine 2011; 8: 195-203.
20. Koprivova J, Congedo M, Raszka M, Prasko J, Brunovsky M, & Horacek J. Prediction of treatment response and the
effect of independent component neurofeedback in obsessive-compulsive disorder: A randomized, sham-controlled,
double-blind study. Neuropsychobiology 2013; 67: 210-223.
21. Kouijzer ME, van Schie HT, Gerrits BJ, Buitelaar JK, & de Moor JM. Is EEG-biofeedback and effective treatment in
autism spectrum disorders? A randomized controlled trial. Appl Psychophysiol Biofeedback 2013; 38: 17-28.
22. Lande RG, Williams LB, Francis JL, Gragnani C, & Morin ML. Efficacy of biofeedback for post-traumatic stress
disorder. Complementary Therapies in Medicine 2010, 18, 256-59.
23. Lansbergen MM, van Dongen-Boomsma M, Buitelaar JK, & Slaats-Willemse D. ADHD and EEG-neurofeedback: A
double-blind randomized placebo-controlled feasibility study. J Neural Transm 2011; 118: 275-284.
24. Meisel V, Servera M, Garcia-Banda G, Cardo E, & Moreno I. Neurofeedback and standard pharmacological
intervention in ADHD: A randomized controlled trial with six-month follow-up. Biological Psychology 2013; 94: 1221.
25. Monastra VJ, Monastra DM, & George S. The effects of stimulant therapy, EEG biofeedback, and parenting style on
the primary symptoms of attention-deficit/hyperactivity disorder. Applied Psychophysiology and Biofeedback 2002;
27(4): 231-249.
26. Moriyama TS, Polanczyk G, Caye A, Banaschewski T, Brandeis D, & Rhode LA. Evidence-based information on the
clinical use of neurofeedback for ADHD. Neurotherapeutics 2012; 9: 588-598.
27. Pliszka S, AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children
and adolescents with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and
Adolescent Psychiatry 2007; 46(7): 894-921.
28. Reiff, M.I. (Eds.). ADHD: What every parent needs to know; 2011. Elk Grove Village, IL: American Academy of
Pediatrics.
29. Schoenberg PL, & David AS. Biofeedback for psychiatric disorders: A systematic review. Appl Psychophysiol
Biofeedback 2014; 39: 109-135.
30. Sibley MH, Kuriyan AB, Evans SW, Waxmonsky JG, & Smith BH. Pharmacological and psychosocial treatments for
adolescents with ADHD: An updated systematic review of the literature. Clinical Psychology Review 2014; 34:
218-232.
31. Sonuga-Barke EJ, Brandeis D, Cortese S, Daley D, Ferrin M, Holtmann M, . . .Sergeant J. Nonpharmacological
interventions for ADHD: Systematic review and meta-analyses of randomized controlled trials of dietary and
psychological treatments. American Journal of Psychiatry 2013; 170(3): 275-289.
32. Steering Committee on Quality Improvement and Management, Subcommittee on Attention-Deficit/Hyperactivity
Disorder. Appendix to ADHD Clinical Practice Guideline: Implementing the key action statements: An algorithm
and explanation for process of care for the evaluation, diagnosis, treatment, and monitoring of ADHD in children
and adolescents. Supplemental information. Pediatrics 2011; 128(5): SI1-21.
Neurofeedback/Biofeedback for Behavioral and Substance Use Disorders
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33. Steiner NJ, Frenette EC, Rene KM, Brennan RT, & Perrin EC. Neurofeedback and cognitive attention training for
children with attention-deficit hyperactivity disorder in schools. Journal of Developmental and Behavioral Pediatrics
2014a; 35: 18-27.
34. Steiner NJ, Frenette EC, Rene KM, Brennan RT, & Perrin EC. In-school neurofeedback training for ADHD:
Sustained improvements from a randomized control trial. Pediatrics 2014b; 133(3): 483-492.
35. Studer P, Kratz O, Gevensleben H, Rothenberger A, Moll GH, Hautzinger M, & Heinrich H. Slow cortical potential
and theta/beta neurofeedback in adults: Effects on attentional processes and motor system excitability. Frontiers
in Human Neuroscience 2014; 8: 555.
36. van Dongen-Boomsma M, Vollebregt MA, Slaats-Willemse D, & Buitelaar JK. A randomized placebo-controlled trial
of electroencephalographic (EEG) neurofeedback in children with attention-deficit/hyperactivity disorder. Journal
of Clinical Psychiatry 2013; 74(8): 821-827.
37. Vollebregt MA, van Dongen-Boomsma M, Buitelaar JK, & Slaats-Willemse D. Does EEG-neurofeedback improve
neurocognitive functioning in children with attention-deficit/hyperactivity disorder? A systematic review and a
double-blind placebo-controlled study. Journal of Child Psychology and Psychiatry 2014; 55(5): 460-472.
ADDITIONAL RESOURCES
Clinical Protocols
Optum maintains clinical protocols that include the Level of Care Guidelines and Best Practice Guidelines which
describe the scientific evidence, prevailing medical standards, and clinical guidelines supporting our determinations
regarding treatment. These clinical protocols are available to Covered Persons upon request, and to Physicians and
other behavioral health care professionals on www.providerexpress.com.
Peer Review
Optum will offer a peer review to the provider when services do not appear to conform to this policy. The purpose of a
peer review is to allow the provider the opportunity to share additional or new information about the case to assist the
Peer Reviewer in making a determination including, when necessary, to clarify a diagnosis.
Second Opinion Evaluations
Optum facilitates obtaining a second opinion evaluation when requested by an member, provider, or when Optum
otherwise determines that a second opinion is necessary to make a determination, clarify a diagnosis or improve
treatment planning and care for the member.
Referral Assistance
Optum provides assistance with accessing care when then provider and/or member determine that there is not an
appropriate match with the member’s clinical needs and goals, or if additional providers should be involved in
delivering treatment.
HISTORY/REVISION INFORMATION
Date
12/16/2016
•
Version 1 (Approved by UMC)
Action/Description
Neurofeedback/Biofeedback for Behavioral and Substance Use Disorders
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