Attention
Deficit/Hyperactivity Disorder: EEG Biofeedback as a Viable Treatment
Option
Cheryl H.
Alexander, Ph.D.
Attention Deficit/Hyperactivity Disorder (ADHD) is one of the most
prevalent and perplexing disorders of childhood and is estimated to
affect three to five percent of school-age children (American
Psychiatric Association, 1994, p. 82). The fourth edition of the
Diagnostic and Statistical Manual of Mental Disorders (DSM-IV)
describes the essential feature of ADHD as “a persistent pattern of
inattention and/or hyperactivity-impulsivity that is more frequent and
severe than is typically observed in individuals at a comparable level
of development” (American Psychiatric Association, 1994, p. 78).
Attention Deficit/Hyperactivity Disorder can lead to emotional and
behavioral problems, difficulty with peer relationships, difficulty
within the family, and can be one of the reasons for academic and
school difficulties (Silver, 1993).
Existing in
all countries and cultures, ADHD is a pervasive lifelong disorder
which is not curable although it is manageable (Lubar, Swartwood,
Swartwood & O’Donnell, 1995). Historically, treatment of the
hyperactive child has predominantly consisted of either stimulant drug
therapy or the utilization of behavior modification and operant
conditioning techniques. Both stimulant drug therapy and behavior
modification therapy have been effective in treating some of the
symptoms of ADHD such as those related to motor function and
undesirable behaviors, but have been relatively ineffective in
treating attentional deficits, high distractibility, low frustration
tolerance, information processing, and emotional lability (Tansey &
Bruner, 1983). Research also indicates that long term effects of the
widely used stimulant medication Ritalin on certain academic or
cognitive tasks such as reading are limited (Barkley & Cunningham,
1978). In addition, when stimulant drug therapy is discontinued and
the medication is out of the body, ADD/ADHD behaviors return (Lubar &
Lubar, 1999).
Currently,
there is much concern over the widespread use of medication as a
treatment for ADHD; it is estimated that several million children are
currently taking stimulant medications in order to control
hyperactivity and inattention. Many people feel that stimulant
medications are overprescribed to ADHD children in an attempt to
relieve parents and teachers from the difficult task of dealing with
the symptoms associated with this disorder.
Because behavior
modification and drug therapy are of limited benefit for the treatment
of ADHD and because there may be repercussions and adverse
side-effects associated with drug therapy, it is important that more
effective, alternative therapies are available for the treatment of
ADHD.
Research
indicates that the primary symptoms of Attention Deficit/Hyperactivity
Disorder (inattentiveness, impulsiveness, and hyperactivity, as well
as their various manifestations) are secondary symptoms resulting from
an underlying neurological disorder. Lubar (1991), Tansey (1993), and
Lubar et al. (1995) have reported that electroencephalographic (EEG)
biofeedback treatment can be an appropriate and efficacious
treatment for children with ADHD. This treatment involves measuring
brainwaves with an EEG and then feeding this information back to the
patient in an effort to increase the patient’s voluntary control over
these physiological responses.
Brainwaves are measured in
Hertz (Hz), or cycles per second and are usually divided into four
major frequency bands: beta (above 12 Hz), alpha (8 - 12 Hz), theta (4
- 8 Hz), and delta (1 - 4 Hz). Each frequency band is traditionally
associated with generalized behavioral correlates. For example, the
fastest frequency band, beta, is associated with focused attention,
active concentration, and is considered a high arousal level. Alpha, a
non-drowsy state, is associated with relief from attention and
concentration. Theta is associated with drowsiness and dreaming, and
is considered a low arousal level. The slowest frequency band, delta,
is normally associated with deep, dreamless sleep.
Research
indicates that children receiving EEG biofeedback training to inhibit
theta (4 - 8 Hertz) and increase beta (13 - 30 Hertz), showed
significant and sustained improvements in school performance and
psychometric measures such as grade point average and achievement
tests (Lubar & Lubar, 1984). A possible behavioral theory that may
account for these results is that through the process of learning EEG
biofeedback, the children are also learning skills to improve their
concentration and attention-spans. Another theory is that the EEG
biofeedback training increases activity in parts of the brain where
there has been a lack of activity. This increase in activity causes
the brain to form new neural pathways and therefore new learning,
which may be demonstrated as improved performance on achievement
tests.
REVIEW OF LITERATURE
In this section,
the history of the disorder which is now known as Attention
Deficit/Hyperactivity Disorder is reviewed. The most relevant
research and theory that provides a rationale for the treatment of
ADHD children with electroencephalographic (EEG) biofeedback
techniques is presented.
The first
description of children who were hyperactive was given in a series of
lectures in 1902 by an English pediatrician, George Still (Ross &
Ross, 1976). These children were labeled as having “defects in moral
control” and this concept remained intact until after the severe
influenza outbreak of 1918. Hohman (1922) and Kennedy (1924) noted
that many children who recovered from influenza-related encephalitis
developed hyperactive behavior, inattentiveness and impulse control
problems. These children were referred to as “organically driven”
because it was discovered that they had suffered brain damage as a
result of the encephalitis. It was thus inferred at this time that
hyperactivity in children was a direct result of brain damage.
In the 1940’s,
it became widely recognized that not all hyperactive children had
suffered some form of overt brain damage. Since it was believed that
even when brain damage could not be demonstrated it could be presumed
to be present, Strauss and Lehtinen (1947) developed the concept of
minimal brain dysfunction (MBD).
In order to help
clarify the diagnosis of minimal brain dysfunction, neurologists began
searching for abnormalities within the EEG records of MBD children.
Jasper, Soloman, and Bradley (1938) presented evidence that MBD
children had abnormalities in their EEG records, primarily in terms of
slow EEG activity (4 - 8 Hertz). A number of other individuals such
as Cohn and Nardin (1958) have also reported EEG abnormalities in MBD
children.
By the early
1970’s, it became clear that the concept of the MBD syndrome
encompassed several different disorders including the hyperkinetic
disorder, specific learning disabilities (LD), disorders of attention,
and disorders of conduct. As MBD became too broad a label for children
with attention and hyperactivity disorders, the term hyperkinetic
disorder replaced minimal brain dysfunction syndrome.
Also during the
early 1970’s, a hypothesis that became known as the “low-arousal
hypothesis” of hyperkinesis was proposed by Satterfield and Dawson
(1971) and Satterfield, Lesser, Saul, and Cantwell (1973). The idea of
arousal can be traced back to Pavlovian ideas of the excitatory
strength of the nervous system (Harre & Lamb, 1983). However, it was
Hans J. Eysenck (1967) who theorized that individuals differ in
habitual levels of arousal in the cortex. For example, Eysenck
proposed that extroverts have a lower level of arousal and hence are
more excitable and seek more stimulation. Following along these lines
of reasoning, it was proposed by Satterfield and his colleagues that
hyperkinetic children easily habituated to sensory stimulation and
therefore constantly sought stimulation because of their low arousal.
This hypothesis made sense of the well known but little understood
fact that stimulants had a paradoxical effect on hyperkinetic
children.
Inspired by
Satterfield’s work and M. B. Sterman’s work, Lubar conducted a study
using EEG biofeedback employing sensorimotor rhythm training to
determine if this might be a viable modality for helping children with
hyperkinesis (Lubar & Shouse, 1976). The results from Lubar’s blind
crossover study provided the first clear evidence that this was a
powerful modality for working with the hyperkinetic disorder.
In 1984, Lubar
and Lubar found ADHD children had significant and sustained
improvements in school performance and on psychometric measures after
participating in a combination of sensorimotor rhythm (SMR) training
followed by training to increase beta and inhibit theta. Lubar’s work
has been replicated by Michael Tansey and his colleagues (Tansey &
Bruner, 1983; Tansey, 1990).
Other studies
have shown that ADHD children have increased theta and decreased beta
present in their EEG records. For example, Mann, Lubar, Zimmerman,
Miller, and Muenchen (1992) found, by looking at the sixteen-channel
topographic brain maps of 25 nine to twelve-year-old right-handed
males with ADHD, increased theta and decreased beta as compared to 27
controls matched for age and grade level.
In a different
type of study, Zametkin, Nordahl, Gross, King, Semple, Rumsey,
Hamburger, & Cohen, (1990) used positron-emission tomography (PET) to
measure cerebral glucose metabolism in hyperactive adults and normal
adult controls. The metabolism of glucose (a sugar which is used as
an energy supply for the brain) as measured by the PET, indicates
areas in the brain that are active. They found that both global and
regional glucose metabolism was reduced in the hyperactive adults,
specifically in regions of the brain that have been postulated to be
involved in the control of attention and motor activity. This study
represents independent medical verification of frontal hypometabolism
in hyperactives and thus lends support to the use of EEG biofeedback
as a treatment modality for ADHD children.
The reviewed
studies (Lubar & Shouse, 1976; Lubar & Lubar, 1984; Tansey & Bruner,
1983; and Tansey, 1990) indicate that EEG biofeedback training that
focuses on inhibiting theta and increasing beta is an effective
treatment for children with Attention
Deficit/Hyperactivity Disorder.
REFERENCES
Alexander, C. H. (1997). The
impact of EEG biofeedback treatment sessions on the theta/beta ratio
of children with attention deficit/hyperactivity disorder.
American Psychiatric
Association. (1994). Diagnostic and statistical manual of mental
disorders (4th ed.). Washington, DC: Author.
Barkley, R. A., &
Cunningham, C. E.(1978). Do stimulant drugs improve the academic
performance of hyperkinetic children? Clinical Pediatrics, 8,
137 - 146.
Cohn, R., & Nardin, J.
(1958). The correlation of bilateral occipital slow activity in the
human EEG with certain disorders of behavior. American Journal of
Psychiatry, 115, 44 - 54.
Eysenck, H. J. (1967. The
biological basis of personality. Illinois: C. C. Thomas.
Harre, R., & Lamb, R.
(Eds.). (1983). The encyclopedic dictionary of psychology (p.
29). Massachusetts: MIT Press.
Hohman,
L. B. (1922). Post-encephalitic behavior in children. Johns Hopkins
Hospital Bulletin, 33, 372 - 375.
Jasper, H. H., Soloman, P., &
Bradley, C. (1938). Electroencephalographic analysis of behavior
problems in children. American Journal of Psychiatry, 95, 641 -
658.
Kennedy, R. (1924).
Prognosis of sequelae of epidemic encephalitis in children.
American Journal of Diseases of Children, 28, 158 - 172.
Lubar, J. F. (1991).
Discourse on the development of EEG diagnostics and biofeedback for
attention-deficit/hyperactivity disorders. Biofeedback and
Self-Regulation, 16 (3), 201 - 225.
Lubar, J. F., & Shouse, M.
N. (1976). EEG and behavioral changes in a hyperactive child
concurrent with training of the sensorimotor rhythm (SMR). A
preliminary report. Biofeedback and Self-Regulation, 1, 293 -
306.
Lubar, J. F., Swartwood, M.
O., Swartwood, J. N., & O’Donnell, P. H. (1995). Evaluation of the
effectiveness of EEG neurofeedback training for ADHD in a clinical
setting as measured by changes in T.O.V.A. scores, behavioral ratings,
and WISC-R performance. Biofeedback and Self-Regulation, 20
(1), 83 - 99.
Lubar, J. O., & Lubar, J. F.
(1984). Electroencephalographic biofeedback of SMR and beta for
treatment of attention deficit disorders in a clinical setting.
Biofeedback and Self-Regulation, 9 (1), 1 - 23.
Lubar, J. O., & Lubar, J. F.
(1999). Neurofeedback assessment and treatment for Attention
Deficit/Hyperactivity Disorders. In J. R. Evans & A. Abarbanel
(Eds.), Introduction to Quantitative EEG and Neurofeedback.
San Diego: Academic Press.
Mann, C. A., Lubar, J. F.,
Zimmerman, A. W., Miller, C. A., & Muenchen, R. A. (1992).
Quantitative analysis of EEG in boys with
attention-deficit-hyperactivity disorder: controlled study with
clinical implications. Pediatric Neurology, 8 (1), 30 - 36.
Ross, D., & Ross, S. (1976).
Hyperactivity: Research, theory, and action. New York: John
Wiley.
Satterfield, J. H., &
Dawson, M. E. (1971). Electrodermal correlates of hyperactivity in
children. Psychophysiology, 8, 191 - 197.
Satterfield, J. H., Lesser,
L. I., Saul, R. E., & Cantwell, D. P. (1973). EEG aspects in the
diagnosis and treatment of minimal brain dysfunction. Annals of the
New York Academy of Sciences, 205, 274 - 282.
Silver, L. B. (1993). Dr.
Larry Silver’s advice to parents on attention-deficit hyperactivity
disorder. Washington, DC: American Psychiatric Press.
Strauss, A. A., & Lehtinen,
L. E.(1947).Psychopathology and education of the brain-injured
child. New York: Grune and Stratton.
Tansey, M. A. (1990).
Righting the rhythms of reason: EEG biofeedback training as a
therapeutic modality in a clinical office setting. Medical
Psychotherapy, 3, 57 - 68.
Tansey, M. A. (1993).
Ten-year stability of EEG biofeedback results for a hyperactive boy
who failed fourth grade perceptually impaired class. Biofeedback
and self-regulation, 18 (1), 33 - 44.
Tansey, M. A., & Bruner, R.
L. (1983). EMG and EEG biofeedback training in the treatment of a
10-year-old hyperactive boy with a developmental reading disorder.
Biofeedback and self-regulation, 8 (1), 25 - 37.
Zametkin, A. J., Nordahl, T.
E., Gross, M., King, A. C., Semple, W. E., Rumsey, J., Hamburger, S.,
& Cohen, R. M. (1990). Cerebral glucose metabolism in adults with
hyperactivity of childhood onset. The New England Journal of
Medicine, 323 (20), 1361 - 1366.
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