WHAT IS NEUROFEEDBACK: AN UPDATE
D. Corydon Hammond
Physical Medicine & Rehabilitation, University of Utah School of Medicine, Salt Lake City, Utah, USA
Written to educate both professionals and the general public, this article provides an update
and overview of the ﬁeld of neurofeedback (EEG bi ofeedback). The process of assessment
and neurofeedback training is explained. Then, areas in which neurofeedback is being used
as a treatment are identiﬁed and a survey of research ﬁndings is presented. Potential risks,
side effects, and adverse reactions are cited and guidelines provided for select ing a legiti-
mately qualiﬁed practitioner.
In the late 1960s and 1970s it was learned that
it was possible to recondition and retrain
brainwave patterns (Kamiya, 2011; Sterman,
LoPresti, & Fairchild, 2010). Some of this work
began with training to increase alpha brainwave
activity for the purpose of increasing relaxation,
whereas other work originating at University of
California, Los Angeles focused ﬁrst on animal
and then human research on assisting uncon-
trolled epilepsy. This brainwave training is
called EEG biofeedback or neurofeedback.
Prior to a more detailed discussion, the author
will review some preliminary information about
brainwave activity. Brainwaves occur at various
frequencies. Some are fast, and some are quite
slow. The classic names of these EEG bands are
delta, theta, alpha, beta, and gamma. They are
measured in cycles per second or hertz (Hz).
The following deﬁnitions, although lacking in
scientiﬁc rigor, will provide the general reader
with some conception of the activity associated
with different frequency bands.
Gamma brainwaves are very fast EEG
activity above 30 Hz. Although further research
is required on these frequencies, we know that
some of this activity is associated with intensely
focused attention and in assisting the brain to
process and bind together information from
different areas of the brain. Beta brainwaves
are small, relatively fast brainwaves (above
13–30 Hz) associated with a state of mental,
intellectual activity and outwardly focused
concentration. This is basically a ‘‘bright-eyed,
bushy-tailed’’ state of alertness. Activity in the
lower end of this frequency band (e.g., the
sensorimotor rhythm, or SMR) is associated
with relaxed attentiveness. Alpha brainwaves
(8–12 Hz) are slower and larger. They are
generally associated with a state of relaxation.
Activity in the lower half of this range represents
to a considerable degree the brain shifting into
an idling gear, relaxed and a bit disengaged,
waiting to respond when needed. If people
merely close their eyes and begin picturing
something peaceful, in less than half a minute
there begins to be an increase in alpha brain-
waves. These brainwaves are especially large
in the back third of the head. Theta (4–8 Hz)
activity generally represents a more daydream-
like, rather spacey state of mind that is associa-
ted with mental inefﬁciency. At very slow
levels, theta brainwave activity is a very relaxed
state, representing the twilight zone between
waking and sleep. Delta brainwaves (.5–
3.5 Hz) are very slow, high-amplitude (magni-
tude) brainwaves and are what we experience
Received 1 August 2011; accepted 15 August 2011.
Address correspondence to D. Corydon Hammond, PhD, Physical Medicine & Rehabilitation, University of Utah School of
Medicine, 30 North 1900 East, Salt Lake City, UT 84132-2119, USA. E-mail: firstname.lastname@example.org
Journal of Neurotherapy, 15:305–336, 2011
Copyright # Taylor & Francis Group, LLC
ISSN: 1087-4208 print=1530-017X online
in deep, restorative sleep. In general, different
levels of awareness are associated with domi-
nant brainwave states.
It should be noted, however, that each of us
always has some degree of each of these various
brainwave frequencies present in different parts
of our brain. Delta brainwaves will also occur,
for instance, when areas of the brain go ‘‘off
line’’ to take up nourishment, and delta is also
associated with learning disabilities. If someone
is becoming drowsy, there are more delta and
slower theta brainwaves creeping in, and if
people are somewhat inattentive to external
things and their minds are wandering, there is
more theta present. If someone is exceptionally
anxious and tense, an excessively high fre-
quency of beta brainwaves may be present in
different parts of the brain, but in other cases
this may be associated with an excess of inef-
ﬁcient alpha activity in frontal areas that are
associated with emotional control. Persons
with Attention-Deﬁcit=Hyperactivity Disorder
(ADD, ADHD), head injuries, stroke, epilepsy,
developmental disabilities, and often chronic
fatigue syndrome and ﬁbromyalgia tend to have
excessive slow waves (usually theta and some-
times excess alpha) present. When an excessive
amount of slow waves are present in the execu-
tive (frontal) parts of the brain, it becomes
difﬁcult to control attention, behavior, and=or
emotions. Such persons generally have prob-
lems with concentration, memory, controlling
their impulses and moods, or hyperactivity.
They have problems focusing and exhibit
diminished intellectual efﬁciency.
As the reader can see, there can be com-
plexity involved in how the brain is operating.
Research (Hammond, 2010b) has found that
there is heterogeneity in the EEG patterns
associated with different diagnostic conditions
such as ADD=ADHD, anxiety, or obsessive-
compulsive disorder. For example, scientiﬁc
research has identiﬁed a minimum of three
major subtypes of ADD=ADHD, none of which
can be diagnosed from only observing the
person’s behavior and each of which requires
a different treatment protocol. The picture
can become even more complicated by the
fact that sometimes there are other comorbid
problems present, and not simply ADD=ADHD
alone. Therefore, appropriate assessment is
important prior to beginning to do neurofeed-
back to determine what EEG frequencies are
excessive or deﬁcient, or if there are problems
in processing speed or coherence, and in what
parts of the brain. Proper assessment allows the
treatment to be individualized and tailored to
Neurofeedback training is EEG (brainwave)
biofeedback. During typical training, one or
more electrodes are placed on the scalp and
one or two are usually put on the earlobes.
Then, high-tech electronic equipment provides
real-time, instantaneous feedback (usually audi-
tory and visual) about your brainwave activity.
The electrodes allow us to measure the electri-
cal patterns coming from the brain—much like
a physician listens to your heart from the surface
of your skin. No electrical current is put into
your brain. Your brain’s electrical activity is
relayed to the computer and recorded.
Ordinarily, patients cannot reliably inﬂu-
ence their brainwave patterns because they lack
awareness of them. However, when they can
see their brainwaves on a computer screen a
few thousandths of a second after they occur,
it gives them the ability to inﬂuence and gradu-
ally change them. The mechanism of action is
generally considered to be operant condition-
ing. We are literally reconditioning and retrain-
ing the brain. At ﬁrst, the changes are
short-lived, but the changes gradually become
more enduring. With continuing feedback,
coaching, and practice, healthier brainwave
patterns can usually be retrained in most
people. As is reviewed later in the article, most
research suggests that signiﬁcant improvements
seem to occur 75 to 80% of the time. The pro-
cess is a little like exercising or doing physical
therapy with the brain, enhancing cognitive
ﬂexibility and control. Thus, whether symptoms
stem from ADD=ADHD, a learning disability, a
stroke, head injury, deﬁcits following neurosur-
gery, uncontrolled epilepsy, cognitive dysfunc-
tion associated with aging, depression,
anxiety, obsessive-compulsive disorder, autism,
or other brain-related conditions, neurofeed-
back training offers additional opportunities
306 D. C. HAMMOND
for rehabilitation through directly retraining the
electrical activity patterns in the brain. The
exciting thing is that even when a problem is
biological in nature, there is now another treat-
ment alternative to simply relying on medi-
cation. Neurofeedback is also being used
increasingly to facilitate peak performance in
‘‘normal’’ individuals, executives, and athletes.
More than a decade ago, Frank H. Duffy,
MD, a professor and pediatric neurologist at
Harvard Medical School, stated in the journal
Clinical Electroencephalography that scholarly
literature had already suggested that neurofeed-
back ‘‘should play a major therapeutic role in
many difﬁcult areas. In my opinion, if any medi-
cation had demonstrated such a wide spectrum
of efﬁcacy it would be universally accepted and
widely used’’ (Duffy, 2000, p. v). ‘‘It is a ﬁeld to
be taken seriously by all’’ (p. vii). Considerable
research has been published since that time.
This article, written to educate both profes-
sionals and the general public about the ﬁeld
of neurofeedback, provides an overview of this
literature without seeking to cite every publi-
cation with all their methodological details.
ASSESSMENT PRIOR TO
Some people wish that they could simply buy
their own neurofeedback equipment and train
themselves or their children. As is explained
later in this article, this is fraught with potential
for harm or ineffectiveness. To be done prop-
erly, neurofeedback needs to be conducted
or supervised by someone with specialized
expertise concerning brain function and who
is knowledgeable about much more than sim-
ply how to operate equipment and software.
As just mentioned, for training to be successful
and side effects avoided, it is vitally important
for an assessment to be performed and the
training to be individualized to the distinctive
brainwave patterns and symptoms of each per-
son. Everyone does not need the same training
at the same locations, and research has shown
that a person’s brainwave patterns simply
cannot be distinguished by only observing the
person’s behavioral symptoms. Therefore, prior
to doing neurofeedback training, legitimate
licensed clinicians will want to ask questions
about the clinical history of the client or
patient. Occasionally in more serious cases
they may suggest doing neuropsychological or
psychological testing. Competent clinicians
(Hammond et al., 2011) will also do a careful
assessment and examine brainwave patterns.
Some practitioners may do an assessment by
placing one or two electrodes on the scalp
and measuring brainwave patterns in a limited
number of areas. Other clinicians perform a
more comprehensive evaluation by doing a
quantitative electroencephalogram (QEEG)
brain map where 19 or more electrodes are
placed on the scalp.
A QEEG is an assessment tool to objectively
and scientiﬁcally evaluate a person’s brainwave
function. The procedure usually takes about 60
to 75 min and consists of placing a snug cap on
the head, which contains small electrodes to
measure the electrical activity coming from
the brain. This is done while the client is resting
quietly with his or her eyes closed, eyes open,
and sometimes during a task. Afterward, a
careful process is used to remove as completely
as possible artifacts that occurred when the
eyes moved or blinked, from body movement,
or tension in the jaw, neck, or forehead. The
brainwave data that were gathered are then
statistically compared to a sophisticated and
large normative database that provides scien-
tiﬁcally objective information on how the brain
should be functioning at the client’s age. This
assessment procedure allows the professional
to then determine in a scientiﬁc, objective
manner whether a client’s brainwave patterns
are signiﬁcantly different from normal, and if
so, how and where they differ.
Since the 1970s and 1980s there has been
a great deal of research with QEEG for a wide
range of problems. Abundant evidence, sum-
marized in Thatcher (2010), has veriﬁed the
reliability of QEEG evaluation, and hundreds
of scientiﬁc studies have been published using
QEEG evaluations. These studies have found
the QEEG to have documented ability to aid
in the evaluation of conditions such as mild
traumatic brain injury (TBI; and sports-related
WHAT IS NEUROFEEDBACK 307
concussions), ADD=ADHD, learning disabilities,
depression, obsessive-compulsive disorder,
anxiety, panic disorder, drug abuse, autism,
and a variety of other conditions (including
schizophrenia, stroke, epilepsy, and dementia;
e.g., Alper, Prichep, Kowalik, Rosenthal, & John,
1998; Amen et al., 2011; Barry, Clarke,
Johnstone, McCarthy, & Selikowitz, 2009;
Clarke, Barry, McCarthy, & Selikowitz, 2001;
Clarke et al., 2007; Harris et al., 2001; Hoffman
et al., 1999; Hughes & John, 1999; Newton
et al., 2004; Thatcher, 2010; Thatcher et al.,
1999). QEEG has even been able to predict
treatment outcomes from interventions with
conditions such as ADD=ADHD (Sufﬁn &
Emory, 1995), and alcoholism and drug abuse
(Bauer, 1993, 2001; Prichep, Alper, Kowalik,
John, et al., 1996; Prichep, Alper, Kowalik, &
Rosenthal, 1996; Winterer et al., 1998). The
American Psychological Association has also
endorsed QEEG as being within the scope of
practice of psychologists who are appropriately
trained, and the International Society for
Neurofeedback and Research (ISNR) has simi-
larly endorsed its use by qualiﬁed health care
professionals who are appropriately trained
(Hammond et al., 2004) and created standards
for the use of QEEG in neurofeedback. Persons
who are certiﬁed in this assessment specialty
may be identiﬁed through either the EEG &
Clinical Neuroscience Society (http://www.
ecnsweb.com/provider-directory.html) or the
Quantitative Electroencephalography Certiﬁ-
cation Board (http://www.qeegboard.org).
Once the assessment is complete and treat-
ment goals have been established, most com-
monly one or more electrodes are placed on
the scalp and one or more on the earlobes for
neurofeedback training sessions. The trainee
then usually watches a display on the computer
screen and listens to audio tones, sometimes
while doing a task such as reading. These train-
ing sessions are designed assist the person to
gradually change and retrain their brainwave
patterns. For example, some persons may
need to learn to increase the speed or size of
brainwaves in speciﬁc areas of the brain,
whereas other individuals need training to
decrease the speed of and amplitude of their
brainwaves. Commonly initial improvements
begin to be noticed within the ﬁrst ﬁve to 10
sessions. Length of treatment may only be 15
to 20 sessions for anxiety or insomnia, but with
other conditions such as ADD=ADHD or learn-
ing disabilities it will more often involve 30 to
50 sessions, depending on the severity of the
problem. Each session usually lasts about 20
to 25 min once equipment is attached. In treat-
ing very complex conditions or when multiple
disorders or diagnoses are present, a clinician
cannot always stipulate in advance how many
treatment sessions may be required.
SPECIALIZED TYPES OF
There are also several innovative forms of
neurofeedback that should be explained. They
each differ in distinctive ways from the tra-
ditional neurofeedback methods that have just
been described, and yet each represents impor-
tant and fascinating advances in our technology.
Slow Cortical Potentials Training
Speaking very technically for a moment, slow
cortical potentials are the positive or negative
polarizations of the EEG in the very slow
frequency range from .3 Hz to usually about
1.5 Hz. They may be thought of as the direct
current baseline on which the alternating cur-
rent EEG activity rides. There is generally a
negative shift in direct current potentials that
occurs during cognitive processing (to create
excitatory effects) and positive slow cortical
potentials occur during inhibition of cortical
networks. During and prior to an epileptic seiz-
ure, for example, the cortex is electronegative,
and this same kind of hyperexcitability tends
to be seen before many migraines. After a
seizure, when the cortex is fatigued, it tends
to be electro-positive. Slow cortical potential
neurofeedback training has been done (e.g.,
Kotchoubey, Blankenhorn, Froscher, Strehl, &
Birbaumer, 1997; Kotchoubey et al., 2001;
Strehl et al., 2006), particularly in Europe, with
308 D. C. HAMMOND
epilepsy and ADHD. This type of neurofeed-
back may also hold strong potential in the
treatment of migraine (Kropp, Siniatchkin, &
Gerber, 2002). In this training, one electrode
is placed in the center of the top of the head
and one behind each ear, while the client
focuses on changing a visual display on the
computer (Strehl, 2009).
THE LOW ENERGY
The Low Energy Neurofeedback System (LENS;
Hammond, 2007b; Larsen, 2006; Ochs, 2006)
is a unique and passive form of neurofeedback
that produces its effects through feedback that
involves a very tiny electromagnetic ﬁeld, which
only has a ﬁeld strength of 10
This feedback is so small that it is the equivalent
th of the strength of the input we
receive from simply holding an ordinary cell
phone to the ear and only about the intensity
of the output coming from a watch battery. It
is delivered in 1-s intervals down electrode wires
while the patient remains relatively motionless,
usually eyes closed. This feedback is adjusted
16 times a second to remain a certain number
of cycles per second faster than the dominant
brainwave frequency. Most preliminary
research and clinical experience are encour-
aging with articles published on LENS treatment
of conditions such as TBI (Hammond, 2010c;
Schoenberger, Shiﬂett, Esdy, Ochs, & Matheis,
2001), ﬁbromyalgia (C. C. S. Donaldson, Sella,
& Mueller, 1998; Mueller, Donaldson, Nelson,
& Layman, 2001), anger (Hammond, 2010a),
restless legs syndrome (Hammond, in press),
ADD=ADHD, anxiety, depression, insomnia
and other conditions (Larsen, 2006; Larsen,
Harrington, & Hicks, 2006). LENS has even
been used to modify behavioral problems in ani-
mals (Larsen, Larsen, et al., 2006). Advantages of
the LENS approach include that it commonly
seems to produce results faster than traditional
neurofeedback, and it can be used with very
young children and with individuals who are less
motivated and who do not have the impulse
control or stamina required with other neuro-
There are two different hemoencephalography
(HEG) systems that provide feedback, which is
believed to inﬂuence cerebral blood ﬂow
(Toomim & Carmen, 2009). Preliminary
research consisting of case series reports on
the HEG applications appears encouraging
(Carmen, 2004; Coben & Pudolsky, 2007b;
Duschek, Schuepbach, Doll, Werner, & Reyes
Del Paso, 2010; Friedes & Aberbach, 2003;
Mize, 2004; Sherrill, 2004; Toomim et al.,
2004), perhaps especially with migraine.
Live Z-Score Neurofeedback Training
Live Z-score training is a more recent innovation
that usually utilizes two, four, or more electrodes
on the head. Continuous calculations are being
computed comparing the way that the brain is
functioning on different variables (e.g., power,
asymmetries, phase-lag, coherence) to a scien-
tiﬁcally developed normative database. Feed-
back is then based on these moment-to-
moment statistical comparisons to norms for
the patient’s approximate age group. As with
other methods of neurofeedback, the feedback
that is provided is designed to guide the brain
toward normalized function. This feedback
often consists of observing a DVD where the pic-
ture dims and ﬂickers when the person is not
doing as well and becomes more clear and
bright when his or her brain is functioning closer
to norms. At this point, most of what has been
published on this approach are case series data
(Collura, 2008a, 2008b, 2009; Collura, Guan,
Tarrant, Bailey, & Starr, 2010; Collura, Thatcher,
Smith, Lambos, & Stark, 2009), with the excep-
tion of a new controlled study showing positive
results with insomnia (Hammer, Colbert, Brown,
& Ilioi, 2011), but these preliminary results,
which include pre- and posttreatment QEEGs,
are very encouraging. As this is being written,
an expansion of this approach has become avail-
able wherein an entire electrode cap with 19
electrodes can also be used for training.
LORETA Neurofeedback Training
LORETA refers to low resolution electromag-
netic tomography. This is a kind of QEEG
WHAT IS NEUROFEEDBACK 309
analysis that provides an estimation of the
location of the underlying brain generators
(e.g., the anterior cingulate, insula, fusiform
gyrus) of the patient’s EEG activity within a
frequency band. Very preliminary research
(Cannon & Lubar, 2007; Cannon et al.,
2007; Cannon et al., 2006; Congedo, Lubar,
& Joffe, 2004) has been published about this
approach. It does require more labor-intensive
preparation where an entire electrode cap with
19 electrodes must be applied in every session.
It is believed that this approach may have
potential to improve outcomes in difﬁcult cases
and=or shorten the length of treatment, and a
preliminary report (Cannon & Lubar, 2011)
suggests that changes may be enduring.
Functional MRI Neurofeedback
Functional magnetic resonance imaging (fMRI)
is a very sophisticated type of neuroimaging
that examines brain activation to evaluate
brain functioning (unlike the MRI, which exam-
ines brain structure). A fascinating scientiﬁc
advancement in the last several years has been
utilization of the fMRI for neurofeedback (Caria
et al., 2007; deCharms, 2007; deCharms et al.,
2004; deCharms et al., 2005; Haller, Birbau-
mer, & Veit, 2010; Johnston, Boehm, Healy,
Goebel, & Linden, 2010; Rota et al., 2009;
Weiskopf et al., 2004; Weiskopf et al., 2003;
Yoo et al., 2006). An advantage of fMRI neuro-
feedback is that it can examine functioning at
deep subcortical areas of the brain. However,
the serious practical disadvantage of fMRI
neurofeedback is that it would be incredibly
expensive and with equipment that costs
approximately $1 million or more, as well as
extreme expenses associated with the day-to-
day operation of such equipment, this approach
does not appear to be something that will hold
realistic clinical promise as a treatment option
in the foreseeable future.
AREAS OF APPLICATION FOR
Since the late 1970s, neurofeedback has been
researched, reﬁned, and tested with ADD=
ADHD and learning disabilities. Clinical work
by Dr. Joel Lubar and his colleagues (e.g., Lubar,
1995) at the University of Tennessee as well as
many others has repeatedly demonstrated that
it is possible to retrain the brain. In fact, one
randomized controlled study (Levesque,
Beauregard, & Mensour, 2006) documented
with fMRI neuroimaging the positive changes
in brain function in ADHD children that mir-
rored their behavioral changes following neuro-
feedback treatment. This and the research cited
next all provide strong support that demon-
strate the effectiveness of neurofeedback in
treating ADD=ADHD. Whereas the average
stimulant medication treatment study follow-up
is only 3 weeks long, with only four long-term
follow-up medication studies that lasted 14
months or longer, Lubar (1995) published
10-year follow-ups on cases and found that in
about 80% of clients, neurofeedback can sub-
stantially improve the symptoms of ADD and
ADHD and that these changes are maintained.
Rossiter and LaVaque (1995) found that 20
sessions of neurofeedback produced compara-
ble improvements in attention and concen-
tration to taking Ritalin. Fuchs, Birbaumer,
Lutzenberger, Gruzelier, and Kaiser (2003)
and Rossiter (2005) likewise demonstrated that
neurofeedback produced comparable improve-
ments to Ritalin. Drechsler et al. (2007) found
slow cortical potentials training superior to
group therapy with ADHD children. Neuro-
feedback has also been found in randomized
controlled studies to be superior to EMG
biofeedback (Bakhshayesh, 2007). In a 1-year
follow-up, control group study, Monastra,
Monastra, and George (2002) found that neuro-
feedback produced superior improvements
compared to Ritalin, not requiring continuation
of the medication. In a randomized controlled
study, Leins et al. (2007) demonstrated that
30 sessions of slow cortical potentials training
or of traditional neurofeedback were both
effective in producing cognitive, attentional,
behavioral, and IQ improvements, which
remained stable 6 months after treatment.
Gevensleben et al. (2009b) in a randomized
controlled study documented the superiority of
neurofeedback training (effect size ¼ .60)
310 D. C. HAMMOND
compared with computerized attention skills
training (which would have placebo control
characteristics). Behavioral and attentional
improvements were found to be stable on
6-month follow-up in research studies reported
by Strehl et al. (2006) and Gevensleben et al.
(2010), and the latter found that neurofeedback
training produced superior results to computer-
ized attention skills training, as did Holtmann
et al. (2009).
Two randomized, double-blind placebo
controlled studies (deBeus & Kaiser, 2011;
deNiet, 2011) have documented the effective-
ness of neurofeedback with ADHD. Other
recent, large randomized controlled studies
(Gevensleben et al., 2009a; Wrangler et al.,
2010) should also do much to dispel concerns
that improvements from neurofeedback training
simply reﬂect nonspeciﬁc placebo factors. These
studies demonstrated protocol-speciﬁc changes
in electrophysiological brain function using
EEG and sophisticated event-related potential
measures, replicating some earlier ﬁndings
(Heinrich, Gevensleben, Freisleder, Moll, &
Rothenberger, 2004) and showing distinct
neuronal mechanisms involved with different
training techniques. A 2-year follow-up (Gani,
Birbaumer, & Strehl, 2008) of the Heinrich
research found that not only were improve-
ments in attention and behavior stable but that
some parent ratings had shown continued
improvement during the 2 years. Continuing
improvement on 6-week and 12-week follow-
ups were also found after the completion of
LENS treatment of adult ADD=ADHD by deNiet
(2011) in a randomized, double-blind placebo
controlled study. Thus follow-up evaluations
ranging from 3 months to 10 years after treat-
ment (Gani et al., 2008; Heinrich et al., 2004;
Lubar, 1995; Monastra et al., 2002; Strehl
et al., 2006) provide strong support that
improvements from neurofeedback with ADD=
ADHD should be enduring, unless of course
something such as a head injury or drug abuse
were to occur to negative alter brain function.
A recent meta-analysis (Arns, de Ridder,
Strehl, Breteler, & Coenen, 2009) concluded
that neurofeedback treatment of ADD=ADHD
meets criteria for being classiﬁed as an
efﬁcacious and speciﬁc treatment—the highest
level of scientiﬁc validation (La Vaque et al.,
2002). In comparison to neurofeedback,
a meta-analysis (Schachter, Pham, King,
Langford, & Hoher, 2001) of randomized con-
trolled studies of medication treatment for
ADD=ADHD concluded that the studies were
of poor quality, had a strong publication bias
(meaning that drug company funded studies
that failed to support the effectiveness of their
product tended to never be submitted for pub-
lication), and often produced side effects. They
further indicated that long-term effects (beyond
placebo effects) for longer than a 4-week
follow-up period were not demonstrated.
A recent comprehensive review (Drug
Effectiveness Review Project, 2005) of medi-
cation treatment for ADD=ADHD concluded
that there was no evidence on the long-term
safety of the medications used in ADD=ADHD
treatment and that good quality evidence is
lacking that drug treatment improves academic
performance or risky behaviors on a long-term
basis, or in adolescents or adults. The latter con-
clusions were also reached by Joughin and Zwi
(1999). The largest randomized controlled mul-
tisite study compared medication treatment,
‘‘routine community care,’’ and behavior ther-
apy. Outcome raters were not blinded, introdu-
cing a bias, and most subjects in community
care were also on medications. At 14-month
follow-up (MTA Cooperative Group, 1999), all
groups showed improvements, and medication
produced better improvements in attention
and hyperactivity (the latter only on parent rat-
ings), but not in aggression, social skills, grades,
or parent–child relations. The ratings provided
by the only blinded rater (a classroom observer),
however, showed no difference between
groups, and on 3-year follow-up (Swanson
et al., 2007) there was no difference on any
outcome measures between groups, ﬁndings
that were conﬁrmed on 8 year follow-up
(Molina et al., 2009). Studies (e.g., Swanson
et al., 2007) have conﬁrmed loss of appetite
and growth suppression as a side effect of medi-
cation treatment, along with other side effects
such as increased heart rate and blood pressure,
insomnia, loss of emotional responsiveness,
WHAT IS NEUROFEEDBACK 311
dizziness, headache, and stomachache. In the
MTA study, 64% of children reported side
effects, 11% of them moderately severe and
3% severe. Side effects associated with ADD=
ADHD medications are also so common that
less than 50% of children maintain prescribed
dosages for more than 6 months (Hoagwood,
Jensen, Feil, Vitiello, & Blatara, 2000).
In light of these ﬁndings, neurofeedback
seems well validated as providing a noninvasive
and relatively side effect free treatment alterna-
tive for ADD=ADHD. In the long run it is also
very cost effective. Some individuals express
concern about the cost of neurofeedback being
greater than the expense involved in drug treat-
ment. Research has shown, however, that the
costs associated with medication treatment
are actually quite sizable. For instance, a study
(Marchetti et al., 2001) of six different medica-
tions for ADD=ADHD treatment found that the
average cost per school-aged patient was
$1,678 each year. Another study (Swensen
et al., 2003) examined the health care costs in
more than 100,000 families where ADHD
was either present or not present. They found
that in families where a member had ADHD,
the direct costs of health care expenditures plus
indirect costs (such as work loss) averaged
$1,288 per year higher for the other family
members (who had not been diagnosed as hav-
ing ADD=ADHD) in comparison with members
of families where ADHD was not present. This
would mean that the cost of medication just
cited, combined with indirect costs each year
for a family with two children, one of whom
had ADHD, would be $5,542.
Neurofeedback training for ADD=ADHD
is commonly found to be associated
with decreased impulsiveness=hyperactivity,
increased mood stability, improved sleep pat-
terns, increased attention span and concen-
tration, improved academic performance, and
increased retention and memory, and with a
much lower rate of side effects. It is fascinating
to note that ADD=ADHD or learning disability
studies that have evaluated IQ pre- and
posttreatment have commonly found IQ
increases following neurofeedback training.
These improvements ranged from an average
of 9 IQ points improvement in one study
(Linden, Habib, & Radojevic, 1996), to an
average improvement of 12 IQ points in a
study by L. Thompson and Thompson (1998),
a mean of 19 IQ points in another study
(Tansey, 1991b), and even up to an average
increase of 23 IQ points in a study by Othmer,
Othmer, and Kaiser (1999).
Learning and Developmental
With regard to learning disabilities, Fernandez
et al. (2003) demonstrated in a placebo-
controlled study that neurofeedback was an
effective treatment, and the improvements
were sustained on 2-year follow-up (Becerra
et al., 2006). An additional report by Fernandez
(Fernandez et al., 2007) on 16 children with
learning disabilities documented signiﬁcant
EEG changes 2 months after neurofeedback
compared to a placebo-control group where
there were no EEG changes, and 10 of 11 chil-
dren in the neurofeedback treatment group
showed objective changes in academic perfor-
mance compared with one in ﬁve children in
the placebo group. Other articles have also
been published on the value of neurofeedback
with learning disabilities (Orlando & Rivera,
2004; Tansey, 1991a; Thornton & Carmody,
2005). A randomized controlled study with
children with dyslexia (Breteler, Arns, Peters,
Giepmans, & Verhoeven, 2010) documented
signiﬁcant improvement in spelling, and Walker
(2010a; Walker & Norman, 2006) found signiﬁ-
cant improvements in reading ability in 41
dyslexia cases. In the ﬁrst 12 cases reported
by Walker (Walker & Norman, 2006) after 30
to 35 sessions, all the children had improved
at least two grade levels in reading ability.
Barnea, Rassis, and Zaidel (2005) identiﬁed
improvements in reading ability in learning
disability children after 20 sessions.
Although controlled research has not been
done, Surmeli and Ertem (2007) evaluated
whether QEEG-guided neurofeedback could
be helpful with Down Syndrome children. All
eight children who completed up to 60 treat-
ment sessions (one child dropped out after only
eight sessions) showed signiﬁcant improvement
312 D. C. HAMMOND
in attention, concentration, impulsivity,
behavior problems, speech and vocabulary,
and on QEEG measures. Surmeli and Ertem
(2010) treated 23 children diagnosed with mild
to moderate mental retardation with 80 to
160 QEEG-guided neurofeedback sessions.
Twenty-two of 23 showed clinical improve-
ment on the Developmental Behaviour
Checklist, and 19 of 23 showed improvement
on the Wechsler Intelligence Scale for Children
and a computerized test of attention.
Cognitive and Memory Enhancement
Neurofeedback also has documented results for
cognitive and memory enhancement in normal
individuals (Angelakis et al., 2007; Boulay,
Sarnacki, Wolpaw, & McFarland, 2011;
Egner & Gruzelier, 2003; Egner, Strawson, &
Gruzelier, 2002; Fritson, Wadkins, Gerdes, &
Hof, 2007; Gruzelier, Egner, & Vernon, 2006;
Hanslmayer, Sauseng, Doppelmayr, Schabus,
& Klimesch, 2005; Hoedlmoser et al., 2008;
Keizer, Verment, & Hommel, 2010; Rasey,
Lubar, McIntyre, Zoffuto & Abbott, 1996;
Vernon et al., 2003; Zoefel, Huster, &
Herrmann, 2010). Neurofeedback to enhance
cognitive functioning and to counter the effects
of aging has been referred to as ‘‘brain brighten-
ing’’ (Budzynski, 1996). Ros, Munneke, Ruge,
Gruzelier, and Rothwell (2010) produced
evidence that neurofeedback training with
normal persons may enhance neuroplasticity.
Medication treatment of epilepsy is successful
only in completely controlling seizures in two
thirds of patients (Iasemidis, 2003), and the
long-term use of many antiseizure medications
can have health risks. When medication treat-
ment is not successful, neurosurgery is often
recommended, but it has limited success
(Witte, Iasemidis, & Litt, 2003). In addition,
many epilepsy patients are also women of
child-bearing age who wish to have children
but fear the effects of medications on the fetus.
Therefore, a treatment option other than or in
addition to medication and surgery would be
desired. Research has shown that when medi-
cation is insufﬁcient to control the occurrence
of seizures, neurofeedback can offer an
additional modality that can be added to treat-
ment, which has the potential to assist in bring-
ing seizures under control, allowing dosage
levels of medications to be reduced, and help-
ing to avoid invasive brain surgery.
Research in this area began in the early
1970s and is extensive and rigorous, including
blinded, placebo-controlled, cross-over studies
(reviewed in Sterman, 2000, and in a meta-
analysis by Tan et al., 2009). The samples in
the studies that have been done typically
consist of the most severe, out-of-control,
medication-treatment-resistant patients. How-
ever, even in this most severe group of
patients, research found that neurofeedback
training on average produces a 70% reduction
in seizures. In these harsh cases of medically
intractable epilepsy, neurofeedback has been
able to facilitate greater control of seizures in
82% of patients, often reducing the level of
medication required, which can be very posi-
tive given the long-term negative effects of
some medications. Many patients, however,
may still need to remain on some level of
medication following neurofeedback.
More recently Walker and Kozlowski
(2005) reported on 10 consecutive cases, and
90% were seizure free after neurofeedback,
although only 20% were able to cease taking
medication. In another group of 25 uncon-
trolled epilepsy patients (Walker, 2008),
100% became seizure free following QEEG-
guided neurofeedback, with 76% no longer
requiring an anticonvulsant for seizure control
on follow-up, which averaged 5.1 years.
Walker (2010b) reported on still an additional
20 patients with intractable seizures, 18 of
which were seizure free following neurofeed-
back training, whereas two continued to report
occasional seizures. Two of the 18 patients
remained on a single anticonvulsant medi-
cation. The average length of follow-up in
these cases was 4 years. In this same report,
Walker indicated that he had seen nine
women who wished to stop taking anticonvul-
sants to become pregnant, and all nine
have remained seizure free for an average of
WHAT IS NEUROFEEDBACK 313
TBI and Stroke
Concussions and head injuries that cause
emotional, cognitive, and behavioral problems
occur as a result of many things such as motor
vehicle accidents, war (Trudeau et al., 1998),
and sports (McCrea, Prichep, Powell, Chabor,
& Barr, 2010; McKee et al., 2009), including
football (Amen et al., 2011), doing headers in
soccer (Tysvaer, Stroll, & Bachen, 1989), and
boxing (Ross, Cole, Thompson, & Kim, 1983).
Neurofeedback treatment outcome studies
of closed and open head injuries have been
published (Ayers, 1987, 1991, 1999; Bounias,
Laibow, Bonaly, & Stubbelbine, 2001; Bounais,
Laibow, Stubbelbine, Sandground, & Bonaly,
2002; Byers, 1995; Hammond, 2007a,
2007b, 2010c; Hoffman, Stockdale, Hicks, &
Schwaninger, 1995; Hoffman, Stockdale, &
Van Egren, 1996a, 1996b; Keller, 2001;
Laibow, Stubbelbine, Sandground, & Bounais,
2001; Schoenberger et al., 2001; Thornton,
2000; Tinius & Tinius, 2001), as well as with
stroke (Ayers, 1981, 1995a, 1995b, 1999;
Bearden, Cassisi, & Pineda, 2003; Cannon,
Sherlin, & Lyle, 2010; Doppelmayr, Nosko,
Pecherstorfer, & Fink, 2007; Putnam, 2001;
Rozelle & Budzynski, 1995; Walker, 2007;
Wing, 2001), but further high-quality research
needs to be done. One article (Hammond,
2007b) reported a case of moderate severity
TBI treated with the LENS, which resulted in
the complete reversal of posttraumatic anosmia
(complete loss of sense of smell) of 9
duration, which was previously unheard of,
as well as signiﬁcant clinical improvement in
A recent research review (Thornton &
Carmody, 2008) particularly suggests that
QEEG-guided neurofeedback is superior to neu-
rocognitive rehabilitation strategies and medi-
cation treatment in the rehabilitation of TBI.
Traditionally physical medicine and rehabili-
tation physicians tell head injury patients that
years after a TBI they cannot expect further
improvement and must simply adjust to their
deﬁcits. Clinical experience and research thus
far clearly indicate that neurofeedback may
often produce signiﬁcant improvements even
many years after a head injury. The accumulat-
ing evidence indicates that neurofeedback
offers a valuable additional treatment in the
rehabilitation of head injuries and with athletes
who have suffered concussions.
Alcoholism and Substance Abuse
EEG investigations of alcoholics (and the chil-
dren of alcoholics) have documented that even
after prolonged periods of abstinence, they fre-
quently have lower levels of alpha and theta
brainwaves and an excess of fast beta activity.
This suggests that alcoholics and their children
tend to be hardwired differently from other
people, making it difﬁcult for them to relax.
Following the intake of alcohol, however, the
levels of alpha and theta brainwaves increase.
Thus individuals with a biological predis-
position to develop alcoholism (and their chil-
dren) are particularly vulnerable to the effects
of alcohol because, without realizing it, alco-
holics seem to be trying to self-medicate in an
effort to treat their own brain pathology. The
relaxing mental state that occurs following alco-
hol use is highly reinforcing to them because of
their underlying brain activity pattern. Several
research studies now show that the best predic-
tor of relapse is the amount of excessive beta
brainwave activity that is present in both
alcoholics and cocaine addicts (Bauer, 1993,
2001; Prichep, Alper, Kowalik, John, et al.,
1996; Prichep, Alper, Kowalik, & Rosenthal,
1996; Winterer et al., 1998).
Recently, neurofeedback training to teach
alcoholics how to achieve stress reduction and
profoundly relaxed states through increasing
alpha and theta brainwaves and reducing fast
beta brainwaves has demonstrated promising
potential as an adjunct to alcoholism treatment.
Peniston and Kulkosky (1989) used such training
in a study with chronic alcoholics compared to a
nonalcoholic control group and a control group
of alcoholics receiving traditional treatment.
Alcoholics receiving 30 sessions of neurofeed-
back training demonstrated signiﬁcant increases
in the percentages of their EEG that was in the
alpha and theta frequencies, and increased
alpha rhythm amplitudes. The neurofeedback
314 D. C. HAMMOND
treatment group also demonstrated sharp
reductions in depression when compared to
controls. Alcoholics in standard (traditional)
treatment showed a signiﬁcant elevation in
serum beta-endorphin levels (an index of stress
and a stimulant of caloric [e.g., ethanol] intake),
whereas those with neurofeedback training
added to their treatment did not demonstrate
this increase in beta-endorphin levels. On
4-year follow-up checks (Peniston & Kulkosky,
1990), only 20% of the traditionally treated
group of alcoholics remained sober, compared
with 80% of the experimental group who had
received neurofeedback training. Furthermore,
the experimental group showed improvement
in psychological adjustment on 13 scales of the
Millon Clinical Multiaxial Inventory compared
to the traditionally treated alcoholics who
improved on only two scales and became worse
on one scale. On the 16-PF personality inven-
tory, the neurofeedback training group demon-
strated improvement on seven scales, compared
to only one scale among the traditional treat-
ment group. Similar positive results with 92%
sobriety on 21-month follow-ups were reported
by Saxby and Peniston (1995) in 14 depressed
alcoholics, and encouraging results were
reported on 3-year follow-ups in a treatment
program with native Americans (Kelley, 1997).
Scott, Kaiser, Othmer, and Sideroff (2005)
conducted a randomized controlled study with
121 individuals undergoing an inpatient sub-
stance abuse program. The patients received
40 to 50 treatment sessions. Persons who had
neurofeedback added to their treatment
remained in therapy signiﬁcantly longer—an
important factor in the treatment of substance
abuse. On 1-year follow-up, 77% of patients
receiving neurofeedback remained sober ver-
sus only 44% of traditional treatment patients.
Signiﬁcant differences were found in measures
of attention and in seven scales on the Minne-
sota Multiphasic Personality Inventory–2 com-
pared with improvement on only one scale in
those receiving traditional treatment. Reports
from a similar treatment program (Burkett,
Cummins, Dickson, & Skolnick, 2005) with
270 homeless crack cocaine addicts showed
that the addition of neurofeedback to treatment
more than tripled the length of stay in the
recovery center. On 1-year follow-up of the
94 patients who completed treatment, 95.7%
were now maintaining a residence, 93.6% were
employed or in schooling, 88.3% had no
further arrests, and 53.2% had been alcohol
and drug free 1 year, whereas another 23.4%
had used alcohol or dugs only one to three
times, corroborated by urinalysis.
Arani, Rostami, and Nostratabadi (2010)
compared results from 30 sessions of neuro-
feedback being provided to opioid dependent
patients undergoing outpatient treatment
(methadone or Buprenorpine maintenance),
compared with a control group that received
outpatient treatment alone. Patients receiving
neurofeedback showed signiﬁcantly more
improvements in outcome measures (e.g., of
hypochondriasis, obsessing, interpersonal sensi-
tivity, aggression, psychosis, anticipation of posi-
tive outcome, and desire to use drugs) and on
QEEGs. Preliminary research (Horrell et al.,
2010) has suggested that neurofeedback may
also have potential to reduce drug cravings in
The evidence reviewed validates the
immense potential that neurofeedback treatment
has to likely double if not triple the outcome rates
in alcoholism and substance abuse treatment
when it is added as an additional component to
a comprehensive treatment program (Sokhadze,
Cannon, & Trudeau, 2008). It may have real
potential in not only treating but also remediating
some of the serious damage to the brain that
occurs through drug abuse (e.g., Alper et al.,
1996; Struve, Straumanis, & Patrick, 1994).
and Criminal Justice
Quirk (1995) reported reduced recidivism using
a combination of neurofeedback and galvanic
skin response biofeedback. Smith and Sams
(2005) showed improvements in attention and
behavior in a group of juvenile offenders, and
a study in a Boys Totem Town project with
seven juvenile felons (Martin & Johnson,
2005) improvements were noted on a variety
of measures. Most recently, Surmeli and Ertem
WHAT IS NEUROFEEDBACK 315
(2009) presented a case series of 13 patients
who received from 80 to 100 neurofeedback
treatment sessions guided by QEEG ﬁndings.
Outcomes were measured with the Minnesota
Multiphasic Personality Inventory, a test of
attention, QEEG results, and interviews with
family members. Twelve of the 13 patients
showed signiﬁcant improvement, which was
maintained on 2-year follow-up. The abnormal
representation of learning disabilities, ADHD,
head injuries, childhood abuse, alcoholism,
and substance abuse in an incarcerated
offender population (Wekerle & Wall, 2002;
Wilson & Cumming, 2009) and of alcoholism
and drug abuse in domestic violence (Lin
et al., 2009) would suggest considerable poten-
tial for the use of neurofeedback, particularly
given the high recidivism rates that attest to
the limited effectiveness of traditional psy-
chotherapies and pharmacology treatment. This
will be another fruitful area for further research.
Posttraumatic Stress Disorder
Peniston and Kulkosky (1991) added thirty
30-minute sessions of alpha=theta neurofeed-
back training to the traditional VA hospital
treatment provided to a group of posttraumatic
stress disorder Vietnam combat veterans, and
then compared them at 30-months posttreat-
ment with a contrast group who received only
traditional treatment. On follow-up, all 14 tra-
ditional treatment patients had relapsed and
been rehospitalized, whereas only three of 15
neurofeedback training patients had relapsed.
Although all 14 patients who were on medi-
cation and were treated with neurofeedback
had decreased their medication requirements
by follow-up, among the patients receiving tra-
ditional treatment, only one patient decreased
medication needs, two reported no change,
and 10 required an increase in psychiatric med-
ications. On the Minnesota Multiphasic Person-
ality Inventory, neurofeedback training patients
improved signiﬁcantly on all 10 clinical scales—
dramatically on many of them—whereas there
were no signiﬁcant improvements on any scales
in the traditional treatment group. One study
(Huang-Storms, Bodenhamer-Davis, Davis, &
Dunn, 2006) has also reported positive
improvements in 20 adopted children with
histories of abuse and=or neglect. Improve-
ments were noted in externalizing and interna-
lizing problems, social problems, aggressive and
delinquent behavior, anxiety=depression,
thought problems, and attentional problems.
Neurofeedback seems very promising with
posttraumatic stress disorder, but further corro-
borating research is needed.
Autism and Aspberger’s Syndrome
There is a quite signiﬁcant body of research that
has now appeared on the neurofeedback
treatment of autism and Asperger’s Syndrome
(Coben & Myers, 2010; Coben & Pudolsky,
2007a; Jarusiuwicz, 2002; Knezevic, Thompson,
& Thompson, 2010; Kouijzer, de Moor, Gerrits,
Buitelaar, & van Schie, 2009; Kouijzer, de Moor,
Gerrits, Congedo, & van Schie, 2009; Kouijzer,
van Schie, de Moor, Gerrits, & Buitelaar, 2010;
Pineda et al., 2007; Pineda et al., 2008;
Scolnick, 2005; Sichel, Fehmi, & Goldstein,
L. Thompson, Thompson, and Reid (2010)
reported on a case series of 150 Asperger’s Syn-
drome patients and nine autism spectrum dis-
order patients who received 40 to 60 sessions,
commonly with some supplementary peripheral
biofeedback. They found very statistically sig-
niﬁcant improvements in measures of attention,
impulsivity, auditory and visual attention, read-
ing, spelling, arithmetic, EEG measures, and an
average full scale IQ score gain of 9 points.
Some of the studies just cited were control
group studies. There has also been a placebo-
controlled study (Pineda et al., 2008), and there
have been 6-month (Kouijzer et al., 2010) and
1-year follow-ups (Kouijzer et al., 2009) docu-
menting maintenance of positive results. A
review of neurofeedback with autism spectrum
problems, which includes a review of unpub-
lished papers presented as scientiﬁc meetings,
has been published by Coben, Linden, and
Myers (2010). In an as-yet-unpublished study
cited by those authors using neurofeedback
and HEG training, Coben found a 42%
reduction in overall autistic symptoms, including
a55% decrease in social interaction deﬁcits and
improvements in communication and social
316 D. C. HAMMOND
interaction deﬁcits of 55% and 52%,respect-
ively. Overall, neurofeedback has positive
research support as a beneﬁcial treatment with
autism spectrum problems, with ﬁndings of
positive changes in brain function, attention,
IQ, impulsivity, and parental assessments of
other problem behaviors such as communi-
cation, stereotyped and repetitive behavior,
reciprocal social interactions, and sociability.
Although neurofeedback is certainly not a cure
for these conditions, it appears to usually pro-
duce signiﬁcant improvements in these chronic
Anxiety and Depression
Encouraging preliminary research has been
published for the effectiveness of neurofeed-
back in treating anxiety with 10 controlled stu-
dies that have been identiﬁed (Hammond,
2005c; Moore, 2000). Of the eight studies of
anxiety that were reviewed, seven found posi-
tive changes. Another study (Passini, Watson,
Dehnel, Herder, & Watkins, 1977) used only
10 hr of neurofeedback with anxious alcoholics
and found very signiﬁcant improvements in
state and trait anxiety compared to a control
group, with results sustained on 18-month
follow-up. A randomized, blinded, controlled
study (Egner & Gruzelier, 2003) was done with
performance anxiety at London’s Royal College
of Music. They evaluated the ability of alpha=
theta neurofeedback to enhance musical per-
formance in high-talent-level musicians when
they were performing under stressful conditions
where their performance was being evaluated.
When compared with alternative treatment
groups (physical exercise, mental skills training,
Alexander Technique training, and two other
neurofeedback protocols that focused more
on enhancing concentration), only the alpha=
theta neurofeedback group resulted in enhanc-
ement of real-life musical performance under
stress. Similar randomized controlled studies
reducing performance anxiety have been
conducted with musical performance (Egner &
Gruzelier, 2003), ballroom dance performance
(Raymond, Sajid, Parkinson, & Gruzelier,
2005), and performance in singing (Kleber,
Gruzelier, Bensch, & Birbaumer, 2008; Leach,
Holmes, Hirst, & Gruzelier, 2008). In a rando-
mized, placebo-controlled study with medical
students (Raymond, Varney, Parkinson, & Gru-
zelier, 2005) neurofeedback enhanced mood,
conﬁdence, feeling energetic and composed.
Neurofeedback has also been shown with
objective measures to improve depression
(Baehr, Rosenfeld, & Baehr, 2001; Hammond,
2001a, 2005b; Hammond & Baehr, 2009). The
degree to which depressed patients were able
to normalize their EEG activity during neuro-
feedback has been found to signiﬁcantly corre-
late with improvement in depressive symptoms
(Paquette, Beauregard, & Beaulieu-Prevost,
2009). A blinded, placebo-controlled study
(Choi et al., 2011) demonstrated the superiority
of neurofeedback over a placebo treatment in
reducing depression while improving executive
function. However, more research is needed
on the use of neurofeedback with depression.
A randomized, controlled study (Hoedlmoser
et al., 2008) demonstrated that only 10 neuro-
feedback sessions focused on reinforcing the
SMR resulted in an increase in sleep spindles
and reduced sleep latency. Because memory
consolidation occurs during sleep, this study
also documented improved memory in the sub-
jects. This study replicated ﬁndings some earlier
studies (Berner, Schabus, Wienerroither, &
Klimesch, 2006; Sterman, Howe, & MacDonald,
1970). Hammer et al. (2011) published a
randomized, single-blind controlled study docu-
menting the effectiveness of 20 sessions of live
Z-score training in the treatment of insomnia.
Individualized neurofeedback was also shown
in control group studies by Hauri (1981; Hauri,
Percy, Hellekson, Hartmann, & Russ, 1982) to
have long-lasting effects with insomnia patients.
A recent randomized control group study
(Cortoos, De Valck, Arns, Breteler, & Cluydts,
2010) of primary insomnia patients found an
average of 18 sessions of home neurofeedback
training administered over the Internet pro-
duced a signiﬁcant improvement in the time
required to fall asleep and a signiﬁcant improve-
ment in total sleep time as measured in a sleep
lab compared with a control group. Even three
WHAT IS NEUROFEEDBACK 317
schizophrenic or schizoaffective patients with
disturbed sleep all showed improvement in
sleep quality when compared with a control
group (Cortoos et al., in press).
Headaches and Migraine
Walker (2011) reported on 71 recurrent
migraine cases who consulted a neurological
practice. Forty-six of the patients consented
to QEEG-guided neurofeedback treatment,
whereas 25 chose drug treatment. Excess higher
frequency beta was present in all cases. At
1-year follow-up, 54% of the neurofeedback
group experienced complete cessation of
migraines compared with no one in the medi-
cation treatment group. In the neurofeedback
group, 39% experienced a reduction of greater
than 50% in migraines (compared with 8% with
drug treatment), and a reduction of less than
50% was found in 4% of patients (compared
to 20% with medication treatment). Sixty-eight
percent of the medication treatment group
reported no change in headache frequency,
whereas only one patient (2%) receiving neuro-
feedback reported no reduction in frequency.
Siniatchkin, Hierundar, Kropp, Gerber, and
Stephani (2000) found a signiﬁcant reduction
in the number of days per month with a
migraine in children treated with slow cortical
potentials training versus a waitlist control group.
Carmen (2004) reported improvement of more
than 90% in migraine sufferers who completed
at least six sessions of HEG training. For Stokes
and Lappin (2010), 70% of migraine patients
experienced at least a 50% reduction in fre-
quency on more than 1-year follow-up from a
combination of 40 neurofeedback sessions com-
bined with HEG training. Tansey (1991a) pub-
lished four case reports. Although encouraging,
further controlled research is needed.
Peak or Optimal Performance Training
Neurofeedback is also being utilized in peak
performance training (Vernon, 2005). For
example, in a randomized, blinded controlled
study (Egner & Gruzelier, 2003) neurofeedback
signiﬁcantly enhanced musical performance,
and a similarly designed study (Raymond,
Sajid, et al., 2005) documented signiﬁcant
improvements in ballroom dance performance.
Such results have also been reported with golf
(Arns, Kleinnijenhuis, Fallahpour, & Breteler,
2007), archery (Landers, 1991; Landers et al.,
1994), improving fast reaction time and visuo-
spatial abilities (which has relevance to athletic
performance; Doppelmayr & Weber, 2011;
Egner & Gruzelier, 2004), improving singing
performance (Kleber et al., 2008; Leach et al.,
2008), acting performance (Gruzelier, Inoue,
Smart, Steed, & Steffert, 2010), and improve-
ments in radar-monitoring tasks (Beatty,
Greenberg, Diebler, & O’Hanlon, 1974). One
fascinating study (Ros et al., 2009) compared
training to either increase SMR or alpha and
theta brainwave frequencies in opthalmic
microsurgeons in training, compared to a wait-
list (no-treatment) group. In only eight sessions
of SMR training the physicians demonstrated
signiﬁcant improvements in surgical skill,
decreases in anxiety, and a 26% reduction in
surgical task time. Research documenting
improvements in cognitive and memory perfor-
mance has already been reviewed earlier. The
potential of neurofeedback applications for
optimal performance will be very a fruitful area
for further research.
Other Clinical Applications
of Neurofeedback Training
Preliminary reports have also been published
on the use of neurofeedback with chronic fati-
gue syndrome (Hammond, 2001b); Tourette’s
(Tansey, 1986); obsessive-compulsive disorder
(Hammond, 2003, 2004; Surmeli, Ertem,
Eralp, & Kos, 2011); Parkinson’s tremors (M.
Thompson & Thompson, 2002); tinnitus
(Crocetti, Forti, & Bo, 2011; Dohrmann, Elbert,
Schlee, & Weisz, 2007; Gosepath, Nafe,
Ziegler, & Mann, 2001; Schenk, Lamm,
Gundel, & Ladwig, 2005; Weiler, Brill, Tachiki,
& Schneider, 2001); pain (Ibric & Dragomirescu,
2009; Jensen, Grierson, Tracy-Smith, Baciga-
lupi, & Othmer, 2007; Sime, 2004); physical
balance, swallowing, gagging, and incontinence
(Hammond, 2005a); children with histories of
abuse and neglect (Huang-Storms et al., 2006)
or reactive attachment disorder (Fisher, 2009);
cerebral palsy (Ayers, 2004); restless legs and
318 D. C. HAMMOND
periodic limb movement disorder (Hammond,
in press); physical and emotional symptoms
associated with Type I diabetes mellitus
(Monjezi & Lyle, 2006); essential tremor; and
for ‘‘chemo fog’’ (Raffa & Tallarida, 2010;
Schagen, Hamburger, Muller, Boogerd, & van
Dam, 2001) following chemotherapy or radi-
Mixed results have been found with neuro-
feedback treatment of ﬁbromyalgia. An uncon-
trolled trial (Mueller et al., 2001) with 30
patients with ﬁbromyalgia (using an early version
of LENS) found signiﬁcant improvements in
et al. (1998) used an earlier version of LENS
(and a small amount of EMG biofeedback) and
reported signiﬁcant improvement in 77% of
patients’ long-term follow-ups, but again this
was an uncontrolled case series. In contrast, these
results were not conﬁrmed by Kravitz, Esty, Katz,
and Fawcett (2006) in a double-blind, placebo-
controlled study, and Nelson et al. (2010) found
improvements in pain, fatigue, and cognitive
clouding, and increased activity in comparison
to a sham placebo control group, but the effects
were not enduring. On the other hand, Kayiran,
Dursan, Dursun, Ermutlu, and Karamursel
(2010), in a randomized, blinded, control group
study, compared 20 sessions of neurofeedback
to treatment with Lexapro and found that both
treatments produced signiﬁcant symptomatic
improvements, but the beneﬁts were signiﬁcantly
greater in the neurofeedback group.
Research has shown that it is possible for
schizophrenics to participate in neurofeeback
training (Guzelier, 2000; Gruzelier et al., 1999;
Schneider et al., 1992) and clinical experience
with chronic schizophrenics (Bolea, 2010;
Cortoos et al., in press; M. Donaldson, Moran,
& Donaldson, 2010; Surmeli, Ertem, Eralp, &
Kos, in press) provides encouragement that this
may be an additional treatment intervention
which holds potential.
IS MORE PLACEBO CONTROLLED
Despite the considerable research cited in this
article, there are many areas where more
controlled outcome research is still needed in
the application of neurofeedback to various
problems. Placebo-controlled studies are often
regarded as the very highest level of scientiﬁc
validation. It can be assumed that positive
results from neurofeedback are due to a com-
bination of expectancy (placebo) effects and
effects speciﬁc to the neurofeedback treatment
(Hammond, 2011; Perreau-Linck, Lessard,
Levesque, & Beauregard, 2010), because pla-
cebo effects appear to be an active ingredient
in virtually every therapeutic modality. We
know, however, that there are improvements
very speciﬁc to neurofeedback because there
are several placebo-controlled studies that
have demonstrated signiﬁcant efﬁcacious and
speciﬁc effects beyond placebo inﬂuences in
neurofeedback training (Raymond, Varney,
et al., 2005), including with learning disabilities
(Becerra et al., 2006; Fernandez et al., 2003),
ADD=ADHD (deBeus & Kaiser, 2011; deNiet,
2011), anxiety (Raymond, Varney, et al.,
2005), epilepsy (Lubar et al., 1981), sleep
latency and declarative learning (Hoedlmoser
et al., 2008), cognitive enhancement in the
elderly (Angelakis et al., 2007), autism (Pineda
et al., 2008), and depression (Choi et al.,
2011), although one preliminary study did
not ﬁnd such effects (Lansbergen, van Dongen-
Boomsma, Buitelaar, & Slaats-Willemse, 2010).
Certainly animal studies (e.g., Sterman, 1973;
Larsen, Larsen, et al., 2006) also suggest that
neurofeedback has therapeutic effects inde-
pendent of placebo effects. It would not be
anticipated that cats would form positive
expectancies about being more seizure resist-
ant simply because an experimenter was put-
ting electrodes on their heads.
In spite of the placebo-controlled studies
we have in neurofeedback, some academic
researchers (e.g., Loo & Barkley, 2005),
insurance companies, and proponents of medi-
cation treatment have complained that there
should be more placebo-controlled research
on neurofeedback, even though medical ethi-
cists (Andrews, 2001; Lurie & Wolfe, 1997;
Rothman, 1987), neurofeedback advocates
(La Vaque, 2001), and the Declaration of
Helsinki (World Medical Association, 2000)
WHAT IS NEUROFEEDBACK 319
have expressed the view that requiring
placebo-controlled studies in conditions where
there is a known effective treatment already
available is considered unethical. The primary
beneﬁt of placebo-controlled studies is that
they clarify the mechanism of action by which
a treatment works, but they are not necessary
to determine the effectiveness of a treatment
(e.g., the degree of improvement in attention
and behavior in ADD=ADHD, and in compari-
son with stimulant drugs).
When considering how well validated com-
mon medical and psychiatric treatments actually
are, it is enlightening to learn that only 11% of
2,711 cardiac medical treatment recommenda-
tions are based on multiple randomized con-
trolled studies (Tricoci, Allen, Kramer, Califf, &
Smith, 2009) and only 41% are based on evi-
dence from a single randomized trial or nonran-
domized studies, whereas 48% are simply based
on ‘‘expert opinion’’ or only case studies. As yet a
further example, the public is generally unaware
2010, and Moncrieff, 2009) of psychiatric medi-
cation treatment of depression have concluded
that they are only mildly (18%)moreeffective
than a placebo (and yet frequently associated
with side effects and a withdrawal syndrome).
Despite these facts, insurance companies accept
medication treatment for depress ion and a large
proportion of medical treatments as being well
established and effective. These facts do not
mean that more neurofeedback outcomes stu-
dies are desirable and needed, but it creates an
important perspective that much of current
medical and psychiatric treatment practice does
not rest on as much sound scientiﬁc evidence
as is commonly assumed.
ADVERSE EFFECTS, SIDE EFFECTS, AND
Mild side effects can sometimes occur during
neurofeedback training. For example, occasion-
ally someone may feel fatigued, spacey, or
anxious; experience a headache; have difﬁculty
falling asleep; or feel agitated or irritable. Some-
times such side effects may occur because the
training session is too long (Matthews, 2007,
2011; Ochs, 2007). Many of these feelings pass
within a short time after a training session. If
clients make their therapists aware of such
feelings, they can alter training protocols and
usually quickly eliminate such mild side effects.
Selecting a Qualiﬁed Practitioner
It is possible, however, for more signiﬁcant
negative effects to occur (Hammond & Kirk,
2008; Hammond, Stockdale, Hoffman, Ayres,
& Nash et al., 2001; Todder, Levine, Dwolatzky,
& Kaplan, 2010), particularly if training is not
being conducted or supervised by a knowl-
edgeable, certiﬁed (http://www.bcia.org) pro-
fessional who will individualize the training. A
‘‘one-size-ﬁts-all’’ approach that is not tailored
to the individual will undoubtedly pose a greater
risk of either being ineffective or of producing an
adverse reaction. Due to the heterogeneity in
the brainwave activity (e.g., Clarke et al.,
2001; Hammond, 2010b; Prichep et al.,
1993) within broad diagnostic categories (e.g.,
ADD=ADHD, head injuries, depression, autism,
or obsessive-compulsive disorder) the treatment
requires individualization, and research is
increasingly showing that different treatment
protocols have differential effects (e.g.,
Angelakis et al., 2007; Egner & Gruzelier,
2004; Gevensleben et al., 2009a, 2009b;
Gruzelier & Egner, 2005; Hauri, 1981; Hauri
et al., 1982; Heinrich et al., 2004; Ros et al.,
2010; Wrangler et al., 2010) on the brain.
Thus, it is emphasized once again that
everyone does not need the same treatment
and that if training is not tailored to the person,
the risk is greater of it being ineffective or very
infrequently even detrimental. For instance,
Lubar et al. (1981) published a reversal double-
blind controlled study with epilepsy which
documented that problems with seizure dis-
order could be improved with neurofeedback,
but they could also be made worse if the wrong
kind of training was done. Similarly, Lubar and
Shouse (1976, 1977) documented that ADD=
ADHD symptoms could improve but also be
worsened if inappropriate training was done.
As yet another example in the treatment of
ADD=ADHD, it was found that when a nonin-
dividualized approach was used (Steiner,
320 D. C. HAMMOND
Sheldrick, Gotthelf, & Perrin, 2011) with one
electrode embedded in a helmet compared
with computerized attention training, only
modest equivalent results were found. In con-
trast, when individualized neurofeedback was
compared with computerized attention train-
ing (Gevensleben et al., 2010; Gevensleben
et al., 2009a, 2009b; Holtmann et al., 2009),
neurofeedback was signiﬁcantly more effective
than the skills training.
Therefore, seeking out a qualiﬁed and cer-
tiﬁed professional who will do a comprehen-
sive assessment of brain function (e.g., with a
QEEG or careful assessment of the raw EEG
activity) is deemed to be vitally important. If
the practitioner indicates that they do a ‘‘brain
scan’’ or QEEG, it is important to determine
whether the EEG data are actually being
statistically compared to a normative database
rather than simply being roughly measured.
If you are seeking help for a psychological,
psychiatric, or medical problem like those dis-
cussed in this article, the ISNR (Hammond
et al., 2011) has recommended that you deter-
mine that the practitioner you select is not only
certiﬁed but also licensed or certiﬁed for inde-
pendent practice in your state or province as
a mental health or health care professional.
An increasing number of unqualiﬁed and
unlicensed persons are managing to obtain
neurofeedback equipment and seeking to basi-
cally practice psychology and medicine without
a license. It has unfortunately become a ‘‘buyer
In this regard, some individuals are now
renting and leasing home training equipment.
It is strongly recommended that training with
equipment at home should be done only
under the regular consultation and supervision
of a legitimately trained and certiﬁed pro-
fessional, and preferably home training should
occur only following closely supervised training
that has taken place in the ofﬁce for a period of
time (Hammond et al., 2011). It is important to
caution the public that if this is not done, some
negative effects (and a higher probability of
ineffective results) could occur from such unsu-
pervised self-training. It is important to remem-
ber that the impressive success documented in
most of the research on neurofeedback is
based on work conducted by qualiﬁed profes-
sionals, following individualized assessment,
and with training sessions that are supervised
by a knowledgeable therapist rather than with
unsupervised sessions taking place in an ofﬁce
or at home. Supervised training sessions where
the patient is coached have been found to
produce signiﬁcantly better outcomes than
unsupervised sessions (Hammond, 2000).
Readers may identify certiﬁed practitioners
who are doing neurofeedback training by
consulting the website for the Biofeedback
Certiﬁcation International Alliance (http://www.
bcia.org) and by examining persons who are
licensed and listed in the membership directory
for ISNR (http://www.isnr.org). In addition to
the references included in this article, the ISNR
website also includes a comprehensive bibli-
ography of outcome literature on neurofeed-
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