Some of this will be a little heavy, other parts more digestible. More about treatment options towards the end of the article.
Vestibular Migraines may or may not involve headaches in combination with vestibular symptoms such as vertigo, imbalance, nausea and vomiting.
- Vestibular Migraine can cause vesibualr or balance symptoms without an actual headache
- There is almost always a history of motion sensitivity (such as car sickness) since childhood, and migraine headaches at some point in the person's lifetime, even if hey last occurred decades ago.
- Vestibular migraine isn't fully understood but seems to be a result from overlapping pathways that modulate pain and vestibular inputs into the brain.
- Many of the triggers for migraine headaches can cause a vestibular migraine.
- Because a majority of people who have vestibular migraines do not have vesibular symptoms and headaches occurring at the same time, the onset of dizziness by itself may make it challenging to arrive at a diagnosis. Other diagnositic considerations that can present similarly to vesitbular migraine include:
- Benign paroxysmal positional vertigo (BPPV)
- Meniere's disease
- Transient ischemic attack (TIA) or "mini stroke"
- It is common for vestibular migraine, BPPV and Meniere's disease to coexist, which can make diagnosis adn treatment more challenging. (20)
Functionally what we see in our office is that vestibular signals that are coming into your brain, generated from the inner ear are not processed or gated appropriately in the brain stem or cortex, much like the pain pathways in Migraine. And, since they share the same pathway through the Thalamus, they can overlap, or effect one another. It's important to understand non-vestibular Migraine as the approach is similar, yet additonal regions are involved. Dr. Aaron MacArthur is a board certified Chiropractic Neurologist with a fellowship in Vestibular Rehabilitation as well as a fellowship in Brain Injury and Rehabilitation.
As for a non-Vestibular Migraine- It's all about the Trigeminovascular pathway
The World Health Organization lists Migraine as the sixth most disabling disorder globally, and the most disabling of all neurological disorders (1). Migraine affects females 3:1 (2). Migraines are described as a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment (3). It's a complex and multifaceted disorder of the brain which in its entirety may last over several days (3). It is widely accepted that Migraine involves activation and sensitization of the trigeminovascular pathways, as well as brain stem and diencephalic nuclei (4,5). A primary dysregulation of sensory processing is likely to result in a constellation of neurological symptoms that affect our senses. It has been suggested that migraine may be considered a brain state of altered excitability (6-10).
In about as simple of terms as I can explain, A Migraine is due to an increase, or alteration in activity within your brain pathway that tells you information about your head/face relative to pain.
In real terms, it means that a Migraine is a disruption in normal signaling within a specific pathway in your brain that alters the function of the entire brain. Along this pathway are many areas that may be involved in the brain stem, Mesencephalon, Pons, Medulla and Diencephalon- Specifically the SuS, TCC, RVM, LC, PAG, Hypothalamus, Thalamus, Cortex (ACC, S1, S2, PFC). If you want to know more, reference article (3). It specifically affects the Trigeminal Cervical Complex (TCC), which is your fifth cranial nerve and C1-2 regions. The reason the TCC is so important to your Migraine experience is that it's the one that carries sensory information from your face and head, or PAIN. The "hyperexcitability" refers to the excessive signaling of the trigeminal nerve complex and other regions of the brain that make a person extremely sensitive to sensory input, whether sounds, light, irratibility, pain, movement, etc. It is basically an inability to gait sensory information entering the brain so that we can't weight it appropriately and a small amount of movement or stimulation to the face/head/eyes/ears is experienced as an exaggerated pain, light or sound response, resulting in headache pain. The Thalamus is a part of our brain that gates all sensory information, except smell to the rest of our cortex and is thought to be a major component of Migraine. It is believed to be at the heart of the central processing and integration of nociceptive (pain) information and is regarded as a relay center for handling all incoming sensory information, and even modulating it (3). The path that regulates pain is skewed and exaggerating the signal within the brain, resulting in Migraine. This path can be treated once we locate the culprit(s) along the pathway.
We used to think Migraines were a vascular disorder, but it is much different than that.
The brain is largely insensate, but a rich plexus of nociceptive nerve fibers that originate in the trigeminal ganglion innervate the pial, arachnoid, and dural blood vessels, including the superior sagittal sinus and middle meningeal artery, as well as large cerebral arteries. Activation of these structures, particularly the dura mater, with mechanical, chemical, or electrical stimulation results in headache pain very similar to the pain in migraine, as well as other symptoms associated with migraine, including nausea and photophobia. The normal throbbing of blood vessels leads to head pain because of an error(s) within the Trigeminovascular pathway that includes the PAG, RVM, Locus Coeruleus, Sus, and Diencephalic nuclei, inluding the Hypothalamus, Thalamus, and Cortex (3).
Why do I have throbbing pain in my head?
The pain can be terrible with Migraines, although some people do not experience pain during their cycle, which is known as a silent migraine. Migraine is defined by 4 Phases- Premonitory, Aura, Pain and Postdrome. In my opinion, the most important phase is the premonitory phase as you can either take your medication as early as possible to mitigate the Migraine response, or receive other treatments to restore the trigeminovascular pathway input to a normal functional level (16-18). This where the throbbing head pain comes in, normal activity of dilation and constriction within the blood vessels that supply the meninges that usually does not elicit painful information now becomes painful due to the heightened sensitivity within the trigeminovascular pathway. Somewhere along this pathway, particularly the Thalamus skews the sensory information to the brain and we perceive pain during normal vascular activity instead of normal, painless proprioception. Many medication such as the CGRP monoclonal antibodies aim to block this pain pathway from sending painful information to the brain stem and cortex. However, there may be a better way to get to the source by reducing the hypersensitivity and restoring normal neuronal function along the trigeminovascular pathway by reconnecting the brain's normal signaling network utilizing a combination of neuroplasticity retraining, vestibular rehabilitation, visuomotor rehab, chiropractic, physical therapy and oxygenation.
Phases of Migraine
Phase 1- Premonitory, which may precede the actual headache, or pain phase, by 72 hours (11). Include changes in mood and activity, irritability, fatigue, food cravings, repetitive yawning, stiff neck, and phonophobia (irritation of sounds). These symptoms may endure well into the aura, headache and even podrome phases. This dysfunction is shown to be as a result of the Hypothalamus (3).
Phase 2- Aura, about one third of migrainers experience transient neurological deficits, the migraine aura (12). A transient wave of neuronal depolarization of the cortex, the cortical spreading depression (CSD), is believed to be the pathophysiological brain mechanism underlying the clinical phenomen of migraine aura (3). The ICHD-3 defines the migraine aura as one or more transient, fully reversible neurological deficits. of which at least one has to have a unilateral localization, that develops over 5 min or more and of which each deficit lasts between 5 and 60 min, 26% of patients have at least one of three auras that lasts longer than an hour. Five percent of auras are over 4 h (13). Visual aura is found in over 90% of the cases, and the most common deficit, however sensory, motor, speech, brain stem adn retinal aura symptoms may also occur. Aura symptoms may precede the headache phase but may last well into the headache phase or even initiate during the headache phase. An example of motor aura would be hemiplegic migraine and may last up to 72 hours (14).
Phase 3- Headache, ICHD-3 defines migraine as a headache attack lasting 4-72 h that is accompanied by nausea, photophobia (light sensitivity) and phonophobia (sound sensitivity), or both. The headache is characterized as unilateral, pulsating, of moderate or severe intensity and aggravated by physical activity; two of these characteristics uffice to fulfill the diagnostic criteria. Chronic migraine is defined as a migraine that occurs on 15 or more days per month as compared to episodic, which is less than 15 days per month (15).
Phase 4- Postdrome, this is often referred to as the Migraine hangover and it does reflect some of the symptoms experienced in the premonitory phase.
Migraines due to improper breathing mechanics (Respiration), creating a global hyperexcitability of the brain, increasing that inividual's symptoms, especially pain.
Respiration can greatly affect Migraine sufferers. When Hyperventilation occurs, which often happens if we are lacking proper lumbar lordosis, rib expansion, abdominal strength, sacral flexibility (nutation), we do not fill our lower lobes where most gas exchange occurs and progress into a state of Respiratory Alkalosis. This causes increased binding of Calcium in our blood by a protein known as Albumin. Since Calcium and Sodium compete with one another for neuronal activation, when Ca2+ levels drop, Na+ rises and they now freely enter our brain cells and cause a level of hyperexcitability within those neurons, similar to what we're discussing in regards to Migraine, causing increased activation to the pain pathways on top of an already hypersensitive and dysregulated system. This can be due to abnormal rib activity, posture, spinal misalignment/dysfunction, weakness in abdominal and spinal extensor musculature and responds very well to Chiropractic Neurological Treatment and Physical Therapy.
How do Genetics fit in? You're not limited by them (see last few paragraphs).
Genetics play a role as they affect the voltage gated channels that allow Calcium (Ca2+) into axon terminals to release Neurotransmitters. These genetic errors cause these channels to form improperly, not allowing them to close all the way, leading to an excess of Ca2+ entering the axon terminal and release an excessive amount of Neurotransmitter. This causes the Trigeminal pain pathway to become overactive, or hyperexcitable and causes Migraines.
Technical Migraine Overview
From a genetic predisposition, to brain hyperexcitability, to peripheral and central sensitization, and brain stem and hypothalamus dysfunction. They all contribute to the phenotype of the migraineur. Migraine is a complex, basically inherited variable disorder of brain function. Its afferent pathway arises in the nociceptive durovascular afferents that seemed design to warn not localize. Their projection to the thalamus and cortex, and the regulation of this pathway, importantly at each level, and by multiple systems offers the possibility to understand the complex symptoms and target therapies. Rather than a sequential activaiotn of different brain regions, migriane is a disorder of brain and therefore considered a "brain state," and is a consequence of changes, or dysfunction, in brain stem and hypothalamic regions which contribute to changes in cellular and vascular function in many regions of the brain. Migraine is best described as a consequence of dysfunction in the brain stem and hypothalamic nuclei that normally modulate or gate sensory inputs, including touch, light, sounds, and smells. These brain stem and hypothalamic nuclei can be considered "migraine mediators," and their dysfucntion can lead to the failure of the brain integration and filtering mechanisms. The complex network of connections between regions of the brain stem, which include the PAG, RVM, locus coeruleus, and SuS, and diencephalic nuclei including hypothalamus, thalamus, and cortex can lead to the generation of symptoms throiugh the same core of dysfucntion. Dysfunction in these regions, though descending control of trigeminovascular nociceptive traffic, can lead to the perception of head pain through normal vessels throbbing, and continued dysfunction can lead to central sensitization of trigeminovascular neurons and the exacerbation of pain to normal physical activity as well as cutaneous cephalic and extracephalic allodynia. Convergence of sensory inputs to the thalamus that project to the cortex can explain the hypersensitivity to light, sounds and smells. The same dyfunction can lead to homeostatic changes, controlled by Hypothalamus related to sleep, feeding and activity. The general alteration of cortical and subcortical function can trigger events such as migraine aura, and extend to general inability to function properly. Inherited genetic factors clearly play a role in predisposing migraine susceptibility, as do the role of potential migraine triggers, whose common link seems to play at the heart of brain homeostasis in the hypothalamus and brain stem (3).
How can we diagnose what's causing your Migraine?
By evaluating the brain and nervous system in its entirety, but specifically along the trigeminovascular pathway, we can localize regions that are dysfunctional and misrepresenting sensory information to the brain. Autonomic dysregulation is a hallmark of Migraine dysfunction and we perform careful evaluation of this potential involvement. Oxygenation is an important aspect of Migraine and is also evaluated very carefully. We're essentailly looking at your brain from an integration perspective, ensuring all regions are sending appropriate afferent information to the brain, including the vestibular system, proprioceptive system, visuomotor system, autonomic system, oxygenation system. Our core model of care is multi-modal, ensuring that all potential regions that may contribute to Migraine are properly assessed and treated to allow proper gating and function to occur along the Trigeminovascular pathway. In order to do this, we must reset the Central Integrated State of the dysfunction neuronal regions of the brain to reduce their resting membrane potential to an appropriate level that is healhy and approximately -65 mV, reducing hyperexcitablity. We attempt to achieve this through a specialized program that combines Neurology, Chiropractic, Physical Therapy, Vestibular Rehabilitation, Occupational Therapy and Oxygen.
Migraine Core Testing:
- Videooculography (VOG, sometimes referred to as VNG) that measure eye movements that relate to specific regions of the brain, brain stem and vestibular system.
- Sensitive balance and coordination testing of proprioception and brain using Computerized Assessments of Posturography Systems (CAPS) that allow us to measure dysfunctional areas sensory input related to Migraine.
- Tilt Table Testing
- Autonomic Assessment
- Clinical Examination (Neurology, Proprioceptive, Respiration)
- Gait analysis
- Oxygen evaluation
- Metabolic capacity
- Objective measures
- Spatial and Temporal Summation (Treatment Plan)
Vestibular Migraine Core Treatment:
- Tilt Table Treatment (TTT)
- Non-Invasive Nerve Stimulation (NINS)
- Vagus Stimulation (VS)
- Oculomotor retraining (eye movement exercises) (OMR)
- Vestibular Rehabilitation (VR)
- Occupational Therapy (OT)
- Rib Manipulation (RM)
- Cervicovestibular rehabilitation (CVR)
- Specific Chiropractic Neurological Manipulations for Oxygenation L/S/T (SCNM-O)
- Mild Hyperbaric Oxygen Therapy (mHBOT)
- Postural Restoration (PR)
- Physical Therapy (PT)
- Functional Neurological Rehabilitation/Neuroplasticity Retraining Exercises (FNR/NRE)
- Co-treatment (Botox, Medications, etc..) (CT)
- Migraine dietary recommendations (MDR)
How can our treatments change your Migraine response?
Neurons require Activation, Oxygen and Fuel (glucose) to maintain a healthy state of -65 mV and undergo Immediate Early Gene Response to create more cellular contents such as sodium/potassium pumps, mitochondria for ATP formation, axonal and dendritic connections with neighboring cells, etc. The list you saw is how we target the dysfunctional areas with activation, oxygen and carry fuel to those cells. This has to be done in a very graded, careful manner so as to not exceed the metabolic rate of the neurons involved. We observe metabolic capacity for each individual and maintain levels of treatment that stay below those levels so as to keep a steady progression of healthy return to a normal state of function. Neurons respond through Temporal and Spatial Summation, so we can develop treatment plans based on your severity that will allow maximal response and long-term changes. This is known as Neuroplasticity and is at the core of our Migraine Program. I often tell people, I don't know how much I can help you, but in most cases, we're able to improve Migraine at least 50% with the understanding that our goal is much higher. Your response depends on multiple factors, including genetics, central sensitization (chronicity), following our treatment plan and so forth. We are very open and honest with our patients and do our best to provide accurate information, but it is a functional issue and it is sometimes difficult to be exacting in our predictions.
Can Portland Chiropractic Neurology treat my Migraines successfully?
For many individuals, yes we can, and we've been doing it for over 12 years. However, that can range from 25% improvement to as close to 100% as possible, although most people will agree that an improvement of 50% is life changing. The rest we hope to control through lifestyle changes, dietary changes, Medical intervention such as medications, botox, etc. Our goal is for your results to be long-lasting and permanent without our continued care because we utilize Neuroplasticity appropriately along all aspects of our treatment plan, patients don't return to their previous state when they are finished treatment. That being said, genetics and many other aspects play a role in your Migraine physiology, so it is difficult to determine or know for sure at the beginning of treatment if you are a 50% improved patient or a 100%, or anything in between. Even those with genetic predispositions, which is not always known, respond well to care as our treatment aims to change the phenotypic expression of their migraine genotype, or what your parents passed down to you (genetics). With the proper diagnosis, we can treat the areas that are the primary source of your Migraines through Neuroplasticity Retraining Excercises that will change your brain function along the pathway involved with Migraines (Trigeminovascular pathway).
Please reach out to ask specific questions that you may have at firstname.lastname@example.org or call us at 207-699-5600 to set up a free consult with a doctor.
People with Vestibular Migraines can reduce the number and intensity of episodes by maintaing a regular sleep and meal schedule, avoiding triggers, exercising regularly and managing stress (20).
Migraine Diagnosis Criteria- see International Classification for headache disorders (ICHD)- 3 Beta (19)
- Patient must experience at least five attacks lasting 4-72
- Headache has at least two of the following
- Unilateral location (one sided)
- Pulsating quality
- Moderate or severe pain intensity
- Aggravation by or causing avoidance of routin physical activity (e.g., walking or climbing stairs)
- During headache at least one of the following
- Nausea and/or vomiting
- Photophobia and phonophobia
- Not better accounted for by another ICHD-3 diagnosis
- At least two attacks fulfilling criteria B and C
- One or more of the following fully reversible aura symptoms
- Speech and/or language
- Brain Stem
- At least two fo the following four characteristics
- At least one aura symptom spreads gradually over or equal to 5 min, and/or two or more symptoms occur in succession
- Each individual aura symptom lasts 5-60 min
- At least one aura symptom is unilateral (one sided)
- The aura is accompanied, or followed within 60 min, by headache
- Not better accounted for by another ICHD-3 diagnosis, and transient ischemic attack has been excluded (19).
(1) Global Burden of Disease Study. Global, regional, and national incidence, prevalance and years lived wiht disaiblity for 301 acute and chronic diseases and injuries in 188 coutnires, 1990-2013; a systematic analysis for the Global Burden of Disease Study 2013. Lancet 386: 743-800, 2015
(2) Buse DC, et al. Sociodemographic and comorbidity profiles of chronic migraine and episodic migraine suffers. J Neurol Neurosurg Psychiatry 81: 428-432, 2010.
(3) Goadsby Peter J., et al. Pathophysiology of Migraine: A Disorder of Sensory Processing. Physiol Rev 97 553-622, 2017.
(4) Akerman S, Holland P, Goadsby PJ. Diencephalic and brainstem mechanisms in migraine. Nature Rev Neurosci 12: 570-584, 2011.
(5) Bernstein C, Burstein R. Sensitization of the trigeminovascular pathway: perspective and implications to migraine pathophysiology. J Clin Neurol 8: 89-99, 2012.
(6) Charles A. Migraine: a brain state. Curr Opin Neurol 26: 235-239, 2013.
(7) Coppola G, et al. Is the cerebral cortex hyperxcitable or hyperresponsive in migraine? Cephalgia 27: 1427-1439, 2007.
(8) Coppola G, et al. Reply to the topical review entitled "the phenomenon of changes in cortical exctiabiltiy in migraine is not migraine-specific-unifying thesis" by Anne Stankewitz adn Arne May published in Pain 2009; 145:1407. Pain 149: 407-409, 2010.
(9) De Tommaso M, et al. Altered processing of sensory stimuli in patients with migraine. Nat Rev Neurol 10:144-155, 2014.
(10) Stankewitz A, et al. The phenomenon of changes in cortical excitability in migraine is not migraine-specific-a unifying thesis. Pain 145: 14-17, 2009.
(11) Gifffin NJ, et al. Premonitory symptoms in migraine: an electronic diary study. Neurology 60: 935-940, 2003.
(12) Rasmussen BK, et al. Migarine with aura and migraine without aura: an epidemiological study. Cephalgia 12: 221-228, 1992.
(13) Viana M, et al. Migraine aura symptoms: duration, succession and temporal relationship to headache. Cephalgia 36: 413-421, 2016.
(14) Hansen JM, et al. Migraine headache is present in the aura phase: a prospective study. Neurology 79: 2044-2049, 2012.
(15) Olesen J, et al. New appendix criteria open for a broader concept of chronic migraine. Cephalgia 26: 742-746, 2006.
(16) McNaughton FL, et al. Innervation of intracranial structures: a reappraisal. In:Physiological Aspects of Clincal Neurology, edited by Rose FC. Oxford: Blackwell Scientific, 1977, p. 279-293
(17) Penfield W, et al. Dural headache and the innervatin of hte dura mater. Arch Neurol Psychiatry 44:43-75
(18) Ray BS, et al. Experimental studies on headache. Pain sensitive structures of the head and their significance in headache. Arch Surg 41:813-856, 1940.
(19) Headache Classification Committe of the International Headache Society. The international classification of headache disorders, 3rd edition. Cephalgia 33: 629-808, 2013.