
Neurofeedback Therapy Treatment
for Attention Deficit Disorder
and Other Disorders
|
There is a growing body of research and clinical application
data to support the fact that attention deficit disorder with and without
hyperactivity (ADD), stems from deficits in brain information processing.
In the ADD child's developing brain, cells which normally learn to
interface with one another and take on more and more activity, do not take
on the proper working matrix. This may happen for a variety of reasons and
has no bearing on intelligence. These children have difficulty arousing
brain cell stimulation in an important part of the brain... the
sensorimotor cortex. Arousal is slower than normal and thus the child has
difficulty integrating sensory input from the world with motor reflexes.
When given certain medications such as amphetamine, the brain cells
increase in activity, working at a faster frequency, to communicate
efficiently with one another; the child can now tend to environment
properly and focus attention. Unfortunately this stimulation is short
lived and may have side effects to which some parents are uncomfortable.
Brainwave biofeedback, or neurofeedback, is a specialized field of biofeedback therapy with more than 20 years of research and clinical application. Neurofeedback has been utilized to successfully treat children with certain learning disabilities, ADD, as well as those who exhibit specific developmental disorders in areas such as reading writing, and spelling. More specifically, EEG (electoencephalogram) electrodes are used to measure brainwave activity from the sensorimotor cortex of the brain. The child being measured is given a visual and auditory signal, or feed back, from the computer, and he or she can learn to increase or decrease brainwave activity. With neurofeedback, some children may learn to increase the’stimulation of these sensorimotor neurons, thus facilitating more brain wave activity. Learning to increase amplitude (power) in the 12-32 Hertz (beta, a fast frequency) range while learning to decrease 4-8 Hertz (theta, a slow frequency) are the primary objectives. Once these neurons begin to work properly and network together, they generally will be that way throughout the life of the child and into old age. On Saturday May 16, 1998, National Public Radio's Weekend Edition did a story of Neurofeedback in a Yonkers, New York school district which is using Neurofeedback for its ADD students. You can hear that broadcast by using Real Audio and retrieving it from http://www.npr.org/ramfiles/980516.wesat.09.ram Neurofeedback Yellow Pages lists worldwide providers of Neurofeedback.
Historical Literature Review of EEG Biofeedback (Neurofeedback) In the early 1970s, researchers
proposed several theories and protocols for using neurofeedback as an
assessment and treatment approach for ADHD children. In 1973, Satterfield
proposed a "low-arousal "hypothesis of hyperkinetic children, finding that
under-arousal corresponded to decreased beta amplitudes. Lubar &
Seifert (1975) published the first article dealing with the reduction in
seizure activity by using neurofeedback training. 1976, Lubar & Bahler
published a series of case studies showing the effectiveness of SMR
training in reducing seizures, replicating Sterman's (1973) findings.
These seizure patients also experienced increased attentiveness in school.
The findings led to anther case study by Shouse and Lubar (1976) to
determine the effectiveness of neurofeedback training using SMR
(sensorimotor rhythm) and helping an ADHD child. This blind crossover
study provided the first clear evidence that neurofeedback training,
utilizing SMR with theta inhibition, was an effective way for working with
an ADHD child. In 1976, Lubar began treating ADHD children using
neurofeedback. He found that children with attention and reading
difficulties, but not with hyperactivity problems, produced excessive
theta activity and deficit beta production. In 1985, Lubar, Bianchini,
Calhoun, & Lambert >provided a strong rationale involving theta
suppression. More extensive studies were published following this study,
employing more children (e.g., Janzen, Graap, Stephanson, Marshall, &
Fitzsimmons, 1995; Linden, Habib, & Radojevic, 1996; Lubar 1977,
Lubar, 1991; Lubar & Lubar, 1984; Shouse andLubar, 1978, 1979, Lubar
and Lubar, 1984, Lubar, Swartwood; Swartwood, &O'Donnell, 1995;
Othmer, Kraiser, & Othmer, 1995; Tansey & Bruner, 1983,Tansey,
1984, 1985, 1990). From 1986 to 1991, topographic brain mapping studies
further clarified the difference in EEG's between ADHD and matched
controls. In 1990, Mann, Lubar & Zimmerman, Miller, & Muenchen
found that theta activity was obtained in many locations (frontal and
central) and decreased beta activity was found in many frontal and
temporal locations. These findings demonstrated that ADHD (with
hyperactivity) formed a neurologicallydistinct group from controls.
Furthermore, PET scans found decreased glucose metabolism in areas of the
brain involved in motor activity and attention in ADHD (hyperactive)
versus normal controls (Zametkin, 1986 & Zametkin et al., 1990).
Later, using SPECT (single photon emission computedtomography) Sieg,
Gaffney, & Preston (1995) found brain imaging abnormalities in ADHD.
Using PET and SPECT these researchers also demonstrated that ADHD children
exhibit a maturational delay in the systems affected by. Mann, Lubar,
Zimmerman, et al. (1992) found that the comparison between the brain
mapping of ADHD and non-ADHD boys revealed increased theta production and
decreased beta production in ADHD boys. In addition, the distribution of
EEG >frequency for the ADHD boys corresponded to brain activity
characteristic to younger children. Rossiter and LaVaque (1995)
compared the effectiveness of neurofeedback to stimulant medication in
reducing ADHD symptoms. Their results indicated that neurofeedback is a
viable alternative to the use of stimulant medication. Other more recent
studies (Linden, Habib, & Radojevic, 1996; Lubar, Swartwood,
Swartwood, & O'Donnell, 1995) continue to provide evidence for the
effectiveness of neurofeedback training for ADHD children.
The above section written by Alexander Minevich, M.A. Ontario
Institute for Studies in Education (University of Toronto)
Other applications of Neurofeedback (although considered experimental)
include Substance Abuse Disorders, Depression, Chronic Fatigue Syndrome,
Siezure Disorders, Peak Performance Training and Fibromyalgia.
Publications related to Neurofeedback
Comprehensive Neorofeedback Bibliography
D.Corydon Hammond, Ph.D.
Frank H. Duffy, M.D., a Professor and Pediatric Neurologist at Harvard Medical School, recently stated in an editorial in the January 2000 issue of the journal Clinical Electroencephalography that the scholarly
literature suggests that neurofeedback should play a major therapeutic role in many difficult areas. In my opinion, if any medication had demonstrated such a wide spectrum of efficacy it would be universally accepted and widely used. (p. v) It is a field to be taken seriously by all. (p. vii)
The references below are primarily outcome studies and case reports, with an
occasional reference to significant conceptual papers or reviews. References will occasionally
appear under more than one problem area when the paper deals with more
than one disorder. The following reference provides guidelines for objectively evaluating the
efficacy of neurofeedback treatments:
La Vaque, T.J., Hammond, D. C., Trudeau, D., Monastra, V., Perry, J., Lehrer, P., Matheson, D., &
Sherman, R. (2002). Template for developing guidelines for the evaluation of the clinical efficacy of
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273-281.
Epilepsy
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related techniques for the enhancement of attention.
Applied Psychophysiology &
Biofeedback, 22(2), 111-126.
Sams,
M. W., (1995). Mathematically
derived frequency correlates in cerebral function: Theoretical and
clinical implications for neurofeedback treatment.
Journal of
Neurotherapy,1(2), 1-14.
General Articles on Slow Cortical Potential Neurofeedback
Birbaumer,
N., Elbert, T., Canavan, A. G. M., & Rockstroh, B. (1990).
Slow potentials of the cerebral
cortex and behavior.
Physiological Reviews, 70, 1-41.
Birbaumer,
N., Roberts, L. E.,Lutzenberger, W., Rockstroh, B., & Elbert, T.
(1992). Area-specific
self-regulation of slow cortical potentials on the saggital midline and
its effects on behavior.
Electroencephalography & Clinical Neurophysiology,
84 353-361.
Elbert,
T. (1980). Biofeedback of slow cortical potentials. Part I.
Journal of
Electroencephalography & Clinical Neurophysiology, 48,
293-301.
Elbert,
T., Lutzenberger, W., Rockstroh, B., & Birbaumer, N. (1983).
When regulation of slow brain
potentials fails B A
contribution to the psychophysiology of perceptual aberration and
anhedonia. Advances in
Biological Psychiatry, 13, 98-106.
Kotchoubey,
B., Schleichert, H., Lutzenberger, W., & Birbaumer, N. (1997).
A new method for self-regulation
of slow cortical potentials in a timed paradigm.
Applied Psychophysiology &
Biofeedback, 22(2), 77-93.
Kropp,
P., Siniatchkin, M., & Gerber,W-D. (2002).
On the pathophysiology of
migraine: Links for empirically based treatment
with neurofeedback.
Applied Psychophysiology & Biofeedback, 27(3),
203-213.
Roberts,
L. E., Birbaumer, N., Rockstroh, B., Lutzenberger, W., & Elbert, T.
(1989). Self-report during
feedback regulation of slow
cortical potentials.
Psychophysiology, 26(4), 392-403.
Rockstroh,
B. (1987). Operant control of
slow brain potentials.
Chapter in J. N. Hengtgen, D. Hellhammer, & G. Huppmann (Eds.),
Advanced Methods in Psychobiology.
C. H. Hogrefe, pp.
179-190.
Rockstroh,
B., Birbaumer, N., Elbert, T., & Lutzenberger, W. (1984).
Operant control of spontaneous
EEG, evoked potentials and slow potentials of the brain.
Biofeedback &
Self-Regulation, 9, 139-160.
Rockstroh,
B., Elbert, T., Lutzenberger, W., & Birbaumer, N. (1982).
The effects of slow cortical
potentials on response speed.
Psychophysiology, 19, 211-217.
Siniatchkin,
M., Kropp, P., & Gerber, W-D. (2000).
Neurofeedback
The
significance of reinforcement and the search for an appropriate strategy
for the success of self-regulation.
Applied Psychophysiology & Biofeedback, 25(3),
167-175.
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