Chester Clinic

 

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Journal of Adult Development, Vol. 12, Nos. 2/3, August 2005 ( C Neurofeedback Treatment of Depression and Anxiety
D. Corydon Hammond1,2
A robust body of research documents that there are biological predispositions that oftenexist for depression, anxiety, and obsessive–compulsive disorder. However, new researchhas shown that medication is only mildly more effective than placebo in the treatment ofthese problems. In treating these conditions, neurofeedback (EEG biofeedback) may offer analternative to invasive treatments such as medication, ECT, and intense levels of transcrancialmagnetic stimulation. This paper reviews the neurofeedback literature with these problems,finding particularly positive research support for the treatment of anxiety disorders. Newfindings on the neurofeedback treatment of depression are presented.
KEY WORDS: Neurofeedback; EEG biofeedback; QEEG; depression; anxiety; OCD.
right and left prefrontal cortex. A large number ofEEG studies, summarized by Davidson (1992, 1995, Biological Substrates of Depression,
1998a), have demonstrated that the left frontal area OCD, and Anxiety
is associated with more positive affect and memories,and the right hemisphere is more involved in Speaking as a psychologist, I think that it is negative emotion. When there is a biological predis- not uncommon for us to minimize and, therefore, position to depression, there is a frontal asymmetry neglect the biological aspects of mental health disor- with more left frontal alpha activity, meaning that ders, with the exception of schizophrenia and bipolar the left frontal area is less activated. This means disorder. Our training is primarily in psychologi- that such individuals may be anticipated to be less cal interventions rather than in directly modifying aware of positive emotions while at the same time how the brain functions. However, as I have re- being more in touch with the negative emotions viewed elsewhere (Hammond, 2003), there is strong that are associated with the right hemisphere. It has evidence that obsessive–compulsive disorder has a also been demonstrated (Henriques & Davidson, significant biological component. There can also be 1991) that the left hemisphere is associated with strong biological predispositions to anxiety and panic approach motivation and behavior whereas the disorder (e.g., Heller, Etienne, & Miller, 1995, 1997; right hemisphere is involved in withdrawal behavior.
Wiedemann et al., 1999).
Thus, when the left hemisphere is basically "stuck" A robust body of research has been summarized in an alpha idling rhythm, there is more withdrawal by Davidson (1998a) documenting that depression is behavior in addition to the deficit in positive affect.
associated with an activation difference between the Even the infants of depressed mothers have beenfound to display this same reduced left frontal EEG 1Department of Physical Medicine and Rehabilitation, University activation (Dawson, Grofer Klinger, Panagiotides, of Utah School of Medicine, 30 No. 1900 East, Salt Lake City, Hill, & Spieker, 1992; Dawson, Grofer Klinger, Panagiotides, Spieker, & Frey, 1992), even as young 2To whom correspondence should be addressed at Department of as 3–6 months (Field, Fox, Pickens, & Nawrocki, Physical Medicine and Rehabilitation, University of Utah Schoolof Medicine, 30 No. 1900 East, Salt Lake City, UT 84132-2119; 1995) and 1 month of age (Jones, Field, Fox, Lundy, & Davalos, 1997).

2005 Springer Science+Business Media, Inc.
Baehr, Rosenfeld, and Baehr (1997) and Askew meet the criteria for being both an efficacious and (2001) have expressed the belief that this frontal specific treatment, as established by the American asymmetry may represent a state marker of depres- Psychological Association Clinical Psychology Divi- sion, as well as reflecting a biological or trait marker sion (Chambless & Hollon, 1998; Chambless et al., of a vulnerability (Henriques & Davidson, 1990, 1991) to depression. Askew (2001) found a strong Monastra's (2002) recent research found neu- correlation between alpha asymmetry scores and the rofeedback to be significantly more effective than Beck depression Inventory (p < 0.0001) and on the ritalin in changing ADD/ADHD, without having to MMPI-II Depression Scale (p < 0.0001). Davidson remain on drugs. Other studies (Fuchs, Birbaumer, (1998b) expressed his belief that such an asymmetry Lutzenberger, Gruzelier, & Kaiser, 2003) have found is not necessary or sufficient for the production of a comparable improvements with 20 h of neurofeed- specific type of affective style or psychopathology, back training (forty 30-min sessions) to those pro- but that differences in prefrontal asymmetry may duced by ritalin, even after only twenty 30-min be most appropriately viewed as diatheses that bias sessions of neurofeedback (Rossiter & LaVaque, a person's affective style, and then in turn modu- late someone's vulnerability to develop depression.
Davidson (1998b) does not subscribe to a strictlybiological model of depression, but he believes that the asymmetry does predict a vulnerability to depres- OF ANXIETY AND DEPRESSION
sion so that when negative life events occur over aprolonged period of time to such a person, there is an Neurofeedback for Anxiety
increased probability of them becoming depressed.
Not all persons with this frontal alpha asymmetry will Moore (2000) reviewed the literature on neu- be depressed, and someone can experience negative rofeedback treatment for anxiety disorders. He life events and still become depressed in the absence reviewed eight studies of generalized anxiety disor- of this asymmetry. This EEG asymmetry is best seen der (GAD), three with phobic anxiety disorder, two when the EEG is examined with an average refer- studies of obsessive–compulsive disorder, and one ence or a reference on the vertex at Cz (Baehr et al., published report with post-traumatic stress disorder 1997; Davidson, 1998a,b; Rosenfeld, Cha, Blair, & (PTSD). There were several problems with this lit- Gotlib, 1995).
erature. One problem in the literature is that moststudies only utilized very brief training. For instance,in the GAD studies that listed length of training, it only averaged 3.2 h! As a clinician, I will mostcommonly utilize 7–12 h of neurofeedback training EEG biofeedback (neurofeedback) has been with anxiety problems. Nonetheless, seven of the found to be effective in modifying brain function eight studies produced positive changes in clinical and producing significant improvements in clini- cal symptoms in several clinical areas, including The finest studies were the three studies of epilepsy, ADD/ADHD, learning disabilities, and phobic (test) anxiety (Garrett & Silver, 1976), that head injuries. For example, Sterman (2000) compre- included random assignment, alternative treatment hensively reviewed the literature on the neurofeed- control groups, and a wait-list control group. In back treatment of uncontrolled epilepsy. Overall, one experiment, the group receiving alpha EEG en- this literature documented that 82% of the most se- hancement training produced 33% more alpha post- vere, uncontrolled epileptics demonstrated a signifi- treatment, and all three feedback groups demon- cant reduction in seizure frequency, with an average strated significant reductions in test anxiety, while of a 70% reduction in seizures. Two studies even the untreated control group and the relaxation train- measured sleep EEG pre- and post-training and doc- ing group experienced no significant reduction. In umented significant normalization of brain activity another experiment, participants received phases of even when patients were asleep. Another new con- alpha enhancement training and EMG biofeedback trolled study (Kotchoubey et al., 2001) validated the training. The alpha training increased alpha produc- effectiveness of neurofeedback compared to med- tion from 64 to 78%, and anxiety scores dropped ication and placebo. These neurofeedback studies significantly (p < 0.001) for this combined treatment Neurofeedback Treatment of Depression and Anxiety
group compared to a non-treatment group. Thus, ac- ical scales—dramatically on many of them—while cording to APA Clinical Psychology Division criteria there were no significant improvements on any scales for efficacious treatments, neurofeedback for phobic in the traditional treatment group. An additional anxiety qualifies for the status of possibly efficacious.
study, not originally reviewed by Moore (2000), was Moore's review (2000) also concluded that a placebo done by Peniston, Marrinan, Deming, and Kulkosky effect was certainly present in these neurofeedback (1993). They randomly selected 20 chronic PTSD studies, but that alpha and theta enhancement train- Vietnam veterans, who also had alcohol abuse, from ing provided additional effects beyond placebo and a VA hospital population. They were treated with are effective treatments of anxiety disorders.
thirty 30-min sessions of alpha/theta neurofeedback There were two studies that was not reviewed training. On 26-month follow-up, only 4 of the 20 by Moore (2000). Passini, Watson, Dehnel, Herder, patients reported a few (1–3) instances of recurrence and Watkins (1977) compared 25 anxious alcoholics of nightmares/flashbacks, and the other 16 patients with a matched control group before and after 10 h had no recurrence of PTSD symptoms.
(over a 3 week period) of alpha neurofeedback train- Moore (2000) reviewed two published studies of ing. Alpha neurofeedback training produced signif- OCD that used alpha enhancement training, without icant (p < 0.001) changes in state and trait anxiety positive results. However, these studies utilized a compared with controls. Patients receiving neuro- naive treatment approach of only doing alpha en- feedback training increased their eyes-closed alpha hancement training, and literature since that time production from 38 to 55%, while controls dropped has shown that there are at least three subtypes slightly. In an 18-month follow-up (Watson, Herder, of EEG patterns that are found in OCD. More & Passini, 1978), essentially identical results were recently, I have reported on successful treatment still found, indicating that the anxiety changes from with lengthy follow-ups of three consecutive cases alpha neurofeedback were enduring. A new random- of OCD, utilizing protocols that were individualized ized, blinded, controlled study (Egner & Gruzelier, through using a quantitative EEG assessment. In 2003) at London's Royal College of Music evaluated the first publication, (Hammond, 2003) scores on the the ability of alpha/theta neurofeedback to enhance Yale–Brown Obsessive–Compulsive Scale (YBOCS) musical performance in very high level musicians and the Padua Inventory normalized following treat- when they were performing under stressful condi- ment. The patients showed 3.7 and 3.0 standard devi- tions. When compared with alternative conditions ation improvements on the YBOCS. This is particu- (physical exercise, mental skills training, Alexander larly significant because a meta-analysis (Ackerman Technique training, beta1 neurofeedback, and SMR & Greenland, 2002) of 25 drug studies found that neurofeedback), only the alpha/theta neurofeedback even the most effective pharmacologic treatment group resulted in enhancement of real-life musical for OCD (clomipramine) only produced an average performance under stress.
treatment effect on the Y-BOCS of a 1.33 standard Two neurofeedback studies focused on chronic deviations improvement (uncorrected for placebo PTSD. In a randomized, control group study, effects), and about one-half that much improve- Peniston and Kulkosky (1991) added thirty 30-min ment across studies with Prozac. Improvements were sessions of alpha/theta EEG biofeedback training to also documented with an MMPI, with follow-ups the traditional VA hospital treatment provided to of the two cases at 15 and 13 months after treat- a group of 15 PTSD Vietnam combat veterans, and ment. Figure 1 shows the pre–post improvements compared them at follow-up with a contrast group of in one of these cases. Maintenance of change was 14 veterans who only received traditional treatment.
also externally validated through contacts with fam- On 30-month follow-up, all 14 traditional treatment ily members. I have now followed-up the third case patients had relapsed and been rehospitalized, while (Hammond, 2004) for 10 months. Figure 2 displays only 3 of 15 neurofeedback training patients had his MMPI pre-treatment, mid-treatment, and at the relapsed. Although all 14 patients treated with neu- conclusion of treatment. It may be seen that his Pt rofeedback had decreased their medication require- scale decreased from 115 t-scores to 60 t-scores. His ments by follow-up, among traditionally treated pa- Y-BOCS improved from his original score of 16 to tients, only one patient decreased medication needs, a score of 3, representing a 2.2 standard deviation two reported no change, and 10 required more psy- improvement. He had originally scored 6 on the chiatric medications. On the MMPI, neurofeedback compulsions subscale, and now scored zero, and his training patients improved significantly on all 10 clin- score had improved from 10 to 3 on the obsessions Fig. 2. Pre–Post MMPI changes in a case of obsessional OCD.
Fig. 1. MMPI Changes in an OCD case after 25 h of neurofeed-
subscale. Once again, external validation of improve- Gotlib, Ranganath, & Rosenfeld, 1999; Henriques & ments and their maintenance was obtained by talking Davidson, 1990; Kwon, Youn, & Jung, 1996) have with his family.
found that following drug treatment that producedremission of the depression, the frontal alpha asym-metry remained, indicating a continued vulnerability Neurofeedback for Depression
to future depression.
Several years ago (Hammond, 2000) I likewise Based on the large volume of research reviewed reported a case study with an eight and a half month earlier that validates the role of the frontal alpha follow-up of the effective alleviation of severe de- asymmetry in depression, Rosenfeld (1997) devel- pression using my own neurofeedback protocol for oped a neurofeedback protocol for modifying this modifying frontal alpha asymmetry. This protocol asymmetry. His ALAY (standing for alpha asymme- utilizes electrode sites Fp1 (on the left forehead) try; F4−F3/F3+F4, with a reference electrode at Cz) and F3, which is approximately 2.5–3 inch. straight protocol rests on very firm theoretical ground and above Fp1. In this protocol, we inhibit slow alpha and the preliminary results from case studies (Rosenfeld theta activity, while reinforcing 15–18 Hz beta for the et al., 1995; Baehr, Rosenfeld, & Baehr, 2001, 1997) first 20–22 min of each training session, after which are encouraging, although no controlled research the frequency band being reinforced is decreased to has yet been completed. There have been long-term 12–15 Hz during the final 8–10 min of each session.
follow-ups, however. Baehr et al. (2001) reported Since the publication of the original report, I have on 1–5 year follow-ups on patients treated with the continued to use this same protocol for the treatment Rosenfeld protocol, documenting that the substan- of depression.
tial changes were not only enduring, but also that A new sample reported in this paper consists the frontal alpha asymmetry had not only changed, of nine consecutive, white, middle class (mean age but remained eliminated on long-term follow-ups.
43.5; range 34–50 years) patients. Informed consent This is particularly significant because a variety was obtained from all patients, all of whom presented of studies (Allen, Iacono, Depue, & Arbisi, 1993; with a primary complaint of depression, which was Neurofeedback Treatment of Depression and Anxiety
confirmed through administration of the MinnesotaMultiphasic Personality Inventory. The only otherselection criterion was that they were each screenedwith the Rosenfeld protocol for the presence of thefrontal alpha asymmetry associated with a predispo-sition to depression. Rosenfeld (Baehr et al., 2001)has found that percentage scores greater than 60 in-dicate that there is not a predisposition to depression,while scores of 58 or less indicate the presence of apredisposition. The mean percentage score for thissample was 40.05, and the mean of this sample on theMMPI Depression scale was 93.75 t-scores. Whereaspatients in drug studies are often more moderatelydepressed, 7 of the 8 patients in this series werejudged to be seriously to severely depressed, withonly one that was moderately depressed. In contrast,the case reports cited earlier (Baehr et al., 1997, 2001)that used the Rosenfeld neurofeedback protocol in-volved relatively mild depression in the 62–64 t-scorerange on the MMPI, with an percentage score of only51.3.
Eight patients completed training, requiring an average of 20.75 thirty-minute sessions (10.4 h) ofneurofeedback, with no other psychotherapy pro-vided. Seven of eight patients made very substan- Fig. 3. Neurofeedback for depression: Average MMPI Pre-post
tial improvements, and one dropped out after five changes for eight cases.
sessions because he was too busy. The drop-outshowed signs of questionable motivation from thebeginning, seeming to be in treatment primarily to SUMMARY AND CONCLUSIONS
please his wife and daughter. Many of the patientswere on medication at the time of initial testing, but Through the years I found it irritating that psy- were no longer on medication at the completion of chiatrists tell patients that they have a "biological depression" without any objective validation, seem- Pre–post changes on the MMPI may be seen in ingly as a justification to then simply write a pre- Fig. 3, with a mean decrease in the depression scale scription. Yet, startlingly, pharmacologic treatment of 28.75 t-scores. One patient improved from severely for depression (Antonuccio, Danton, DeNelsky, depressed to normal and two progressed from being Greenberg, & Gordon, 1999; Greenberg, Bornstein, seriously depressed to normal. Three improved from Greenberg, & Fisher, 1992; Kirsch, Moore, Scoboria, severe to mild depression, and one improved from & Nicholls, 2002; Kirsch & Sapperstein, 1998; moderately depressed to mildly depressed. One case Krisch, Scoboria, & Moore, 2002; Moncrieff, 2001; who was severely depressed only showed mild im- Walach & Maidhof, 1999), anxiety (Khan, Khan, provement. This was an individual who had lost his & Brown, 2002), and obsessive–compulsive dis- wife to cancer a year earlier and issues surrounding order (Ackerman & Greenland, 2002; Goodman, this loss seemed likely to need to be addressed, and McDougle, & Price, 1992) has been found to be he was referred for psychotherapy for these issues.
only mildly effective over and above placebo effects.
Categorizing this last case and including the drop- Nonetheless, there is a robust literature validating out as failures, this represents 77.8% of cases who that in fact there are biological predispositions that made significant improvements. The average length exist to depression, OCD, and anxiety.
of follow-up for these cases was about 1 year, with a Neurofeedback is an encouraging development range from 2 years in two cases, to 4 months in the that holds promise as a method for modifying bi- case of the individual who only mildly improved.
ological brain patterns associated with a variety of mental health and medical (e.g., stroke, head injury, effects of aging) disorders–particularly because un-like drugs, electroconvulsive therapy, and intense Ackerman, D. L., & Greenland, S. (2002). Multivariate meta- transcranial magnetic stimulation, it is non-invasive analysis of controlled drug studies for obsessive–compulsive and seldom associated with even mild side effects.
disorder. Journal of Clinical Psychopharmacology, 22(3),309–317.
Echoing similar sentiments, Frank H. Duffy (2000), Allen, J. J., Iacono, W. G., Depue, R. A., & Arbisi, P. (1993). Re- a Professor and Pediatric Neurologist at Harvard gional electroencephalographic asymmetries in bipolar sea- Medical School, recently stated that scholarly litera- sonal affective disorder before and after exposure to brightlight. Biological Psychiatry, 33, 642–646.
ture now suggests that neurofeedback "should play a Antonuccio, D. O., Danton, W. G., DeNelsky, G. Y., Greenberg, major therapeutic role in many difficult areas. In my R. P., & Gordon, J. S. (1999). Raising questions about antide- opinion, if any medication had demonstrated such pressants. Psychotherapy and Psychosomatics, 68, 3–14.
Askew, J. H. (2001). The diagnosis of depression using psycho- a wide spectrum of efficacy it would be universally metric instruments and quantitative measures of electroen- accepted and widely used" (p. v). "It is a field to be cephalographic activity. Unpublished doctoral dissertation, taken seriously by all" (p. vii). Despite the promise University of Tennessee.
Baehr, E., Rosenfeld, J. P., & Baehr, R. (1997). The clinical use of of neurofeedback, however, Duffy also noted the an alpha asymmetry protocol in the neurofeedback treatment need for improved and higher quality research. This of depression: Two case studies. Journal of Neurotherapy, is particularly true in the application of neuro- Baehr, E., Rosenfeld, J. P., Baehr, R., & Earnest, P. (1998). Com- feedback to the treatment of anxiety and affective parison of two EEG asymmetry indices in depressed patients vs. normal controls. International Journal of Psychophysiol- Since the completion of the successive cases ogy, 31, 89–92.
Baehr, E., Rosenfeld, J. P., & Baehr, R. (2001). Clinical use of reported in this paper, I have personally treated an alpha asymmetry neurofeedback protocol in the treatment approximately 15 additional patients suffering with of mood disorders: Follow-up study one to five years post depression, but sometimes without post-treatment therapy. Journal of Neurotherapy, 4(4), 11–18.
Chambless, D. L., Baker, M. J., Baucaom, D. H., Beutler, L. E., testing and lengthy follow-up. It is my impression Calhoun, K. S., Crits-Christoph, P., et al. (1998). Update on from both this case series and from my subsequent empirically validated therapies II. The Clinical Psychologist, clinical experience that the use of this neurofeed- Chambless, D., & Hollon, S. D. (1998). Defining empirically sup- back protocol results in significant, enduring im- ported therapies. Journal of Consulting and Clinical Psychol- provements approximately 80% of the time when ogy, 66, 7–18.
patients have the frontal alpha asymmetry that re- Davidson, R. J. (1992). Emotion and affective style: Hemispheric substrates. Psychological Science, 3, 39–43.
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