What is a Migraine?

Jul 28

Migraine headaches are some of the most common and most disabling neurological disorders, affecting millions of people on a daily basis. Migraines can be debilitating neurological conditions.

Migraines are disorders with a diverse array of symptoms, including severe headaches, nausea, dizziness, vomiting, and hypersensitivity to sensory stimuli. In particular, light and sound can severely provoke the pain of a migraine. Migraine can be preceded by an aura, in which one can experience visual symptoms as much as an hour before the migraine pain sets in.

Migraines typically affect one side of the face and head and can last for a few minutes, several hours, or even days at a time. During a migraine attack people often need to drop whatever they are doing, seek refuge in a dark, quiet, cool environment, and wait for the symptoms to gradually subside.

How Common are Migraines?

Migraines affect 1 billion people worldwide. There are 39 million people in the US that suffer from migraines.

Everyone either knows someone who suffers from migraine, or struggles with migraine themselves.

Migraine is the 3rd most prevalent illness in the world.
Nearly 1 in 4 U.S. households includes someone with migraine.
12% of the population – including children – suffers from migraine.
18% of American women, 6% of men, and 10% of children experience migraines.
Migraine is most common between the ages of 18 and 44.
Migraines tend to run in families. About 90% of migraine sufferers have a family history of migraine (1)

What Causes Migraines?

Migraines can be caused by trauma, hormonal changes, food sensitivities, and autonomic dysregulation, among many factors. We often see migraines secondary to traumatic brain injury or as part of post-concussive syndrome.

Genetics play a significant role in the development of migraines. It is becoming increasingly clear in research that much of the vulnerability to migraine is inherited (5). There is evidence of genetic changes in ion pumps that regulate sodium and potassium concentrations in neurons. These are critical for maintaining proper frequencies of neuronal activation.

These genetic factors lead to dysfunction in specific ion channels that regulate calcium ion flow into neurons, which mediate serotonin release in the midbrain (6). Serotonin is an important regulator of blood vessel diameter, and is also involved in a number of pain-modulating mechanisms. Dysfunction of these channels likely impairs serotonin release and predisposes patients to migraine. Magnesium also appears to play an important role, as magnesium blocks the excessive calcium channel activity seen in migraine, and magnesium deficiency has been demonstrated in the cortex of migraine patients (7).

Migraine is a complex primary brain disorder that involves a cascade of events that lead to recurrent inappropriate activations of the trigeminocervical pain system. The initiating events are currently the focus of study and may prove to be invaluable targets for future preventative treatments.

What are the Symptoms of Migraines?

Migraine symptoms involve a throbbing or pulsing head pain, usually on one side of the head. This can also cause light and sound sensitivities along with visual disturbances like flashes of light in the visual field. Migraines can also cause tingling of the face and speech difficulties. For some individuals, these symptoms begin as early as childhood and can progress through their life. Not all people living with migraines will experience all of these symptoms. (2)

Acute migraine attacks occur in the context of an individual’s inherent level of vulnerability. The greater the vulnerability or 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 which lead to the generation of a migraine headache.

There are up to five clinical phases of a migraine attack. Many sufferers experience vague fatigue, cognitive difficulties or mood changes up to 24 hours prior to the onset of a migraine attack. This phase is called the prodrome.

The aura phase consists of focal neurological symptoms that persist up to one hour. Symptoms may include visual, sensory, or language disturbance as well as symptoms localizing to the brainstem.

Within an hour of resolution of the aura symptoms, the typical migraine headache usually appears with its unilateral throbbing pain and associated nausea, vomiting, and light or sound sensitivity. 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 straining. This phase is sometimes called the migraine hangover.

What are the Consequences of Migraines?

Migraine is the 6th most disabling illness in the world.
Every 10 seconds, someone in the U.S. goes to the emergency room complaining of head pain, and approximately 1.2 million visits are for acute migraine attacks.
While most sufferers experience attacks once or twice a month, more than 4 million people have chronic daily migraine, with at least 15 migraine days per month.
More than 90% of sufferers are unable to work or function normally during their migraine.

Depression, anxiety, and sleep disturbances are common for those with chronic migraine.
Over 20% of chronic migraine sufferers are disabled, and the likelihood of disability increases sharply with the number of comorbid conditions (1).

What Happens in the Brain During a Migraine?

There are several competing theories regarding the pathophysiology of migraines. Our understanding of how the headache of migraine is initiated is a work in progress. There is evidence of inappropriate activation of both pain receptive neurons and higher order neurons within the pain modulatory system. Any event that activates the system is capable of causing a headache.

In all models of migraine, the Trigeminovascular system becomes activated. The trigeminal nerve, which innervates the meningeal covering of the brain, is intricately involved in migraine. How the migraine is triggered and the cascade of events following the original activation of migraine are not completely understood. However, there is increasing evidence that events inside the cerebral cortex are capable of affecting the pain-sensitive meningeal vascular structures. If this is the case, then this might explain on way in which the headache is activated in individuals experiencing the aura.

Pain signals are transmitted through the Trigeminal nerve to the Spinal Trigeminal Nucleus. This is the relay nucleus in the lower brainstem that receives pain inputs from your head, face, upper cervical spine, and the blood vessels in your brain. When this nucleus becomes activated, pain signals are relayed into your brain, and you experience some form of headache.

Most historical models of migraine are based on inappropriate control of blood flow. In the vascular model of migraine, some neurons in your brain become overstimulated. Often these are neurons in your occipital cortex, the area that processes vision. Bright lights cause these neurons to fire faster, and they need additional resources to keep up. In a normal brain, the overstimulated neurons yell down into the brainstem and say “give me some more blood, and fast!” The brainstem responds by activating areas that control blood pressure, and these selectively shunt blood up to the struggling areas. This provides the oxygen and glucose necessary for the neurons to keep up, and everything is good.

In a vascular migraine, this reflex fails to respond at an appropriate level. The blood supply to the cortex is insufficient, and neurons begin to run out of resources. Often the last thing a neuron does before it fails is fire as fast as it can, in a process known as anoxic depolarization.

This excessive firing of the neurons was long assumed to be the basis of the aura that many people experience just before their head pain develops. If the visual areas of the brain are running out of oxygen, people see wavy lines or flashing lights. If areas in the temporal lobe are the source of the migraine, people may experience an aura consisting of odd smells or tastes. People often experience speech difficulties, cognitive challenges, and nausea.

Once the neurons involved fail, they dump out waste products and noxious chemicals that irritate pain neurons that surround the blood vessels in the brain. These pain fibers become sensitized, and the throbbing sensation you feel is the pulse of blood moving through your brain.

The symptoms of migraine aura are spectacular and sometimes frightening. Although most migraine patients will never have an aura, much attention has been focused on the phenomenon. The classical, slow progression of symptoms is experienced by only 15%, whereas less specific disturbances cover the whole visual field in about 25% of patients.

A positron emission tomography (PET) study of spontaneous migraine demonstrated a spreading, bilateral decreases in cerebral blood flow, which establishes that the phenomenon exists in migraine sufferers (10). Headache starts when blood flow is still reduced (9).

More current research has demonstrated that the migraine aura is not produced by decreased blood flow. Vascular changes follow changes in neuronal activity during the visual aura, not the other way around. More likely, it is the result of aberrant patterns of firing of neurons and related cellular elements characteristic of cortical spreading depression (11). Cortical spreading depression (CSD), is a slow-moving wave of excessive neuronal firing, followed by a suppression of brain activity in the same neuronal systems. It is a complex process that involves dramatic changes in neural and vascular function (21). CSD can activate the trigeminal pain system both peripherally and centrally. A primary neuropeptide of the trigeminal system is calcitonin gene-related peptide, which is a potent dilator of blood vessels. Research shows several potential vascular and neural connections between calcitonin gene-related peptide and cortical spreading depression (22). In essence, spreading depression is almost like a focal seizure, in that affected neurons fire as fast as they can, creating aura symptoms. These move extremely slowly through the cerebral cortex, with a characteristic slow march of symptoms to be 3 mm/min (1). A slow progression of decreased cerebral blood flow has been observed during auras (8,9).

There is a connection between cortical spreading depression (CSD) and activation of trigeminal nerve afferents. Activation of the trigeminal nerve evokes a series of meningeal and brainstem events that provoke the pain of a migraine attack.

Triggering CSD leads to a long-lasting blood flow increase within the middle meningeal artery. This increase in blood flow is dependent upon trigeminal nerve and brainstem parasympathetic activation. This reactive dilation of blood vessels triggers the pain-sensitive neurons surrounding blood vessels, leading to transmission of pain via the trigeminal nerve (12).

It is also possible that migraines can be triggered by inappropriate activation of brainstem systems. Certain aminergic brainstem nuclei, nucleus locus coeruleus, and dorsal raphe nucleus can alter brain blood flow and are involved in pain control, as well as other modulation of other sensory modalities. Research shows that stimulating the periaqueductal grey matter can evoke a migraine-like headache (13), and stimulating the locus ceruleus reduces cerebral blood flow in a frequency-dependent manner (14). These findings allowed the development of the central neural hypothesis of migraine (15, 16). Brain imaging studies suggest that important modulation of the trigeminovascular pain input stems from dorsal midbrain, periaqueductal grey and the dorsal raphe nucleus, and the pons, the locus coeruleus (17).

In the neuroinflammation model of migraine, there is a higher-than-normal release of inflammatory chemicals in the brain known as cytokines. These include chemicals such as TNF-⍺, IL-6. There is also release of neuropeptides including CGRP, Substance P, and several others. Plasma levels of these neuropeptides are increased with stimulation of the trigeminal ganglion, leading to increased levels of pain (18).

Local inflammation of blood vessels and meninges in the brain can directly activate the trigeminal nucleus and produce the pain of migraine. Several mechanisms can provoke brain inflammation. One of the most common is when a patient experiences a compromise in their blood-brain barrier. This is a network of blood vessels and supporting cells called astrocytes that create a wall between the brain’s internal environment and the rest of the body. When this breaks down, inflammatory chemicals in the rest of the bloodstream can cross the blood-brain barrier. Any inflammation anywhere in the body can lead to cytokines crossing the BBB. This can be from an injury, or from something as benign as a food allergy. These cytokines will activate brain immune cells called microglia. Activated microglia release inflammatory chemicals of their own, which increases the firing of pain neurons.

Central sensitization is another important aspect of chronic migraine. It involves dysfunction of brain-stem pathways that normally modulate sensory input. The key pathway for the pain is the trigeminovascular input from the meningeal vessels. These nerves pass through the trigeminal ganglion and synapses on second-order neurons in the trigeminocervical complex, which then project to the thalamus and brain for perception of pain.

In essence, when pain fibers anywhere are fired for extended periods of time, they become better at what they do, which unfortunately is to transmit pain signals to the brain. Pain neurons around your blood vessels can become sensitized such that it takes much less of a stimulus to make them fire, they fire at higher levels, and take longer to calm back down. The receptive fields of these neurons will expand, and your pain will expand throughout your head, face, scalp, and neck. Central sensitization is an important mechanism in any form of chronic pain, but particularly so in chronic migraine (3).

Most migraine patients exhibit increased pain called allodynia inside and outside their pain- referred areas during migraine attacks. A few minutes after the initial activation of the patient’s system, cranial hypersensitivity develops on the side of the migraine pain. This is another form of central sensitization, leading ultimately to allodynia on the opposite side of the head and forearm within 2 hours of the migraine onset (19).

There are most likely combinations of all of these mechanisms in any unique migraine, and often all of these are present at the same time. The character of migraine usually changes through a person’s life, most likely due to shifts between these different mechanisms as the condition progresses.

In summary, migraine is a primary brain disorder most likely involving an ion channel in brainstem nuclei, a form of neurovascular headache in which neural events result in dilation of blood vessels aggravating the pain and resulting in further nerve activation. It involves dysfunction of brainstem pathways that normally modulate sensory input. The key pathway for the pain is the trigeminovascular input from the meningeal vessels.

Migraine is now largely accepted to be an inherited tendency for the brain to lose control of its inputs. Migraines develop due to a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment. In the initial prodrome phase that precedes headache, brainstem and thalamic systems modulating afferent signals, become dysfunctional. This leads to light and sound sensitivity, and eventually to the onset of the pain phase, and slowly progresses towards pain resolution and the hangover phase (20).

How are Migraines Usually Treated?

Migraines are often treated through preventative measures, such as proper hydration, exercises, and relaxation techniques. Alternative therapies offered also suggest acupuncture, cognitive behavioral therapy, and supplementation. Frontline migraine therapy is usually medication management, involving over the counter analgesics like ibuprofen and acetaminophen. Prescription medications are also commonly employed including narcotics and barbituates to block pain, and triptans or ergotamines to prevent blood vessel changes. In some cases, Botox injections can be employed to decrease muscle spasms that can be migraine triggers. (2)

How is the NeuroRescue Program Different?

There are a number of pathways in the brain that exist to modulate the activation of the trigeminal nucleus. There are anti-nociceptive pathways that originate in several different areas of the brain and brainstem that function to shut down the trigeminal pain system and block the transmission of pain signals to the brain. Deficiencies in any of these systems can lower your migraine threshold and increase the frequency and intensity of migraine attacks.

In the NeuroRescue Program, we precisely evaluate the function and fatiguability of all of these systems, and design a protocol of specific exercises and stimuli to restore optimal function in these pathways.

We design your unique NeuroRescue program to address every structural and neurological factor involved in your migraines. We also evaluate the influences of metabolism, inflammation, and other chemical factors that may be promoting your pain. We evaluate the function of all of the muscles, joints, ligaments, and nerves in your cervical spine and temporomandibular joints, which are frequent contributors to trigeminal nucleus activation. We assess the neurological mechanisms that control their function, and the central brain and brainstem systems that normally function to shut off pain.

We combine all of this information into a comprehensive protocol that does not just help you mask your headache symptoms. Instead, we get to the unique root of your problem, address it at a foundational level, and help you rebuild the functional integration necessary for your migraines to finally be resolved.

One essential function of the brain is the ability to localize your body in space, a necessary step to be able to respond appropriately to the environment. The brain does this through a series of maps that allow us to put together information from our eyes, inner ear, muscles and joints into a coherent picture of where we are in space. We also have motor maps that allow us to control movement. Our brains feature sensory and motor maps in our parietal and frontal lobes, and ideally these maps are saying the same thing at all times. Research shows that in migraine sufferers there is a distinct impairment of functional connectivity between sensory and motor maps. This lack of connectivity has been hypothesized as resulting in an increased perception of migraine pain (4).

The aspects of the brainstem that function in antinociceptive mechanisms are integrated with neuronal pools that are involved in the generation of specific types of eye movements. Much research has revealed deficiencies in specific classes of eye movements in migraine patients. Fast movements between targets known as saccades, and saccades away from presented targets (anti-saccades) have been demonstrated to be impaired in migraine sufferers (23). The slower reaction time in saccades and frequent errors on anti-saccades demonstrate an impairment in inhibitory control mechanisms that varies with the severity of the migraine. These appear to imply dysfunction in the cerebellum, parietal and frontal lobes, and associated interconnections (24). We focus heavily on rehabilitation of these systems, and regularly see significant improvement in migraine frequency and intensity when these eye movement functions are restored.

We employ a wide variety of neuromodulation strategies that have been shown in neuroscience research to help reduce migraine symptoms and attacks (25). These may include transcutaneous vagus nerve stimulation (26), transcranial direct current stimulation (27), transcutaneous occipital nerve stimulation (28), or transcranial magnetic stimulation (29). All of these have been proven to be safe and effective interventions in reducing pain and preventing recurrence of migraine attacks.

We may employ hyperbaric oxygen therapy (30), or photobiomodulation with LED and low-level laser therapy (31). We may also include nutritional interventions such as magnesium (32), riboflavin (33), and assorted nutraceutical supplementation (34), or promote ketogenic diets (35) to provide metabolic support and decrease frequency of attacks.

We will almost always address any structural factors that may be provoking activation of your trigeminal pain system. These involve the muscles and joints of the upper cervical spine and jaw. Physical rehabilitation (36) and manual therapies (37) have been shown to be effective in reducing migraine attacks by resolving structural triggers.

No two migraine presentations are alike, and the same holds true for the NeuroRescue program. A cookie-cutter approach will be doomed to fail in a condition as complicated as migraine. All of our therapy protocols are dictated by your unique history, examination, and diagnostic testing. Every NeuroRescue program is tailored to the unique needs of the individual.

How Does the NeuroRescue Program Work?

We design your unique NeuroRescue Program to be among the most comprehensive diagnostic and therapeutic protocols available today. We create individual NeuroRescue Programs based on a comprehensive analysis of every relevant neurological system and pathway, using gold-standard, cutting edge neurodiagnostic technologies and examination procedures and state-of-the-art therapies.

We begin with your Discovery Day, wherein we perform a comprehensive history of not only your condition, but your life on a timeline. This allows us to dive deeply into your case and see all of the factors that led to where you are now. It helps us uncover hidden problems and associated conditions that may be making it difficult for you to move your recovery forward.

Our examination allows us to identify the areas and pathways of your brain that have been impacted by your condition. We begin by precisely quantifying the function of your visual, vestibular, and proprioceptive systems through computerized analysis of your eye movements, your inner ear reflexes, and your ability to balance in a host of different sensory conditions.

We employ technologies including Videooculography and Saccadometry to measure several classes of eye movements. We use Video Head Impulse Testing to measure the function of your inner ear, and Computerized Dynamic Posturography to assess your balance in different sensory conditions.

We use NeuroSensoryMotor Integration testing to evaluate hand-eye coordination and cognition, and Virtualis testing to assess dynamic eye tracking and perception of vertical in a virtual reality environment.

We combine all of this with a comprehensive physical and neurological examination of your sensory, motor, autonomic, and cognitive systems. We review any relevant laboratory testing, radiological imaging, and prior neurodiagnostic testing, and integrate that information with our findings.

We use this information to identify which parts of your brain are working properly, which systems are struggling, and the precise point at which your systems fatigue.

We can then design a NeuroRescue Program that is unique and specific to your brain, and yours alone. Your NeuroRescue Program works to rejuvenate and reintegrate the damaged neurons and pathways in your brain. It works to improve energy, endurance, and functional capacity within your fragile systems.

We use our technologies and procedures to not only see what we need to address, but also when it is time to stop and let you rest. We address your impaired neurological function from multiple angles of therapy, and provide metabolic support to improve neurological recovery.

While we cannot bring back neurons that have been lost, your NeuroRescue Program allows us to take the pathways that remain and maximize their efficiency and endurance. And by focusing on the integration of systems, we can do more than just get pathways working better, we can get them working together again. This gives us our best opportunity to return you to living a healthy, vibrant, and fulfilling life.