What is a Migraine?

Migraine

Migraine is one of the most common and most disabling neurological conditions in the world, affecting millions of people every day.

Migraine can cause a wide range of symptoms, including severe headache, nausea, vomiting, dizziness and strong sensitivity to light, sound and other sensations. Light and sound can make migraine pain much worse. Some migraines are preceded by an aura, which can bring visual symptoms up to an hour before the pain begins.

Migraine pain often affects one side of the head and face, and attacks can last from a few hours to several days. During an attack, many people have to stop what they’re doing, find a dark, quiet, cool place and wait for the symptoms to pass.

Some headaches need emergency care. Call 911 if you have a sudden, severe headache that feels like the worst of your life, or a headache with weakness or numbness on one side, trouble speaking, confusion, vision loss, a stiff neck or fever, especially if it’s different from your usual migraines. These can be signs of a stroke or other emergency.

How Common Is Migraine?

According to the Migraine Research Foundation (1):

Migraine affects about 1 billion people worldwide and about 39 million people in the U.S.

Nearly 1 in 4 U.S. households includes someone with migraine.

About 12% of people, including children, have migraine.

About 18% of American women, 6% of men and 10% of children have migraine.

Migraine is most common between the ages of 18 and 44.

Migraine tends to run in families. About 90% of people with migraine have a family history of it.

What Causes Migraine?

Migraine can be influenced by many factors, including hormonal changes, certain foods, changes in the autonomic nervous system and head injuries. Migraine can also develop after a traumatic brain injury or as part of post-concussion syndrome.

Genetics play a major role. Research increasingly shows that much of the tendency toward migraine is inherited (2). Some genetic changes affect the pumps and channels that control sodium, potassium and calcium in nerve cells, which help keep nerve cell activity at the right level.

Some of these genetic changes affect calcium channels that help control the release of serotonin in the brainstem (3). Serotonin helps regulate blood vessel size and is involved in controlling pain. Problems with these channels may affect serotonin release and make migraine more likely. Magnesium also appears to play a role. It helps calm overactive calcium channels, and low magnesium levels have been found in the brains of people with migraine (4).

Migraine is a complex brain disorder involving a chain of events that repeatedly activates the trigeminal pain system, which carries pain signals from the head and upper neck. What starts that chain is an active area of research and may lead to better ways to prevent migraine in the future.

What Are the Symptoms of Migraine?

Migraine usually causes throbbing or pulsing head pain, often on one side. It can also cause sensitivity to light and sound and visual changes like flashes of light. Some people have tingling in the face or trouble speaking. Migraine can begin in childhood and may change over a person’s life. Not everyone with migraine has all of these symptoms (5).

Everyone has a different threshold for migraine. The lower your threshold, the more often attacks happen. An attack begins when internal or outside triggers are strong enough to set off the chain of events that leads to a migraine.

A migraine attack can have up to five phases:

Prodrome. Many people feel tired, foggy or moody up to 24 hours before a migraine starts.

Aura. Some people have neurological symptoms lasting up to an hour, such as visual changes, numbness or tingling, or trouble with language.

Headache. Usually within an hour after the aura ends, the headache begins, often with one-sided throbbing pain, nausea, vomiting and sensitivity to light or sound. Without treatment, it can last up to 72 hours.

Resolution. The headache often ends with deep sleep.

Postdrome. For up to a day afterward, many people feel unwell and tired, and the pain may briefly return with coughing, sudden head movement or straining. This is sometimes called the migraine hangover.

How Does Migraine Affect Your Life?

According to the Migraine Research Foundation (1):

Migraine is among the most disabling illnesses in the world.

Every 10 seconds, someone in the U.S. goes to the emergency room with head pain, and about 1.2 million visits a year are for migraine attacks.

Most people with migraine have attacks once or twice a month, but more than 4 million people have chronic migraine, with at least 15 headache days a month.

More than 90% of people with migraine can’t work or function normally during an attack.

Depression, anxiety and sleep problems are common in people with chronic migraine.

More than 20% of people with chronic migraine are disabled, and the risk rises sharply with each additional health condition.

What Happens in the Brain During a Migraine?

Researchers are still working to understand exactly how migraine starts, and there are several theories. Most likely, a combination of these mechanisms is involved in any one person’s migraine, and the mix may change over a lifetime.

The trigeminal pain system. In every model of migraine, the trigeminovascular system becomes activated. The trigeminal nerve supplies the meninges, the protective coverings around the brain, and their blood vessels. Pain signals travel through the trigeminal nerve to the spinal trigeminal nucleus, a relay station in the lower brainstem that also receives pain input from the face, upper neck and the brain’s blood vessels. When this nucleus is activated, pain signals are sent up into the brain, and you feel headache pain.

The blood vessel model. Older models of migraine focused on blood flow. In this model, nerve cells in part of the brain, often the vision-processing area in the back of the brain, become overstimulated, for example by bright lights. They need more oxygen and glucose to keep up. Normally, the brainstem responds by sending more blood to those areas. In this model, that reflex doesn’t respond well enough, the nerve cells run short of resources, and they fire abnormally. This was long thought to cause aura: wavy lines or flashing lights when the visual areas are involved, or odd smells or tastes when the temporal lobe is involved. Chemicals released by these struggling cells irritate the pain nerves around blood vessels, and the throbbing you feel is the pulse of blood moving through sensitized vessels.

Most people with migraine never have an aura. Brain imaging has shown slowly spreading decreases in blood flow during aura, and headache can begin while blood flow is still reduced (6, 7, 8).

Cortical spreading depression. Newer research shows that aura isn’t caused by reduced blood flow. Instead, changes in nerve cell activity come first, and blood flow changes follow (9). Aura is now thought to be caused by cortical spreading depression, a slow wave of intense nerve cell activity followed by a period of quiet that moves across the brain’s surface at about 3 millimeters per minute (1, 10). This explains the slow “march” of aura symptoms. Spreading depression can activate the trigeminal pain system. One of the key chemicals released by the trigeminal system is CGRP, which strongly widens blood vessels, and research has found several links between CGRP and spreading depression (11). Spreading depression can also trigger a long-lasting increase in blood flow in an artery supplying the meninges, which activates the pain nerves around it (12).

The brainstem model. Migraine may also start with abnormal activity in the brainstem. Certain brainstem areas, including the locus coeruleus and dorsal raphe nucleus, help control blood flow in the brain and help regulate pain and other senses. Stimulating an area called the periaqueductal gray can cause a migraine-like headache (13), and stimulating the locus coeruleus can reduce blood flow in the brain (14). These findings led to the idea that migraine starts in the brain itself (15, 16). Brain imaging suggests that areas in the midbrain and pons play an important role in controlling trigeminal pain input (17).

The inflammation model. In this model, the brain releases higher-than-normal levels of inflammatory chemicals, along with pain-related chemicals such as CGRP and substance P. Levels of these chemicals rise when the trigeminal ganglion is stimulated, increasing pain (18). Inflammation of the blood vessels and meninges can directly activate the trigeminal system. Researchers are also studying how inflammation elsewhere in the body, and changes in the blood-brain barrier, may influence migraine by activating the brain’s immune cells, called microglia.

Central sensitization. When pain nerves fire over and over for long periods, they get better at their job, which unfortunately is sending pain signals. Pain nerves can become so sensitized that it takes less to make them fire, they fire more strongly, and they take longer to calm down. The area they respond to can also grow, so pain spreads across the head, face, scalp and neck. Central sensitization is important in many types of chronic pain, especially chronic migraine (19).

Many people with migraine develop allodynia during attacks, meaning normal touch becomes painful. Within minutes of an attack starting, the skin on the side of the pain can become sensitive, and within about two hours, this sensitivity can spread to the other side of the head and even the forearm (20).

In summary, migraine is now widely understood as a brain disorder that involves an inherited tendency for the brain to have trouble controlling incoming sensory information. This tendency likely cycles over time and is influenced by genetics and environment. In the prodrome phase, brainstem and thalamus systems that filter incoming signals stop working normally, leading to light and sound sensitivity, then the pain phase, and eventually recovery (21).

How Is Migraine Usually Treated?

Migraine is diagnosed and treated by healthcare providers. Prevention often includes staying hydrated, exercising, managing stress and avoiding known triggers. Some people also use acupuncture, cognitive behavioral therapy or supplements. Over-the-counter pain relievers like ibuprofen and acetaminophen are often used first. Prescription options include triptans and other medications that stop an attack, along with preventive medications, newer medications that target CGRP, and Botox injections for chronic migraine (5). Taking pain relievers too often can make headaches more frequent, so talk with your doctor if you’re using them often.

How the NeuroRescue Program Can Help

Our care is designed to work alongside your physician, neurologist and other providers, never in place of them. Please don’t change or stop any medication without talking with your prescriber.

Your brain has several pathways that work to calm the trigeminal pain system and block pain signals before they reach your awareness. These start in different areas of the brain and brainstem. When any of these systems isn’t working well, your migraine threshold may drop, which can make attacks more frequent and more intense.

We carefully evaluate how these systems work and how quickly they tire, and we design a program of specific exercises and therapies aimed at improving how they function. We also evaluate the muscles, joints, ligaments and nerves of your neck and jaw, which can feed input into the trigeminal pain system, along with the nervous system pathways that control them.

One of the brain’s most important jobs is figuring out where you are in space so you can respond to the world around you. It does this using maps that combine information from your eyes, inner ear, muscles and joints. It also has movement maps that control how you move. These sensory and movement maps, located in the parietal and frontal lobes, need to agree with each other. Research has found reduced connections between these sensory and movement maps in people with migraine, which researchers believe may increase how strongly migraine pain is felt (22).

The brainstem areas that help control pain are closely connected with areas that produce certain eye movements. Research has found differences in specific eye movements in people with migraine, including saccades, which are fast eye movements between targets, and antisaccades, which involve looking away from a target (23). Slower saccade reaction times and more antisaccade errors suggest reduced inhibitory control that varies with migraine severity, and they may point to involvement of the cerebellum and the parietal and frontal lobes (24). Eye movement testing and training are an important part of our care.

Depending on your needs and test results, your program may include:

Non-invasive neuromodulation, which has been studied for reducing migraine symptoms and attacks (25), such as transcutaneous vagus nerve stimulation (26) and transcutaneous occipital nerve stimulation (27).

Care for the muscles and joints of your upper neck and jaw, including chiropractic adjustments when appropriate. Physical rehabilitation (28) and manual therapies (29) have been studied for reducing migraine frequency.

Light therapy, also called photobiomodulation, using LED and low-level laser (30).

Nutritional guidance. Magnesium (31), riboflavin (32) and other nutritional supplements (33), as well as ketogenic diets (34), have been studied for reducing how often migraines happen. Talk with your physician before starting supplements or making major diet changes, especially if you take medication or are pregnant.

Transcranial magnetic stimulation (TMS), which has been studied for migraine (35). At our clinic, TMS is provided by our psychiatric mental health nurse practitioner, who will evaluate whether it may be appropriate for you.

Some programs include mild hyperbaric therapy as a structured recovery option between more demanding therapy sessions.

No two cases of migraine are alike, and the same is true for your NeuroRescue Program. The therapies we recommend are always chosen based on your history, testing and exam findings.

How the NeuroRescue Program Works

Your NeuroRescue Program begins with your Discovery Day. We start with a detailed history of your condition and your life on a timeline. This helps us understand the factors that may have contributed to where you are now, and identify related conditions that may be making it harder to move forward.

We measure how your visual, vestibular and balance systems are working through computerized analysis of your eye movements, inner ear reflexes and balance under different conditions. Our testing includes videonystagmography and saccadometry to measure several types of eye movements, the video head impulse test to measure inner ear reflexes, and CAPS computerized posturography to assess your balance under different sensory conditions. We also use NeuroSensoryMotor Integration testing to evaluate hand-eye coordination and cognition, and Virtualis testing to assess dynamic eye tracking and your perception of vertical in a virtual reality environment.

We combine this with a thorough physical and neurological exam of your sensory, motor, autonomic and cognitive systems. We also review any relevant lab work, imaging and prior testing, and integrate it with our findings.

Together, this helps us understand which parts of your nervous system are working well, which are struggling, and how quickly they tire. We use that information to design your personal NeuroRescue Program, aimed at improving function in the systems that need support and helping them work together. Our testing also helps us decide when to push and when to let you rest.

Our goal is to help raise your migraine threshold and reduce how often and how severely attacks happen, so you can spend fewer days in a dark room and more days living your life.

Your Next Step

Living with migraine can be exhausting and isolating, but you don’t have to keep searching alone. To find out if the NeuroRescue Program is right for you, contact one of our patient care coordinators to schedule your Discovery Day.

It’s never too late to take the next step.

References

1. https://migraineresearchfoundation.org/about-migraine/migraine-facts/

2. https://americanheadachesociety.org/wp-content/uploads/2018/05/NAP_for_Web_-_Pathophysiology_of_Migraine.pdf

3. https://pubmed.ncbi.nlm.nih.gov/8848121/

4. https://pubmed.ncbi.nlm.nih.gov/2584000/

5. https://www.mayoclinic.org/diseases-conditions/migraine-headache/symptoms-causes/syc-20360201

6. https://pubmed.ncbi.nlm.nih.gov/7908596/

7. https://pubmed.ncbi.nlm.nih.gov/2285266/

8. https://pubmed.ncbi.nlm.nih.gov/7969360/

9. https://pubmed.ncbi.nlm.nih.gov/11287655/

10. https://pubmed.ncbi.nlm.nih.gov/24042483/

11. https://pubmed.ncbi.nlm.nih.gov/29695168/

12. https://pubmed.ncbi.nlm.nih.gov/11821897/

13. https://headachejournal.onlinelibrary.wiley.com/doi/abs/10.1111/j.1526-4610.1987.hed2708416.x

14. https://pubmed.ncbi.nlm.nih.gov/7139303/

15. https://pubmed.ncbi.nlm.nih.gov/1889975/

16. https://pubmed.ncbi.nlm.nih.gov/7585147/

17. https://www.nejm.org/doi/10.1056/NEJMra010917

18. https://pubmed.ncbi.nlm.nih.gov/1699472/

19. https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-019-1066-0

20. https://pubmed.ncbi.nlm.nih.gov/10908199/

21. https://pubmed.ncbi.nlm.nih.gov/28179394/

22. https://link.springer.com/article/10.1007/s00415-017-8404-4

23. https://pubmed.ncbi.nlm.nih.gov/21628442/

24. https://pubmed.ncbi.nlm.nih.gov/33897613/

25. https://pubmed.ncbi.nlm.nih.gov/29601305/

26. https://pubmed.ncbi.nlm.nih.gov/26156114/

27. https://pubmed.ncbi.nlm.nih.gov/28428093/

28. https://pubmed.ncbi.nlm.nih.gov/31813696/

29. https://pubmed.ncbi.nlm.nih.gov/21298314/

30. https://pubmed.ncbi.nlm.nih.gov/33636371/

31. https://link.springer.com/article/10.1007/s12011-019-01931-z

32. https://pubmed.ncbi.nlm.nih.gov/32067520/

33. https://pubmed.ncbi.nlm.nih.gov/28527067/

34. https://pubmed.ncbi.nlm.nih.gov/31228957/

35. https://pubmed.ncbi.nlm.nih.gov/28028801/

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