European Heart Journal Advance Access originally published online on June 7, 2006
European Heart Journal 2006 27(14):1756-1757; doi:10.1093/eurheartj/ehl070
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Closure of ASD: what aggravates the migrainous diathesis?
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Mortelmans et al.1 report new onset of migraine with aura (MA+) and migraine without aura (MA–) following percutaneous closure of atrial septal defect (ASD). Sudden or immediate worsening of MA+ attacks following closure of ASD has also been noted.2,3 Because closure of ASD cannot possibly have any influence on brain neuronal function or cortical spreading depression, the widely favoured pathogenetic paradigm, or paradoxical embolism or paradoxical transfer of putative headache-provoking neurotransmitters, such aggravation of the tendency to develop migraine has important pathophysiological implications.
De novo development of migraine or dramatic aggravation of migraine following atrial shunt closures indicates a substantial or definitive alteration of some physiological variable with a critical influence on the primary pathophysiological process in migraine.2–4 In ASD, the reduced filling pressure of the left ventricle causes a smaller than normal stroke volume and reduced cardiac output; consequently, a relatively small aorta is commonly seen. Following closure of large atrial shunts, immediate improvement in left ventricular stroke volume and cardiac output occurs. Precipitation of migraine following the closure of atrial septal defect suggests that a higher stoke volume/cardiac output might worsen or unmask a migrainous diathesis.
Recently, the theoretical basis for a non-neuronal non-vascular origin of migraine has been elucidated.5,6 A selective involvement of the ophthalmic division of the trigeminal nerve is likely in migraine and other primary headaches; mechanical deformation of the corneo-scleral envelope by ocular choroidal venous congestion and rise of intraocular pressure (IOP) have been proposed to underlie both the scintillating scotoma and the headache of migraine. In contrast to the brain, the eye is a low-volume but far more highly vascularized organ; the eye is anatomically less capable of accommodating any sudden increase in stroke volume. The cardiac output increasing effect of closure of larger atrial shunts is somewhat comparable to the immediate peripheral arterial perfusion-enhancing effect of glyceryl trinitrate (GTN) manifested by flushing of face and throbbing headache.4 GTN is the best available experimental human model for migraine; it generally causes migraine headache a few hours after consumption,7 at which time substantial venous pooling likely develops at the ocular choroidal venous plexus in migraine patients due to an intrinsic regional ocular sympathetic hypofunction. Propranolol, atenolol, metoprolol, nadolol, clonidine, flunarizine, and verapamil lower the IOP, further supporting the nexus between migraine, autonomic dysfunction, IOP, and glaucomatous visual field deficits.5,6 Immediate aggravation of migraine attacks after closure of atrial shunts spontaneously regresses after a few months;2 ocular tissue creep at the level of the corneo-scleral envelope likely dissipates the headache-provoking effect of increased cardiac output in patients post-ASD closure.4,5
Like trait or basal autonomic function, endogenous pain control mechanism, and corneo-scleral distensibility, increase in cardiac output after atrial shunt closure is likely to be a highly variable, idiosyncratic function. Additionally, the effects of a variable state or situational ocular autonomic function in migraine patients will variably affect ocular handling of increased stroke volume post-ASD closure in individual patients. The ocular tamponade effect of IOP limits ocular choroidal congestion.8 In those patients whose ASD closure appears to remit migraine, a higher basal IOP linked to a higher cardiac output may reduce the frequency of migraine attacks by limiting intermittent or periodic choroidal congestion. Systemic blood pressure, and therefore cardiac output, is closely linked to IOP.9 Remission or exacerbation of the migrainous diathesis after ASD closure probably depends on alterations of ocular hydrodynamics that, in turn, decrease or increase the tendency to develop headache-provoking antidromic ophthalmic-trigeminal division discharges, respectively. The eye probably links the cardio- and the cranio-vascular systems in this clinical situation.
References
- Mortelmans K, Post M, Thijs V, Herroelen L, Budts W. (2005) The influence of percutaneous atrial septal defect closure on the occurrence of migraine. Eur Heart J 26:1533–1537.
[Abstract/Free Full Text] - Yankovsky AE and Kuritzky A. (2003) Transformation into daily migraine with aura following transcutaneous atrial septal defect closure. Headache 43:496–498.[CrossRef][ISI][Medline]
- Gupta VK. (2004) Percutaneous closure of patent foramen ovale reduces the frequency of migraine attacks. Neurology 63:1760–1761.
[Free Full Text] - Gupta VK. Clopidogrel and atrial shunt closure for migraine: why is migraine aggravated immediately? Heart Published online ahead of print December 13, 2005. http://heart.bmjjournals.com/cgi/eletters/91/9/1173#869.
- Gupta VK. (2006) Migrainous scintillating scotoma and headache is ocular in origin: a new hypothesis. Med Hypotheses 66:454–460.[CrossRef][Medline]
- Gupta VK. Glyceryl trinitrate and migraine: nitric oxide donor precipitating and aborting migrainous aura. J Neurol Neurosurg Psychiatry Published online ahead of print October 22, 2005. http://www.jnnp.com/cgi/eletters/76/8/1158#708.
- Thomsen LL, Kruuse C, Iversen HK, Olesen J. (1994) A nitric oxide donor (nitroglycerin) triggers genuine migraine attacks. Eur J Neurol 1:73–80.
- Gupta VK. Intraocular pressure, systemic blood pressure, and headache: occult pathophysiological link? Br J Ophthalmol A Published online ahead of print December 21, 2005. http://bjo.bmjjournals.com/cgi/eletters/89/3/284.
- Klein BEK, Klein R, Knudtson MD. (2005) Intraocular pressure and systemic blood pressure: longitudinal perspective: The Beaver Dam Eye Study. Br J Ophthalmol 89:284–287.
[Abstract/Free Full Text]
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