Migraine is a debilitating illness with long term consequences for the brain. Researches had explored the origins of migraine and suggest that it is an electrical phenomenon initiated in the occipital cortex. Assessments of the brain using the EEG have found abnormal electrical activity supporting this idea. Neurofeedback for migraines is a treatment targeting electrical firing patterns in the brain. Many research data had shown that NFB training/treatment successfully suppresses abnormal brain wave activity leading to a significant decrease in migraine frequency and improvement in associated psychoneurological states such as anxiety, depression, and sleep.
WHAT IS MIGRAINE? CAUSES, SYMPTOMS, AND PATHOPHYSIOLOGY.
Migraine is a severe health problem which is the second most common one among the primary headaches, which affects 3-10 to 30-38% of the world’s population and which affects the quality of life negatively. Migraine is a disabling neurological condition characterized by episodic attacks of usually unilateral headache, with pulsating character and light and sound intolerance, associated with nausea and vomiting.
The tendency to suffer from migraine has a genetic component, but attacks can be triggered by a series of internal and external factors.
Migraine is a disease with many faces. The most common form is migraine without aura, occurring in about 80% of patients, while migraine with aura occurs in about 20% of the patients.
The annual costs of migraines such as diagnosis, treatment, reduced productivity, and absence from work are estimated to be 5 billion euros in the European Union and about 29 billion in the USA.
The incidence of migraine before puberty is greater in boys than in girls. It grows up to 12 years in both sexes and is the highest in the age range of 30–40 years. After puberty, the ratio changes and increases in favor of women, and with 40 is 3.5:1. After 40 years, the strength of the symptoms is reduced (except for women in perimenopause), and the beginning of migraine headaches in the fifties are rare.
Migraine trigger checklist
The main symptoms of migraine are recurring, severe, most often localized in one half of the head (hemicrania), and throbbing headache, which can last from 4 to 72 hours. It usually begins in the temporal region, in the eyeballs, or in the frontal region. Pain may also occur in the face, and neck. During a migraine attack, visual disturbances, increased sensitivity in the hands, dizziness, tinnitus, and increased sensitivity to light or noise may be observed. At the end of an attack, nausea and vomiting may occur.
There are migraines with and without aura. Aura is a complex of neuropsychological symptoms that anticipate the onset of pain, become the first signs of a migraine, or develop simultaneously with a headache. They are caused by a spasm of cerebral vessels, which occurs at the initial stage of an attack.
Symptoms associated with Migraine are:
- Severe pain in the head or eyes;
- Being worse on one side of the head;
- Nausea
- Vomiting;
- Dizziness ;
- Perceiving an aura;
- Blurred or tunnel vision;
- Seeing auras;
- Photophobia (sensitivity to light);
- Phonophobia (sensitivity to sound);
- Osmophobia (sensitivity to smells);
- Poor concentration;
- Ringing in the ears;
- Sweating;
- Feeling very hot or very cold;
- Abdominal pain (which can sometimes cause diarrhea);
- A frequent need to urinate.
The pathogenesis of migraine
The pathogenesis of migraine has long been a subject of discussion among scientists. It has been considered that typical headaches are caused by intracranial vasodilation preceded by vasoconstriction causing aura—vascular theory. Today it is known that this is not the case, and although new findings have emerged, the exact mechanism and genetic determinants are not yet fully clarified.
For a long time, it was thought that the cause of the aura, which precedes headaches, is cerebral vasoconstriction. Today, this theory is denied, and the aura is explained by neural dysfunction rather than ischemia due to vasoconstriction.
The frequency with which migraine attacks occur may vary from once in a lifetime to almost daily, an indication that the degree of migraine predisposition varies individually. It is necessary to consider both the factors that influence the threshold of a person’s susceptibility to a migraine attack and also the mechanisms that trigger the attack and the associated symptoms.
Acute migraine attacks occur in the context of an individual’s inherent level of vulnerability. The greater the vulnerability/lower the threshold, the more frequent attacks occur. Attacks are initiated when internal or environmental triggers are of sufficient intensity to activate a series of events that culminate in the generation of a migraine headache. Many migraineurs experience vague vegetative or affective symptoms as much as 24 hours before the onset of a migraine attack. This phase is called the prodrome and should not be confused with the aura phase.
The aura phase consists of focal neurological symptoms that persist for up to one hour. Symptoms may include visual, sensory, or language disturbance, as well as symptoms, localizing to the brainstem.
Within an hour of the resolution of the aura symptoms, the typical migraine headache usually appears with its unilateral throbbing pain and associated nausea, vomiting, photophobia, or phonophobia. Without treatment, the headache may persist for up to 72 hours before ending in a resolution phase often characterized by deep sleep.
For up to twenty-four hours after the spontaneous throbbing has resolved, many patients may experience malaise, fatigue, and transient return of the head pain in a similar location for a few seconds or minutes following coughing, sudden head movement, or Valsalva movements. This phase is sometimes called the migraine hangover (postdrome).
It is becoming increasingly clear that much of the vulnerability to migraine is inherited.
Migraine is, in essence, a familial episodic disorder whose key marker is a headache, with certain associated features. One of the most important aspects of the pathophysiology of migraine is the inherited nature of the disorder. It is clear from clinical practice that many patients have first-degree relatives who also suffer from migraines. Transmission of migraines from parents to children has been reported as early as the seventeenth century, and numerous published studies have reported a positive family history.
In approximately 50% of the reported families, Familial hemiplegic migraine (FHM) has been assigned to chromosome 19p13. The biological basis for the linkage to chromosome 19 is mutations involving the Ca 2.1 (P/Q) type voltage-gated calcium channel CACNA1A gene. Dysfunction of these channels might impair serotonin release and predispose patients to migraine or impair their self-aborting mechanism.
Migraine aura
A migraine aura is defined as a focal neurological disturbance manifesting as visual, sensory, or motor symptoms. It is seen in about 30% of patients, and it is neurally driven. Visual aura has been described as affecting the visual field, suggesting the visual cortex, and it starts at the center of the visual field, propagating to the periphery at a speed of 3 mm/min. Blood flow studies in patients have also shown that focal hyperemia tends to precede the spreading of oligemia. However, some researchers conclude that migraine aura is evoked by aberrant firing of neurons.
Shown is the entire hemisphere, from a posterior-medial view. The aura-related changes appeared first in extrastriatal cortex. The spread of the aura began and was most systematic in the representation of the lower visual field, becoming less regular as it progressed into the representation of the upper visual field.
WHAT KIND OF CHANGES IN THE BRAIN CAUSE THE MIGRAINE?
The study of anatomy and physiology of pain-producing structures in the cranium and the central nervous system modulation of the input have led to the conclusion that migraine involves alterations in the subcortical aminergic sensory modulatory systems that influence the brain widely.
Available research data had shown that no structural differences have been found in individuals with migraine compared to individuals without migraine. This research suggests that migraine is an electrical phenomenon initiated within the cortex of the brain. This phenomenon is known as Cortical Spreading Depression (CSD) referring to a wave of electrophysiological hyperactivity that spreads through the brain from the occipital lobes forward. This wave affects the cortex in several ways: altering the electrical polarity of neurons, decreasing blood flow and associated levels of oxygen in the cortex and altering the degree of vasodilation within the vascular system of the cortex. These changes release of nerve irritating chemicals into the brain. These chemicals irritate the pain transmitting the “trigeminal” nerve system in the meninges, the sensitive membranes that cover the brain. The result is severe blinding pain.
Consequences of migraine to the brain are:
- impaired ability in tests of short and long-term memory,
- small areas of stroke-like damage to the brain,
- with a high frequency of Migraine (more than three attacks per month) show significantly more areas of damage than those with fewer attacks,
- with a history of Migraines, longer than 15 years were found to have more changes in the brain than those with a shorter history,
- higher frequency migraines show abnormalities in both white and gray matter of the brain,
- people with migraine are more at risk for future strokes,
- show a predilection toward damage in the following sites:
– frontal lobe
– limbic system
– parietal lobes
– brainstem
– cerebellum
Chronic migraine comorbidities
WHAT EEG CHANGES CAN BE OBSERVED IN PEOPLE WITH MIGRAINES?
There are two ways in which anomalies in the EEG have been associated with migraine: via the relationship of migraine to seizure activity and as a function of slow brain waves found elsewhere in the brain. Migraine and epilepsy frequently coexist and are often difficult to differentiate. Both migraine and seizure-prone individuals show abnormal occipital discharges that are typically high voltage (200–300 mV), with a diphasic morphology, and a unilateral or bilateral occipital and postero-temporal distribution.
Migraine has been associated with abnormal EEG activity elsewhere in the brain. Both unilateral and bilateral increased delta wave activity has been recorded during a hemiplegic migraine and attacks of migraine with disturbed consciousness. It is shown that in the waking, non-migraine state there are slow waves in the theta range (48 hertz). Neurofeedback for migraines has been used to target and suppress this slow-wave activity in both adults and children with a concomitant reduction in frequency and intensity of migraine. Some research has shown that neurofeedback blood flow-up training in the frontal cortex results in a 70% reduction in the frequency of migraines compared with a 50% reduction using medication alone. NFB training is also associated with decreases in anxiety, depression, and improved sleep, each of which has been associated with migraines.
Newer methods, i.e. EEG frequency analysis and topographic brain mapping, are promising tools in this field. So far, mostly small studies have been published with somewhat inconsistent results. A pattern of increased alpha rhythm variability (and/or asymmetry) in the headache-free phase seems to emerge, however. Significant asymmetry of alpha and theta during headache has been reported in a topographic brain mapping study.
The EEG patterns observed in migraine patients seem to suggest a possible physiological connection between sleep, hyperventilation, and migraine.
EEG activity seems to change shortly before the attack. This suggests that migraineurs are most susceptible to attack when anterior QEEG delta power and posterior alpha asymmetry values are high.
Occipitoparietal and temporal alpha power were more asymmetric before the attack compared with the interictal baseline
Different research found the increased power in 19 cortical areas in delta (1.5-3.5 Hz), theta (4.0-7.5 Hz), and high-frequency beta (21-30 Hz) bands. Multiple types of research have shown significant abnormalities in the high-frequency beta band (21-30 Hz) in the parietal, central, and frontal regions.
How Neurofeedback Training Manage Migraines?
Despite a large number of medications being used to treat migraine today, only 20% of patients report their effectiveness. Many develop resistance to medications, and therefore the dose of the drug is gradually increasing, which is required to achieve the effect of relieving headache. Often the medication is accompanied by side effects.
In patients with migraine, changes in the biological parameters of brain activity, brain waves, are often recorded. Neurofeedback is a recently developed technology for treating migraines based on recording these changes in brain wave activity and transmitting information about their condition in the form of audio and video signals to the patient. Based on these audio and video signals, the patient learns how to manage his condition to regulate brain wave activity and normalize it. Normalization of wave activity leads to a significant decrease in both the frequency and intensity of headaches. At first, these changes are not stable but gradually become stable and permanent. It becomes possible (after about 10 sessions of treatment) to manage the condition without the support of special equipment and computer programs.
Migraine research points to electrophysiological anomalies in the brain as correlates of migraine headaches. Neurofeedback, as a therapy, is specifically designed to target dysregulated firing patterns in the brain. Research has demonstrated the ability of NFB to successfully treat anomalous brainwave patterns in a variety of conditions most specifically with migraines.
After performing diagnostic scanning and getting brain mapping patterns of the patients with migraine some clinicians provide neurofeedback training with an increase of SMR and low beta 12-15 Hz and decreased theta (4-7Hz) and high beta (21-30 Hz) at each affected site; 5 sessions for each affected site.
qEEG Before and after Neurofeedback for Migraines
Electrode Placement and Detailed Neurofeedback Protocols for Migraine Management
Key Electrode Sites for Migraine Neurofeedback
1. Fz (Frontal Midline):
• Location: Frontal lobe, on the midline, 20% of the distance from the nasion (bridge of the nose).
• Relevance: Associated with emotional regulation and autonomic control. Targeting this site can help manage stress and reduce the frequency and intensity of migraines.
2. Cz (Central Midline):
• Location: The scalp vertex, halfway between the nasion and inion and equally spaced between the left and right preauricular points (just above the ears).
• Relevance: Central region involved in general arousal regulation. Often used as a reference or active site for enhancing overall neural stability.
3. Pz (Parietal Midline):
• Location: Parietal lobe, on the midline, 50% of the distance from the nasion to the inion.
• Relevance: Involved in sensory processing and pain perception. Targeting Pz can help modulate sensory processing related to migraine pain.
4. T3 (Left Temporal Lobe):
• Location: Temporal lobe, 20% above the preauricular point.
• Relevance: Associated with stress and emotional regulation. Training in this area can help manage triggers related to emotional stress.
5. T4 (Right Temporal Lobe):
• Location: Temporal lobe, analogous to T3 on the right side.
• Relevance: Similar to T3, it helps balance activity related to emotional stress and can assist in reducing migraine frequency.
Neurofeedback Protocols for Migraine
The protocol involves training individuals to increase or decrease specific brainwave activity at the targeted locations to promote relaxation, improve stress management, and reduce migraine symptoms.
1. Alpha Enhancement Protocol
This protocol focuses on increasing alpha (8-12 Hz) activity to promote relaxation and reduce stress, which are common migraine triggers.
• Target Brainwaves: Alpha waves (8-12 Hz)
• Goal: Increase alpha activity to enhance relaxation and reduce stress-related migraine triggers.
Procedure:
1. Electrode Placement: Place electrodes at Fz and Pz with Cz as the reference.
2. Baseline Recording: Record baseline alpha activity for 5-10 minutes.
3. Feedback Mechanism: Provide real-time feedback using visual (e.g., calming images) or auditory (e.g., soothing sounds) cues. Positive feedback is given when alpha activity increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use headache frequency and intensity diaries along with follow-up qEEG to assess changes.
2. SMR Training Protocol
This protocol focuses on increasing sensorimotor rhythm (SMR, 12-15 Hz) activity to promote calmness and reduce hyperarousal that can trigger migraines.
• Target Brainwaves: SMR (12-15 Hz)
• Goal: Increase SMR activity to enhance motor inhibition and promote calmness.
Procedure:
1. Electrode Placement: Place electrodes at Cz with reference electrodes at mastoids (A1 and A2).
2. Baseline Recording: Record baseline SMR activity for 5-10 minutes.
3. Feedback Mechanism: Provide real-time feedback using visual or auditory cues. Positive feedback is given when SMR activity increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use headache frequency and intensity diaries and follow-up qEEG to monitor changes.
3. Theta/Beta Ratio Training
This protocol aims to balance theta (4-8 Hz) and beta (15-20 Hz) wave activity to improve cognitive control and reduce stress, which can contribute to migraine frequency.
• Target Brainwaves: Theta (4-8 Hz) and Beta (15-20 Hz)
• Goal: Decrease theta activity and increase beta activity to improve cognitive control and reduce stress.
Procedure:
1. Electrode Placement: Place electrodes at T3 and T4 with Cz as the reference.
2. Baseline Recording: Record baseline theta and beta activity for 5-10 minutes.
3. Feedback Mechanism: Provide feedback using visual or auditory stimuli. Positive feedback occurs when theta decreases and beta increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use headache frequency and intensity diaries along with follow-up qEEG to track progress.
4. Alpha/Theta Training
This protocol focuses on increasing alpha (8-12 Hz) and theta (4-8 Hz) waves to promote relaxation and reduce anxiety, which are common migraine triggers.
• Target Brainwaves: Alpha waves (8-12 Hz) and Theta waves (4-8 Hz)
• Goal: Increase alpha and theta activity to reduce stress and improve overall emotional regulation.
Procedure:
1. Electrode Placement: Place electrodes at Fz and Cz (reference).
2. Baseline Recording: Record baseline alpha and theta activity for 5-10 minutes.
3. Feedback Mechanism: Use calming visual or auditory feedback. Positive feedback is provided when alpha and theta waves increase.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use headache frequency and intensity diaries along with follow-up qEEG to monitor changes.
Frequently used Neurofeedback Protocol for migraine management as follows:
Left-sided headaches – at C3 (T3)
- down-trained: 2-7 Hz and high-frequency beta
- up-trained: 15-18 Hz
Right-sided headaches – at C4 (T4)
- down-trained: 2-7 Hz and high-frequency beta
- up-trained: 12-15 Hz
An average number of neurofeedback sessions to get a significant change to occur are around 20-30 sessions. A person can get a neurofeedback session as much as twice a day with at least a two-hour break in between. It is recommended that a person try to do neurofeedback at least two or three times a week until the sessions are completed. Results appear to solidify and happen faster when done more frequently.
How effective is neurofeedback for migraines?
Neurofeedback for migraines can help with dysfunctions in the central nervous system, such as the increased excitability of the cerebral cortex. Because of working directly with the central nervous system, Neurofeedback training can be very effective in stabilizing the excitability of the cerebral cortex what will result in reduced headaches, less sensitivity, and improvements in other symptoms associated with Migraine.
The researchers concluded, “Neurofeedback appears to be dramatically effective in abolishing or significantly reducing headache frequency in patients with recurrent migraine”.
Walker (Walker, J. E. (2011). QEEG‐Guided Neurofeedback for Recurrent Migraine Headaches. Clinical EEG and Neuroscience, 42(1), 59‐61. doi:10.1177/155005941104200112) examined the effects of neurofeedback therapy versus drug therapy in 71 patients with recurrent migraine headaches. After completion of a quantitative electroencephalogram (QEEG) procedure, all results indicated an excess of high-frequency beta activity (21‐30 Hz). Twenty‐five patients chose to continue with drug therapy for their recurring migraines, whilst 46 of the 71 patients selected neurofeedback training. Of those who chose neurofeedback therapy, the majority (54%) reported complete abolishment of their migraines, 39% experienced a significant reduction in migraine frequency of greater than 50%, and 4% experienced a decrease in the frequency of less than 50%. Only one patient did not report a reduction in headache frequency. The control group of participants who opted 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%). Overall, the study demonstrates that neurofeedback is significantly effective in abolishing or substantially reducing the frequency of headaches in patients with recurrent migraines.
Effectiveness of Neurofeedback vs. Drug Management of the Migraine
Effectiveness of Neurofeedback for Migraines
Effectiveness of Drug Therapy for Migraines
After Neurofeedback for migraines, the reduction of frequency and intensity of headaches usually was sustained at the 14.5 months follow‐up assessment.
Some of the benefits of neurofeedback for migraines:
- It helps to retrain the brain and or optimize the functioning of the entire brain by removing barriers and improving the connections and brainwave activity in a certain region of the brain or among different regions of the brain.
- It releases the old stuck or abnormal patterns to create new and more effective, stronger, and organized patterns.
- Training protocols are generated from the initial QEEG brain mapping. Training involves audiovisual feedback that INVOLUNTARILY teaches the individual to self-regulate the abnormal brain wave patterns that are presented to them on a computer screen in several ways.
- There are no contraindications or side effects of neurofeedback for migraines.
Effective Use of Various Biofeedback Modalities for Migraine Management
Various modalities of biofeedback, including Electromyography (EMG), Heart Rate Variability (HRV), Temperature, and Galvanic Skin Response (GSR), can also be effectively utilized in the management of migraines. EMG biofeedback helps individuals become aware of and reduce muscle tension, which can alleviate headache symptoms. HRV biofeedback trains individuals to regulate their heart rate variability, promoting autonomic balance and reducing stress, a common migraine trigger. Temperature biofeedback involves monitoring peripheral skin temperature to enhance relaxation and decrease physiological arousal, thus helping to prevent migraines. GSR biofeedback measures the skin’s electrical conductance, which varies with sweat gland activity, providing insights into stress and arousal levels. By learning to modulate these physiological responses, individuals with migraines can manage their symptoms more effectively, complementing traditional neurofeedback approaches. For more detailed information regarding various biofeedback modalities used in Migraine Management, please visit the Article “Biofeedback for Migraines. How to choose”.
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