There is a
100-year history on the EEG. Compare the quality of research with what
is typical for Educators determining programs and curriculum. How much
stronger is this evidence using the "data based decision making"
criteria of No Child Left Behind?
Educators and Psychologists -- All Aboard!!
Neurofeedback in Psychological Practice
Author: Masterpasqua, Frank; Healey, Kathryn N. Source: Professional Psychology: Research and Practice December 2003 Vol. 34, No. 6, 652-656 ISSN: 0735-7028 Number: pro346652
Neurofeedback, also known as EEG biofeedback or EEG operant
conditioning, is an emerging modality with the potential of becoming an
important part of effective psychological practice. Neurofeedback is a
process whereby individuals learn to self-regulate their brain waves.
Preliminary findings indicate that teaching individuals to alter
electrocortical activity may have beneficial effects for
attention-deficit/hyperactivity disorder (ADHD). Other research is
ongoing to determine the effectiveness of neurofeedback for other
disorders as well, including depression and schizophrenia. Its promise
notwithstanding, neurofeedback has been virtually ignored by the
mainstream investigators and clinicians. Even accounting for the absence
of conclusive empirical efficacy, a process that combines two pillars
of psychology-operant conditioning and brain function-deserves greater
attention from the psychological community. With this article we hope to
call attention to this modality by presenting some of the history and
research pertaining to brain wave self-regulation.
A Brief History of Electroencephalography and Neurofeedback
Observations of electrical activity of the brain were first reported in 1875 when British physician Richard Caton observed electrical signals while probing the exposed cortices of animals. Fifty years later Hans Berger (1929)
showed that electrocortical activity could be detected from the surface
of the human scalp. It was Berger who first used the term electroencephalogram
(EEG) and who identified different frequencies of brain waves
measurable from the scalp. He also found that certain frequencies were
characteristic of different states of attention. If subjects sat quietly
with eyes closed, Berger observed frequencies around 10 cycles per
second (10 Hz); if they were asked to focus on a mathematics problem
with eyes open, frequencies were more likely to be in the range of 15
Berger's work encouraged others to determine whether particular
features of an EEG were diagnostic for neurological or psychological
disorders (see Robbins, 2000).
Although there was some success linking EEG patterns to brain trauma
and seizure disorders, early research was largely unsuccessful in
relating EEG to psychopathology. Later in this article we report on more
recent developments in the use of sophisticated techniques such as
quantitative EEG (QEEG) that have revealed electrocortical correlates of
a number of psychological and neurological disorders (Cantor, 1999; Hughes & John, 1999).
Following Miller's (1969)
seminal work demonstrating that autonomic functions can be operantly
conditioned, psychologists were the first to discover that animals and
humans could likewise learn to control their brain waves via contingent
feedback (Robbins, 2000). A long series of studies by Sterman and his colleagues (Sterman & Friar, 1972; Sterman, Macdonald, & Stone, 1974)
demonstrated that both cats and humans were able to learn to increase
the amplitude of frequencies in the 12-15-Hz range recorded in the area
of the sensorimotor cortex. Sterman (2000)
found that patients with seizure disorders could use operant
conditioning to increase these so-called SMR (sensorimotor rhythm)
frequencies and thereby reduce seizure activity. As we report below, Sterman and Friar's (1972) work with seizure disorders led directly to the first use of EEG biofeedback for ADHD (Lubar & Shouse, 1976).
At about the same time as Sterman and Friar's (1972) work with frequencies in the 12-15-Hz range, Kamiya (1969)
reported that the amplitude of slower brain waves in the 8-11-Hz range
(so-called alpha waves) could also be increased through contingent
feedback. Kamiya attached electrodes to the surface of the scalp to
determine whether humans could correctly identify when there was a
predominance of alpha waves (8-12 Hz) in the area of the occipital lobe.
His participants were able to identify the state associated with alpha
in relatively short order and were able to increase the amplitude of the
alpha frequency when signaled to do so.
work precipitated great interest in the operant conditioning of slower
frequencies, both alpha and 4-7-Hz (theta), and the 1960s and 1970s
witnessed a large number of studies designed to determine the efficacy
of alpha/theta operant conditioning. Outcomes assessed ranged from
enhancing peak performance, drug and alcohol abuse, and posttraumatic
stress disorder (Evans & Abarbanel, 1999).
Neurofeedback could not withstand the multitude of claims made for
its efficacy. The modality quickly became associated with the
psychedelic, altered states of consciousness movement that was perceived
as a fringe element of scientific psychology. It is not surprising then
that it only required a few negative findings for neurofeedback to fall
out of favor within the mainstream psychological community (Budzynski, 1999).
Neurofeedback in a New Technological Era
At about the same time that early efforts at EEG biofeedback were
falling into disrepute, initial strides were being made in brain imaging
techniques. In the past 20 years there has been a revolution in
neuroscience, resulting in large part from advances in neuroimaging.
Neuroimaging as well as progress in computerized neurophysiology, also
known as QEEG, provide tools that may elucidate the mechanisms
Positron emission tomography (PET) and single photon emission
computed tomography (SPECT) assess blood flow and activity patterns in
the brain. The procedures require injection of small amounts of
radioactive material that allow for visual representation of brain
oxygen and glucose utilization. Functional magnetic resonance imaging is
a more recent noninvasive technique that, along with PET scans, allows
researchers to apprehend brain activity during cognitive tasks (see Sarter, Bernston, & Cacioppo, 1996).
In QEEG, electrodes are placed on multiple predetermined sites on the
scalp, and data from these sites are submitted to computer analyses and
"brain mapping." The kinds of results available from conventional EEG
and QEEG include but are not limited to distribution of electrical
frequencies in various brain regions, the amplitude and shape of these
frequencies, and the symmetry of frequencies, amplitudes, and wave
shapes on homologous sites on each hemisphere. By comparing these
measures to normative databases, researchers are able to identify brain
wave patterns that are characteristic of various clinical populations.
On the basis of a review of over 200 studies, Hughes and John (1999)
concluded that QEEG qualifies as an assessment tool for cerebrovascular
disease, dementia, learning and attention disorders, mood disorders,
postconcussion syndrome, schizophrenia, and substance abuse. In the
discussion that follows, we show how some of these advances in EEG
assessment are being used as the bases for neurofeedback interventions.
We focus our discussion of the association between altered
electrocortical activity and psychological disorder on ADHD and, to a
lesser extent, depression. We do so because of recent work showing that
each of these disorders can be distinguished by characteristic QEEGs and
the existence of outcome studies implicating their responsiveness to
QEEG and Neurofeedback for ADHD
Three independent research teams have now documented that individuals
with ADHD can be differentiated from nonclinical samples by means of
QEEG (Chabot & Serfontein, 1996; Janzen, Graap, Stephenson, Marshall, and Fitzsimmons, 1995; Monastra, Lubar, & Linden, 2001).
Research consistently reveals that elevation in the average amplitude
of slow brain wave frequencies (4-7 or 8-11 Hz) and a corresponding
decrease in amplitude of higher frequencies (12-15 or 15-18 Hz),
especially over the prefrontal or medial central cortex, is a
distinguishing feature in ADHD subjects. These subjects show an even
greater relative elevation in slow brain wave activity compared with
faster activity when cognitively challenged (Lubar & Lubar, 1999).
The QEEG studies showing slower brain function among ADHD patients are corroborated by brain imaging research. Using PET scans, Zametkin et al (1990)
reported a slowing of frontal cortex glucose metabolism in ADHD
subjects. Much like the QEEG findings, those of Zametkin et al. showed
that the slowing was especially noticeable during cognitive tasks. Using
SPECT imaging, Amen and Carmichael (1997)
also reported lower rates of metabolism in frontal and/or parietal
lobes among their ADHD participants. Thus, the findings of relatively
slower brain waves among subjects with ADHD are confirmed by brain
imaging research showing relatively slower rates of metabolism at
similar brain locations in similar populations.
The neurofeedback procedure.
Regardless of disorder, the neurofeedback procedure is relatively
consistent across studies. Neuroelectrical activity is detected via
surface electrodes; this activity is then amplified and processed by
software programs that provide contingent auditory, tactile, and/or
visual feedback to the patient via a game simulation on a computer
monitor. For instance, a Pac-Man figure advances and sounds a tone
whenever a client maintains waves in the 15-18-Hz range above a certain
amplitude threshold while keeping waves in the 4-7 Hz range below a
certain threshold. Amplitude thresholds are established for each
individual so as to optimize motivation and learning. In this example, a
reward would occur whenever the client maintains 15-18-Hz above
predetermined amplitude 70% of the time while keeping the 4-7-Hz
frequency above a predetermined amplitude only 20% of the time.
Outcomes using single-case designs.
Neurofeedback for ADHD began as an extension of Sterman and Friar's (1972) groundbreaking work with epilepsy. Lubar and Shouse (1976)
reasoned that increasing the sensorimotor rhythm through neurofeedback
might serve to quiet motor responses in "hyperactive" children (as they
were then called), much as it did for Sterman's epileptic patients.
Using a blinded ABA reversal design, Lubar and Shouse (1976)
provided the first empirical evidence for the value of neurofeedback
for ADHD. In this ABA design, a 9-year-old child first learned to
improve EEG patterns and behaviors associated with ADHD (as assessed by
observers who were blind to the procedure), then to return measures to
baseline values, followed by a return to improved behavioral and EEG
status. The authors reported that medication was permanently ended
following the study and that the child continued to function well
without medication long after the study's termination. Using the blind
ABA design with other children, Shouse and Lubar (1979) and Tansey (1993)
replicated these findings. They also reported long-term positive
effects of neurofeedback for these clients that lasted years after
treatment, a finding with special significance, because the benefits of
psychostimulants are known to last only while the patient is medicated.
Nash reviewed a number of other multiple-case studies (e.g., Alhambra
et al., 1995; Tansey & Bruner, 1983; Thompson & Thompson, 1998
[all cited in Nash, 2000])
in which pre- and postneurofeedback assessments demonstrated
improvements on measures including intelligence, academic skills,
continuous performance tests, and behavioral rating scales.
Results of single-case designs and case studies can tell much about
treatment effectiveness under real-world circumstances, but controlled
studies comparing the treatment with placebo or other modalities are
required to demonstrate efficacy of specific interventions (Chambless & Hollon, 1998).
In the following section, we review results from published controlled
group studies from four different research teams that are suggestive of a
role for neurofeedback for ADHD.
Controlled group studies.
Rossiter and LaVaque (1995)
compared neurofeedback and stimulant therapy in 46 patients (ages 8-21
years) who had self-selected participation in either neurofeedback or
stimulant therapy conditions. Although assignments were not random,
there were no significant pretest differences between groups on measures
of age, gender, intelligence, ADHD subtype, frequency of other
diagnoses, or type of school placements. The neurofeedback group
received 20 sessions over a 3-month period; the medication-only group
received doses of either methylphenidate or dextroamphetamine as
prescribed by their personal physicians. Both neurofeedback and
stimulant groups showed improvements from pre- to posttest on behavioral
ratings completed by mothers using the Behavior Assessment Scale for
Children (Reynolds & Kamphaus, 1992) and on a continuous performance measure, the Tests of Variables of Attention (TOVA; Greenburg & Dupuy, 1993).
Results indicated positive effects for both medication and
neurofeedback and an equal contribution from both therapies for symptom
Linden, Habib, and Radojevic (1996)
randomly assigned 18 patients (ages 8-21 years) to either a
neurofeedback treatment or a wait-list control group. The treatment
group learned to suppress theta (4-7 Hz) while enhancing beta waves
during 40 sessions of feedback extending over 6 months. Neither group
received medication. Compared with the control group, the neurofeedback
group demonstrated significant pre- to posttest reductions in
inattentive behaviors as assessed with the Swanson, Nolan, and Pelham (1988) measure and the Iowa Conners (Atkins & Milich, 1987) rating scales, as well as a significant increase in scores on the Kaufman Brief Intelligence Test (Kaufman & Kaufman, 1990).
Monastra, Monastra, and George (2002)
compared the effects of Ritalin, EEG biofeedback, and parenting styles
on the primary symptoms of ADHD in 100 children ages 6-19 years. All
subjects participated in a 12-month comprehensive intervention that
included Ritalin, parent counseling, and academic support at school.
Fifty-one of the 100 children also received weekly sessions of
neurofeedback modeled on the Lubar protocol designed to increase
amplitudes in the 12-18 Hz range while decreasing amplitudes in the 4-11
Hz range at the central midline cortex (Lubar & Lubar, 1999).
Pre- and posttreatment assessment included the Attention Deficit
Disorders Evaluation Scales (ADDES, home and school versions; McCarney, 1995), TOVA, and a QEEG measure previously shown to distinguish children with ADHD (Monastra et al., 2001).
No significant pretreatment differences existed for the two groups.
After one year, children were assessed while taking Ritalin and while
not taking the medication. While not taking Ritalin, only children who
had received neurofeedback sustained the gains in the ADDES and TOVA. In
addition, only children who received neurofeedback showed posttreatment
improvement on the QEEG measure of neurophysiological changes. Thus, by
"dismantling" the effects of neurofeedback from other forms of
treatment, Monastra et al. (2002)
demonstrated that only children who displayed changes in cortical
arousal maintained improvements while not taking Ritalin and that only
children who received neurofeedback training manifested those changes.
Fuchs, Birbaumer, Lutzenberger, Gruzelier, and Kaiser (2003) assigned 8-12-year-old children with ADHD to either a neurofeedback (n = 22) or methylphenidate (n
= 12) condition on the basis of parents' preference. The authors
reported that both groups showed significant improvements on all
subscales of the TOVA and on the d2 Attention Endurance Test (Brickenkamp, 1994).
In addition, both groups showed significant declines in disordered
behaviors as assessed by the German version of the Iowa Conners Behavior
Rating Scale (Atkins & Milich, 1987).
On all measures, improvements in outcomes from pre- to posttreatment
were comparable between neurofeedback and methylphenidate.
In summary, four different research teams have performed controlled
trials showing the efficacy of neurofeedback for ADHD. Each of these
teams used a variation of Lubar's original protocol designed to help
children to increase frequencies ranging from 12-18 Hz while inhibiting
frequencies in the 4-7 Hz or 8-11 Hz range. What is more, findings from
one study (Monastra et al., 2002)
suggested that neurofeedback provided for sustained changes in
underlying EEG patterns, thereby indicating a potential mechanism for
the effects of neurofeedback on behavior. Indeed, one of the
implications of the Monastra et al study (2002)
is that, unlike methylphenidate, neurofeedback's benefits are retained
when children are not receiving treatment. Although more research is
required, we believe that these findings begin to demonstrate the role
that neurofeedback can play in a multimodal approach to ADHD.
Neurofeedback for Other Disorders
It has been known for some time that damage to the left frontal lobe
often leads to symptoms of depression, whereas damage to right frontal
lobe is more likely to lead to symptoms of mania (Gainotti, 1972; Robinson & Downhill, 1995; Robinson, Starr, & Price, 1984). Recently, Davidson and colleagues (Davidson, 1993, 1994; Davidson, Jackson & Kalin, 2000)
showed that alpha wave asymmetry between the frontal lobes can be
diagnostic for mood disorders. Positive affect was associated with
relatively lower amplitudes of frequencies in the 8-12 Hz (alpha) range
in the left frontal cortex compared with the right frontal cortex.
Conversely, negative affect corresponded to lower amplitudes of the
alpha range in the right frontal compared with the left frontal lobes.
Actively depressed patients as well as participants in current remission
who had previously experienced depressive episodes showed relatively
more left than right frontal alpha activity. The latter finding is
consistent with a diathesis-stress model of depression, inasmuch as a
person's affective style appears to predispose him or her to depressive
Using alpha asymmetry as a starting point, Baehr, Rosenfeld, and
colleagues sought to determine whether changing alpha asymmetry through
neurofeedback could reduce symptoms of depression (Baehr, Rosenfeld, Baehr, & Earnest, 1999; Rosenfeld, 2000).
In the Baehr et al. protocol, the subject hears a clarinet tone only
when the amplitude of alpha (8-12 Hz) measured from the right frontal
cortex is relatively greater than that of alpha measured from the left
frontal cortex. Individuals were asked to maintain the tone and to
increase its pitch for as long as possible during a session lasting
15-30 min. Baehr, Rosenfeld, and Baehr (2001)
recently reported follow-up data on 3 of 6 depressed patients treated
with the alpha asymmetry protocol. Patients showed positive changes in
alpha asymmetry and on the Beck Depression Inventory both immediately
after and 1-5 years following treatment. Similar clinical case studies
(e.g., Hammond 2001; Rosenfeld, Baehr, Baehr, Gotlib, & Ranganath, 1996)
are suggestive of the potential benefits of neurofeedback for the
treatment of depression. Although a mechanism underlying the potential
efficacy of neurofeedback has been articulated and clinical case studies
are suggestive, controlled group outcomes are clearly required. Similar
preliminary findings exist for other disorders, including schizophrenia
(Gruzelier, 2000) and anxiety disorders (Moore, 2000).
It is not possible to make unqualified or categorical conclusions
about the value of neurofeedback as a therapeutic modality. There are
varying degrees of certainty about what is known. First, we have known
for over 100 years that electrocortical activity can be measured and for
over 50 years that different frequencies reflect different states of
arousal. Second, we have known for 25 years that both animals and humans
can learn to alter their brain waves through operant conditioning and
thereby reduce seizures. Third, the work of Hughes and John (1999),
among many others, documents that a number of psychological disorders,
including ADHD, mood disorders, and schizophrenia, may be discriminated
by characteristic patterns of the QEEG. Fourth, although still in its
early stages, research documenting the efficacy of neurofeedback for
ADHD is beginning to accumulate; four different research teams have
demonstrated its efficacy using controlled trials. Finally, outcome
research concerning the efficacy of neurofeedback for other disorders is
still either experimental, or preliminary at best. On the basis of
these findings, we suggest that clinicians begin to give greater
consideration to neurofeedback as part of a multimodal approach,
especially in the treatment of ADHD. We agree with Oubré (2002), who concluded the following:
Neurofeedback is perhaps best viewed not as an alternative to
conventional psychopharmacological agents but rather as one component of
a multimodal approach. When used as an adjunctive treatment in
combination with standard medication, neurofeedback may improve clinical
outcomes in some psychiatric patients. (p. 8)
It is also important to point out that the neurophysiological
mechanisms purported to underlie neurofeedback are consistent with an
emerging model in the neurosciences. This model is based on findings
that timing of electrical activity throughout the brain and between
various regions of the brain play a basic role in the emergence of
psychopathology (Llinas, Ribary, Jenmonod, Kronberg, & Mitra, 1999; McCormack, 1999; Varela, Lachaux, Rodriquez, & Martinerie, 2001).
We encourage practicing psychologists to educate themselves more
fully about the potential of neurofeedback; helping clients to learn to
self-regulate neuronal function can become an important addition to
psychological practice. Recent changes in billing codes include
biofeedback (and EEG biofeedback) as reimbursable, either alone or in
combination with psychotherapy. There are venues that provide clinicians
with training, and most offer continuing education credits approved by
the American Psychological Association. Private groups such as EEG
Spectrum International (www.eegspectrum.com) and Thought Technology
(www.thoughttechnology.com) offer introductory and advanced training in
the skills necessary to begin to integrate neurofeedback into practice.
In addition, the International Society for Neuronal Regulation sponsors
the Journal of Neurotherapy and an annual conference. For those
practitioners interested in referring their clients to clinicians
trained in neurofeedback, the society's Web site (www.snr-jnt.org) lists
providers throughout the world. The Association for Applied
Psychophysiology and Biofeedback focuses on the more general practice of
biofeedback but includes a journal and annual conference that offer
education in EEG biofeedback (www.aapb.org).
Unlike other biological treatment modalities, neurofeedback is
steeped in the history and ethos of psychology. Especially for ADHD,
practicing psychologists would do well to further educate themselves
regarding the modality, as it shows promise as a therapeutic option in
managing this condition.
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