EEG-Driven Stimulation (EDS) is a form of EEG neurofeedback that involves monitoring and analyzing EEG signals read through surface electrodes on the scalp, and uses the EEG itself to guide the feedback by means of low-intensity light stimulation. The feedback signal is of very low power but produces measurable reaction in the EEG, and in brain function. The EEG signals influence the feedback, and the feedback, in turn, changes the EEG pattern.
Whereas EEG neurofeedback trains the person to alter brain wave activity, the Flexyx EEG-Driven Stimulation (EDS) system directly trains the brain itself. First developed in 1990 by Dr. Len Ochs at the University of California in Los Angeles (now owner of Flexyx LLC & Ochs Labs, Walnut Creek, California), the Flexyx EDS system uses photic (or light) stimulation to directly effect the brain waves through a process called “EEG entrainment”.
EEG entrainment refers to the well-known observation that brain waves tend to follow rhythms or frequencies in approximately the range of 1-30 Hz. That is, the brain will tend to produce an increase in EEG voltage or amplitude at the same frequency at which it is stimulated. For example, listening to a metronome steadily beating at 4 beats per second (a frequency of 4 Hz) will tend to cause an increase in brain wave activity at approximately 4 Hz frequency, whereas listening to a metronome at 10 beats per second (10 Hz) will cause an increase in faster 10 Hz brain waves. Similarly, looking at a light that is flashing at a certain rate or frequency will tend to increase brain wave activity at that same frequency— speed up or slow down the flash rate of the light and the brain waves will tend to follow.
Just as in EEG neurofeedback, the EDS system measures brain wave activity from electrodes placed on the scalp and sends this raw data to a computer for analysis. By means of special proprietary software developed by Flexyx LLC, the brain wave data is analyzed to determine the single frequency from 1-40 Hz that is the most powerful at any given moment— that is, the dominant EEG frequency. This calculated dominant frequency is then used to control the frequency of a set of flashing LED lights built into a set of eyeglasses worn by the patient. The flashing lights can be set by the therapist to lead or lag the EEG dominant frequency by some amount. The therapist can also change the brightness of the flashing lights.
With EDS there is a complex interaction between the patient’s brain waves and the flashing lights in the eyeglasses. This is because the frequency of the flashing light stimulus changes with the EEG dominant frequency— as the dominant moves to a faster frequency, the light stimulus flashes faster; as the dominant moves to a lower frequency, the light stimulus flashes slower— but the frequency of the flashing lights also tends to control the frequency of the EEG dominant through the process of entrainment. When the therapist sets the flashing lights to lead the EEG dominant by some fixed amount— say 5 Hz— the lights will always flash at 5 Hz faster than the EEG dominant frequency and this will tend to move the EEG dominant into a higher frequency range. Similarly, when the therapist sets the flashing lights to lag the EEG dominant by some fixed amount— say 3 Hz— the lights will always flash at 3 Hz slower than the EEG dominant and tend to move the dominant into a lower frequency range.
The Flexyx EDS system has been clinically demonstrated to be a very effective technique for treating problems that appear to be associated with brain wave patterns that are more or less stuck in one part of the total EEG spectrum. For example, clinical evidence suggests that most patients with fibromyalgia or chronic fatigue show excessive amounts of lower frequency delta (0-4 Hz) and theta (4-8 Hz) brain wave activity with measured EEG dominant activity that infrequently moves above alpha (8-12 Hz) into the beta (12-30 Hz) range of the total EEG spectrum (e.g., Chaudhuri, Holden, & Donaldson, 1996; Donaldson, Sella, & Mueller, 1998; Mueller, Donaldson, Nelson, & Layman, 2001).
How Does EDS Differ From AVE and EEG Neurofeedback?
EDS differs from EEG neurofeedback in that EDS does not require the patient to understand the meaning of, or consciously attend to, the feedback signals in order to control them and, thereby, benefit from treatment. No attentional, discrimination, or conscious learning demands are placed on the EDS patient. The feedback goes directly to the brain by way of the optic nerve and the occipital cortex and its connections with the rest of the brain. The pattern of photic stimulation is processed by the brain and facilitates adjustment of ongoing background brain activity without the patient’s conscious awareness.
EEG neurofeedback involves learning through operant conditioning; whereas EDS is a form of Pavlovian or classical conditioning.
EDS also differs from commercially available audio visual entrainment or AVE devices in that the light strobing frequency is directly controlled by the patient’s own EEG activity. The stimulation frequency of the consumer AVE systems is pre-programmed and changes in ways that are unrelated to the user’s own brain wave activity. With these commercial AVE devices the user may be able to select from a variety of pre-set programs designed to entrain brain waves in some particular manner to enhance relaxation, or meditation, or deep sleep, or mental energy and creativity, etc. but the program cannot adjust itself to ensure that the user becomes entrained. EDS customizes the stimulation from moment-to-moment on the basis of the patient’s own changing EEG. AVE devices are not biofeedback devices.
How Does EDS Work?
EDS works by continuously monitoring (128 times/second) brainwave activity (EEG) from one scalp location at a time and using these readings to determine the frequency of low intensity strobing lights directed in front of the subject’s closed eyes. The frequency of the strobing lights can be set to lead or lag the subject’s moment-to-moment dominant EEG frequency by some set amount from ±1 Hz to ±20 Hz. Variables that may be modified in the session are: (1) amount of frequency lead or lag in each of 4 periods per cycle; (2) length of time per period; (3) light intensity in each period; (4) duty cycle of lights in each period; (4) percent synchrony/asynchrony of light flashes to right versus left eye; (5) number of cycles per session; (6) colour of strobing light; and (7) location of EEG recording.
What Does EDS Do?
The purpose of EDS is to reduce the amplitude and variabilty (including spiking) of the EEG activity across the 1-30 Hz spectrum at each of the standard International 10/20 system sensor sites. Although EDS takes advantage of the brain’s tendency to follow or entrain to frequencies in 1-30 Hz range, the purpose of EDS is not to entrain the brain to any specific frequency nor to increase some specific waveband while decreasing some other, but to quiet the EEG and increase dominant ranging. In this sense, EDS is actually a disentrainment device. With increasing EDS sessions, the EEG becomes increasingly less hyper-reactive to stimulation-- both from the EDS lights and from other internal and external sources.
Why Should We Do This?
There is increasing clinical and research literature pointing to a group of neurological or neurosomatic disorders which are characterized by slowing of the EEG-- i.e., increased amplitudes of low frequency delta, theta & slow alpha activity with reduced movement of the moment-to-moment dominant frequency above low alpha (10 Hz) levels. These disorders include: Attention Deficit Disorder (ADD), Minor Head Trauma (MHT) and Post-Concussive Syndrome (PCS), Toxic Trauma (TT), Chronic Fatigue Syndrome (CFS), Fibromyalgia Syndrome (FMS), Pre-Menstrual Syndrome (PMS), Post-Polio Syndrome (PPS), and Post-Traumatic Stress Disorder (PTSD). Reduced overall EEG amplitudes and a high theta:beta ratio have also been noted from left-hemisphere locations in persons who are depressed. Symptoms commonly associated with such EEG slowing are: irritable, anxious and depressed mood, low mental and physical energy, sleep disorder, decreased cognitive functioning (mental fogginess), and increased pain sensitivity with reduced localization.
Clinical experience with EDS has shown that “normal” asymptomatic persons sitting comfortbly at rest with eyes closed demonstrate a relatively flat EEG (amplitudes <3.0 microvolts) with frequent and free ranging of dominant frequency from 1-30 Hz with a mean dominant frequency in the high alpha-low beta range (12-16 Hz) as recorded from all locations under barely visible levels of light stimulation. Delta;Theta;Beta ratios are generally very close to 1:1:1. In contrast, persons with neurosomatic disorders demonstrate abnormally high amplitudes (>4.0 microvolts) of lower frequency activity (1-10 Hz) with dominant frequency rarely ranging above 10 Hz from primarily frontal, prefrontal and central sites under barely visible levels of light stimulation. It is not uncommon to see Delt:Theta:Beta ratios equal to or greater than 3:2:1. Symptomatic individuals also tend to initially demonstrate more “irritable” EEGs to increasing light stimulation levels than do normals.
When chronic pain subjects first enter EDS treatment, they tend to see themselves as overly sensitive to many things. In fact, these persons are better described as over-reactive and relatively insensitive. These persons are so reactive to external and internal stimuli and so caught up in the emotional, cognitive, glandular, vascular, and motoric elements of their reactions to these stimuli that there is literally no opening for being aware of the actual stimuli. Persons who view themselves as hypersensitive are rarely aware of their true situations or their true feelings. They are instead highly aware of their reactions to these situations and feelings and often become overwhelmed by the distress and discomfort of their reactions or overwhelmed by the difficulty of taking things in.
So How Does EDS Really Work?
While the final determination on how EDS really works must rest with a great deal of further research, we presently believe that EDS works to break up the rigid, self-protective way that the brain has of responding after psychological stress or physical trauma. There is evidence that during any kind of trauma, the brain protects itself from seizures and overloads by releasing various chemicals that reduce these risks. Unfortunately, this protective mechanism also reduces functional capacity, not unlike the effect of inflammatory swelling on joint articulation. Long after the trauma is over and the danger is past, the “protection” may remain turned on. The person can, therefore, become stuck in various kinds of disabilities due to the reduced neural flexibility.
We believe that the effect of trauma on the brain is to reduce the impermeability of the cortex to stimulation from lower centres, particularly the thalamus and limbic systems. The cortex loses some of its integrative ability and permits unprocessed stimulation to leak through.
We believe that the hyper-reactivity commonly seen in neurosomatic patients is a function of increased cortical permeability to inputs from the thalamus and limbic systems that results from neurochemical changes in response to psychological stress or physical trauma to the brain. It has been frequently observed that individuals with chronic central nervous system dysfunctioning have higher levels of recordable low frequency electrical activity at scalp sites. It has further been observed that, as the functioning of the individual improves with treatment, the amplitude of the low frequency EEG diminishes. We believe that a traumatized brain undergoes neurochemical changes that increase cortical permeability and allow low frequency signals from the thalamus and limbic systems to come through the cortex relatively unintegrated. EDS functions to decrease cortical permeability by increasing the integrative functioning of the cortex. By feeding back frequency information that is different from that which is measured at the scalp site, but nonetheless perfectly correlated with the measured frequency, may place different neurochemical demands on the synapses which feed the measured activity. If there is post-traumatic inhibitory neurotransmitter activity interfering with cortical function, (i.e., increasing cortical permeability) and if the mechanism perpetuating this activity is disturbed and altered, then the synaptic neurochemical mix might also be altered top once again permit decreased cortical permeability and proper integrative functioning of the cortex.
Who Can Benefit From EDS?
People suffering the effects of head injury, extreme stress, anxiety attacks, depression, emotional trauma, attention deficit disorder, autism, explosive disorders, Alzheimer’s and fibromyalgia have benefited greatly. Post-stroke deficits have also improved with FNS. Potential benefits can be evaluated by a specialized three-hour examination.
How Long Does Treatment Take?
A person’s sensitivity, and the complexity and duration of symptoms determine how long treatment lasts. Effects of a single upset may be resolved in as few as three or four sessions. Lifelong or complex problems may take 40 or more. A single session lasts approximately 30-45 minutes.
Is EDS Proven? And Do The Effects Last?
EDS has been studied clinically since 1990 with many thousands of patients. Approximately 70-75% of patients treated with EDS have experienced significant improvements in their CNS symptoms, and the benefits gained seem only to sustain or increase, unless new trauma occurs. Although clinical and experimental research continue, and more experimental research is planned, on very limited scientific research on EDS has seen publication to date.
References and Suggested Further Reading
Anderson, D. (1989). The treatment of migraine with variable frequency photo-stimulation. Headache, 29, 154-155.
Boersma, F. & Gagnon, C. (1992). The use of repetitive audiovisual entrainment in the management of chronic pain. Medical Hypnoanalysis Journal, 7 (3), 80-97.
Cady, R. & Shealy, N. (1990). Neurochemical responses to cranial electrical stimulation and photo stimulation via brain wave synchronization. Available from Shealy Institute of Comrehensive Health Care, Springfield, Missouri.
Charter, J. & Russell, H. (1992). Effects of EEG frequency control training on boys with significant WISC-R Verbal vs. Performance IQ discrepancies. Journal of Biofeedback & Self-Regulation.
Chaudri, B., Holden, W., & Donaldson, S. (1996). Electroencephalogram (EEG) Driven Stimulation (EDS) to Improve Fibromyalgia Pain Symptoms. Unpublished poster presentation at the 31st Annual Meeting of the National Congress of Neurological Sciences, June 25-29, 1996, London, Ontario.
Chijiiwa, M., Yasushi, M., Saito, S., et al. (1992). Application of photic feedback system to psychosomatic medicine. Japanese Journal of Biofeedback Research, 19, 49-56.
Donaldson, C.S. (1999). The pain of fibromyalgia: A message to the practitioner. Biofeedback, 27(3), 11-12.
Donaldson, C.S., Sella, G.E., & Mueller, H.H. (1998). Fibromyalgia: A retrospective study of 252 consecutive referrals. Canadian Journal of Clinical Medicine, 5(6), 116-127.
Donaldson, C.S., Sella, G.E., & Mueller, H.H. (submitted). The neural plasticity model of fibromyalgia: Theory, assessment and treatment. American Journal of Pain Management.
Donaldson, M.., Mueller, H.H., Donaldson, C.S., Sella. G.E. (2003). QEEG patterns, psychological status and pain reports of fibromyalgia patients. Clinical findings. American Journal of Pain Management, 13(2), 60-73.
Fox, P. & Raichle, M. (1985). Stimulus rate determines regional blood flow in striate cortex. Annals of Neurology, 17, 303-305.
Kumano, H., Harumi, H., Tomoko, S., et al. (1996). Treatment of Depressive Disorder Patient with EEG-Driven Photic Stimulation. Biofeedback & Self-Regulation, 21(4), 323-334.
Mueller, H.H. (1998). Brain waves. The key to curing fibromyalgia? Feel Good Magazine, March/April 1998, 24.
Mueller, H.H., Donaldson, C.S., Nelson, D., & Layman, M. (2001). Treatment of fibromyalgia incorporating EEG-driven stimulation: A clinical outcomes study. Journal of Clinical Psychology, 57(7), 933-52.
Mueller, H.H., Holden, W., & Layman, M. (2000). EEG neurotherapy: New kid on the block. PAA Psymposium, 9 (5), 26-28.
Noton, D. (1996). PMS, EEG and Photic Stimulation. Unpublished poster presented at the 1996 nAnnual Meeting of the Association for Applied Psychophysiology and Biofeedback, March 1996, Albuquerque, New Mexico. See AAPB Proceedings.
Ochs, L. (1992). EEG treatment of addictions. Biofeedback, 20 (1), 8-16.
Fibromyalgia Patients Treated With
EEG-Driven Stimulation and
Myofascial Physical Therapies
at Myosymmetries Edmonton
SUMMARY OF CLINICAL OUTCOMES
Dr. Horst H. Mueller, RPsych, CRHSPP, FBCIA-EEG
Clinic Director & Senior Consulting Psychologist
Myosymmetries Edmonton Inc.
The overall effectiveness of combining treatment modalities focused on both central and peripheral nervous systems in alleviating the complex psychological and somatic complaints associated with fibromyalgia was demonstrated by a recent clinical outcomes study of a series of 30 consecutive fibromyalgia patients treated at Myosymmetries Edmonton (see Mueller, Donaldson, Nelson & Layman, 2001). Another 16 patients were subsequently added to the end of October 2002, for a grand total of 46 fibromyalgia patients for whom treatment outcomes data is summarized in this report.
All patients (41 female, 5 male; aged 49.1 ± 10.7 years) included in this study had been previously diagnosed with fibromyalgia by a treating physician, fully met the American College of Rheumatology classification criteria for fibromyalgia as determined by both their history and a physical examination with tender point palpation and dolometry, and were actively symptomatic at the time of their intake to treatment. Disease chronicity averaged 5.5 ± 4.6 years.
Although there was some individual variation, patients were generally treated 3-5 times per week with an advanced form of EEG neurotherapy— EEG-Driven Stimulation (EDS) (Flexyx LLC, Walnut Creek, California)— exclusively until their in-session self-reports began to reveal a positive change in perceived mental clarity, mood, and restorative sleep as well as a shift from experiencing “all-over-body” pain to more localized aches and pains. Once this shift in self-reported symptoms became apparent (i.e., mean of 16 ± 6 weeks; range 6-29 weeks), the number of EDS sessions per week were gradually reduced and 2-3 weekly sessions of physical therapies were added. Physical therapies included some combination of trigger point massage, intramuscular stimulation, myofascial and positional release, stretch and spray, sEMG-assisted neuromuscular retraining, prescribed muscle stretching and strengthening exercises, dependent on each patient’s individual needs. As a group, these patients averaged 36 ± 16 hours of EDS and 8.9 ± 9.5 hours of physical therapies over the course of approximately 4-6 months of treatment. The cost of treatment varied significantly between patients, with an average cost of CAD$4300 ± $1960.
Significant pre- versus post-treatment changes were obtained on the Symptom Check List 90-R (SCL-90-R) (Derogatis, 1994), the Fibromyalgia Impact Questionnaire (FIQ) (Burckhardt, Clark, & Bennett, 1991), repeated patient self-reports of selected key symptoms using a 10 centimeter visual analog scale (VAS), spectral EEG bandwidth power, number of positive tender points, mean pain threshold over tender points, and total percent of body perceived as painful. Patients rated themselves as an average of 66.1% ± 19.5% improved overall (range 20%-90%) at the time of their follow-up, an average of 9.7 ± 5.1 months after treatment was terminated.
Treatment was associated with significant improvement in SCL-90-R Global Severity Index scores, as well as 7 of 9 subscales; with greatest change in those symptoms included within the Somatization, Obsessive-Compulsive, Depression, and Anxiety subscales. Broadly, SCL-90-R profiles shifted from clinical to normal levels. Similarly, patient VAS ratings for sleep quality, pain intensity, level of fatigue, level of cognitive clouding, level of depression, and level of anxiety improved significantly from intake to discharge (i.e., 145%, 56%, 50%, 67%, 71%, and 71% improved, respectively).
EDS therapy was associated with a significant decrease in average levels of cortical delta (1-4 Hz), theta (4-8 Hz), and alpha (8-12 Hz) power as measured in pre- versus post-treatment brain maps (i.e., 35%, 32%, and 19% reductions, respectively). Changes in low beta (12-18 Hz) and mid beta (18-24 Hz) power were not significant at less than 2%.
Treatment also resulted in a significant decrease in the average percent of the body perceived as painful, from a mean of 31.2% ± 12.1% at intake to 9.6% ± 9.5 % at discharge. Similarly, treatment resulted in a significant reduction in number of positive tender points (from 15 ± 3 at intake, to 7 ± 3 at discharge) for the group; with all patients meeting the criteria of at least 11 of 18 tender points positive for pain at less than 4.0 kg/cm2 of pressure on intake and only 4 patients still meeting this criteria on discharge. As a group, the mean pain threshold over the 18 fibromyalgia tender point locations increased significantly; from 2.6 ± 0.7 kg/cm2 to 3.9 ± 0.6 kg/cm2 of pressure.
Finally, there were significant increases in patients’ “activities of daily living” (over 50%), average days per week in which patients “felt good” (from 1.1 to 4.8 days), and average number of nights per week patients “slept well” (from 1.8 to 5.4 nights) as reported on the FIQ at treatment intake versus at follow-up, an average of 9.7 months post-treatment.
Because all patients received differing amounts of the different therapy modalities, it was not possible to determine which therapy accounted for the majority of the patients’ improvements. However, it was noted that reductions in EEG delta and theta amplitudes correlated significantly with improvements in SCL-90-R Global Severity Index, Somatization, Depression, and Anxiety scores as well as with improved ability to perform activities of daily living, increased number of days in which patients felt good, and increased number of nights patients slept well as indicated on the FIQ. Number of sessions of EDS therapy correlated most strongly with patients’ self-report of reduced pain and improved sleep over the course treatment sessions. Time spent in physical therapies was most strongly correlated with reductions in patients’ number of positive tender points, increased pain threshold, and decreased percent of the body experienced as painful.
These outcomes based on 46 fibromyalgia patients seen for therapy at Myosymmetries Edmonton are broadly consistent with observations on a larger number of such patients seen at Myosymmetries Calgary (see Donaldson, Sella & Mueller, 1998).
Donaldson, C.C.S., Sella, G.E., & Mueller, H.H. (1998). Fibromyalgia: A retrospective study of 252 consecutive referrals. Canadian Journal of Clinical Medicine, 5 (6), 116-127.
Donaldson, M., Mueller, H.H., Donaldson, C.C.S., & Sella, G.E. (2003). QEEG patterns, psychological status, and pain reports of fibromyalgia sufferers. American Journal of Pain Management, 13(2), 60-73.
Mueller, H.H., Donaldson, C.C.S., Nelson, D.V., & Layman, M. (2001). Treatment of fibromyalgia incorporating EEG-driven stimulation: A clinical outcomes study. Journal of Clinical Psychology, 57(7), 933-952.
Copyright Myosymmetries Edmonton 2003. Last revised 10/03