Dear Anthony, you mentioned that "Allodynia has been alleviated by caloric stimulation (running water at certain temperatures into the ear canal)." Do you have any article goes with this concept.

Acta Neurol Scand. 2009 Jun;119(6):404-9. doi: 10.1111/j.1600-0404.2008.01106.x. Epub 2008 Oct 6.

Post-stroke tactile allodynia and its modulation by vestibular stimulation: a MEG case study.

Abstract

BACKGROUND:

There is behavioural evidence that caloric vestibular stimulation (CVS) can alleviate central pain. Several such patients have also noted that it reduces tactile allodynia, an especially ill-understood phenomenon in these patients.

AIMS OF THE STUDY:

The first aim is to use magnetoencephalography (MEG) to study neural activity associated with tactile allodynia in central post-stroke pain (CPSP). The second is to assess how this would be affected, if at all, by CVS. The third is to assess the ability of the VESTAL solution for MEG to detect anterior cingulate activation.

METHODS:

A 58-year-old woman with CPSP, and marked unilateral tactile allodynia, participated in a MEG study with imaging pre- and post-CVS.

RESULTS:

Tactile simulation within the patient's allodynic area resulted in contralateral activation of the primary motor and anterior cingulate cortices, which had normalized 24 h post-CVS.

CONCLUSIONS:

We suggest that the unexpected primary motor cortex activation in response to light touch in the allodynic area arises from inappropriate activation of a normal mechanism, which may occur when a threat to homeostasis is present, to lower motor thresholds and allow for more rapid performance of corrective actions. We propose this may be mediated by the interoceptive cortex in the dorsal posterior insula.

 Dear Anthony, tha's a very interesting topic. It seems to me that a hypereactive state of the inner ear cannot explain per se several features of migraine attacks and interictal migraine cycle. First of all, it cannot explain migraine symptoms other than auditory (visual aura, motor aura, photophobia etc). Second it cannot explain cortical phenomena as modified excitability and reduced habituation to EPs in visual, somatosensory and also cognitive processes. Also the auditory componentsna and auditory changes found in EPs could be explained by a disfunction at the cortical level as shown in several papers on corical AEPs and IDAP. Lately, at present, allodynia is the clinical representation of central sensitization which appears to be due to a thalamic involvement. Whichever it is the mechanism that facilitate the coritcal dysfunction and if subocrtical structures can contribute is still under evaluation. Personally, I don't see why auditory system should partecipate more than other sensory ssystems (e.g. visual, somatosensory).

"First of all, it cannot expolain migraine symptoms other than auditory (visual aura, motor aura, photophobia etc)."

I have just checked through my recent migraine references, and found 7 where vestibular abnormalities were commoner in those with aurae.  I am sure many visual hallucinations are of vestibular origin (eg in alcoholic hallucinoisis).

I find photophobia a very frustrating symptom.  I suspect it is, like occasional transitory blindness, due to aberrant vestibular reflexes.  Certainly, I don't know of a better alternative explanation for it. 

In development, the vestibular system develops early and drives development of other sensory systems,  I think it still has an overriding influence in adults on sensory and arousal systems. 

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"Personally, I don't see why auditory system should partecipate more than other sensory systems"

Agreed, but there is every reason to suspect the vestibular system.

"Whichever it is the mechanism that facilitate the coritcal dysfunction and if subocrtical structures can contribute is still under evaluation."

This highlights a general chicken and egg problem in many neurological and psychiatric conditions.  For example, I think brain changes in schizophrenia are far more likely the result than the cause of the disease, reflect subcortical drivers, and are shaped in the first instance by the symptoms.

"Second it cannot explain cortical phenomena as modified excitability and reduced habituation to EPs in visual, somatosensory and also cognitive processes"

A whole panoply of bizarre sensory and motor phenomena are seen in the sensorimotor induction syndrome.  The only proven pathology, in some cases at least, is damage to the inner ear.  Halpern gives a typical case report in Neurology 1954;4:233.  Her trouble started with attacks of dizziness, fulness in the ears, blurred vision, and general weakness.  This can only be Meniere Spectrum Disorder, ie endolymphatic hydrops, at least to begin with.

"it cannot expolain migraine symptoms other than auditory (visual aura, motor aura, photophobia etc)"

I have just come across the newly-described disorder, visual snow, often (mis)diagnosed as migraine aura.    It is not due to eye or brain disease, but there are many clues on the Internet implicating inner ear disorder, eg vertigo, tinnitus, depersonalisation, Meniere's disease, etc, so it looks like another example of vestibular interference with vision.

Allodynia is the result of central sensitization and don't the result of pathology of vestibular system. Vertigo and dyziness very rare in my practice among the migraine patients. And allodynia as hyper sinsitive of head scin, photophobia, phonophobia and osmophobia are usial and very often

"Allodynia is the result of central sensitization and don't the result of pathology of vestibular system"

These two processes are not contradictory.  For example, tinnitus, which always starts in or near the cochlea, often rewires and sensitises the cortical analysers. 

"phonophobia and osmophobia are usial and very often"

Phonophobia (audiosensitivity) is due to cochlear hypersensitivity, not to any primary central cause. Whilst I have not tested persons during migraines, in every other condition producing audiosensitivity I found abnormal stapedial reflexes.

To all readers of this thread : ALLODYNIA  is not necessarily a manifestation of central sensitization,  and the idea that it is mediated by the thalamus is incorrect. I have trained under the individual who characterized the thalamic responses to visceral versus somatic pain in non-human species via electrophysiology and continued the work with neuroimaging in humans (AV Apkarian), and there is no strong evidence to even seriously consider this hypothesis. 

Only DYNAMIC MECHANICAL ALLODYNIA is indicative of SPINAL central sensitization (which is the only kind, read Clifford Woolf's work), meaning that the pressure stimulus must be moving across the skin. Direct pressure that indents the skin, which is the most common for of allodynia, is not the same animal and can co-exist with dynamic mechanical allodynia.

"a hypereactive state of the inner ear cannot explain per se several features of migraine attacks and interictal migraine cycle. First of all, it cannot explain migraine symptoms other than auditory (visual aura, motor aura, photophobia etc)."

It has occurred to me that a good way to sort out the relative contributions of visual and vestibular causes of visuoperceptual disorders or phenomena is to look at sleep, where (mis)information from the ear is far more likely than from the eye or visual environment. A quick check on Google has found plenty of evidence for a vestibular driver, eg  see JM Windt Dreaming (2015):

"In dreams, vestibular processing -- prompted by ambiguous signals from the otoliths -- drives the integration of visual imagery and at the same time heightens sensitivity to real-body input.  Vestibular processing, alongside emotion, may thus be a primary factor of dream production."

I

"It seems to me that a hypereactive state of the inner ear cannot explain per se several features of migraine attacks and interictal migraine cycle. First of all, it cannot explain migraine symptoms other than auditory (visual aura, motor aura, photophobia etc)."

As usual, whenever I think I have come up with a good original idea, I eventually find that someone else thought of it first.  Here it is Gelle in Ann Ophthalmol Otol 1896;5;1180-96.  I do not recall any similar article on the detailed description of auricular vertigo, based on careful observations of hundreds of patients.

"There exists a veritable aura, premonitory of the approach of vertigo; and that this offers special and distinct characteristics which certainly refer it to hallucinatory phenomena" ...

"Vertigo begins frequently with visual disturbances...dazzling lights...flames, zigzag fires, as in ophthalmic migraine...sudden abatement of vision...he sees butterflies, clouds, caverns...veritable hallucinations, rapid fantastic visions..."

"This picture of sensorial phenomena, sensitive or motor, premonitory to the access of auricular vertigo, shows us clearly that the irritations of the auditory nerve produce in man not only the perturbations of equilibrium and movement that the experimentor studies in the laboratory, and which are so well known, but that, moreover, they act upon the psychic centres, provoking the appearance of veritable hallucinations of the senses and movements that only clinical observation can teach us".

"Labyrinthitic vertigo is oftenest secondary to maladies of the ear and petrous bone; these cause an abnormal sensibility of the nervous portion of the organ, a hyperaesthesia more or less accentuated, and a consecutive hyperexcitability". 

"Migraine, a vertiginous affection, is frequently transformed by age into Meniere's vertigo".

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I can add nothing to such a rich phenomenology, indeed much of it comes as a surprise to me as much as it will to others.  The only important thing I can add to the extended syndrome is a simple physiological basis, perilymphatic hypotension.

   Another example here of how the vestibular system can affect visual perception.   So it is not valid to dismiss an inner ear cause for migraine because it supposedly cannot explain visual disturbances.

"Flashing "search" button affects my medical condition

The flashing "search" button is affecting my equilibrium. I have a medical condition, too complicated to explain, but I'm thinking that this flashing button, or anything flashing on here, may also affect people with Epilepsy. I can't look at anything that's flashing due to an inner ear, vestibular disorder. The inner ear works with the brain and eyes to keep a person in balance, equilibrium. When things are flashing, the brain can't look at things around it as a target to keep a person stable and upright. Please, please, please get rid of all flashing things."

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In migraine, cutaneous allodynia is likely reated to central sensitization, and posterior nuclei of the thalamus are involved in spread and extracephalic allodynia. Peripheral and central sensitization of trigeminal nucleus cannot explain it. For a reference, please see Goadsby et al. 2017 Physiol Rev 97:553-622. Quite long, but extremely beautiful and very useful for people that are not into migraine.

In migraine.."

Since there is no agreement as to the cause of migraine, the migraine literature cannot be used to refute a peripheral trigger. There are definitely peripheral vestibular abnormalities in many migraineurs. So if one postulates a central cause, one then has to have a double pathology, both in the ear and brain. At least the labyrinthine reflex(es) theory is parsimonious, only proposing one trigger area.

Here is strong evidence that migraine is not a neurological disorder:

"Psychiatric Disorders Share an Underlying Genetic Basis

NEUROSCIENCE NEWS JUNE 21,

Psychiatric disorders such as schizophrenia and bipolar disorder often run in families. In a new international collaboration, researchers explored the genetic connections between these and other disorders of the brain at a scale that far eclipses previous work on the subject. The team determined that psychiatric disorders share many genetic variants, while neurological disorders (such as Parkinson’s or Alzheimer’s) appear more distinct.

Published today in Science, the study takes the broadest look yet at how genetic variation relates to brain disorders. The results indicate that psychiatric disorders likely have important similarities at a molecular level, which current diagnostic categories do not reflect...

The final results indicated widespread genetic overlap across different types of psychiatric disorders, particularly between attention-deficit/hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder, and schizophrenia. The data also indicated strong overlap between anorexia nervosa and obsessive-compulsive disorder (OCD), as well as between OCD and Tourette syndrome.

In contrast, neurological disorders such as Parkinson’s and multiple sclerosis appeared more distinct from one another and from the psychiatric disorders — except for migraine, which was genetically correlated to ADHD, major depressive disorder, and Tourette syndrome."