Electroencephalographic (EEG) Neurofeedback: Another approach to treat ADHD

Neurofeedback: Other

Treatment for ADHD

Only in the last 20 years, Attention Deficit Hyperactivity Disorder (ADHD) has

become "leaders U.S. childhood psychiatric disorder. Approximately 2% to 6% of school-age children are diagnosed with ADHD (Raz 2004). According to Barkley (1998), the number of children affected by ADHD can vary from 1% to 20%, depending on how you choose to define the study population, geographic location survey, etc. ADHD is characterized by the inability to self-regulate the spotlight. Children are impulsive and hyperactive behavior disinherited. The condition development is disabling, if not controlled persist into adolescence and adulthood (Edwards, 1995).

Frontal lobe and ADHD

Research suggests a neurological basis for ADHD, specifically, frontal lobe dysfunction. frontal lobe functions are of a executive, and are involved in developing plans and organizing resources. They are also critical in mediating behaviors such as inhibitory control engine performance and focus on the inhibition of distracting or irrelevant stimuli. Evidence suggesting a right frontal lobe dysfunction as the basis of attention deficit disorders is substantial (Chelune, Ferguson, Koon, and Dickey, 1986, Gualtieri and Hicks, 1985; Hynd, et.al 1990, Lou, et.al., 1989).

There has been a growing interest in the relationship between the prefrontal cortex function and ADHD. Children with frontal lobe lesions show hyperactive impulsive behavior (Grattan and Eslinger, 1991), and adolescents with ADHD show decreased activity in the frontal lobe anterior tomography emission tomography (Zametkin et al., 1993). Performance on neuropsychological tests purportedly to test functioning frontal cortex is deficient in children with ADHD (Barkley et al., 1992). The study examined the frontal lobe functioning in adolescents with ADHD Schandl (2001) found a presence and magnitude reflect dysfunction frontal lobe in children with ADHD aged between 12 and 17. The results of the study by Fredericksen et al. al. (2002) was consistent with previous reports of reduced volumes of the frontal lobe, associated with the study of ADHD. Schmidt (1999) shows that children with ADHD exhibit a less frontal activation pattern right lateralized The normal control children. Halperin (2006) found that brain activation gradients in ventrolateral prefrontal cortex of adolescents with ADHD. Research Recent morphological using advanced brain imaging procedures has shown that ADHD children are not normal asymmetry has the right-most left at the mass of the frontal lobes (Hynd, Hem, Voeller, and Marshall, 1991). Consistent with this finding, quantitative computerized electroencephalographic (EEG) analysis shows significantly more slow wave (theta) and significantly less fast wave activity (beta) activity mainly in frontal regions for ADHD children compared with age-and sex-matched normal (Mann, et al, 1992).

Neurofeedback Training for ADHD

The neurofeedback training, also known as EEG Biofeedback or Neurotherapy, uses an electroencephalogram (EEG), a device that detects and records electrical activity in the brain, called brain waves. An EEG can detect brain waves and discern if they are strong or weak (amplitude) or fast or slow (frequency). Scientists identify brain waves commonly into four categories: –

Beta, the faster brain waves 14-32 Hz, is focused on daily activities and the activities of care and thought.

Alpha, a brain wave slow, between 8 and 12 hertz. This rhythm is a characteristic of a relaxed but alert state of consciousness.

Theta, the next slow wave range 4-8 Hz. This rhythm is often associated with images of a dream, drowsiness and deep relaxation.

Delta, the most Slow waves, 0-4 Hz, predominates during dreamless sleep.

EEG accepts the neurological basis of ADHD (ie lobe dysfunction front). Recognizing that patients with ADHD produced more theta activity and less beta-wave activity, compared with non-ADHD patients (Barabasz et al, 1993; Mann et al, 1992). The objective of the training is to alter EEG abnormal brain waves, theta waves decreased, while simultaneously increasing beta waves. The Advocates of this technique believe that the theta and beta brain waves carry sound closer to patterns leads to a reduction of ADHD symptoms.The EEG monitors and records different brain waves of the patient, who learns to increase or reduce certain types of brain waves. EEG training is to teach patients to normalize brainwave responses to stimuli.

In the EEG neurofeedback training, the therapist explains to the patient the connection between what is happening in the cortex and what is recorded in the EEG. Then, the therapist helps the patient learn to gain control over her / brainwaves. The therapist places electrodes on the head EEG detect different types of brain waves produced by the patient and send the information to a data logger. Each time the desired brain wave is identified, the device sends neurofeedback a signal to the patient – auditory or visual feedback – to encourage the production of similar brain waves. Auditory or visual feedback vary sounds easy to make computer graphics made the game look like, where the generation of brain waves would add excitement to action and carries any reward. Neurofeedback training usually takes 30-40 sessions depending on the severity of the disease and other comorbid symptoms present. The first six sessions are completed as quickly as possible and then the frequency of training is reduced to two or three times a week. With regular attendance, Total Training can be completed in four to six months. Each training session lasts approximately 30-45 minutes.

The procedure is based on a study early Sterman and Friar (1972), who found that brain-wave feedback has to learn to inhibit seizures by enhancing low-beta (12-16), which is called the sensory motor rhythm (SMR). As in the current neurofeedback protocols ADHD, Sterman and Friar patients were also trained while minimizing theta. The first preliminary study for the application of this procedure for hyperkinetic children was Lubar and Shouse (1977). The effects neurofeedback appear to provide a change in performance without external intervention continues. Chartier and Kelly (1991) examined the effects of neurofeedback for ADHD in more 200 children treated by Dr. Joel Lubar at the University of Tennessee, Dr. John Carter of the University of Texas and Dr. Michael Tansey of Sommerville, New Jersey. Chartier and Kelly neurofeedback training were found to provide important and sometimes "dramatic" clinical improvements in children with attention deficit disorder. Parents and teachers of children receiving EEG neurofeedback training have reported dramatic improvements in behavior, such as:   end tasks, listen better, less impulsivity, greater motivation and focus, and greater self-esteem. In some cases, medications are completely discontinued and in others they have significantly reduced.

Although the review suggests that EEG neurofeedback approach is an effective intervention to address the behavior, listening, impulsivity and attention problems in ADHD, more research is needed to define the optimal information for training sessions and follow the procedures currently neurofeedback limitations include: 1) the need for more controlled experimental studies showing effects that are independent maturation of the development and potential confounding of therapists and care of parents during the course of treatment, and 2) the large number of sessions (Up to 80, 6-8 months) required academic standing and clinical changes occur. While the field awaits further investigation, however, training Current EEG could be used separately or can be combined with one or more of one of the other traditional treatment methods to eliminate or reduce some of the drawbacks possible.

References

• Barabasz, A. (1993). Address: processes isolation of Antarctica and attention: implications for research professionals. Presented at the Fifth International Conference on REST, Seattle, WA, 26 until February 28.
• Barkley, RA, Anastopoulos, AD, Guevara, DG, and Fletcher, KF (1992). Adolescents with hyperactivity disorder and attention deficit disorder: mother-adolescent interactions, family beliefs and conflicts, and maternal psychopathology. Journal of Abnormal Psychology, 20, 263-288
• Barkley, RA (1998). Attention Deficit Hyperactivity Disorder: A Handbook for the Diagnosis and Treatment (2 nd ed.). New York Guilford.
• Chartier, D., & Kelly, N. (1991). Neurofeedback treatment of attention Deficit hyperactivity disorder. Grand Rounds Presentation, Rex Hospital, Raleigh, North Carolina
• Chelune, GJ, Ferguson, W., Koon, R., and Dickey, T. 0. (1986). Frontal lobe disinhibition in attention deficit disorder. Child Psychiatry and Human Development, 16, 221-232.
• Edwards, R. (1995). Hyperactivity is the label applied too often? Monitor of the American Psychological Association, 26, 44-45.

• Fredericksen KA, Cutting, LE, Kates WR, Mostofsky, SH, Singer, HS

Cooper, KL, et al. (2002). Disproportionate increases white matter of right

frontal lobe in Tourette syndrome. Neurology, 58, 85-89.

• Grattan LM, Eslinger PJ. (1991). Frontal lobe damage in children and adults:

comparative. Developer Neuropsychol, 7: 283-326.

• Gualtieri, CT, and Hicks, RE (1985). Neuropharmacology of methylphenidate and a substitute for the nerves to childhood hyperactivity. The psychiatric clinics of North America, 8, 875-892.
• Halperin, J. M & Schulz, PK (2006). Review of the role of the prefrontal cortex in

Pathophysiology of attention-deficit/hyperactivity disorder (ADHD). Psychological

Bulletin, 132, 560-581.

• Hynd, GW Hem, Voeller KL, K_ K_ And Marshall, RM (1991). Neurobiological basis of attention deficit disorder and hyperactivity disorder (ADHD). School Psychological Review, 20.174-186.
• Hynd, GW, Semrud-Clikeman, M., Lorys, A., Novey, ES, and Eliopulos, D. (1990). Brain morphology in developmental dyslexia and attention deficit disorder / hyperactivity. Archives of Neurology, 47, 919-926.
• Lou, HC, Henriksen, L., Bruhn, P., Bomer, H., and Nielsen, J. (1989). Striatum. dysfunction in attention deficit and hyperkinetic disorder. Archives of Neurology, 46, 48-52.
• Lubar, JF and ~ Shouse, MN (1977). The use of biofeedback and the treatment of seizure disorders and hyperactivity, Advances in Clinical Child Psychology. New York: Plenum, 1, 204-251.
• Mann CA, Lubar, JF, Zimmerman, AW Miller, CA and Muenchen, RA (1992). A quantitative analysis of EEG in children with deficit disorder Attention-Deficit/Hyperactivity Disorder: Clinical Neurology implications.Pediatric controlled, 8, 30-36.
• Raz, A. (August 2004). Data ADHD brain image. Psychiatric Times. Issue 9 Vol XXI.
• Schandl, S. (2001). Frontal lobe functioning in adolescents with disorder hyperactivity and attention deficit disorder – Statistical data included. Adolescence
• Schaughency, EA, and GW Hynd, (1989). Care and control of impulses in attention deficit disorder (ADD). Learning and Individual Differences, 1, 423-449.
• Sterman, MB, and brother, L. (1972). Suppression of seizures by following sensorimotor EEG feedback training. Electroencephalography and Clinical Neurophysiology, 33, 89-95.
• Zametkin AJ, Liebenau LL, Fitzgerald GA, King AC, Minkunas DV, Herscovitch P, Yamada EM, Cohen RM (1993). Brain metabolism in adolescents with hyperactivity disorder attention deficit. Arch General Psychiatry 50:333-340.

About the Author

Dr. Kamal Sesalem
Professor of Special Education
Dept. of Teacher Education
McNeese State University
Lake Charles, LA 70609

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