Vestibular migraine (VM) is a migraine disorder characterised by the overlapping presence of vestibular and migraine symptoms, which may include vertigo, visual disturbances, headache, sensitivity to sound and light, or visual aura.
Even though formal guidelines for diagnosis were only developed in 2012, vestibular migraine is now recognised the most common cause of spontaneous episodic vertigo1 , yet remains a poorly understood and significantly under-diagnosed condition. Though BPPV is at least half as common2 , it is better understood and hence diagnosed 3-4 times more often.3
Vestibular migraine is listed in the appendix of the ICHD-3, for entities that ‘are believed to be real but for which better scientific evidence must be presented before they can be formally accepted’. Amazingly some neurologists argue it doesn’t even exist.4
At the Melbourne Headache Centre not only do we know that it exists, but we understand and treat one of the most important sources of input that connects not only to the vestibular nucleus (creating dizziness and vertigo), but also to the trigeminal nucleus (headache, photophobia, phonophobia), cuneate nucleus (visually associated symptoms) and solitary nucleus (nausea and vomiting).
Whilst many other clinics, and indeed doctors, will have barely heard of vestibular migraine, our experience and expertise at the Melbourne Headache Centre allows us to identify a key cause of dysfunction and treat it rapidly, safely and effectively. We also understand how easily many people with VM can be triggered by overly aggressive neck treatment. Experience counts for everything!
Diagnosis & Symptoms
Vestibular migraine is ‘owned’ by two disciplines – Neurology and Otology (Vestibular), and as such the classification was jointly agreed to by both the International Headache Society and the Committee for Classification of Vestibular Disorders of the Bárány Society. The two versions differ slightly which in itself is interesting, but presented here is the version described in the appendix of the ICHD-3 under episodic syndromes that may be associated with migraine.
A. At least five episodes fulfilling criteria C and D
B. A current or past history of migraine with or without aura
E. Not better accounted for by another ICHD-3 diagnosis
Vestibular symptoms include:
- Positional vertigo, occurring after change in head position
- Visually-induced vertigo, triggered by a complex or large moving stimulus
- Head motion-induced vertigo, occurring during head motion
- Head motion-induced dizziness with nausea.
If 5 episodes have occurred with at least some of the above occurring in different episodes (not all symptoms need to be present all the time) in the absence of other diagnosable conditions, then a diagnosis of vestibular migraine will be given.5
A diagnosis of ‘probable Vestibular Migraine’ will be given if only one of conditions C. or D. are satisfied.
Vestibular Migraine has been previously known as:
- Migraine-associated vertigo/dizziness
- Migraine-related vestibulopathy
- Migrainous vertigo
0%of people with BPPV
0%of VM sufferers
As a newly emerged diagnostic entity (first official diagnostic criteria decided in 2012) there are few studies using the formal classification. A study in the USA looking combining definite and probable VM found a 1-year prevalence of 2.7%.6 Only 10% of those had received a diagnosis of vestibular migraine.
With stricter criteria (limited to co-occurrence of migraine with vertigo – i.e. no head motion-induced dizziness with nausea) are used the 1-year prevalence drops to 1.98%.7
Even at these levels Vestibular Migraine is the leading cause of vertigo with BPPV at 1.5%8 and Meniѐre’s disease between 0.5% and 1.3%,9 however this strict criteria for classification are drawn up for research purposes. In the clinic we see:
- 87% of patients with benign recurrent vertigo (no structural cause) have migraine10
- 15-38% of patients attending dizziness clinics have migraine
- 51-72% of those attending migraine clinics report dizziness and/or vertigo11
- The prevalence of vestibular migraine has been estimated at 7% among consecutive clients attending a dizziness clinic, and 9 % among consecutive patients attending a migraine clinic.12
- 70% have had medical review involving diagnostic testing in the past 12 months
- 30% of these had multiple tests
- Only 10-21% of those examined receive the diagnosis of Vestibular Migraine despite meeting the criteria.
- 40% report sick leave from work due to VM
- 79% report significant impact on daily life (severe 33%, moderate 46%)
- 40% took medications, with only one third of these reporting a good response.
At the Melbourne Headache Centre:
we treat the one input that can feed into every part of the vestibular migraine symptoms profile (see causes below). During the assessment we are looking for three key factors:
- Do you have a small fault which creates spasm in the sub-occipital muscles?
- Can we treat the fault and correct the muscle spasm?
- Is it relevant to your condition?
The vast majority of people with VM have a sensitivity driven by the muscles in the top of the neck and can be
At the Melbourne Headache Centre, we specialise in providing treatment for vestibular migraine we are used to treating people with chronic issues and sensitive necks. We understand that many of our clients seeking treatment for vestibular migraine may have been aggravated with the ‘press and guess’ approach some standard manual therapies employ.
Treating OCI is not about ‘deep and painful’ manual stretching techniques. By treating the source of the spasm we can do so with minimal aggravation and maximum impact, and it’s also the reason why we typically see rapid changes with vestibular migraine, and often don’t need to do a lot in terms of hands on treatment.
Many people have this fault in the top of the neck. If you are sensitive to the ‘noise’ it creates you will potentially have symptoms associated with headache, migraine or some of its variations including vestibular migraine.
The current guidelines for vestibular migraine follow the same pharmacological approach as for non-vestibular migraine. Given the obvious differences in pathophysiology (i.e. involvement of the vestibular nucleus) seems to be lacking from the outset. Medication studies in this space have not undergone suitable randomised controlled trials, with the majority of data available from retrospective chart reviews, and treatment trials that lack placebo control. We know placebo can account for 20-35% response rates in medication trials, so judging the effectiveness of these medications and weighing the benefits versus the risks is very difficult based on the evidence available.
Changes to the impact of dizziness (measured by Dizziness Handicap Index) have shown across a number of studies to be marginally positive at best and possibly no effect at all. The aim is to help the vestibular system to adjust (habituation) or find alternative pathways (adaptation), rather than deal with the underlying sensitivity, but with no real side effects, highly recommended.
Like other forms of migraine we have an incomplete understanding of the pathophysiology of vestibular migraine, but we understand which parts of the brainstem control the symptoms we see. The symptoms of vestibular migraine can be accounted for by the vestibular nucleus (vertigo, dizziness), trigeminal nucleus (headache, photophobia, phonophobia), solitary nucleus (nausea), and cuneate nucleus (visually induced symptoms).
Currently the neurological model attempts to explain vestibular migraine within the context of the current model of migraine – a combination of abnormal processing of shared pain and vestibular pathways, abnormal thalamic function, genetic factors, migraine aura (cortical spreading depression) and the latest – CGRP release presumably into the brainstem, or independently into the dural blood vessels AND inner ear. While these theories all have some merit, none offer a logical starting point – that remains a mystery, and only offer partial explanation. Cobbled together they may provide a complete picture – relying on dysfunction in multiple brainstem nuclei and multiple sites of spontaneous CGRP release. Possible, but highly complicated and unlikely.
Often the simple explanation is the right one – but unfortunately neurologists are not specialists in, or even have reasonable knowledge of the one anatomical pathway that connects directly to all the areas involved. The upper cervical spine.
Nerve endings from the top of the neck feed directly into key brainstem areas that if dysfunctional will cause:
- Dizziness and vertigo
- Sleep disturbance, lethargy
- Brain Fog
- Orthostatic intolerance
The small muscles under the base of your skull – known as the sub-occipital triangle (obliquus capitis inferior, obliquus capitis superior and rectus capitis major and minor) play a major role in proper vestibular function and in coordinating head and eye movements and finely controlled movements of the head with the trunk. To do this they are jam packed with muscles spindles – the sensory part of the muscle. In fact they have the highest muscle spindle density of any muscle group in the body.
Dysfunction in these muscles is very common, and can be extremely disruptive. Whilst it doesn’t always cause neck pain, for many there will be a stiffness or pressure under the base of the skull. This is why many migraineurs and vestibular migraineurs will have neck pain as part of their presentation – but being treated using techniques designed to ‘loosen stiff joints’ can be far too aggressive and provoke episodes. Especially in VM, we often see people scared of having anyone push on their neck!
Using the Watson Headache ® Approach we are able to assess and correct the fault that OCI is reacting to. In other words the position indicated above can be corrected within about 30 seconds or so during the assessment, and can show you how to keep it stable. Properly identifying and treating the cause for this muscle spasm is a critical step that is often missed, and has a profound effect on the response to treatment.
NB: In the hands of a skilled practitioner this fault is able to be assessed manually. If you have x-rays by all means being them to the assessment, but they are not required to identify this fault, and cause needless exposure.
Vestibular Migraine Differential Diagnosis – What else could it be?
BPPV – Benign paroxysmal positional vertigo – comes in at second as a cause of vertigo. – this is number one. This is a more common presentation and should be ruled out by testing with a vestibular (ENT) specialist or Physiotherapist specialising in vestibular therapy.
Meniѐre’s disease – a condition with recurrent vertigo accompanied by fullness or ringing in the ears (tinnitus) and deafness. Symptoms include vertigo, dizziness, nausea, vomiting, loss of hearing (in the affected ear), and abnormal eye movements. It is caused by dysfunction of the semi-circular canals of the inner ear.
The best distinguishing characteristic of MD from VM is unilateral, low-frequency, progressive, or fluctuating, sensorineural hearing loss (SNHL). A patient with a long history of episodic vertigo with aural symptoms who only has mild, symmetrical hearing loss most likely has VM
Transient Ischaemic Attacks – TIA’s
A number of studies show that dizziness and vertigo, even when isolated (only symptom) are the most common premonitory symptom of a vertebrobasilar TIA, in the days and weeks preceding posterior circulation stroke. In the majority of cases vertigo lasted longer than 1 hour, but is very hard to distinguish from VM in the initial presentation.
For this reason any new presentation, especially with patients with cardiovascular risk factors should be reviewed by a doctor, and preferably a neurologist, or neurootologist.
Migraine with Brainstem Aura: there must be at least 2 posterior circulation symptoms (vertigo, diplopia, tinnitus, impaired hearing, ataxia or encephalopathy (lasting between 5-60 minutes and be followed by migraine headache. Most patients with VM’s vestibular symptoms do not fit the aura time window, and fewer experience immediately before headache onset.
Binocular Vision Dysfunction
This occurs when the eyes are very slightly misaligned or unable to coordinate properly. It is not as obvious as strabismus (visible turned eye) and may be more a functioning problem that a structural one.
More acute causes should be ruled out with MRI at the onset of new symptoms, such as a brain tumour or Multiple Sclerosis.
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