Nearly 13% of the adult population of the United States has migraine (Lipton et al, 2002). About 1/3 of persons with migraine headaches report dizziness (Kayan and Hood, 1984; Selby and Lance, 1980). Headache and dizziness often appear independently (Cutrer and Baloh, 1992). Strict criteria suggest that about 1.5% of the German population has migraine associated dizziness (Newhauser et al, 2006). As strictness can cause underestimation errors, in our judgment, a reasonable estimate is that about 3% of the adult population of the United states has migraine associated dizziness.
Migraine is an extremely common condition. Some authors suggest that 100% of the population could develop a "migraine", given the right stimuli. Stress, a bottle of bad red wine, lots of chocolate, and plenty of MSG - -who wouldn't get a migraine ? Given that the prevalence is potentially 100%, statistics and inferences have to be based on frequency rather than single episodes that meet incident criteria. That aside, the main idea here is that migraine is not a "disease", but a normal human response.
Litchman and Sanamandra (2019) listed 5 theories of pathogenesis for migraine, showing that we have a collection of symptoms here with no dominant theory.
Logically, Migraine wouldn't be so common if it were not good for something. But how could pain and sensory exaggeration be a good thing ? Our idea is that Migraine is a safety circuit. Pain in the head -- from the eyes, teeth, neck, face -- is all collected together in the nucleus caudalis - the descending nucleus of the Vth nerve (Yin et al, 2009). In other words -- toothache, earache, sinus etc -- all of these inputs go to the nucleus caudalis. The funneling in of all head pain input resulting in a common final pathway for headache is called the "convergence hypothesis" (Cady, 2007). It explains the overlap between Migraine and tension headache. (Olesen, 1991). While the convergence hypothesis is plausible, it is not a popular hypothesis in the migraine literature.
When there is too much pain -- the nucleus activates a central hypersensitivity positive feedback "machine" to draw more attention to the pain. Everything becomes more sensitive -- sound, light, movement, and hurts more. The skin hypersensitivity is called "allodynia". Positive feedback causes a "runaway" shutdown, with the whole system being reset by sleep.
There are several obvious flaws with this hypothesis. It is difficult to understand why any useful circuit could create migraine aura, or cause stroke (see below). Either the hypothesis is wrong, or there are more things going on -- for example, several disorders being lumped into one big Migraine pot.
Other than drawing attention to dangerous things, there are many other possibilities why Migraine might be useful. It has been suggested that women with migraine are more fertile, although against this suggestion, fertility is not affected in women with cluster headache (Rozen et al, 2012). The sensory hyperacuteness that appears in migraineurs might have some survival value. Someone with supersonic hearing, might hear danger before others. Someone who can smell something rotten early on, might confer a survival advantage to themselves or group. Individuals with migraine tend to be more "sensitive" in general, making them more creative -- this may confer an advantage too.
It is common for speakers regarding migraine associated vertigo to say that nobody really knows how migraine causes dizziness. It is more accurate to say -- "its complicated". Part of the problem may be that migraine is a "committee diagnosis", and may include within it many diseases with different mechanisms. Following are some potential mechanisms for how migraine might be associated with dizziness.
Sensory amplification is very common in migraine --
Phonophobia (hyperacusis) is common in migraine (Vingen et al. 1998). Sensitivity to light (photophobia) is also commonly present. (Boulloche et al., 2010) Photophobia is not specific to migraine, and can also accompany eye disorders of course, and other conditions with headache such as meningitis, and and post-traumatic headache. An obvious question here is -- if all headaches use migraine circuitry, aren't these just migraines with infection or trauma as the drive ?
Other sensory amplifications which are common in persons with migraine include allodynia (pain from stimuli that are not painful in most people), smell sensitivity, sensitivity to weather changes and seasons (Brewerton et al, 1990), motion sensitivity, and medication sensitivity (Miller, 2001). Allodynia is very common, affecting roughly 60% of migraine patients (Lipton et al, 2008; Young et al, 2009). Sensitivity to smell (Blau and Solomon, 1985) is very specific to migraine (Kelman, 2004). Osmophobia in children with headache is highly predictive of evolution into migraine (De Carlo et al, 2012).
The sensory amplification is "hard wired" as well as increased during a migraine, and causes positive feedback.
When you barbeque, you may run into positive feedback. The meat on the grill gets hot, fat drips into the coals, the fat starts to burn, everything gets hotter, more fat ... positive feedback ! Positive feedback loop as shown in control systems. Input (x) goes through gain G. A portion of it gets fed back with positive sign. If the feedback gain (H) is high, this system can "runaway", or with a delay in the loop, may break into oscillation.
Persons with migraine -- which make up a large percentage of the population, are "hard wired" to have lower thresholds to many sensory stimuli. Aurora et al (2007), have pointed out using MRI scans that the part of the brain that processes sensory input is larger in persons with migraine. Aurora also reviewed the magnetic stimulation literature that suggests that persons with migraine have lower thresholds, even when they are not having a headache.
During a flare up in migraine activity, brainstem circuits increase this sensitivity. (Denuelle et al, 2011). This creates a "positive feedback" process as shown above. If it "runs away", it ends up with shutdown -- the person with migraine going to bed, turning out the lights, and turning off all noise.
Persons with migraine are not just hypersensitive when they are having a headache. Headache is not the cause -- it is the consequence. While hypersensitivity gets worse when one is far into "runaway" -- i.e. headache, many persons with migraine are extra sensitive 24/7 (Gunaydin et al, 2006; Aurora and Wilkinson, 2007).
Jeong et al (2010) suggested in a thoughtful paper, that "Instead, innate hypersensitivity of the vestibular system may be an underlying mechanism of motion sickness and increased TC in MD/MV. " Here "TC" means increase time constant.
Migraine patients also are slower to habituate.
Perhaps of some importance regarding treatment, especially vestibular rehabilitation that relies heavily on training, patients with migraine do not "learn" as quickly as normal persons to suppress sensory input (Allena et al, 2007). This would imply that persons with MAV might be slower to respond to VRT or motion sickness habituation protocols. In our practice in Chicago, we prefer to use medications for migraine rather than habituation protocols or vestibular rehabilitation for migraine.
Sensory amplification causes motion sickness.
As shown above, normally individuals combine together input from multiple streams of input to develop an estimate of position and movement of their body, from which to base future plans.
- eyes (including both visual motion, and depth)
- ears (vestibular)
- joint sensation -- proprioception (especially neck and feet)
- internal estimate of where they are in space
Frequently these streams conflict. For example, while texting from the back of a car, one's eyes are focused on the cell phone, while one's ears are getting information about bumps in the road and turns. These two streams conflict, which makes this type of activity a highly likely one to induce motion sickness.
Normally, one can turn off one of the conflicting streams - - probably the vestibular one, to reduce the motion sensitivity.
Persons with migraine get overloaded with sensory input, and can develop a constant "motion sickness". Motion sickness is much more common in persons with migraine. (Barabas et al, 1983)
Migraine is associated with several other causes of dizziness.
Meniere's disease and Migraine -- the interrelationship causing dizziness in migraine. Maybe in a few.
Basilar artery migraine is quite difficult to distinguish from Meniere's disease because the "aura" can include 3 of the 4 diagnostic features of Meniere's disease. Migraine associated vertigo, for the subcase where there is no headache, overlaps nearly 100% with the criteria for Menieres.
About 50% of persons with Meniere's disease also meet the criteria for migraine. (Radke et al, 2002; Rassekh et al, 1992), essentially meaning that they have headaches in addition to their Meniere's symptoms. In our Dizzy practice in Chicago, we agree with this general estimate.
As about 10% of the population has migraine (Lipton et al, 2002), this is a 5:1 increased risk. Going the other way, about 2/1000 persons in the population have Meniere's disease. As about 3/100 persons in the population have migraine associated vertigo (see above), there cannot be a substantial # of persons with MAV who also by chance alone have Meniere's disease.
Basilar artery migraine (BAM) is essentially migraine plus an assortment of symptoms that can include those commonly found in Meniere's disease -- see above (Bickerstaff, 1961). Practically, given that headaches are not required to diagnose Migraine associated vertigo, the distinction between Meniere's and basilar artery migraine (BAM), is mainly made by permanent hearing loss noted in Meniere's, and transient hearing symptoms in BAM. In our practice, we attribute symptoms that change synchronously in both ears -- such as low tone hearing loss or tinnitus -- to Migraine, rather than to Meniere's.
BPPV and Migraine causing dizziness and migraine -- some evidence in a few.
Studies report that there is a higher frequency of BPPV in persons with Migraine, as well as vice versa (Ishiyama et al, 2000; Uneri 2004; Chu et al, 2015).
About half of persons with BPPV onset before the age of 50 meet criteria for migraine. There is no reasonable explanation for this association and we are dubious that it exists. Need more data here !
In a large study in Taiwan by Chu et al (2013), migraine roughly doubled the risk of being diagnosed with BPPV. "The results showed that patients with migraine had a 2.03-fold increased risk of developing BPPV compared with age- and sex-matched controls." They commented that BPPV was not a very large cause of dizziness in migraine, but there is some connection. We agree with this.
In our practice, we frequently observe "bitorsional nystagmus", which resembles the nystagmus of BPPV, in persons with migraine. We doubt that these people truly have bilateral BPPV, but rather suspect that they are experiencing changes in central processing in their brainstem or cerebellum that modifies the strength of modulation of otolithic signals.
Positional nystagmus is very common in active migraine (Polansek et al, 2010). Any direction seems to be possible. Again, we suspect that this is due to changes in central circuitry.
We suspect that the association of BPPV with migraine is in part due to clinical errors mixing up bitorsional with BPPV.
Brain tumors and Migraine causing dizziness in migraine -- almost never.
Occasionally of course, patients with migraine will have other disorders such as brain tumors. Go HERE to see an example of this rare situation. The association works like this: Migraine, per se, does not cause brain tumors, but the headaches of brain tumors can be mistaken for migraine, or occur in the same person that has migraine.
"Neurogenic inflammation" causing dizziness in migraine. Its quite a stretch.
Some authors suggest that the trigeminal nerve system that is activated in migraine can cause "neurogenic inflammation" and "local plasma extravasation" (Vass et al, 2001). This conclusion was drawn from a study of guinea pigs whose trigeminal ganglion was stimulated with electrical shocks or pepper extract (capsaicin). They showed that the arteries that supply the inner ear were affected -- in essence -- inflamed, by these stimuli. Capsaicin in particular causes vasodilation. Several papers by this group developed this theme.
Espinosa-Sanchez and Lopez-Escamez (2015) also offered this hypothesis, suggesting that "The neurogenic inﬂammation triggered by activation of the trigeminal-vestibulocochlear reﬂex, with the subsequent inner ear plasma protein extravasation and the release of inﬂammatory mediators, can contribute to a sustained activation and sensitization of the trigeminal primary afferent neurons explaining VM symptoms."
Logically though, this is an unlikely mechanism. It takes a huge leap to conclude that because inner ear arteries of guinea pigs are affected by pepper extract and shocks applied to the trigeminal ganglion, that migraine causes dizziness through the same mechanism. In other contexts where cochlear blood vessels are dilated (e.g. treatment with betahistine), the logic is actually applied the other way -- suggesting that vasodilation improves inner ear function. As a general rule, increased blood supply is a good thing.
Thus, for this to work, something else would have to happen -- perhaps production of inimical substances -- cytokines -- that affect inner ear function. This idea would suggest that a subtype of vertigo and/or hearing loss due to migraine is caused by reduced blood flow to the inner ear. Seems possible, but not especially likely. There are just too many tenuous connections. Why would this mechanism selectively affect the inner ear causing hearing loss, tinnitus or vertigo, without causing a lot of other collateral damage ?
Perhaps this mechanism is a little piece of the puzzle in a subset of the broad group of people who are lumped into the migraine spectrum.
Persons with migraine can sometimes experience a stroke, especially in the cerebellum -- the main balance part of the brain, and thus there can be dizziness due to vascular disturbances. Strokes from migraine are called "complicated migraines". As only about 1% of persons with Migraine experience a stroke, and not all strokes are in the balance part of the brain, this is an unusual situation.
The well known association between strokes and Migraine has caused some difficulties for mechanistic systems thinkers. It is difficult to see any value to a disorder that causes stroke, and also difficult to see how neural circuitry involved in modulating pain could cause a stroke either. Perhaps we are dealing with more than one disorder here ?
Persons with migraine also frequently exhibit MRI findings suggestive of small strokes, or multiple sclerosis. (Evans and Olesen, 2003; De Benedittis and Lorenzetti, 1995). At this writing, it seems unlikely that these lesions are of any functional significance.
Persons with migraine have fluctuating levels of serotonin, and medications that manipulate serotonin, such as some of the antidepressants, are very powerful agents to control migraine. Dizziness is a moderately common side effect of antidepressants in general, including many of those that manipulate serotonin.
If serotonin mechanisms were important in migraine associated vertigo, one would anticipate that medications that manipulate serotonin such as triptans, would be effective treatment of migraineous vertigo. Furman et al (2011) reported that one triptan (rizatriptan), reduces motion sickness in migraineurs. In an uncontrolled study, Cassano (2015) reported about 50% response to a triptan as well. While we have been in clinical practice for many years, seeing many migraine patients/week, we have rarely encountered this situation. Still, our take on this idea, as of 2020, is that it is worth trying, with low-risk triptans (such as frovatriptan)..
We have, however, encountered patients who can treat their photophobia/phonophobia with nonsteroidals. This would be in favor of the general idea that one can treat for migraine pain, and sometimes alleviate other symptoms.
The cerebellum in part, controls balance. Persons with migraine often exhibit unsteadiness with a cerebellar pattern. Persons with severe migraine may develop profound ataxia, sometimes requiring use of a walker or cane, without any signs of inner ear disturbances. Cerebellar findings are sometimes reported in migraine (e.g. Oh et al, 2009), although this is of very little importance as focal neurological deficits could certainly occur in any disorder that can cause stroke. In our otoneurology clinical practice, we occasionally see gaze and rebound nystagmus in individuals with migraine, but this is by no means a universal finding.
Inner ear testing in migraine, is generally normal. In fact, rotatory chair testing usually shows that inner ear function is excellent. The cerebellum has within it circuitry that could cause nystagmus.
In other words, in our opinion, a common mechanism for migraineous dizziness is changes in cerebellar metabolism.
We are dubious that there is a strong association between autonomic disturbances and migraine. We think that this association is largely explained by the well known age and gender associations of migraine - -Migraine is more common in women of childbearing age, and this group is also more likely to have low-normal blood pressure.
A special group are women of perimenopausal age, who have hot flashes. In these situations, it seems plausible that the vasomotor fluctuations associated with hot flashes, could also modulate blood pressure.