Neurofeedback, also called electroencephalogram (EEG) biofeedback or neurotherapy, is an adjunctive treatment used for psychiatric conditions such as attention-deficit/hyperactivity disorder, generalized anxiety disorder, posttraumatic stress disorder, phobic disorder, obsessive-compulsive disorder, bipolar disorder, depression and affective disorders, autism, and addictive disorders (Moore, 2000; Rosenfeld, 2000; Trudeau, 2000).
In an interview with Psychiatric Times, Siegfried Othmer, Ph.D., chief scientist at EEG Spectrum International Inc., described neurofeedback as neuroregulation in the time and frequency domains through the use of bioelectrical operant conditioning. Like repetitive transcranial magnetic stimulation (rTMS), neurofeedback is an innovative form of electrotherapeutics that complements neurochemical interventions for mood disorders. "With the use of anticonvulsants as mood stabilizers," Othmer said, "we have seen a convergence of psychiatry and neurology in the field of pharmacology. Similarly, neurofeedback signals a convergence of psychiatry and neurology in bioelectrical approaches to treating affective disorders. By stabilizing the brain and rewarding it for holding particular states, neurofeedback acts as a natural anticonvulsant." The rationale for using neurofeedback therapeutically is that it corrects deficits in brain cerebral regulatory function related to arousal, attention, vigilance and affect (Othmer et al., 1999).
During neurofeedback sessions, patients learn to produce desirable brain wave patterns displayed on a computer screen by controlling the activity of a computerized game or task seen on a second screen. Increases in the amplitude of slow spindle activity are instantaneously rewarded. The reward corresponds to the earned score, similar to scores accumulated in a computer game (Othmer, 1999).
Neurofeedback represents a window of opportunity for assessing and shifting any given brain state (Manchester et al., 1998). The designated frequency band determines which brain state is rewarded (Othmer, 1999). Beta (15 Hz to 18 Hz) training usually produces a slightly upward shift in arousal levels, leading to increased wakefulness and attentiveness or to decreased depression. The sensorimotor rhythm (SMR) (12 Hz to 15 Hz) elicits a slightly downward shift in arousal. The SMR is associated with subjective feelings of relaxation, emotional calm and centeredness (Othmer, 1999). Combined left-side, ß-SMR and right-side - neurofeedback is often used to treat brain wave dysregulation associated with traumatic memories. Right-side training is also employed for social and emotional deficits such as conduct disorder, autism and reactive attachment disorder (Othmer, 2000; Othmer et al., 1999).
Assessment of Clinical Evidence
The efficacy of neurofeedback in the treatment of seizure and pseudoseizure disorders has been well documented in peer-reviewed literature for over 25 years (Lubar, 1997; Swingle, 1998). On the whole, however, clinical support for the effects of neurotherapy is limited and based primarily on case studies, rather than randomized, controlled, blinded studies. While Joel Lubar, Ph.D., professor of psychology at University of Tennessee in Knoxville, recognizes the shortage of randomized trials on neurofeedback, he told PT that matched-group studies conducted in accordance with the Declaration of Helsinki are more appropriate than controlled trials for studying hyperactivity. He noted that 1,500 groups worldwide currently use neurofeedback for psychiatric applications, including attention-deficit/hyperactivity disorder (ADHD) and comorbidities. Since the 1970s, his team has investigated various interventions for treating hyperactivity in children and found EEG to be superior.
Lubar and his colleagues (1995) evaluated the effects of neurofeedback treatment on ADHD in 19 youth, ages 8 years to 19 years, under relatively controlled conditions. The subjects received one-hour sessions of ß brain wave training daily for up to 40 hours over a two- to three-month period. The goal of the therapy was to increase 16 Hz to 20 Hz (ß) activity while reducing the amplitude of brain waves (4 Hz to 8 Hz). Compared to pre-training results, post-training changes showed improvements in Test of Variables of Attention (TOVA) scores, Attention Deficit Disorders Evaluation Scale (ADDES) behavior ratings and Weschler Intelligence Scale for Children-Revised (WISC-R) performance. Twelve out of 18 subjects with pre-/post-TOVA scores had EEG-responsive improvements on an average of three of four possible scales. This change was comparable to pre-/post-medication differences in TOVA scores in youth with ADHD.
While TOVA scores typically return to baseline when the effects of pharmacotherapy wear off, the TOVA scores of the EEG-responsive subjects remained at the improved level. Significant post-test increases in IQ scores were observed in 10 EEG-responsive subjects who had been tested on the WISC-R two years earlier. Parental and teacher ratings of the children's behavior also improved following neurofeedback training. Thus, in the EEG-responsive youth, behavioral improvements corresponded with increased scores on TOVA and WISC-R. Lubar and his associates cautiously concluded that EEG neurofeedback training is a powerful adjunctive technique for treating ADHD when used as part of a multi-component therapeutic approach.
Additional research suggests that EEG neurofeedback may be an effective alternative to psychostimulants in the treatment of ADHD if medication is ineffective or has adverse effects or if patients are noncompliant (Rossiter and La Vaque, 1995). In one case study, a 36-year-old female diagnosed with ADHD, temporal seizure disorder and borderline personality disorder received 30 weekly sessions of SMR neurofeedback training and carbamazepine (Tegretol) (Hansen et al., 1996). The patient initially was reluctant to take carbamazepine but became compliant after starting neurofeedback training. However, because of the drug's side effects, she stopped, restarted and then again discontinued her medication. Following 17 sessions of neurofeedback, her quantitative EEG (QEEG) showed relative powers within normal ranges. Carbamazepine increased the favorable effect of neurofeedback on TOVA performance in the early phase of treatment. Although the subject's TOVA scores fluctuated as she went on and off carbamazepine, all four scales were normal months after she ceased taking carbamazepine. At that time, her TOVA performance showed no evidence of attentional deficit.
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