Timothy C. Hain, MD, Chicago IL. •Page last modified: May 31, 2020
Patients with migraine (defined as individuals who meet the IHS criteria for migraine) are commonly intolerant of higher levels sensory inputs, and report pain from intensity of input that normal subjects find "under the radar screen" (Aurora and Wilkinson, 2007; Harriott et al, 2014). The dislike for these stimuli are often called "phobias" for fear of the sensory input, as shown below. They are distinct from having lower thresholds (meaning ability to detect smaller levels of the input).
While those with extreme sensory intolerances are generally considered just idiosyncratic migraines, one might also reasonably argue that these groups could be considered as separate subvariants of migraine (such as hemiplegic migraine), or perhaps they are just genetic variants that are grouped into the rather broadly drawn and inclusionary criteria for "migraine". If so, they might actually reflect a different biochemical and neurological wiring arrangement. In other words, perhaps we are dealing with a lot of different diseases, put by the lumpers of the International Headache Society into one big pot called migraine. This is a problem with "committee illnesses", such as migraine and psychiatric disorders.
Although some patients are very certain that sensory input trigger their migraines, the Neurology headache establishment does not appear as certain about this. Pelligrino et al (2017), in a meta-analysis, reported an immense number of potential triggers. Our take on this is that "primary headache disorder" are not really a disease at all, but just a collection of symptoms with many different genetic substrates.
Nevertheless, at least some of these patients are "hard wired" for enhanced sensation as some authors report larger volumes of sensory brain tissue (e.g. Kim et al, 2014).
|Sense||Lower threshold||Greater Discomfort||Measure|
|Sound||Hyperacusis||Phonophobia||LDL (loudness discomfort)|
|Smell||Smell sensitivity||Osmophobia||UPSIT (mainly for reduced smell)|
|Weather||Barosensitivity||? Barophobia ?|
|Motion sensitivity||Motion sickness, kinesophobia||Various questionnaires|
|visceral hypersensitivity||food, medication sensitivity||? IBS ?|
There are separate pages on these topics (see links above).
Inability to regulate sensory input has been reported in a number of psychiatric illnesses, especially autism and schizophrenia. Patient with fibromyalgia, who are similar to migraine patients, also have some reports of lack of habituation. Anomalies in COMT enzyme function are reported to affect sensory gating in the cerebral cortex. Some hallucinogenic drugs also affect sensory input and may lead to overload.
Braff and Geyer (1990) stated that "Clinically, schizophrenic patients report oversensitivity to sensory stimulation that theoretically correlates with stimulus overload and leads to cognitive fragmentation. Animal model studies demonstrate that increased systemic aminergic activity and increased nucleus accumbens dopamine tone causes sensorimotor gating failure, similar to that seen in schizophrenic patients
Baruth et al (2010) stated "It has been reported that individuals with autism spectrum disorder (ASD) have abnormal responses to the sensory environment. For these individuals sensory overload can impair functioning, raise physiological stress, and adversely affect social interaction. Remington and Fairnie (2017) reported that "Autistic people were better at detecting additional unexpected and expected sounds (increased distraction and superior performance respectively). This suggests that they have increased auditory perceptual capacity relative to non-autistic people. " Ronconi et al (2018) reported that persons with autism have superior visual processing.
Regarding drugs, Vollenweider (2001) noted that hallucinogens often act on serotonin receptors located in cortico-thalamic circuitry.
According to Tommasio et al (2014), electrophysiological investigations of episodic migraine have provided "three main sets of observations". First, between attacks, there is a increase in photic driving (presumably this is correlated with photophobia). Second, there is a deficit in habituation of cortical electrical responses to repetitive non-noxious sensory stimuli, which normalizes during attacks. Third, reflexes from noxious stimuli also do not habituate between attacks, but this does not normalize during an attack.
In chronic migraine, the physiology is different. Responses do show substantial habituation. When patients go from episodic to chronic migraine, as a result of medication, the electrophysiology changes back and forth in the same person. These authors proposed that " the pathogenesis of migraine seems to be driven by complex dysfunction of thalamocortical connectivity and temporal activation of neuronal networks." We don't think this sheds much light on the situation.
Harriott (2014), suggested that "Aberrant cortical excitation, lack of habituation, and sensitization of somatosensory and pain pathways are evident between migraine attacks and may relate to the severity and accompanying symptoms that occur during the attack. " We think this is a fair summarization, but not one that sheds much light on the situation.
A common observation in migraine patients is that there is potentiation of one sense by another. Potentiation usually means that there is a multiplication effect rather than just addition, but sometimes the word is just used in a loose way to mean that there is a positive interaction. For example, " exposing migraineurs to light while measuring pain thresholds within locations innervated by the trigeminal nerve results in more sensitivity to painful stimuli than if the light is absent" (Harriott, 2014). Similarly, responses to light are accentuated with thermal pain to the face.
This suggests that it is not just the sum of sensory input that triggers a "shutdown", but rather in migraine, some senses seem to get into other input channels, one sense can or change the scaling factor between other senses and perception of the other senses. This expresses two different concepts -- additive interaction and multiplicative interaction. Consistent with the multiplicative theory, King et al (2014) reported in an open source journal that persons with vestibular migraine have increased sensitivity to dual vestibular inputs (i.e. otolith and canal) compared to normal subjects and non-vestibular migraine. Of course, as is common with migraine studies, these results are very scattered and given the reliance of the diagnosis of migraine on subjective critiera, one wonders what exactly is being studied.
In either case, it would seem likely then "not asking for trouble" and avoiding sensory stimuli would be rational for someone who knows a migraine is coming. "Toughing it out" might not be the best strategy. Shutting down inputs -- avoiding light and loud noise, taking a pain medication, avoiding strong smells -- these would seem more likely to abort an attack.
One would wonder how the triptans (which work on the trigeminal pathway), or nonsteroid pain medications such as ibuprofen could possibly affect sensory input from non-trigeminal pathways (such as sound, light, or smell). Perhaps by reducing somatosensory input, they downmodulate these other senses.