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Edmonton Neurotherapy
Treatment of Migraine
EEG & HEG Neurofeedback Approaches




What is Migraine Headache?

Migraine is a complex and heterogeneous disorder, in which genetics and environment interact to generate dysfunctioning paths and loops at several levels of the nervous system.

A migraine headache is a severe, often debilitating headache with throbbing pain; usually worse on one side of the head near the temples, forehead, and eyes that is often preceded or accompanied by sensory warning signs (called migraine "aura") such as flashes of light, blind spots, tingling in the arms and legs, nausea, vomiting, and increased sensitivity to light and sound. The excruciating pain that migraines bring can last for hours or even days and can result in substantial functional impairment that can have both physical and psychological ramifications.

Migraine is not just an "extreme headache" nor is it a psychosomatic condition. It is a neurological condition with episodic attacks that has potential to progress to more frequent and severe patterns; possibly to even chronic migraine.   

Migraine is a common disorder in Canada, affecting about one in ten of all Canadians, including one in six women. Before puberty, the prevalence of migraine is similar in boys and girls. However, post-puberty, migraine becomes increasingly common in women, at a rate that is 2.5 to 3 times higher than in men. The preponderance in women, which persists throughout adulthood is believed related to hormonal factors. Although, since the gender disparity persists beyond menopause, other factors must be involved that are as yet not well understood. Age is also a factor, with incidence rates increasing after age 12 and peaking at approximately age 40. 

In 2001, the World Health Organization (WHO) cited migraine as the 19th leading cause of years lived with disability among both males and females of all ages combined and the 12th leading cause of of years lived with disability among females of all ages. Missed work and lost productivity from migraine create a significant public burden. More than 60% of diagnosed migraineurs report their headaches leave them severely impaired, while more than 90% report at least some headache-related disability.

Due to poor understanding about the condition, migraine is often misdiagnosed or not diagnosed at all. It is frequently mistaken for tension-type headache or sinus headache, even though the latter is actually quite rare. Less than half of individuals with migraine are diagnosed by their primary care physician and less than 15% have been seen by a headache specialist. As a consequence migraine remains largely underdiagnosed and undertreated.

To see a brief YouTube video on diagnosing and treating migraine headache in Canada, please click on this link... http://www.youtube.com/watch?v=YEtbbHrJj08 


Current Pathophysiological Understanding

The exact cause of migraines is still not well understood, but the problem is considered neurological (i.e., related to the nervous system). It is believed that various brain chemicals, blood vessels, and nerves of the brain are involved.

The still commonly held idea that migraines are simply a vascular event has been largely shown to be inadequate. The more current thinking is that migraines are a complex neurological process involving the brain cortex and the trigeminovascular system.

The current understanding is that migraine is a neurochemical chain reaction that involves a number of distinct phases of a neurological process -- prodrome, aura (which my or may not be noticable), mild, moderate, or severe pain, and postdrome.

Once the reaction is triggered, fluctuation in neuronal activity in a hyperexcitable cortex may activate the trigeminovascular system in the meninges. Once activated, the trigeminal nerve can release various vasoactive peptides, producing an inflammatory response that probably causes the actual head pain.

In turn, the inflammatory response lowers the sensory threshold of the trigeminal nerve, increasing the flow of sensory traffic to the second-order neurons in the brainstem, especially the trigeminal necleus caudalis. This sensory input is allowed to reach higher brain centers of the thalamus and be transmitted up into the cerebral cortex -- the central areas of pain perception.

Migraine symptoms follow the escalating neuronal process. Migraine attacks tend to build in pain intensity and frequency over hours or days. The activation of the trigeminal system also explains facial and neck pain that can occur during migraine and that are not infrequently mistaken for symptoms of either sinus or tension-type headache.

Up to 20 percent of migraineurs experience an aura as part of their episodes and this is believed to be caused by cortical spreading depression (CSD) with extreme glutamate release. Cortical spreading depression is a slowly propagating wave of depolarization involving neuronal and glial cells in the cerebral cortex followed by a longer lasting suppression of brain activity characterized by massive changes in ionic concentrations and slow chemical waves. CSD is a remarkedly complex complex event that involves dramatic changes changes in neural and vascular function and has been hypothesized to be the underlying mechanism of the migraine aura. In more simplified terms, the electrical change tht occurs with CSD results in stress that triggers changes in the brain, which cause the neurotransmitter serotonin to be released, which constricts thaen dilates blood vessels, causing secondary inflammation and neurogenic pain.


Cortical spreading depression (CSD) is a slowly propagated wave of depolarization
followed by suppression of brain activity.

Brain imaging and brain stimulation research is increasingly supporting the idea that virtually all migraine headaches are cortical in origin and that a neuroinflammatory mechanism could not be involved in the initiation of the headache. The neuroinflammatory response appears to be secondary but may be important in the maintenance of the headache and other secondary symptoms involving the sympathetic nervous system.

It is a well-known fact that brain excitability is abnormal in migraine during the interictal period and the current evidence suggests that the migraine headache arises from abnormal neural impulse activity in the pyramidal cells in the outer layers of the cerebral cortex and it is such cells in the primary somatosensory area (S1) that are responsible for the actual headache. The presence of multiple symptoms preceding or during the headache are believed due to independent islands of cortical hyperactivity. While the actual cause of the neural hyperactivity remains unknown, it is likely to involve individual and gender-based genetic and molecular mechanisms.

Migraine attacks also commonly activate the sympathetic nervous system in the body. The sympathetic nervous system is often thought of as the part of the nervous system that controls primitive responses to stress and pain, the so-called "fight or flight" response, and this activation causes many of the symptoms associated with migraine attacks; for example, the increased sympathetic activity in the intestine causes nausea, vomiting, and diarrhea.

  • Sympathetic activity also delays emptying of the stomach into the small intestine and thereby prevents oral medications from entering the intestine and being absorbed.
  • The impaired absorption of oral medications is a common reason for the ineffectiveness of medications taken to treat migraine headaches.
  • The increased sympathetic activity also decreases the circulation of blood, and this leads to pallor of the skin as well as cold hands and feet.
  • The increased sympathetic activity also contributes to the sensitivity to light and sound sensitivity as well as blurred vision.

Some people who suffer from migraines can clearly identify triggers or factors that set off the headaches, but many cannot. Some of the more commonly reported potential migraine triggers include:

  • Allergies and allergic reactions
  • Bright lights, loud noises, and certain odors or volitile aerosol chemicals such as in perfumes
  • Physical or emotional stress/distress
  • Changes in sleep patterns or irregular sleep
  • Smoking or exposure to smoke
  • Skipping meals or fasting
  • Alcohol consumption, especially red wine and brandy
  • Menstrual cycle fluctuations, birth control pills, hormonal fluctuations
  • Tension headaches
  • Foods containing the amino acid tyramine, monosodium glutamate, or nitrates
  • Other foods such as chocolates, nuts, peanut butter, avocado, banana, dairy, pickles, etc.

Not all migraines appear to have specific triggers, and avoiding common triggers does not always prevent migraines. 

Symptoms of migraine can occur a while before the headache, immediately before the headache, during the headache, and after the headache. Although not all migraines are the same, typical symptoms include:

  • Moderate to severe pain, usually confined to one side of the head, but switching in successive migraines.
  • Pulsing and throbbing head pain.
  • Increasing pain during physical activity.
  • Inability to perform regular activities due to pain.
  • Nausea, vomiting, diarrhea
  • Increased sensitivity to light, sound, odors

Many migraineurs experience migraine auras just before or during the onset of headache, but most do not. Auras are perceptual disturbances such as confusing thoughts or experiences and the perception of strange lights, sparkling or flashing lights, lines in the bvisual field or blind spots, pins and needles in the arms or legs, or unpleasant smells.

Migraineurs may also have premonitions called "prodromes" that can occur several hours or even a day or more before the headache. These prodromes may consist of feelings of elation or intense energy, cravings for sweets, thirst, drowsiness, irritability, or depression.

To see a brief YouTube video with information on the pathophysiology of migraines, please click on this link...  https://www.youtube.com/watch?v=dFsfzLV8ZEw


EEG Neurofeedback for Migraine
Training the brain to stabilize itself and down-regulate cortical hyperexcitability

Although neuroimaging studies using MRI are usually normal in uncomplicated migraine, QEEG assessment will often show abnormalities in persons with recurrent migraine (Bjork, et al., 2009; Sprenger, 2010; Sprenger & Goadsby, 2009) and when followed up by EEG neurofeedback to normalize the abnormal QEEG findings, a majority of migraineurs will experience significantly fewer and less severe headaches and some will become drug-free and no longer experience headaches.

Routine clinical EEG, done between episodes of headache, has not proven to be useful in the evaluation of patients with headaches. However, QEEG abnormalities have been reported in a number of studies. Most recently, Dr. Jonathan Walker (Walker, 2011) reported finding significantly increased high-frequency Beta (21-30 Hz) activity in a few cortical areas; most commonly in central, centro-parietal, and parietal regions.

In the Walker study (Walker, 2011), 71 patients (aged 17-62 yrs) with recurrent migraine headaches, from one neurological practice, completed a QEEG assessment. All QEEG results indicated an excess of high-frequency beta activity (21-30 Hz) in anywhere from one to four cortical areas. Forty-six of the 71 patients selected neurofeedback training while the remaining 25 chose to continue on drug therapy. Neurofeedback protocols consisted of reducing 21-30 Hz activity and increasing 10 Hz activity (5 sessions for each affected site). All the patients were classified as migraine without aura. For the neurofeedback group the majority (54%) experienced complete cessation of their migraines, and many others (39%) experienced a reduction in migraine frequency of greater than 50%. Only 4% experienced a decrease in headache frequency of less than 50% and only one patient failed to experience any reduction in headache frequency. The control group of subjects who chose to continue drug therapy as opposed to neurofeedback experienced no change in headache frequency (68%), a reduction of less than 50% (20%), or a reduction greater than 50% (8%).

Based on Dr. Jon Walker's recent study, QEEG-guided neurofeedback appears to be dramatically effective in abolishing or significantly reducing headache frequency in patients with recurrent migraine. Drug therapy of any kind rarely eliminates migraine headaches. Peripheral biofeedback procedures such as temperature training or muscle relaxation training or pulse training, may decrease the frequency of migraines but rarely eliminates them (see Nestoriv & Martin, 2007).

An earlier clinical study by Stokes and Lappin in 2008 examined the effectiveness of two types of neurofeedback--i.e., EEG and HEG neurofeedback--combined with a more conventional peripheral biofeedback therapy--i.e., temperature biofeedback from the fingers--in the treatment of migraine headache. In their study, 37 migraine patients were given an average of 30 EEG and 10 HEG neurofeedback training sessions combined with 5-10 finger temperature biofeedback training sessions (to train handwarming) over an average six-month period. They reported that 62% of their patients obtained major improvement or total remission of their migraines, 18% obtained moderate improvement, and only 21% obtained slight improvement. Fully 70% of the patients obtained a greater than 50% reduction in the frequency of their headaches and no patient experienced a worsening of their headaches. As well, most patients also experienced significant improvements in their sleep, mood, and mental focus.

Many neurotherapy practitioners also support heart rate variability (HRV) biofeedback training in conjunction with EEG neurofeedback as way of increasing the effectiveness of treatment. 

To see brief news reports on EEG neurofeedback for migraine, please click on these links...  



To see brief Youtube videos of migraineurs talking about their success with EEG neurofeedback treatment, please click on these links... 




What is HEG Neurofeedback and How Can It Help Migraines?

HEG neurofeedback involves placing an infrared sensor on the middle of the forehead. The sensor gives a reading of the amount of oxygen being carried by the blood vessels in the frontal lobes of your brain (i.e., the part of your brain just behind your forehead).

For more detailed information on HEG neurofeedback, GOTO: http://www.edmontonneurotherapy.citymax.com/neurofeedback_therapies.html 

Learning to increase the activity of the frontal lobes reduces the number and/or severity of migraines and can even stop a migraine when it's happening.

The frontal lobes are largely inhibitory and regulatory, meaning they put the brakes on other parts of our brain when necessary and help "balance" the activities of the brain as a whole. So by training the frontal lobes to be more active and efficient, they seem to control/reduce the spasms of the trigeminal-vascular system. This results in either less frequent spasms (i.e., fewer headaches) and /or quicker control of the migraine (i.e. shorter headaches, even "silent migraines").

Dr. Jeffrey Carmen has completed a study of 100 people with migraines over 4 years who were taught to increase the blood flow to their frontal lobes using HEG. He found that over 90% of those who completed at least 6 sessions got significant relief from their headaches. There have been a number of other studies that have found similar results.

What are the Side-Effects?

There is a chance of "side-effects" after initial sessions of HEG neurofeedback if you work too hard or too long. These effects will look like less efficient frontal lobes: maybe a migraine, extreme irritability, attention problems, etc. Even if they happen, you will likely feel back to normal or better after a good night's sleep. The good news is that these are easily avoided by being gentle during the first couple sessions and stopping when you feel you are tired and, even if they happen, you will likely still get improvements from the session after the temporary side-effects go away.

The really good news is that the long-lasting "side-effects" of HEG neurofeedback training for migraines include: improved attention and concentration, less emotional sensitivity when it's not needed (e.g., irritability, tears, anxiety), better planning and organization -- all associated with improved frontal lobe functioning.


Bjork, M., Stovner, L., Nilsen, B., Stjern, M., Hagen, K., Sand, T. (2009). The occipital alpha rhythm related to the "migraine cycle" and headache burden: A blinded, controlled longitudinal study. Clinical Neurophysiology, 120(3): 464-471.

Nestoriuc, Y. & Martin, A. (2007). Efficacy of biofeedback in treating migraine: A meta-analysis. Pain, 128: 111-127.

Nestoriuc, Y., Martin, A., Rief, W., et al. (2008). Biofeedback treatment for headache disorders: A comprehensive efficacy review. Applied Psychophysiology & Biofeedback, 33: 125-140.

Sprenger, T. (2010). Abnormal brain activity in migraineurs is not restricted to attacks. Paper presented at 52nd Annual Scientific Meeting of the American Headache Society.

Sprenger, T., Goadsby, P. (2009). Migraine pathogenesis and pharmaceutical treatment options. BMC Medicine, 7:71.

Stokes, D. & Lappin, M. (2008). EEG biofeedback, hemoencephalographic biofeedback, and thermal biofeedback with 37 migraineurs. EEG Spectrum Clinical Interchange Conference, Los Angeles, CA. April 25, 2008.

Stokes, D. & Lappin, M. (2010). Neurofeedback and biofeedback with 37 migraineurs: A clinical outcome study. Behavioral & Brain Functions, 6(9): 2-10.

Tansy, M. (1991). A neurobiological treatment for migraine: Response of four cases of migraine to EEG biofeedback training. Headache Quarterly: Current Treatment & Research, pp. 90-96.

Walker, J. (2011). QEEG-guided neurofeedback for recurrent migraine headaches. Clinical EEG & Neuroscience, 42(1): 59-61.


Transcranial Direct Current Stimulation (tDCS)
A Promising Investigational Treatment for Migraine.

In the light of the changing understanding of migraines as primarily a neurological event involving hyperexcitability and dysregulation of neuronal activity within the cerebral cortex, there has been an increasing interest in the use of neuromodulation techniques in the treatment of migraine.

Although randomized controlled trials are scarce and large sample size studies are as yet nonexistent, some preliminary clinical research results are encouraging and peripheral and central nervous system neuromodulation techniques are considered promising alternatives to pharmacological treatment. Among these various techniques, repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) are the focus of the greatest clinical interest.

While both rTMS and tDCS are able to durably modify the excitability of underlying cortical neurons and could potentially correct the functional abnormalities found in migraine patients, tDCS has the great advantage of being a much less complex and relatively inexpensive technology that can be quite safely used by the patient at home for self-treatment with proper guidance and supervision from a knowledgeable health practitioner.

Transcranial direct current stimulation (tDCS) uses weak DC electrical currents, applied via electrodes attached to the scalp, to modify the resting membrane potential of cortical neurons in the stimulated and interconnected brain regions. Anodal (i.e., positive pole) stimulation increases neuronal excitability, while cathodal (i.e., negative pole) stimulation inhibits neuronal excitability.

A recent therapeutic study by Alessandro Vigano and colleagues at the Headache Research Unit, Department of Neurology, University of Liege in France, using anodal tDCS to treat a small sample of episodic migraineurs (minimum of 4 attacks per month) was very encouraging. Vigano, et al. (2013) administered twice-weekly 15-minute anodal tDCS treatments to the occipital region (visual cortex) of 10 migraineurs for a period of 8 weeks. At week 12 (4 weeks post-tDCS treatments), this group of migraineurs experienced an average 38% reduction in headache frequency, 60% reduction in headache duration, and 48% reduction in number of headache days. There was no significant change in average pain intensity during attacks. Migraine medication use use dropped an average 28%. These results were obtained without any adverse treatment effects.

Even more recent studies of small numbers of chronic migraine patients by Rocha, et al. (2015) and Schoenen, et al. (2016) have confirmed that tDCS over the visual cortex can be effective in significantly reducing the number, duration and intensity of migraine headaches and reduce the need for "rescue" medications in a majority of those treated.

DaSilva et al. (2012) compared tDCS over the primary motor cortex with sham stimulation in 13 chronic migraine patients. Treatment consisted of ten 20-minute anodal tDCS treatments over the primary motor cortex over a 30-day period. Post hoc analyses at one month and three months post-treatment showed a significant reduction in pain intensity (averaging 32%) and length of headaches (averaging 50%) but no significant change in headache frequency in those patient receiving active tDCS. The sham treatment group did not see any significant changes. Follow-up revealed that the active treatment group showed a trend toward increasing improvement over time after treatment was completed a finding that was suggested to be due to the slow modulation of pain matrix structures. Further studies are required to determine whether or not tDCS is effective in migraine. 

For more information on tDCS, GOTO... http://www.edmontonneurotherapy.citymax.com/brain_stimulation_therapies.html


DaSilva, A., Mendonca, M., Zaghi, S., et al. (2012). tDCS-induced analgesia and electrical fields in pain-related neural networks in chronic migraine. Headache pp.1-13.

Rocha, S., Melo, L., Boudoux, C., et al. (2015). Transcranial direct current stimulation in prophylactic treatment of migraine based on interictal visual cortex excitability abnormalities: A pilot random control trial. J. of Neurological Science, 349(1-2): 33-39.

Schoenen, J., D'Ostlio, A., Nonis, R., et al. (2016). Transcranial direct current stimulation and transcranial occipital nerve stimulation on chronic migraine: A pilot comparison of therapeutic and electrophysiological effects. Neurology, 86:16.

Vigano, A., D'Elia, T., Sava, S., et al. (2013) Transcranial direct current stimulation (tDCS) of the visual cortex: A proof-of- concept study based on interictal electrophysiological abnormalities in migraine. The Journal of Headache & Pain, 14: 23-32.

The Edmonton Neurotherapy approach to treating migraine combines HRV biofeedback training of "heart coherent breathing" with transcranial direct current stimulation. EEG neurofeedback and HEG neurofeedback may also be applied in select cases. In those cases where there is also a strong emotional response to the migraines, BAUD therapy may be added to the mix as a means of ameliorating the emotional suffering aspect of the migraine response. For more information on BAUD therapy go to the "Brain Stim Therapies" tab on this website and scroll down the page to the section on BAUD therapy.



Edmonton Neurotherapy.  Dr. Horst H. Mueller, RPsych, CRHSP, BCN, ICPP.

Information contained on this website is intended for educational and informational purposes only and does not constitute medical advice or diagnosis. Nothing on this site is intended nor should be taken as a substitute for the advice provided by your physician or other qualified healthcare professional. You should not use the information on this website for self-diagnosing or self-treating any health problem or disease, or self-prescribing any medication or other treatment.