The Scientific Review of Mental Health Practice

Objective Investigations of Controversial and Unorthodox Claims in Clinical Psychology, Psychiatry, and Social Work


Reply to Kline, Brann, and Loney (2002), "A Cacophony in the Brainwaves"

I have read with concern the paper by Kline, Brann, and Loney (2002) entitled "A Cacophony in the Brainwaves." Neurofeedback treatment for attention deficit disorder (ADD) has grown enormously since the early 1990s, even though the groundwork was laid in our original studies published in the 1970s. More than 2,000 practitioners are using these approaches in the United States, China, Japan, Israel, Australia, and many European countries. The International Society for Neuronal Regulation (ISNR) now has close to 700 members employing neurotherapy as well as more than 600 members in the EEG Biofeedback Division of the Association for Applied Psychophysiology and Biofeedback. Many practitioners use neurotherapy to treat ADD and other disorders. It is often true in clinical practice that techniques are used before all of the necessary scientific studies have been completed. However, I wish to point out where considerable progress has been made.

The main impetus of our earlier studies was to initiate the field and to show that there is a rationale, specifically, that EEG differences exist between individuals with ADD and nonclinical controls. Furthermore, training these differences toward the normal range results in considerable improvement. It is true that the earlier studies, with one exception, were not highly controlled in terms of being randomized, double-blind crossover studies or matched, randomized group studies. Actually, our first study was published in 1976 on a single case. A 1977 chapter that I wrote for the first volume of Advances in Clinical Child Psychology reviews our initial studies in the area of epilepsy research as well as research on ADD. The ADD study described is the only ABA crossover blind study that has been conducted. If it had not yielded the positive results it did, I would probably have not pursued developing this area. The blind component involved independent observers in the classroom who had no knowledge of which portion of the study the patients were engaged in, and the patients were blind in terms of not knowing which conditions were being reinforced and inhibited. Unfortunately, because of the Declaration of Helsinki we are now no longer allowed to conduct studies of this kind because we are subjecting individuals to a condition that might be deleterious, namely, the reversal of the positive feedback conditions. However, other designs are equally appropriate.

In my workshops and writings, I have been critical of the early studies because, as I pointed out, they often lacked adequate controls. However, a great deal of work has been conducted since then. Therefore, I will briefly discuss some of the newer studies that have been carried out. Monastra, myself, and others published two studies in Neuropsychology in which we developed a single- channel database with more than 800 cases. If one examines these studies, one will see that there is a very large and statistically significant difference in terms of theta-beta power ratio measures for individuals with ADD compared with nonclinical controls. In our second study, we cross-validated these measures with more conventional measures that are used in the initial evaluation of individuals to place them into the appropriate group, namely, ADD or non-ADD. Although there are problems with the test of variables of attention (TOVA), the Connors, and the integrated audio and visual test (IVA) as continuous performance measures, we have obtained similar results using at least the IVA and the TOVA in terms of identifying many individuals with ADD. We have also used such additional measures as the Paced Serial Auditory Addition Test (PASAT), drawing tasks, puzzle tasks, and the Wisconsin Card Sorting Test.

I would like to particularly encourage readers to examine the research of Thomas Fuchs, which is a replication of our work, and which yields results very similar to those of Rossiter and LaVaque. The results obtained with neurofeedback and no treatment are comparable with those obtained with methylphenidate (Ritalin) and no treatment. Because of the positive outcome of this study, these investigators are engaged in a large, multicenter study involving a number of European centers. This study should greatly strengthen the argument that neurofeedback is not a placebo and holds its own under controlled conditions. The other study will soon be published in Applied Psychophysiology and Biofeedback. This is a superb investigation of 100 subjects by Monastra's group, which compares the effectiveness of EEG feedback and Ritalin under tightly controlled conditions. Furthermore, this study shows that EEG feedback produced better results than medication alone, with other variables being held constant. There is another study in progress in a military academy, under highly controlled conditions, in which one group is receiving noncontingent feedback and the other group is receiving contingent neurofeedback, with all other influences held constant in terms of medication, counseling, psychotherapy, and other variables.

One of the concerns I had in reading Kline et al.'s paper was the criticism of the databases. I believe that we are on extremely strong ground in this area. Only the study of Kupferman et al. (1996) did not yield the same results as all the other studies, including ours. There are now two studies, including a 1998 study by Clarke et al. and Chabot and Serfontain (1996) with over 400 cases, that replicate our findings. It is now clear that there is a primary pattern associated with ADD seen in many cases of excessive central and frontal theta activity or a combination of theta and low alpha activity. In adults, we see increased 8-10 hertz activity with decreased beta in many cases. A subgroup of individuals (possibly with a combination of ADD and oppositional defiant disorder) is characterized as irritable, in which there is excessive frontal beta. However, many of these individuals also have excessive central theta. The point is that with discriminant function analysis and careful quantitative EEG evaluation, we are approaching 90% accuracy in terms of discriminating ADD and non-ADD individuals, as measured by other "gold standard" techniques. Another implication of Kline et al.'s review is that some of the theta activity that is often reported is due simply to posterior migration of artifact from eye movements and eye blinks. It is important to point out that those of us who have worked in this area for more than 30 years include myself, Robert Thatcher, Jay Gunkleman, Cory Hammond, E. Roy John, Robert Chabot, William Hudspeth, and others. Many of us perform EEG analyses on a daily basis and have examined thousands of EEGs. We are very well versed in the area of artifact evaluation and reduction. I have employed guard channels for EMG and eye movements to determine whether this increases our ability to discriminate artifacts. We have found a number of ways of preparing patients for recording EEG whereby most of these artifacts are tremendously reduced. In addition, we have developed programs that allow us to remove from the EEG any frontal artifact due to eye movement, blinks, and tongue movement that can occur and can be represented even more posteriorly. We can identify and remove bursts of muscle activity and other non-EEG types of activity. The implication that people who have had years of experience in evaluating EEGs are missing artifacts and that the increased theta activity is simply a reflection of artifacts in the EEG is unwarranted. This implication leaves the readers with the impression that those of us who perform quantitative EEG analyses are not well trained in our ability to detect artifacts and remove them.

If one examines all of the studies involving quantitative EEG, PET, SPECT and FMRI, there is no doubt that ADD is a substantially neurological disorder. In a July 2000 presentation, Russell Barkley acknowledged openly that ADD is associated with brain damage, is serious, is neurological, and that people who have ADD should be evaluated neurologically by PET scanning and related methods. This is a radical departure from his earlier point of view that ADD is merely a behavioral disorder, or from earlier models that it is due to poor parenting. Kenneth Blum and his colleagues, David Cummings, Eric Braverman, and others have shown that specific alleles on chromosome 6 and 11 associated with dopamine D2 and D4 receptors are markers for ADD and that these alleles occur in approximately 50% of individuals with ADD. There are studies now under way to examine the relationship between quantitative EEG and genetic expression of these dopamine alleles. Because it is clear that ADD/HD and its subtypes are neurological and substantially heritable, and that neurological markers for this disorder exist in terms of quantitative EEG, neurofeedback has a clear rationale. Readers will find that as the controlled studies become better and appear more frequently, it may be necessary for Kline et al. to reverse or retract many of their assertions. In addition, the longest long-term study of the effectiveness of Ritalin mentioned at the meeting of the Academy of Pediatrics was only 18 months. In 1995 I published a chapter in the book Biofeedback: A Clinician's Guide (Schwartz, 1995), which included data on 51 individuals who were followed for up to 10 years and who were evaluated blindly by an independent professional evaluator using telephone interviews so that the samples were not selected. Using the Conner's Teacher Rating Scale, we found long-term significant improvements in all of the domains assessed by this scale. Individuals who are treating ADD are reporting excellent clinical results and long-term follow-ups. Kline et al. did not even mention the 1999 paper by Thompson and Thompson published in Biofeedback and Self Regulation, which included approximately 100 cases. I have also compiled a listing of peer-reviewed published studies on QEEG evaluation and neurofeedback. This list was updated in August 2002. Kline et al. did not cite many of the studies on this list.

We believe that it is important for Kline et al. and their colleagues to consider attending some of the meetings and workshops offered by the professional organizations in the neurofeedback area and to interact with us directly. If they do, I believe that they will be persuaded that this field has advanced rapidly, that it is satisfying increasingly stringent scientific standards, and that it should not be associated with the term "pseudoscience" in any way.

Joel F. Lubar, Ph.D.
Professor of Psychology and Clinical Psychophysiologist
President Elect of the International Society for Neuronal Regulation


Chabot, R., & Serfontain, G. (1996). Quantitative electroencephalographic profiles of children with attention deficit disorder. Biological Psychiatry, 40, 951-963.

Clarke, A., Barry, R., McCarthy, R., & Selikowitz, M. (1998). EEG analysis in attention-deficit/hyperactivity disorder: A comparative study of two subtypes. Psychiatric Research, 81, 19-29.

Kline, J. P., Brann, C. N., Loney, B. A. (2002). A cacophony in the brainwaves. The Scientific Review of Mental Health Practice, 1(1), 44-54.

Lubar, J. F., & Shouse, M. N. (1977). Use of biofeedback in the treatment of seizure disorders and hyperactivity. In B. B. Lahey and A. E. Kazdin (Eds.), Advances in child clinical psychology (pp. 204-251). New York: Plenum Publishing Company.

Lubar, J. F. (1995). Neurofeedback for the Management of Attention Deficit Hyperactivity Disorders. In M. S. Schwartz (Ed.), Biofeedback: A practitioner's guide (2nd ed., 493-522). New York: Guilford Publications, Inc.

Lubar, J. F., & Shouse, M. N. (1976). EEG and behavioral changes in a hyperkinetic child concurrent with training of the sensorimotor rhythm (SMR): A preliminary report. Biofeedback and Self Regulation, 3, 293-306.

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Monastra, V. J., Lubar, J. F., Linden, M., VanDeusen, P., Green, G., Wing, W., Phillips, A., & Fenger, T. N. (1999). Assessing attention deficit hyperactivity disorder via quantitative electroencephalography: An initial validation study. Neuropsychology, 13(3), 424-433.

Monastra, V. J., Lubar, J. F., & Linden, M. K. (2001). The development of a quantitative electroencephalographic scanning process for attention deficit-hyperactivity disorder: Reliability and validity studies. Neuropsychology, 15(1), 136-144.

Rossiter, T. R., & LaVaque, T. J. (1995). A comparison of EEG biofeedback and psychostimulants in treating attention deficit hyperactivity disorder. Journal of Neurotherapy, 1(1), 48-59.

Schwartz, M. (1987). Biofeedback: A practitioner's guide (2nd ed.). New York: Guilford Press.

Thompson, L., & Thompson, M. (1998). Neurofeedback combined with training in metacognitive strategies: Effectiveness in students with ADD. Applied Psychophysiology and Biofeedback, 23(4), 243-263.

Editor's Note: Kline and his colleagues were afforded the opportunity to respond, but declined.

You can read this correspondence in
The Scientific Review of Mental Health Practice, vol. 2, no. 1 (Spring/Summer 2003).
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