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A Clinical Outcome Study Of Neurofeedback And Biofeedback For Migraine Headache

In a recent meta-analysis involving biofeedback for the treatment of migraine, Grade A evidence [6] was found for the efficacy of the above methods which proved stable over a 17 month follow-up phase [5]. Numerous studies explore peripheral biofeedback [5], but scant studies exist on using neurofeedback methods to treat migraine [7-11]. Although the current study discussed today looks at neurofeedback, it is not the sole intervention. Instead of providing only neurofeedback protocols as the sole modality, the lead author, who is a clinician in private practice, decided early on to utilize evidence-based thermal biofeedback methods in addition to the neurofeedback in order to maximize the patient’s chances of success.

Introduction/Background
Migraine is a common, disabling and often progressive disorder characterized by increased excitability of the central nervous system [1, 2]. It occurs in 18% of women and 6% of men in the US with peak prevalence in individuals between the ages of 25 and 55 [3]. Economic burden of migraine in the US is estimated to be approximately 13 billion annually [4]. Biofeedback is a common intervention in pain management. For migraine treatment, the most frequently used biofeedback methods have been peripheral skin temperature biofeedback, blood-volume-pulse and electromyography feedback [5].

Neurotherapy is a broad term referring to the many types of biofeedback used to deliver information about the central nervous system which involve blood flow, thermal output from the brain or electrical activity. Neurofeedback (also called neurobiofeedback or EEG biofeedback) usually refers to frequency-based biofeedback that uses an EEG to give clients information about their brainwaves and gradually and subtly teaches people how to alter their brainwave activity. Sensors are attached to the scalp and the raw EEG signal is amplified, the frequency spectrum is extracted via a Fourier transform and selected frequency components are displayed through a user interface such as a video game. Unlike peripheral biofeedback that monitors the status of peripheral aspects of the sympathetic and parasympathetic nervous systems (e.g. respiration, galvanic skin response), neurofeedback monitors central nervous system activity.

Abnormalities in electrophysiological activity have commonly been found in the brains of migraine patients [16-21], therefore it is plausible that interventions involving the EEG might be of benefit [16]. Children afflicted with migraine, those with and without aura, demonstrate increased theta frequencies compared to normal controls [17]. One popular neurofeedback protocol for migraine emphasizes protocols rewarding 12-15 HZ at the temporal lobes at sites T3 and T4 [22]. Siniatchkin and colleagues demonstrated a significant reduction in migraines in 10 young migraineurs after 10 sessions of neurofeedback at midline frontal and central areas teaching them to control slow cortical potential activity representing cortical sensitivity and reactivity [7]. Michael Tansey enabled four migraineurs to eliminate their migraines after neurofeedback training along midline frontal and central areas which showed that low frequencies became less dominant and higher frequencies were augmented [8]. An older study found that thermal biofeedback was no more effective than EEG alpha biofeedback and self hypnosis in treating migraine [9]

Neurofeedback training also includes a newer method called hemoencephalography, which targets the frontal lobe [23]. Passive infrared hemoencephalography (pIR HEG) is a form of biofeedback for the brain that measures and feeds back information on the thermal output of the frontal lobe [10,23]. Unlike electromyographic (EMG) feedback which involves lowering the tension of the frontalis or trapezius muscles, pIR HEG involves increasing the forehead temperature by watching a movie for feedback. The movie is in operation when the measured forehead temperature rises and the movie stops when the temperature drops. The therapist will increase the threshold as the client learns how to raise their forehead temperature. Clients are instructed to calmly concentrate on making the movie continue to play. Increases in the pIR HEG signal reflect a composite of thermal activity generated by vascular supply, vascular return and brain cell activity. 100 International Headache Society (IHS)-diagnosed migraineurs reduced the frequency of their headaches using this form of biofeedback [10, 24,25].

Methods
This is a single group outcome, open label study in a clinical setting where both the patients and those administering treatment were aware of the treatment being given. Patients were given Informed Consent for biofeedback methods administered as well as Informed Consent to Research as put forth by the lead author’s ethics committee of the American Psychological Association and the Association of Applied Psychophysiology and Biofeedback.

Participants
The total sample included 37 migraine patients (29 females and 8 males). Ages ranged from 9 to 79, with the majority (56%) between the ages of 16 and 52, and the remainder evenly split between the younger group (22% were between 9 and 15) and the older group (22% were between 55 and 79). In terms of medical history, most patients had long, stable histories of migraine and had tried multiple pharmaceutical treatments prior to neurotherapy. All were having at least one migraine per month and taking at least one type of medication (preventive, abortive or rescue) for their migraines and were not required to discontinue these during the study (See Table 1).

Table 1 (click to enlarge). Number of patients on each type of migraine medication

Initial Assessments
A personal and family headache history was taken at initial evaluation and a diagnostic interview was performed by a licensed psychologist to confirm the IHS-diagnosis of migraine with or without aura and to assess other symptoms and conditions. For patients who did not have at least two weeks of headache diaries, they were asked to wait two weeks to begin treatment in order to keep a baseline daily diary to record headache frequency and severity. At the first session and every 10 sessions thereafter, clients were asked to complete a non-standardized checklist to indicate changes in headaches as well as other symptoms (e.g., anxiety, insomnia, other pain types, depression, and behavioral problems).

Follow up data collection
The data reported in this study were collected 3 months to 2 years after patients stopped coming to the neurotherapy center, either because they had completed the recommended number of  treatment sessions or because they discontinued treatment on their own.  The data were collected through follow-up telephone surveys conducted by a research consulting firm not affiliated with The Better Brain Center.

Treatment Protocol

neurofeedback
The study involved treatment using EEG biofeedback, pIR HEG biofeedback and hand warming biofeedback for an average total of 40 sessions. Average length of time in treatment was 6 months. Subjects underwent an average of 30 frequency-based neurofeedback sessions and 10 pIR HEG sessions for 30 minutes at least twice weekly. Eleven patients had an interruption in their treatment after the initial 20 sessions of up to several weeks but returned for their remaining sessions.  Previously recorded baseline EEG measures were used to guide neurofeedback training protocols by targeting frequency ranges with the highest amplitude. All migraine patients were trained to reduce the amplitude of the targeted frequencies. The EEG training primarily occurred at 5 sets of homologous sites (T3-T4, C3-C4, F3-F4, FP1-FP2 and P3-P4). These homologous sites were chosen according to the lead author’s training in neurofeedback in which years of clinical experience in treating migraines by other experienced clinicians is taught [22].  Electrode placements at homologous sites were used and training always began as a single channel placement using the first site as the signal and the second site as reference (example: T3-T4).

pIR HEG biofeedback
For most patients 30 minutes of pIR HEG biofeedback was introduced at approximately their tenth visit. This involved the patients wearing a headset which is designed to be worn at FPZ (center of forehead) and watching a movie and being challenged to keep the movie playing as the reward threshold was re-set to higher temperatures.

thermal hand warming
Thermal hand warming biofeedback was also used simultaneously along with the EEG biofeedback during clinic sessions.

Please review the original article for a more detailed explanation for treatment rationale, neurofeedback/pIR HEG/biofeedback protocol, and reward/inhibit criteria.

Results
Table 2 shows the age and gender of everyone in the full sample and the pre-treatment and post-treatment migraine frequency estimates. The estimates are based on participant reports of the average number of migraines they experienced per month in the 6 months prior to treatment, and the 6 months immediately preceding the follow-up telephone survey.

The small number of participants (n=7) who had completed treatment only 1 to 5 months before the follow-up interview, reported migraine frequency for this shorter post-treatment time period. The pretreatment mean frequency was 7.6 migraines per month (S.D = 5.1) the post-treatment mean was 2.9 migraines per month (S.D=2.8), and the mean difference was 4.72 (S.D.=4,32) few migraines per month. The standardized effect size (derived by dividing the mean difference score by the standard deviation of the difference scores) is 1.09, an effect size considered in the literature to be very large. Since many migraine studies include only those who experience 2 to 14 migraines per month we also calculated effect size eliminating the 5 patients with 15 to 20 migraines/month and the 4 who experienced only one per month. This produced and even larger effect size: 1.23. We next added in 3 “dummy” cases showing no change to address concerns that those who fail to complete the minimum number of sessions (the minimum was 20, most had at least 40) might have been non-responders. This effort to approximate an “ intention to treat” analysis, assuming a 10% non-completer rate, reduced the 1.23 effect size in the restricted , 2 to 14 migraine sample, to 1.00, still a very large effect size.

Table 2 (click to enlarge). Sample characteristics and average number of migraines per month pre- and post-treatment

For each individual we also calculated the percent reduction in migraine frequency by dividing the difference between that individual’s pre- and post-treatment migraine frequency estimates by the average number of pre-treatment migraines they experienced. As illustrated in Figure 1, 70% of the sample (or 26/37) showed a 50% or greater reduction in the frequency of their migraines, and only 16% (or 6/37) failed to improve at all.

The significance of the observed changes was examined using the Wilcoxon signed ranks test, a non-parametric alternative to the t-test for small sample studies where the dependent variable is not normally distributed. In the Wilcoxon signed ranks test the differences between pre- and post-treatment scores are rank ordered, and the significance test is based on ranks, eliminating the potential biasing effects of large, spurious differences in either direction. If the treatment has no effect the sum of the ranks where the difference is positive should be nearly equal to the sum of the ranks where the difference is negative.

Figure 1 (click to enlarge). Percent reduction of migraine frequency.

In the present case, there was a large difference; in 31 cases post-treatment scores (average number of migraines per month) were less than pre-treatment scores, in 6 cases scores were equivalent, and there were no cases where post-treatment scores were greater than pre-treatment scores. The resulting z-score of -4.86 was statistically significant at the p<.001 level. Although the focus of this study was on migraine headaches, patients seeking neurotherapy are typically experiencing more than one problem, and migraine patients are no exception.

In the follow-up interviews we asked participants to (a) indicate which of several other common symptoms they were experiencing when they first sought treatment, and then (b) use a 5-point scale to rate the level of improvement they experienced following neurotherapy treatment. The response scale options were “no improvement” (0), “slight (10-30%) improvement” (1), “moderate (40%-60%) improvement” (2), “major (70-90%) improvement” (3), and “total (90- 100%) improvement” (4). Table 3 shows the number of individuals rating the 6 most common symptoms (migraine is included and the N of 34 indicates that we did not get ratings from 3 of the migraineurs who provided headache frequency data), and the percent reporting three levels of improvement. The first group includes those who selected either the “No improvement” or the “Slight (10-30%) improvement” response options, the middle group includes those who selected the “Moderate (40-60%) response option, and the third group includes those who selected “Major (70-90%) or Total (100%) improvement. Migraines were the most improved symptom based on this scale, with 62% or 23/37 reporting major or total improvement, followed by “other headaches,” where 50% or 19/37 reported major or total improvement. The percent reporting major or total improvement on other symptoms ranged from 32% to 41%. Sleep problems were least likely to be substantially improved.

Table 3 (click to enlarge). Ratings of improvement on migraine and other presenting problems.

Discussion
The concept of an under or over-aroused nervous system was first proposed by Nobel Laureate Walter Rudolph Hess who in the 1950s experimented with electrical stimulation of the brain which led to changes in arousal [26]. It has been theorized that disorders of attention, affect and pain are due either to over or underaroused brain states, and that neurofeedback is effective for a variety of symptoms or symptom clusters because it improves the brain’s ability to regulate these arousal states [13]. Neurofeedback treatment protocols address the underlying arousal problem, obviating separate validation studies for every medical diagnosis [13].

In this study, it appears that the biofeedback enabled the patients to gradually learn to control their susceptibility to getting headaches. Generally, they began to notice gradual improvements early on in treatment, particularly in their ability to manage stress, which was impetus for continuing treatment. This was assessed every 10 sessions by a written checklist and by interviews with a psychologist at each session. By session 20, most began to be aware of their ability to control or prevent their headaches. In most cases, by session 40, patients felt a sense of increased mastery over being better able to recognize when they were at risk (increased autonomic arousal in reaction to stress) and to take appropriate measures to be able to prevent headaches. 40 sessions happened to be the average number of sessions undertaken in the study.

Number of sessions ranged from 20-67 and was determined by what treatment provider and each patient felt they needed in order to ultimately learn to control migraines. These patients described the biofeedback as helping them to acquire the ability to better self-regulate by learning to control their EEG and reducing muscle tension, slowing the rate of their breathing and warming their hands and forehead, all of which were necessary for the types of biofeedback they had undergone. When asked how they thought they were better able to prevent headaches during interviews at each session and on checklists after every 10 sessions, many would explain that during potentially stressful conditions they would imagine hearing or visualizing the neurofeedback games and this appeared to help them invoke the physiological state elicited during the actual sessions.

We have observed that thermal biofeedback devices (pIR HEG machine and the hand warming units) can often be powerful migraine abortives once patients learn to raise their hand or forehead temperatures. All clients, whether or not they were successful at reducing their migraines, demonstrated an ability to warm their hands and foreheads and decrease their elevated EEG amplitudes of both slow and fast-wave activity. Patients related during session interviews that these techniques have eventually enabled them to automatically learn to abort their headaches without having to use the actual devices. Of the 37 patients in the study, five had fifteen or more migraines a month and all five improved significantly which may show promise that these methods can be useful for preventing the progression from episodic to chronic migraine.

Central nervous system dysfunction may play a key role in the pathogenesis of migraine [16-21]. As there are no apparent structural disturbances, clinical neurophysiological methods may be well-suited to study its pathophysiology [16]. In both migraine with and without aura, somatosensory evoked potential studies show that lack of habituation in cortical information processing between attacks is a reproducible central nervous system abnormality with this population [19]. Siniatchkin et al demonstrated the vulnerability of the migraine brain by measuring the effects of experimentally-induced stress on the contingent negative variation (CNV) response, which is a slow cortical potential believed to reflect altered excitability. This study showed a susceptibility to stress-induced migraine provoking agents before an actual attack [20]. Additionally, it has been observed that abnormal behavioral patterns such as hypersensitivity and perfectionism are often characteristic among migraine sufferers yet these psychological features may be the result of an innate cortical hypersensitivity in addition to associated social learning processes [21]. In this study neurofeedback appears to have improved stress resilience and susceptibility to migraines in the migraine participants. This may be due to the increase in self regulation brought about by the process of long term potentiation that may result from the operant conditioning of the EEG during the neurofeedback training [12].

Migraine has a comorbid association with a number of psychiatric conditions, including bipolar disorder, anxiety states, and depression, all of which are associated with perturbations in the serotonin and norepinephrine neurotransmitter substances [27,28]. Depression is often comorbid with migraines and anti-depressants are often used to treat both conditions [29]. Evidence that many neurological conditions are comorbid and alleviated by identical or very similar drugs supports three important principles in the spectrum paradigm: a) different symptoms are often manifestations of the same underlying instability or in balance, b) symptoms manifest differently depending on where they fall along the continuum of the underlying dysfunction, c) treatments need not be “disease specific” to be helpful [13]. Neurologist Oliver Sacks’ speculation that brainwave biofeedback might prove useful for migraines after showing promise in treating seizures supports the spectrum concept of related disorders responding to one mode of treatment [30].

Migraine and tension type headache were linked after both types showed a significant response to sumatriptan. A convergence hypothesis was proposed speculating that the entire clinical spectrum of headache may share a common physiological pathway based on one type of medication exerting an effect on two distinctly different types of headache [31,32]. Similarly, an older study shows that neurofeedback was effective for tension type headache [11] and our study finds that several types of biofeedback have an effect on migraines, other types of headache and other comorbidities. Biofeedback used with medications appears to outperform medications alone [5, 33,34]. In our study involving biofeedback with clients using medications, we saw the frequency of usage of the abortive and rescue medications drop along with the frequency of headaches.

Conclusions
Migraine may be progressive disorder with an excellent response to preventive early interventions [33,34]. Yet none of the pharmaceutical options are exceptionally effective or without side effects. The best result that medication has achieved has been only about a 50% reduction in approximately 50% of migraine patients [34]. Our study outperforms this by achieving a 50% or more reduction in 70% of the participants based on follow-up data collected on average, 14 months after patients had completed at least the minimum recommended 20 treatment sessions. The treatment effect sizes we obtained (1.09) are greater than those reported in a recent meta-analysis for either EEG-biofeedback (about .4) or temperature training feedback (about .5) or blood volume pulse feedback (about .7) alone, or temperature feedback plus electromyographic feedback (about .6) [5]. Although we did not have a control group, and thus cannot completely rule out placebo effects in this study, it may be unusual for a placebo effect to last 6 months to two years.

Despite the different types of intervention used in our study (manipulation of the EEG, forehead temperature or hand temperature), the retrospective reports of migraine frequency and the absence of a control group, the statistically and clinically significant improvements observed in this patient population attests to the promise biofeedback based treatment modalities hold for migraine patients. It is our hope that this study will generate an interest in performing larger scale controlled studies in the non-invasive neurotherapies to treat migraine and other chronic and/ or progressive disorders.

Citation:
Material adapted by CFisher from:

Stokes, D., & Lappin, M. (2010). Neurofeedback and biofeedback with 37 migraineurs: A clinical outcome study. Behavioral and Brain Functions, 6(9).

References:
1.  Lipton R, Bigal M:  Migraine: epidemiology, impact and risk factors for progression. Headache  2005, (Suppl):S3-S13.
2.  Ambrosini A, deNoordhout AM, Sandor PS, Schoenen J:  Electrophysiological studies in migraine: a comprehensive review of their interest and limitations. Cephalalgia 2003,23 (Suppl1):13-31.
3.  Lipton R, Bigal M, Diamond M, Freitag F, Reed ML, Stewart WF: Migraine prevalence, disease burden, and the need for preventive therapy.  Neurology 2007,68(5):343-349.
4.  Hu XH, Markson LE, Lipton RB, Stewart WF, Berger ML:  Burden of migraine in the United States: disability and economic costs. Arch Intern Med 1999, 159:813-8.
5.  Nestoriuc Y, Martin A, Rief, W, Andrasik, F:  Biofeedback treatment for headache disorders: a comprehensive efficacy review. Appl Psychophysiol Biofeedback 2008, 33:125-140.
6.  Silberstein, S: Practice parameter: Evidence based guidelines for migraine headache (an evidence-based review): report of the quality standards subcommittee of the American Academy of Neurology. Neurology 2000,55:754-762.
7.  Siniatchkin M, Hierundar A, Kropp P, Gerber WD, Stephani U: Self regulation of slow cortical potentials in children with migraine: an exploratory study.  Appl Psychophysiol Biofeedback 2000,25(1),13-32.
8.  Tansey MA: A neurobiological treatment for migraine: the response of four cases of migraine to EEG biofeedback training.   Headache Q- Curr Trea  1991,90-96.
9.  Andreychuk, T, Skriver, C: Hypnosis and biofeedback in the treatment of migraine headaches.  Int J Clin Exp Hypn 1974,23(3):172-83.
10. Carmen J: Passive infrared hemoencephalography: four years and 100 migraines.  J Neurotherapy 2004,8(3)23-51.
11. McKenzie R, Ehrisman W, Montgomery PS, Barnes RH: The treatment of headache by means of electroencephalographic feedback.  Headache 1974,13,164-172.
12. Duffy, F:  The state of EEG biofeedback (EEG operant conditioning: an editor’s opinion.  Clin Electroencephalogr 2000, Jan;31(1):V-VII.
13. Othmer S, Othmer S, Kaiser D:  EEG biofeedback: an emerging model for its global efficacy.  In: Evans JR, Abarbanel A, eds.  Introduction to Quantitative EEG and Biofeedback.  San Diego, CA: Academic Press; 1999, 259-262.
14. Hammond DC:  What is neurofeedback? J Neurotherapy 2005,10(4):25-36.
15. Hammond DC: Comprehensive neurofeedback bibliography: 2007 update. J  Neurotherapy 2008,11(3):45-60.
16. Kropp P, Siniatchkin M, Gerber WD:  On the pathophysiology of migraine- links for “empirically based treatment” with neurofeedback.  Appl Psychophysiol Biofeedback
2002,27(3);203-213.
17. Genco S, deTommaso M, Prudenzano AM, Savarese M, Puca FM:  EEG features in juvenile migraine: topographic analysis of spontaneous and visual evoked brain electrical activity: A comparison with adult migraine.  Cephalalgia 1994,14(1),41-46.
18. Schoenen J: Neurophysiological features of the migrainous brain.  Neurol Sci 2006,27:Suppl 2 S277-81.
19. Coppola G, Vandenheede M, DiClemente L, Ambrosini A, Fumal A, DePasqua V, Schoenen J: Somatosensory evoked high frequency oscillations reflecting thalamocortical activity are decreased in migraine patients between attacks. Brain 2005,Jan;128(1):98-103.
20. Siniatchkin M, Averkina N, Andrasik F, Stephani U, Gerber WD: Neurophysiological reactivity before a migraine attack. Neurosci Lett 2006 May 29; 400(1-2).
21. Gerber WD, Schoenen J: Biobehavioral correlates in migraine: the role of hypersensitivity and information-processing dysfunction. Cephalalgia 1998,Feb 18,(Suppl 21):5-11.
22. EEG Spectrum International:  Neurofeedback in a clinical practice Training manual. Canoga Park, CA: 2005,3-18.
23. Toomim H, Carmen J: Hemoencephalography (HEG).  Biofeedback 1999,27(4)10-14,27.
24. Headache Classification Committee of the International Headache Society.  Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain.  Cephalalgia 1988,8(Suppl7):19-28.
25. Headache Classification Committee of the International Headache Society.  The international classification of headache disorders, 2nd edition.  Cephalalgia 2004,24 (Suppl 1),1-151.
26. Hess WR:  Diencephalon: autonomic and extrapyramidal functions. New York, NY: Grune & Stratton; 1954.
27. Breslau N, Davis G:  Migraine, major depression and panic disorder: a prospective epidemiologic study of young adults. Cephalalgia 1992,12:85-90.
28. Jarman J, Fernandez M Davies P:  High incidence of endogenous depression in migraine: confirmation by tyramine test.  J Neurol Neurosurg Psychiatr 1990,53:573-575.
29. Silberstein S, Dodick D, Freitag F, Pearlman S, Hahn S, Scher A, Lipton R: Pharmacological approaches to managing migraine and associated comorbidities- clinical considerations for monotherapy versus polytherapy.  Headache 2007, 47:585-599.
30. Sacks O:  Migraine. Berkeley, CA: University of California Press; 1992: 265.
31. Cady R, Schreiber C, Farmer K, Sheftell F:  Primary headaches:  a convergence hypothesis. Headache 2002,42:204-216.
32. Cady R, Gutterman D, Saiers J, Beach M:  Responsiveness of non-IHS migraine and tension-type headache to sumatriptan.  Cephalalgia 1997,17:588-590.
33. Silberstein SD: Preventive treatment of headaches.  Curr Opin Neurol 2005,3:289-292.
34. Solomon S:  Major therapeutic advances in the past 25 years.  Headache 2007,47(Suppl1):S20-S22.

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