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Applications of EEG - Neurofeedback for Attention Deficit Disorder T. Druckman, M.Ed., A. Minevich, M.A. 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 demonstrating a reduction in seizure activity by using neurofeedback training. Lubar & Bahler (1976) published a series of case studies showing the effectiveness of Sensorimotor Rhythm (SMR) training in reducing seizures, replicating Sterman's (1973) findings. These seizure patients also experienced increased attentiveness in school. The findings led to another case study by Lubar and Shouse (1976) to determine the effectiveness of neurofeedback training using SMR 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. Lubar noticed that those children with ADHD, with or without hyperactivity, demonstrated a difference in specific types of brain waves. For example, the "Beta" brain wave was found to be significantly lower in shape and frequency compared to "Theta" activity, which was higher in amplitude. More specifically, he found those children with attentional 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 and Lubar, 1979; Lubar and Lubar, 1984; Lubar, Swartwood; Swartwood, & O'Donnell, 1995; Othmer, Kraiser, & Othmer, 1995; Tansey & Bruner, 1983; Tansey, 1984, 1985, 1990). Recently, Lubar et al. (1995) have concluded that for children, under the age of 14, the reduction in Theta activity seems to be the key component correlated with betterment in ADHD. These authors suggest that there is a maturational lag that is reflected in the persistence of excessive Theta activity for ADHD subjects when compared to age-dependent norms. For adults, the findings have shown that increasing the amplitude and duration of Beta brain wave activity seems to be of primary importance. From 1986 to 1991, topographic brain mapping studies further clarified the difference in EEG's between ADHD and matched controls. In 1992, 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 neurologically distinct 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 -- cited in Lubar seminar AAPB fall workshop 1996); Zametkin et al., 1990). Later, Sieg, Gaffney, & Preston (1995) used SPECT (single photon emission computed tomography) and found brain-imaging abnormalities in ADHD. These researchers have demonstrated that ADHD children exhibit a maturational delay in the systems affected by attention in ADHD revealed through the PET and SPECT. 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 those of more immature brain activity, exhibited by younger children. Mann et al. (1991) and Lubar et al. (1995) have also supported these finding. Rossiter and LaVaque (1995) compared the effectiveness of neurofeedback to stimulant medication in reducing ADHD symptoms. The 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. Terminology This section includes key terms necessary in understanding the process and application of Neurofeedback. ADHD Defined Children, adolescents and adults with ADHD, with or without hyperactivity, have difficulty concentrating. They often underperform in school and at work even though they are quite bright. They also suffer from poor self-esteem due to the way they learn. The primary characteristics of ADHD include inattention, impulsivity, and hyperactivity. What distinguishes ADHD children from others is the prevalence, and severity of these symptoms, in a wide range of situations and circumstances. The DSM-IV criteria for classification of ADHD are grouped into Inattention, Hyperactivity, and Impulsivity (see table 1 for a more detailed description of DSM-IV criteria for ADHD classification). Inattention
Hyperactivity Impulsivity
TABLE 1 Source: American Psychological Association DSM-IV ADHD checklist criteria Neurofeedback and it's Uses for Treating ADHD In recent years Topographic Brain-Mapping studies have been used to identify regions of the brain, which are associated with increased activity during specific states (e.g., MRI, PET). Another such device is called an electroencephalogram (EEG). An EEG is a device that measures the natural activity or electricity produced by the brain. A brainwave is the recording of electrical activity that comes from the brain. Some researchers have classified a bandwidth of electrical activity by names such as Beta, Theta, SMR, EMG, Alpha and Beta (see table 2). Classifying bandwidths allows researchers to relate different states to one or more of these bandwidths. What Happens During Neurofeedback? Sensors are attached to the scalp and ear using conductive paste. These sensors measure frequencies and amplitudes produced by the brain. The computer then converts this information into visual and auditory feedback. This way the person can begin to experience how their brain is reacting during different situations, and learn how to change their brain wave patterns. By continuously practicing, the individual learns to change and control their brain patterns. Neurofeedback training is a facilitator of this change. During neurofeedback training, individuals are thought to increase their fast wave activity (e.g., Beta and SMR) and decrease their slow wave activity (e.g., Theta).
Table 2 Assessment Tools (pre-post) These assessment tools have been utilized by various studies in ADHD research:
Cites and Locations Some researchers use "Scull Caps" to assess subjects. This device is similar to a swimming cap. The cap, which contains 19 electrodes, fits over an individual's head. Each electrode is placed upon one cite identified in Figure 1. Research has shown that certain areas of the brain exhibit more activity associated with attention (see Table 3). Some researchers use a "Bi-polar" placement. This method involves placing two electrodes over specific cites (brain regions). Others use "Mono-polar" placement, which involves using one electrode over one brain region. Both have been shown to be efficient methods of conducting neurofeedback. Cite Placement
Figure 1 LEGEND
Cite Locations and Protocols
Table 3 Source: Fifth annual winter conference on Brain Function-EEG, modification and training; advanced meeting colloquium, (Palm Springs February 1997) This table does not include all published research. Other cites such as C3 and C4 have been used in Neurofeedback for ADHD without hyperactivity. For example, Othmer (1995) uses mono-polar placement at C3 Cz C4. Janzen et al., (1995) cite Fitzsimmons, who uses linked-ear C3 C4 CZ P3 P4 Pz Fz due to the distance from locations that exhibit muscle artifact. Subjects and Session # ADHD neurofeedback treatment has been applied to both children and adults, ranging between 20-50 sessions of approximately 40-50 minutes. In addition, some studies have incorporated an educational component with feedback. Table 4 represents various research paradigms used in neurofeedback training for ADHD. Equally important, some studies control factors such as location of cites and training times.
Table 4 Conclusions and Directions for Future Research Despite only a few decades of scientific research, neurofeedback is quickly growing into a mature science. In particular, the application of neurofeedback has become recognized as a valuable tool in the treatment of ADHD. This growth has been aided by factors such as advancement of technology and better understanding of ADHD. However, since most early studies that examined the efficacy of neurofeedback for the treatment of ADHD were composed of small sample sizes, conclusions difficult to extrapolate. Hence, future research must utilize larger sample sizes and employ more standardized methodology. In addition, subject selection should also be more rigorous. The use of appropriate control groups and the recruitment of pure ADHD without comorbidity of other disorders are necessary. Moreover, when selecting subjects, maturational shifts should be taken into account. Furthermore, methodological differences should be drawn between pure neurofeedback versus neurofeedback and academic training. Lastly, long term follow-up studies are necessary to track the efficacy of Neurofeedback. In conclusion, neurofeedback offers numerous possibilities for the future. The possibilities for application toward human cognition and peek performance are enormous. The ability to control our neural responses will allow individuals to have a better quality of life. In particular, the application of neurofeedback promises a viable treatment modality for the treatment of ADHD without the use of medication. References: Janzen, T., & Fitzsimmons, G. Theta: An electrophysiological marker of attention deficit. Unpublished Manuscript. Janzen, T., Graap, K., Stephanson, S., Marshall, W. & Fitzsimmons, G. (1995). Differences in baseline EEG measures for ADD and normally achieving preadolescent males. Biofeedback and Self-Regulation, 20, 65-82. Linden, M., Habib, T., & Radojevic, V. (1996). A controlled study of the effects of EEG biofeedback on cognition and behavior of children with attention deficit disorders and learning disabilities. Biofeedback and Self-Regulation, 21, 35-49. Lubar, J. (1991). Discourse on the development of EEG diagnostics and biofeedback for attention deficit/hyperactivity disorders. Biofeedback and Self-Regulation, 16, 201-225. Lubar, J. F., Bianchini, B. A., Calhoun, W. H., & Lambert, E. W. (1985). Spectral analysis of EEG differences between children with and without learning disabilities. Journal of Learning Disabilities, 18, 403-408. Lubar, J. & Lubar, J. (1984). Electroencephalographic biofeedback of SMR and beta for treatment of deficit disorders in a clinical setting. Biofeedback and Self-Regulation, 9, 1-23. Lubar, J. & Shouse, M. (1976). EEG and behavioral changes in a hyperactive child concurrent with training of sensorimotor rhythm (SMR). A preliminary report. Biofeedback and Self-Regulation, 1, 293-306. Lubar, J. F. & Shouse, M.N. (1977). Use of biofeedback in the treatment of seasure disorders and hyperactivity. In B.B. Lahey & A. E. Kazdin (Eds), Advances in clinical child psychology, (pp. 203-265). New York: Plenum Press. Lubar, J. F. Swartwood, M. O., Swartwood, J. N., & ODonnell, P. H. (1995). Evaluation of the effectiveness 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. Mann, C., Lubar, L. F., Zimmerman, A. W., Miller, C. A., & Muenchen, R. A. (1992). Quantitative analysis of EEG in boys with Attention Deficit-Hyperactivity Disorder (ADHD): A controlled study with clinical implications. Pediatric Neurology, 8, 30-36. Othmer, S. & Othmer, S. F. (1995). EEG biofeedback for attention deficit hyperactivity disorder. (Available from EEG Spectrum, Inc., 16100 Ventura Blvd., Encino, CA 91436). Othmer, S. Kraiser, & Othmer, S. F. (1995). EEG biofeedback training for attention deficit disorder: A review of clinical findings using the T.O.V.A. as a measure. (Available from EEG Spectrum, Inc., 16100 Ventura Blvd.,Encino, CA 91436). Rossiter, T. & LaVague, T. J. (1995). A comparison of EEG biofeedback and psychostimulants in treating attention deficit hyperactivity disorders. Journal of Neurotherapy, (Summer, 1995),48-59. Sieg, K. G., Gaffney, G. R., Preston, D. F., & Hellings, J. A. (1995). SPECT brain imaging abnormalities in attention deficit hyperactivity disorder. Clinical Nuclear Medicine, 20(1), 55-60. Sterman, M. B. (1996). Physiological origins and functional correlates of EEG rhythmic activities: Implications for self-regulation. Biofeedback and Self-Regulation, 1996 Mar; 21 (1): 3-33. Schwartz, M.S., & Associates (1995). Biofeedback a practitioner's guide (2nd edition). The Guilford Press. (pp. 493-522). Shouse, M. N. & Lubar, J. S. (1979). Operant Conditioning of EEG Rhythems and Ritalin in the Treatemtent of Hyperkinesis. Biofeedback and Self Regulation, 4 (4), 299-311. Tansey, M. (1984). EEG sensorimotor rhythm biofeedback training: Some effects on the neurologic precursors of learning disabilities. International Journal of Psychophysiology, 1, 163-177. Tansey, M. (1985). Brainwave signatures- An index reflective of the brains functional neuroanatomy: Further findings on the effects of EEG/SMR biofeedback training on the neurologic precursors of learning disabilities. International Journal of Psychophysiology, 3, 85-89. Tansey, M. (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. & Bruner, R. (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, 25-37. Zametkin, A. J., Nordahl, T. E., Gross, M., King, A. C., Semple, W. E., Rumsey, J., Hamburger, S., & Cohen, R. M. (1990, November 15). Cerebral glucose metabolism in adults with hyperactivity of childhood onset. New England Journal of Medicine, 323, 20, 1361-1366. Please feel free to contact the authors: A. Minevich, M.A. or T. Druckman, M.Ed. or discussion this article on the BiofeedbackZone.com Forums!
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