Dubai Police Medical Services
PO Box 12005
Dubai, United Arab Emirates
Tel: +971 4 3355954
Fax: +971 4 2683701
E-mail address: docgupta{at}emirates.net.ae
Mortelmans et al.1 studied the closure of atrial septal defect (ASD) for preventing migraine. These investigators speculate about small right-to-left shunt (RLS) in ASD during Valsalva or exercise,1 blurring the characteristic haemodynamic difference between patent foramen ovale (PFO)RLS and ASDleft-to-right shunt (LRS).2 Additionally, in contrast to PFO with unpredictable RLS, a predictable LRS is maintained in ASD. Migraine, however, particularly the menstrual variant, is frequently predictable. Secondly, there are no significant differences in the basal haemodynamic values (Table 1)1 that might predict the occurrence of intermittent RLS in this cohort. A higher basal right atrial (RA) pressure might permit intermittent RLS; however, after ASD closure, the lowest RA pressures (Table 3)1 were seen in patients whose migraines persisted or developed de novo. Thirdly, the implication of atrial natriuretic peptide (ANP) in migraine pathogenesis post-ASD correction1 is controversial.2 Falling RA pressure in uncomplicated ASD after correction would correspond with decline in plasma ANP values; in any case, ANP is known to lower central neuronal hyperexcitability.2 Next, larger defects in ASD are likely to be accompanied by larger LRS, a feature that makes intermittent RLS even less likely. Larger ASD sizes, however, as suggested by the size of the Amplatzer device used,1 prevailed in younger patients whose migraines persisted or developed a new post-ASD closure. Also, as with PFO,3 completeness of closure of ASD does not seem to be associated with migraine relief;1 this feature invites yet another pathophysiological assumption involving unpredictable thromboembolism from the left-sided disk of the occluder.1 Finally, atenolola first-line migraine prophylacticdoes not readily cross the intact bloodbrain barrier or significantly influence either brain neuronal function or circulation.4 This pharmacologic absolute does not support a pathogenetic role for embolic brain ischaemia in migraine. Lateralization of headache is a characteristic feature of migraine.4,5 The concept of paradoxical embolization of gas, thrombi, or vasoactive neuromodulators escaping pulmonary filtration/degradation assumes that these potential precipitants of migraine are being streamed regularly over decades to the same brain parenchymal site or circulatory segment in order to produce consistently lateralizing headache.5 After crossing over at the atrial level, however, paradoxical emboli are generally distributed randomly. Furthermore, cluster headache (CH), a strictly lateralized primary headache, is also associated with a strikingly similar incidence of RLS.6 Embolic brain ischaemia has not been invoked in the pathogenesis of CH. Besides, implicating congenital defects such as PFO/ASD in migraine mandates a plausible explanation for the characteristic and predictable late appearance (in the teens or twenties) and spontaneous disappearance (second and third trimesters of pregnancy and the later decades of life), in general, of migraine. The mean age of the subgroup in which migraine disappeared after ASD closure was 52±13.1 Migraine generally remits spontaneously in the fifth and sixth decades, a feature which critically confounds remission of migraine post-ASD closure. Conversely, younger patients developed migraine after ASD closure.1
Optimal size and design of future trials1,3 will not obviate the need for such conceptual groundwork.
References
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