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February 1, 2002 - Psychiatric Times. Vol.
19 No. 2
Alondra Oubré, Ph.D.
Neurofeedback, also called electroencephalogram (EEG)
biofeedback or neurotherapy, is an adjunctive treatment used for
psychiatric conditions such as attention-deficit/hyperactivity disorder,
generalized anxiety disorder, posttraumatic stress disorder, phobic
disorder, obsessive-compulsive disorder, bipolar disorder, depression
and affective disorders, autism, and addictive disorders (Moore,
2000; Rosenfeld, 2000; Trudeau, 2000).
In an interview with Psychiatric Times, Siegfried
Othmer, Ph.D., chief scientist at EEG Spectrum International Inc.,
described neurofeedback as neuroregulation in the time and frequency
domains through the use of bioelectrical operant conditioning. Like
repetitive transcranial magnetic stimulation (rTMS), neurofeedback
is an innovative form of electrotherapeutics that complements neurochemical
interventions for mood disorders. "With the use of anticonvulsants
as mood stabilizers," Othmer said, "we have seen a convergence
of psychiatry and neurology in the field of pharmacology. Similarly,
neurofeedback signals a convergence of psychiatry and neurology
in bioelectrical approaches to treating affective disorders. By
stabilizing the brain and rewarding it for holding particular states,
neurofeedback acts as a natural anticonvulsant." The rationale
for using neurofeedback therapeutically is that it corrects deficits
in brain cerebral regulatory function related to arousal, attention,
vigilance and affect (Othmer et al., 1999).
During neurofeedback sessions, patients learn to produce
desirable brain wave patterns displayed on a computer screen by
controlling the activity of a computerized game or task seen on
a second screen. Increases in the amplitude of slow spindle activity
are instantaneously rewarded. The reward corresponds to the earned
score, similar to scores accumulated in a computer game (Othmer,
1999).
Neurofeedback represents a window of opportunity for
assessing and shifting any given brain state (Manchester et al.,
1998). The designated frequency band determines which brain state
is rewarded (Othmer, 1999). Beta (15 Hz to 18 Hz) training usually
produces a slightly upward shift in arousal levels, leading to increased
wakefulness and attentiveness or to decreased depression. The sensorimotor
rhythm (SMR) (12 Hz to 15 Hz) elicits a slightly downward shift
in arousal. The SMR is associated with subjective feelings of relaxation,
emotional calm and centeredness (Othmer, 1999). Combined left-side,
ß-SMR and right-side - neurofeedback is often used to treat
brain wave dysregulation associated with traumatic memories. Right-side
training is also employed for social and emotional deficits such
as conduct disorder, autism and reactive attachment disorder (Othmer,
2000; Othmer et al., 1999).
Assessment of Clinical Evidence
The efficacy of neurofeedback in the treatment of
seizure and pseudoseizure disorders has been well documented in
peer-reviewed literature for over 25 years (Lubar, 1997; Swingle,
1998). On the whole, however, clinical support for the effects of
neurotherapy is limited and based primarily on case studies, rather
than randomized, controlled, blinded studies. While Joel Lubar,
Ph.D., professor of psychology at University of Tennessee in Knoxville,
recognizes the shortage of randomized trials on neurofeedback, he
told PT that matched-group studies conducted in accordance with
the Declaration of Helsinki are more appropriate than controlled
trials for studying hyperactivity. He noted that 1,500 groups worldwide
currently use neurofeedback for psychiatric applications, including
attention-deficit/hyperactivity disorder (ADHD) and comorbidities.
Since the 1970s, his team has investigated various interventions
for treating hyperactivity in children and found EEG to be superior.
Lubar and his colleagues (1995) evaluated the effects
of neurofeedback treatment on ADHD in 19 youth, ages 8 years to
19 years, under relatively controlled conditions. The subjects received
one-hour sessions of ß brain wave training daily for up to
40 hours over a two- to three-month period. The goal of the therapy
was to increase 16 Hz to 20 Hz (ß) activity while reducing
the amplitude of brain waves (4 Hz to 8 Hz). Compared to pre-training
results, post-training changes showed improvements in Test of Variables
of Attention (TOVA) scores, Attention Deficit Disorders Evaluation
Scale (ADDES) behavior ratings and Weschler Intelligence Scale for
Children-Revised (WISC-R) performance. Twelve out of 18 subjects
with pre-/post-TOVA scores had EEG-responsive improvements on an
average of three of four possible scales. This change was comparable
to pre-/post-medication differences in TOVA scores in youth with
ADHD.
While TOVA scores typically return to baseline when
the effects of pharmacotherapy wear off, the TOVA scores of the
EEG-responsive subjects remained at the improved level. Significant
post-test increases in IQ scores were observed in 10 EEG-responsive
subjects who had been tested on the WISC-R two years earlier. Parental
and teacher ratings of the children's behavior also improved following
neurofeedback training. Thus, in the EEG-responsive youth, behavioral
improvements corresponded with increased scores on TOVA and WISC-R.
Lubar and his associates cautiously concluded that EEG neurofeedback
training is a powerful adjunctive technique for treating ADHD when
used as part of a multi-component therapeutic approach.
Additional research suggests that EEG neurofeedback
may be an effective alternative to psychostimulants in the treatment
of ADHD if medication is ineffective or has adverse effects or if
patients are noncompliant (Rossiter and La Vaque, 1995). In one
case study, a 36-year-old female diagnosed with
ADHD, temporal seizure disorder and borderline personality disorder
received 30 weekly sessions of SMR neurofeedback training and carbamazepine
(Tegretol) (Hansen et al., 1996). The patient initially was reluctant
to take carbamazepine but became compliant after starting neurofeedback
training. However, because of the drug's side effects, she stopped,
restarted and then again discontinued her medication. Following
17 sessions of neurofeedback, her quantitative EEG (QEEG) showed
relative powers within normal ranges. Carbamazepine increased the
favorable effect of neurofeedback on TOVA performance in the early
phase of treatment. Although the subject's TOVA scores fluctuated
as she went on and off carbamazepine, all four scales were normal
months after she ceased taking carbamazepine. At that time, her
TOVA performance showed no evidence of attentional deficit.
In a survey, 36 children, ages 6 years to 17 years,
receiving EEG neurofeedback as a treatment for attention-deficit
disorder (ADD)/ADHD were evaluated for changes in both subjective
and objective clinical parameters (Alhambra et al., 1995). After
20 sessions, subjective improvement based on parental observations
was 86%. In objective assessments, the overall improvement was 74%
for TOVA score and 78% for favorable changes in QEEG parameters.
Over a 12-month period, neurofeedback was associated with either
a decrease or termination of pharmacotherapy in 16 of 24 patients
receiving medication for ADD/ADHD.
In a retrospective study, 11 females, ages 12 years
to 21 years, diagnosed with dissociative identity disorder (DID)
received 30 neurofeedback and 10 group sessions (Manchester et al.,
1998). The treatment was designed to increase prefrontal ß
activity for alertness and simultaneously enhance activity associated
with a reverie state. The combined increase of ß and brain
waves allowed patients to re-experience their traumatic memories
while in a hypnagogic reverie state but free of the distortions
that arise during dreaming or hypnosis. The ratio of to ß
activity is crucial in this type of training. If activity becomes
too high, patients may sink into an unconscious state and not remember
their past experiences. Three to 27 months following neurofeedback
training, the post-treatment score for the DID group was 82, falling
within the range of normal values. By bringing dissociated information,
affect and sensation into consciousness, neurofeedback training
helped subjects to resolve conflicts that contributed to their dissociative
defense symptoms.
Neurofeedback resulted in favorable changes between
pre- and post-treatment scores on the Minnesota Multiphasic Personality
Inventory-2 (MMPI-2) in a 65-year-old woman diagnosed with a major
depressive disorder and in a 42-year-old woman with chronic psychological
maladjustment (Baehr et al., 1997). The researchers concluded that
even though EEG asymmetry training is not an efficacious stand-alone
therapy for depression, it is an effective adjunct to psychotherapy
for treating certain mood disorders.
Certain neurofeedback protocols may be beneficial
for treating anxiety disorders (Moore, 2000), but the success of
particular neurofeedback protocols for anxiety may depend on which
diagnostic categories are used (Thomas and Sattlberger, 1997). Case
studies on the effects of neurofeedback on bipolar disorder (BD)
have produced mixed results. Although Rosenfeld (2000) was unsuccessful
in treating two patients with BD using a neurofeedback protocol,
Othmer (2001) found neurofeedback to be effective in managing mood
swings in pediatric patients with BD when combined with pharmacotherapy
and psychotherapy. In the Othmer case studies, neurofeedback protocols
that directly affect inter-hemispheric communication were most efficacious
for children diagnosed with BD.
In addition, EEG neurofeedback may have limited applicability
for treating psychotic symptoms. Researchers successfully used neurofeedback
to modulate slow potentials in schizophrenic and schizotypal subjects
in the subacute phase (Gruzelier, 2000). And several studies show
that neurofeedback is efficacious for long-term recovery in substance
abusers (Kaiser et al., 1999; Trudeau, 2000).
Future Directions
Despite positive evidence from case studies, Russell
A. Barkley, Ph.D., professor of psychiatry and neurology at University
of Massachusetts Medical School, disputes claims that EEG neurofeedback
has an effect on ADHD. Barkley told PT that EEG neurofeedback is
not supported by evidence-based medicine. "One chief problem,"
he warned, "is that pre- and post-changes occur in subjects
with ADHD regardless of whether or not they receive neurofeedback."
Barkley attributed reported improvements in objective measures of
ADHD symptoms (such as parent and teacher rating scales of disruptive
behavior) to the practice effect. "Because of the lack of adequately
designed studies, any effects associated with EEG neurofeedback
may be due to the placebo response," Barkley said.
However, Lubar et al's. 1995 study provided comparative
pre- and post-treatment measurements of several parameters in subjects
with ADHD who improved and in those who did not. As noted, the pre-/post-changes
observed in the neurofeedback-responsive treatment group were nearly
equivalent to changes reported for pre-/post-medication in subjects
with ADHD. Other studies comparing the effects of EEG neurofeedback
and psychostimulants reveal that neurofeedback produces post-treatment
changes equal to those associated with pharmacotherapy (Nash, 2000).
Based on these findings, supporters argue that neurofeedback achieves
its therapeutic effects by acting on electrophysiological substrates
of the brain and not via a placebo response (Othmer et al., 1999).
"Critics of EEG neurofeedback hold this treatment
to more rigid standards than many of the drug treatments,"
David F. Velkoff, M.D., medical director of the Drake Institute
of Behavioral Medicine in Los Angeles, who has treated over 1,000
patients with neurotherapy, told the press. "Yet unlike drugs,
neurofeedback is benign." According to Frank H. Duffy, M.D.,
associate editor for Clinical Electroencephalography, any pharmaceutical
drug that had as wide a range of effectiveness as neurofeedback
would be universally accepted and widely used (Duffy, 2000).
Although neurofeedback remains an investigational
therapy (Baydala and Wikman, 2001), the growing number of case studies
on this therapy are compelling enough to warrant controlled clinical
trials with adequate sample sizes that can generate replicable data.
"Alternative research designs involving sham neurofeedback
are already in use as well as comparative investigations of neurofeedback
with both conventional treatments and with combined treatments consisting
of neurofeedback and psychostimulants," according to Lubar.
"The Association for Applied Psychophysiology and Biofeedback
[AAPB] is currently developing application standards for ethical
controlled studies of neurofeedback that simultaneously protect
patients and the integrity of research investigations."
In summary, preliminary evidence suggests that psychopharmacological
and electrophysiological approaches to the treatment of mood and
behavioral disorders are not intrinsically contradictory. 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 certain clinical outcomes in some psychiatric
patients.
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