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Headache Extras

Headache Extras is an occasional series of articles, commentaries and other features inspired by papers published in Headache.

The following extras are available:

 

Interview with poetry author and migraine sufferer, Pam Kress-Dunn

 

Pam Kress-Dunn is the medical librarian at Mercy Medical Center – Dubuque, a community hospital with Magnet status in Dubuque, Iowa. She holds master’s degrees in library science and English, and a master of fine arts degree in poetry writing. She was diagnosed with transformed migraine at the Michigan Head Pain and Neurological Institute in March 2010 and spent over two weeks in the Head Pain unit at Chelsea Hospital. Her once-daily headaches are now much better managed, and she has learned to give herself injections when all else fails. This will, no doubt, be the subject of a future poem. 

Read Pam's poems.

Listen to Pam's interview.

 Listen to Pam read her poetry:

 

Does Low Atmospheric Pressure Alone Trigger Migraine?


Hayrunnisa Bolay, M.D., PhD*and Alan Rapoport, M.D.
*Professor of Neurology, Gazi University, Department of Neurology & Neuropsychiatry Centre, Ankara, Turkey
+Clinical Professor of Neurology, The David Geffen School of Medicine at UCLA, Los Angeles, California, USA
±Founder and Director-Emeritus, The New England Center for Headache, Stamford, Connecticut, USA

    We are now somewhat closer to understanding how external triggers can affect the brain in animals and, ultimately, in humans following the publication of an article by Messingler and colleagues on low barometric pressure as a migraine trigger.1
    Despite a variety of studies conducted, it is not clearly understood if weather or food triggers can affect the peripheral or central nervous system (and whether that in turns leads to a migraine attack). Initiating mechanisms for migraine headache have been partly elucidated and indicate that both peripheral and central mechanisms appear to contribute to attack generation. The available data seem to denote activation of peripheral nociception is a prerequisite. Ethanol, a well known chemical trigger, has been demonstrated to lower the threshold temperature for activation of the pain-producing capsaicin ‘receptor’ TRPV1 channels in the trigeminal nerve endings leading to neurogenic edema in dura mater.2 Migraine attacks triggered by alcohol ingestion, therefore, could be due to the vasodilation of meningeal vessels by TRPV1 activation and CGRP release. Related to this, a recently published study revealed that a specific scent of Umbellularia californica (Californian daphne), also known as the headache tree, induces cluster-like attacks. These attacks are always preceded by a cold sensation localized to the nostril ipsilateral to the side of the pain attack.3 Since cold sensation is mediated either by TRPM8 (activated only by menthol) or TRPA1 channels, U. californica was proposed to trigger the headache attack by activating perivascular trigeminal endings by through TRPA1 channel transduction3.
    Nitroglycerin, a nitric oxide (NO) donor, has been widely used to trigger migraine or cluster headache in clinical trials. Two thirds of migraineurs experience a typical migraine attack 4-6 hours following administration of nitroglycerin. This late headache could be related to the induction of iNOS through the NFκβ mediated inflammatory cascade in dural macrophages and activation of mast cells in the dura mater 4, 5 as well as induction of NFκβ, CamKII and cGMP in trigeminal nucleus caudalis 6,7 resulting in the increased transmission of pain signals.
    Cortical spreading depression (CSD), an intrinsic brain event, also activates perivascular trigeminal nerve fibers and could induce lateralized headache.8 Common migraine triggers such as stress, hunger and sleep deprivation may not be involved with either peripheral mechanisms or CSD as an initial event. It has been suggested that several neuronal pathways originating from subcortical structures such as lateral  hypothalamus, paraventricular hypothalamus and bed nucleus of stria terminalis could be responsive to those common triggers.9 A recent publication on migraine triggers in humans addressed delayed type allergy and IgG antibodies to various foods and treatment of patients with elimination diets.10
    What do we know about the relationship between barometric pressure and migraine attacks? Average sea-level atmospheric pressure is 1013 hPa (hectopascal) and atmospheric pressure determines the wind and weather patterns as well as air movement across the globe. A low pressure situation is simply an area where the atmospheric pressure is lower than that of the surrounding area. Low pressure initiates air movement and is usually associated with high winds and warm air; therefore low pressure areas normally produce clouds, precipitation, storms and hurricanes. The lowest atmospheric pressure records were obtained in the eyes of hurricanes or typhoons. Atmospheric pressure also shows a circadian cycle with amplitude of a few hectopascals.
    Since a change in pressure is accompanied by changes in temperature, wind, humidity, precipitation and rain, clinical studies on weather are complicated to do as it is hard to delineate the effect of each weather component. Several studies have shown that atmospheric conditions can affect well-being and headache/migraine is reported to be the most frequent symptom (61%).11 Atmospheric weather changes including, pressure, humidity, wind and temperature have all been suggested as potential triggers for headaches, though a definite link has not yet been demonstrated. Low barometric pressure and low temperature have been associated with increased pain intensity in humans as well as experimental animals.
    In their article in Headache, Messlinger and colleagues describe the experimental conditions they created to evaluate the effect of low atmospheric pressure in a climate controlled room. They investigated whether rapid (8 min) lowering of the ambient pressure (by 40 hPa) to an extremely low level (comparable to that of a typhoon) induces neuronal activity in the trigeminal nucleus caudalis in rats. Their study revealed that by only changing barometric pressure, there was no triggering of trigeminovascular neurons with receptive fields from dura mater or from both dura mater and cornea. Even the prior sensitization by a nitric oxide donor did not alter their response to low atmospheric pressure. The activation of neurons with receptive fields from dura mater are critical since their activation results in neurogenic inflammation characterized by vasodilation, blood flow increase and plasma protein extravasation in the dura mater. All this is a hallmark of the headache phase of migraine.12 
    Though Messlinger and colleagues concluded that “distinct neurons in the trigeminal nucleus caudalis, particularly with preferential afferent input from the eye, respond to lowering of atmospheric pressure” their finding of a lack of activation in the trigeminal neurons with receptive fields from dura mater, or from both dura mater and cornea, indicate that lowering of barometric pressure does not mediate headache. Their results may be influenced by the short exposure time of 8 minutes, since migraine headache generally begins many hours after exposure to any triggering agent. Some studies have reported that a lowering of the ambient atmospheric pressure for 80 minutes aggravated pain behavior within inner ear dependent mechanisms in rats with neuropathic pain.13
    The Messlinger study suggests that ambient pressure change alone (even to an extreme level) does not trigger headache. But, in what conditions do humans experience low atmospheric pressure? On the Earth’s surface, pressure changes are needed to enable natural air convection. With few exceptions, it is typical to experience this phenomenon on an on-going basis. Dramatic atmospheric pressure changes along with air movement and warm winds, alternatively, produce extreme weather conditions such as hurricanes. In unusual situations, high altitude mountaineers, for example, are exposed to low atmospheric pressure. F-16 pilots practice in special low-pressure rooms.
    High altitude is associated with hypoxia; mountaineers are also subjected to cold temperatures, extreme physical activity, sleep deprivation and inadequate food intake.14 For example, the estimated pressure in spring time at 7000 meters on Mount Everest is approximately 431 hPa. The temperature is -12C and the percentage of oxygen relative to that at sea level (1031 hPa) is 9%. Those figures drop to 319 hPa, -28C, and 6.9% at the peak of Mount Everest. 15 Therefore, the various neurological symptoms experienced at high altitude, including headache, are related not only to pressure changes, but to a combination of many factors.
    We are all exposed to rapidly lowered atmospheric pressure when flying. Cabin pressure is maintained at the equivalent of 2438m above sea level (8,000 feet) according to international regulations. Average cabin pressure during 10 hours of flight was measured around 846 hPa.16 It is noteworthy that migraineurs do not usually complain about headaches when travelling in airplanes and flying is not listed as a migraine trigger.
    Are there any alternative explanations for weather related headache triggers? It has been observed that dust originating from larger deserts can be transported to other continents by atmospheric air, resulting in an adverse effect on public health. Up to 5 billion tons of desert dust travels around the globe each year and 50-75 % of the dust originates from Africa.17 Dust originating from the Sahara Desert contains microorganisms that could initiate a series of reactions upon contact with cloud water and efficient UV light from sun. This may result in the formation of reduced iron (Fe2+), oxalate and various basic amino acids. A recent study shed light on mechanisms related to headache. The simulated conditions of Saharan dustladen air induced a c-fos response in the nociceptive superficial lamina (I and II) in trigeminal nucleus caudalis.18 The nociceptive effect was not mediated by dust itself or living microorganisms, but rather by nanoparticles (smaller than 450nm) probably released during a multiplication of microorganisms.
    How does this data relate to other published studies on the effect of weather conditions triggering migraine? Following low atmospheric pressure conditions, African dust travels in warm weather compatible with findings of Prince et al.19 and Mukamal et al 20 demonstrating warm temperatures can trigger migraine attacks. Warm Chinook winds and pre-Chinook days were similarly shown to increase the risk of migraine attack.21 Mukamal et al demonstrated that migraine attack risk increased on days when the temperature increased by 5 oC. They also noticed that low atmospheric pressure anticipated headache. Not every low atmospheric pressure situation, however, anticipates African desert dust-laden weather. Outbreaks of Saharan dust are seasonal and very frequent between October and May. Their presence may be minimal during the summer. The sunlight in the spring and autumn is efficient to fuel any cloud dependent reaction of microorganisms. Several studies also revealed the correlation of migraine attacks and transitional seasons, particularly springtime.20,22 Precipitation is also an important factor. Therefore, certain weeks or months are more prone to carry Saharan dust and other particles including bioavailable iron. A recent study also confirmed that humidity/rain is important in neoformation of iron nanoparticles.23 It is interesting to note that one of the comorbid diseases with migraine is asthma. Increased acute asthma visits are reported to be associated with increased Saharan dust cover.24
    In summary, the Messlinger paper shows that this previously unknown novel factor in the atmosphere is complementary to known weather conditions that may trigger a migraine attack. We look forward to further basic and human studies which may elucidate the mechanisms and molecules underlying migraine triggers.

REFERENCES


1) Messlinger K, Funakubo M, Sato J, Mizumura K. Increases in Neuronal Activity in Rat Spinal Trigeminal Nucleus Following Changes in Barometric Pressure-Relevance for Weather-Associated Headaches? Headache 2010;50:1449-1463.
2) Nicoletti P, Trevisani M, Manconi M, Gatti R, De Siena G, Zagli G, Benemei S, Capone JA, Geppetti P & Pini LA. Ethanol causes neurogenic vasodilation by TRPV1 activation and CGRP release in the trigeminovascular system of the guinea pig. Cephalalgia 2008;28:9–17.
3) Benemei S, Appendino G, Geppetti P. Pleasant natural scent with unpleasant effects: cluster headache-like attacks triggered by Umbellularia californica. Cephalalgia 2009;30: 744–746.
4) Reuter U, Bolay H, Jansen-Olesen I, Chiarugi A, Sanchez del Rio M, Letourneau R, Theoharides TC, Waeber C, Moskowitz MA. Delayed inflammation in rat meninges: implications for migraine pathophysiology. Brain 2001;124:2490-502.
5) Reuter U, Chiarugi A, Bolay H, Moskowitz MA. Nuclear factorkappaB as a molecular target for migraine therapy. Ann Neurol. 2002;51(4):507-16.
6) Greco R, Tassorelli C, Cappelletti D, Sandrini G, Nappi G. Activation of the transcription factor NF-kappaB in the nucleus trigeminalis caudalis in an animal model of migraine. Neurotoxicology 2005;26:795-800.
7) Varga H, Pardutz A, Vamos E, Bohar Z, Bago F, Tajti J, Bari F, Vecsei L. Selective inhibition of cyclooxygenase-2 attenuates nitroglycerininduced calmodulin-dependent protein kinase II alpha in rat trigeminal nucleus caudalis. Neurosci Lett. 2009;451:170-3.
8) Bolay H, Reuter U, Dunn A, Huang Z, Boas D, Moskowitz MA. Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine
model. Nat Med 2002;8:136–42.
9) Levy D, Strassman A, Burstein R. A Critical View on the Role of Migraine Triggers in the Genesis of Migraine Pain. Headache 2009;49:953-7.
10) Alpay K, Ertas¸M, Orhan E, Kanca D, Lieners C, Baykan B. Diet restriction in migraine, based on IgG against foods: A clinical double-blind,
randomised, cross-over trial. Cephalalgia 2010;30 829–837.
11) Von Mackensen S, Hoeppe P, Maarouf A, Tourigny P, Nowak D. Prevalence of weather sensitivity in Germany and Canada. Int J  Biometeorol. 2005;49:156-66.
12) Moskowitz MA. Neurogenic inflammation in the pathophysiology and treatment of migraine. Neurology 1993;43 (6 Suppl. 3):S16–20.
13) Funakubo M, Sato J, Honda T, Mizumura K.The inner ear is involved in the aggravation of nociceptive behavior induced by lowering barometric pressure of nerve injured rats. Eur J Pain. 2010;14:32-9.
14) Firth PG, Bolay H. Transient high altitude neurological dysfunction: An origin in the temporoparietal cortex. High Alt Med Biol. 2004;5:71-75.
15) Firth PG, Zheng H, Windsor JS, Sutherland AI, Imray CH, Moore GW, Semple JL, Roach RC, Salisbury RA. Mortality on Mount Everest, 1921-2006: descriptive study. BMJ 2008;337:2654.
16) Kelly PT, Seccombe LM, Rogers PG, Peters MJ. Directly measured cabin pressure conditions during Boeing 747–400 commercial aircraft flights. Respirology 2007;12: 511–515.
17) Griffin DW. Atmospheric movement of microorganisms in clouds of desert dust and implications for human health. Clin Microbiol Rev 2007;20:459–77.
18) Doganay H, Akcali D, GoktaƟ T, Caglar K, Erbas D, Saydam C, Bolay H. African dust-laden atmospheric conditions activate the trigeminovascular system. Cephalalgia 2009;29:1059-68.
19) Prince PB, Rapoport AM, Sheftell FD, Tepper SJ, Bigal ME. The effect of weather on headache. Headache 2004;44:596-602.
20) Mukamal KJ, Wellenius GA, Suh HH, Mittleman MA Weather and air pollution as triggers of severe headaches. Neurology 2009;72(10):922-7.
21) Cooke LJ, Rose MS, Becker WJ. Chinook winds and migraine headache. Neurology 2000;54:302-307.
22) Brewerton TD, George MS. A study of the seasonal variation of migraine. Headache 1990;30:511-3.
23) Shi Z, Krom MD, Bonneville S, Baker AR, Jickells TD, Benning LG. Formation of iron nanoparticles and increase in iron reactivity in mineral
dust during simulated cloud processing. Environ Sci Technol. 2009 43:6592-6.
24) Gyan K, Henry W, Lacaille S, Laloo A, Lamsee-Ebanks C, McKay S et al. African dust clouds are associated with increased paediatric asthma accident and emergency admissions on the Caribbean island of Trinidad. Int J Biometeorol 2005;49:371–6.

Click below for the paper this Headache Extra was inspired by: 
Increases in Neuronal Activity in Rat Spinal Trigeminal Nucleus Following Changes in Barometric Pressure—Relevance for Weather-Associated Headaches?
Karl Messlinger MD, Megumi Funakubo DSc, Jun Sato MD, DSc, Kazue Mizumura MD, DSc
October 2010, (Volume 50, Issue 9, Pages 1449-1463)

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