What Is A Vestibular Migraine?

Jul 28

A vestibular migraine is the most common cause of spontaneous episodic vestibular symptoms. A migraine is characterized as typically including a moderate to severe pounding or throbbing headache, but a vestibular migraine may or may not include a headache. Instead, it usually includes vestibular symptoms, such as dizziness, vertigo, sensitivity to motion, unsteadiness and loss of balance (1).

How Common are Vestibular Migraines?

It is estimated that in 1 of 4 United States households there will be someone suffering from migraines. Vestibular migraines tend to affect women more than men, and occur in about 1% of the population, including children (2). It is the 3rd most prevalent illness and 6th most disabling illness in the world (6).

What Causes Vestibular Migraines?

Vestibular migraines are likely the result of genetics, epigenetic and environmental factors. Migraines are often present in other family members, or they may occur after a substantial change in environment, such as exposure to toxic mold or chemicals or a traumatic brain injury.

Migraines are traditionally thought of as the result of rapid changes in blood vessel caliber, leading to blood flow changes in certain areas of the brain. When neurons in the cerebral cortex fire rapidly, they communicate with surrounding blood vessels in the effort to increase blood flow. There are also reflexes from the brainstem that control blood flow to the cortex by regulating blood vessel diameter. For a number of reasons, these reflexes fail, leading to neurons being forced to fire at increased rates without sufficient oxygen and glucose. This promotes what is known as spreading depression, where neuronal function gradually fails and creates aura symptoms as firing rates become dysregulated.

In classic migraines, auras can be wavy lines or flashing lights in visual fields. In vestibular migraines, aura symptoms can be sensations of movement or disequilibrium. Spreading depression leads to the production of chemical substances that irritate pain neurons surrounding blood vessels. When the brainstem reflexes ultimately kick in to cause blood vessels to dilate, the sensitized pain fibers respond to the stretch of the blood vessel wall from pulse pressure waves. This creates the characteristic throbbing pain seen in migraines.

Current research implies that the traditional migraine model may be oversimplified, and that neurochemical and neuroinflammatory changes may have a more important role than blood vessel diameter (22).

Causes of vestibular migraines may vary depending on the person. It has been demonstrated in the literature that changes in neurotransmitters such as serotonin (18), as well as in hormones such as estrogen may both be underlying factors promoting development of migraines (19).

What are the Symptoms of Vestibular Migraines?

Symptoms of vestibular migraines may include any or all of the following:

Dizziness lasting more than a few minutes
Nausea and vomiting
Loss of balance
Extreme motion sensitivity (feeling of sickness when moving the head, eyes or body)
Feeling disoriented or confused
Feeling unsteady on your feet, like you’re rocking on a boat
Sensitivity to sound
Sensitivity to light
Lightheadedness
Pressure sensitivity (changes in atmospheric pressure, such as changes in altitude with flying)
Ringing in the ear
Feeling of fullness in the ear(s)
Pressure in the ear(s)

The duration of these symptoms is usually a few minutes to 72 hours. Often the triggers for vestibular migraines are similar to those of classic migraines, including stress, lack of sleep, dehydration, weather changes or barometric pressure changes like with flying, glaring or flickering lights and menstruation. There are also foods that have been studied to be potential triggers for migraines, including chocolate, red wine, aged cheeses, monosodium glutamate (MSG), processed meats, coffee and sodas with caffeine (3). There is almost always a personal history of motion sickness or migraines, even if it dates back to childhood.

What are the Consequences of Vestibular Migraines?

Migraines are an enormous source of disability and lost productivity. More than 90% of migraine sufferers are unable to work or function normally during a migraine (6). Medication overuse is actually the most common reason for episodic migraines turning chronic with over 20% of chronic migraine sufferers being disabled. Estimated costs of healthcare of lost productivity associated with migraine is as high as $36 billion annually in the United States.

The costs of healthcare for a family with one person suffering from migraines is 70% higher than for a non-migraine affected family (6). This is partly because migraines and vestibular symptoms can have profound impacts on mental health. There are well-established links between chronic headaches and conditions such as depression and anxiety (4). Chronic sleep disruption has been associated with migraines, which reinforces a cycle of depression, further sleep disturbance, and further headache (5).

What Happens to the Brain in Vestibular Migraines?

Cortical spreading depression, which is thought to give rise to migraine with aura, is considered to be part of the pathogenesis of VM in patients, in particular for those suffering with short-duration vertiginous attacks. Spreading depression can produce vestibular symptoms if it arrives in the vestibular areas of the cortex, which are mainly located in the posterior insula and the temporoparietal junction (20).

Changes in the function of neurotransmitters also seems important in vestibular migraine. Some neurotransmitters involved in the pathogenesis of migraine (e.g., calcitonin gene-related peptide, serotonin, noradrenaline, and dopamine) control the activities of the central and peripheral vestibular nerves. Dysfunctional neurotransmitters may thus be responsible for both creating migraines and the specific symptoms seen in VM (21).

Changes in the trigeminal pain system and central sensitization of pain also appear to play an important role in migraines. People usually think of their pain system as a series of on-off switches, in that either something hurts and there is something wrong, or it doesn’t hurt and everything is fine. That’s not really the way your pain system works. A better analogy is that the experience of pain is more like trying to ring the bell at the amusement park. You hit the hammer on the striker, the puck goes up, and if you hit it hard enough, the puck goes all the way up and rings the bell. Your pain receptors are the hammer, and your pain threshold is the height of the bell. We want as little firing of pain receptors as possible, so the hammer does not hit the striker hard. We also want the bell to be as high as possible, so that the hammer needs to hit really hard to send the puck up to ring the bell.

The pain receptors for head and face pain fire through your Trigeminal Nerve (10). This nerve also carries pain inputs from the brain’s blood vessels and meninges. When pain receptors are compressed or irritated by inflammation, they fire inputs into the spinal trigeminal nucleus (11). This collection of neurons functions as the striker for your headache pain. It is always being hit with pain inputs from the trigeminal nerve, from pain receptors being compressed through movement, from chemical waste products, and so on. The only pain receptors in this system that are not constantly firing are the dead ones, and as such we have a series of pathways from the brain that fire down to inhibit the trigeminal nucleus. These make sure that normal background firing rates of your pain receptors are not enough for you to experience pain. This can be seen as the height of the bell.

Your trigeminal nerve doesn’t just map your head, face, and brain. It also receives pain input from the top three segments of your neck. The suboccipital spine at the base of your skull sends input into your spinal trigeminal nucleus. If there is enough pain input from your upper cervical spine, the bell can start to ring and you experience a headache.

If this pain input is bad enough to ring the bell hard, pain can start to refer throughout the trigeminal system. This means that you will experience pain not just at the base of your skull, but behind your eyes, in your forehead, in your jaw, and potentially everywhere else that receives input from this nerve. This pain referral is basically crosstalk within your trigeminal system. In the same way that during a heart attack you can have pain go down your left arm even though there is nothing wrong with your arm, if the pain inputs from your neck are high enough you can experience pain throughout your trigeminal system. Most of the pain receptors in your brain surround blood vessels, and if the trigeminal system is stimulated hard enough, you can start to experience throbbing pain every time blood is pumped through your brain’s arteries. This can be another driver of the pain seen in migraines.

Your pain system works just like everything else in your system, in that if you use it over and over, it gets better at what it does. Unfortunately, that means that if you keep ringing the bell for an extended period of time, the bell gets lower, and it takes less pain input to trigger a migraine.

When the trigeminal system is activated, it begins a cycle of neuroinflammation which spreads to other areas of the brain, causing the bell to get lower and lower very quickly. When the bell gets very low, non-painful stimuli (such as light, sound, soft touch and movement) can then produce pain. The term for this heightened, painful reaction to non-painful stimuli is allodynia. The trigeminal ganglion also innervates the inner ear, where the vestibular and auditory systems exist. Excessive activation and blood flow to these areas explains why patients get vestibular and auditory symptoms with their vestibular migraines. Therefore, vestibular migraines ultimately arise from dysfunction in the brain and brainstem that are supposed to control trigeminal nerve inputs (8). It has been proposed that the reciprocal connections between brainstem vestibular nuclei and the structures that modulate trigeminal pain inputs may underlie the pathophysiology of VM (18).

How are Vestibular Migraines Usually Diagnosed?

A physician will usually perform a history, physical and neurological examination and a vestibular migraine is a clinical diagnosis. Early diagnostic criteria usually include (5):

Episodic vestibular symptoms that occur at a moderate to severe intensity.
Migraines occurring either with or without the presence of vestibular symptoms in the past, or currently.
At least one symptom of migraine (migrainous headaches, photophobia, photophobia or visual aura) during at least two episodes of vertigo.
Other causes ruled out by appropriate imaging and tests.

Imaging such as MRI or CT scan are usually used to rule out the presence of other issues such as a brain tumor or brain bleed but cannot detect vascular changes resulting in migraines (31).

How are Vestibular Migraines Usually Treated?

There are many different types of pharmaceutical treatments for migraines. Most traditional therapies for migraines have limited success. We regularly see patients that have been chasing a solution for their vestibular migraines for years, often seeing dozens of providers and having attempted both conservative and invasive forms of therapies. Oftentimes, their lives have become very restricted, as they are trying to avoid foods and other triggers for their debilitating migraines.

Many people get better with therapy, but unfortunately many others have incomplete recoveries. Millions of people suffer with long-term effects of vestibular migraines, and many of them have given up hope of ever living a life like they once had (31).

We have created the NeuroRescue Program to help these people treat the underlying issues so they can get out of pain and get back to doing what they love.

How is the NeuroRescue Program Different?

We design your unique NeuroRescue program to address every structural and neurological factor involved in your vestibular 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 jaw, the neurological mechanisms that control their function, and the central brain and brainstem systems that normally function to shut off pain and ensure eye movements are stable and accurate. We combine all of this information into a comprehensive protocol that does not just help you mask your migraine 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 of the main things your brain does, and maybe even the primary thing, is help you determine where you are in the world. Your brain uses inputs from your inner ear to figure out where your head is in relation to gravity and how it is moving. It uses inputs from your muscles and joints to figure out where your body is in relation to your head and what your body is doing. It uses inputs from your eyes to figure out where your body is in relation to the visual environment.

Your brain needs to put all of that together to make sense of where the world is, and where you are in relation to the world. It needs to be able to localize you effectively in the environment, in order for you to be able to respond to the environment properly.

When you suffer with chronic vestibular migraines, we regularly see dysfunction to pathways that involve the eyes, the inner ear, muscles and joints, among many others. It is important to understand that vestibular migraines are rarely only about dysfunction in the visual system, the inner ear, or the neck. Perhaps the primary problem in vestibular migraines is dysfunction of the neurological mechanisms that allow all of these systems to work together. In most cases of vestibular migraines, at a foundational level a failure of integration exists between the eyes, the vestibular system, and proprioceptive feedback from muscles and joints. This causes inappropriate levels of firing, either too much or too little, resulting in symptoms that are allowed to get out of control.

This is why many patients fail to fully resolve their vestibular migraine challenges with vision therapy, vestibular therapy, physical therapy, chiropractic treatment, manual or massage therapy, and medication management, even if all of their therapies are performed at the same time. While all of these therapies can help with problems in the individual systems, none of them take the comprehensive NeuroRescue Program approach to address all of the systems involved in vestibular migraines and their ability to work together in harmony.

Eye movements have been shown to be compromised in vestibular migraine. Patterns of spontaneous eye movement called nystagmus has been demonstrated in VM patients during acute attacks, indicative of brainstem dysfunction and chemical changes in occipital lobe function (23). Saccades, which are fast eye movements between targets, have also been shown to be compromised in migraines, with patterns suggesting that inhibitory control is impaired in migraine patients depending on the severity of the migraine (24). Other patterns of saccade dysfunction imply that the cerebellum, which is recently thought to be involved in the pathophysiology of migraine, might be involved in distinct processes such as spatial re-mapping through known interconnections with parietal and frontal cortical areas (25). Rehabilitation of these eye movements has been beneficial for all of our vestibular migraine patients.

Research has also demonstrated changes in pathways involved in the central processing of vestibular inputs in VM. Gray matter volume reduction has been shown in the superior, inferior and middle temporal gyrus, the mid. cingulate, dorsolateral prefontal, insula, parietal and occipital cortices. Gray matter volume reduction has also been observed in areas associated with pain and vestibular processing. Moreover, decreased prefrontal cortex volume has been correlated with headache severity (26). The structure of vestibular processing areas of the cortex has been shown to be altered in VM (27), leading to deficits in both balance and cognition (28). In all VM cases, vestibular rehabilitation is a core component of your NeuroRescue Program. Vestibular rehabilitation has been shown to be effective in reducing frequency and intensity of VM attacks (29).

We employ a wide variety of therapies to help resolve your vestibular migraines. All of our therapies are validated by current neuroscience research. The therapies chosen for you will be determined by the specifics of your case and your diagnostic findings. Your NeuroRescue Program will be unique to only one nervous system, that being yours.

Your therapies may range from rehabilitation of specific types of eye movements that have been shown to be impaired in migraines (12), to exercises to rehabilitate reflexes from the vestibular system that are compromising brainstem function (13). We may engage in specific types of electrical stimulation (14), or direct neurostimulation using transcranial magnetic stimulation (15). We may engage in laser photobiomodulation (16), or hyperbaric oxygen therapy (30), or even exercises conducted in a virtual reality environment (17). Whatever combinations of therapies we choose to employ will be dictated solely by your neurodiagnostic testing data and examination findings.

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 injury. 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 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 in the process of your condition, 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 get your vestibular migraines under control, reduce the frequency and severity of attacks, and return you to living a healthy, vibrant, and fulfilling life.

Your Next Best Step:

Living with vestibular migraines can be challenging, but there is hope for recovery and remission. To see if the NeuroRescue Program is right for you, contact one of our patient care coordinators to schedule your Discovery Day.

And remember, it’s never too late to start getting better.