Allergy tests and migraine

Migraine headaches are more frequent in people who suffer from allergic rhinitis and who have more than 10 positive skin allergy tests.  This finding by Dr. Martin and his colleagues presented at the International Headache Congress last week is not surprising since many of my patients report that their migraines worsen during periods when their allergies flare up.  It is also not surprising because almost any medical condition affecting the head, whether it is an ear infection, a dental problem, or conjunctivitis, can trigger a migraine attack.

  1. Dr. Mauskop says: 05/26/20109:16 pm

    Yes, there are many levels here. As far as reference, Vincent Martin has not published his full paper yet.

  2. Pete Smith says: 05/26/20108:54 pm

    I would appreciate some reference detail here. Full name of presenter and if possible a reference link if there was an online abstract.

    When we understand “allergic pain” I think we will better understand migraine too (also cluster headaches and TMD) . There are so many levels here. Firstly in allergic rhinitis, trigeminal nasal sensory nerves are increased (doubled) and they are increased around blood vessels. In the presence of allergic inflammation, neurotrophins such as NGF and BNDF are increased and they increase both dendrite growth and nociceptor expression. Eosinophils pump out NGF. Specifically NGF increases expression of the multi-modal receptor TRPV1 (this is where histamine works, along with prostinoids, leukotrienes, kinins, TRKs, NK1-3, via phospholipases to cause sensory nerve depolarisation). In animal models of molecular pain, Phospholipase activation of subsequent PKC actions leads to de-activation of opioid receptors -resulting in a hyperalgesic state. Antidromic spread is well documented in nasal trigeminal sensory nerves leading to referred pain. Sensory trigeminal nerves leak out SP and CGRP which have both vascular effects as well as depolarising other sensory neurones. SP can also work on mast cells if they express NK1 receptors (which they only do in the presence of SCF or IL4). Note that CNV brainstem receives all the pain and temperature from the face, nose, external ear and eustachian tube. CNVII does not have it’s own central nucleus ganglion. Trigeminal spread is a concept that has been discussed in migraine. Many of the migraine triggers (and cluster headaches) such as temperature/humidity change, smoke, volatile chemicals and strong odors are common triggers for patients with mixed rhinitis and non-allergic rhinitis. Gustatory triggers such as capsaicin bind specifically with TRPV1 which appears on about 60% of trigeminal sensory nerves and dietary isothiocyantes (mustard, wasabi) specifically activate TRPA1 which co-localise with TRPV1 in up to 90% of trigeminal sensory nerves. The TRPV1 receptor also can be activated by calmodulin and some of the older tricyclics can work via this mechanism in sensory pain, probably more so than 5HT1-3 or antihistamine effects.

  3. Jasmine says: 10/07/200910:33 pm

    Sometimes migraine sufferers experience migraine attacks because of the food that they eat that triggers their allergies. Anyway, you have a great blog, it contains a lot of information. Hopefully, you can visit mine too, My site focuses on natural treatments for migraines.

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