Abstract
Change in migraine headache (MH)-preexisting MH change or development of de novo MH-are known potential complications following percutaneous closure of atrial septal defect (ASD), but consensus on a causal trigger remains elusive. To expose potential MH triggers linked, mainly by timing and occurrence, to the emergence of de novo MH or change in preexisting MH subsequent to percutaneous ASD closure (pASDC). The literature was systematically searched for studies available in English reporting MH status after pASDC published between January 1, 1990 and November 15, 2015. We determined the number and percentage of patients experiencing MH status change within 7 days post procedure and the cumulative total by final follow-up (Mdn = 12 months). Twenty-five studies met the inclusion criteria, which accounted for a total of 1,646 pASDC patients. Pre-procedure MH prevalence was 8% (126/1,646). Change in preexisting MH occurred in a total of 72% (91/126), 12% (11/91) within 7-days after pASDC; within follow-up MH improved in 14% (18/126), resolved in 37% (47/126), but persisted in 63% (79/126). De novo MH incidence ranged between 10 (153/1,520) and 18.3% (153/836); 34% incipience (52/153) was within 7-days of pASDC; females accounted for 80% (63/79) of gender differentiated cases; of type distinguished cases, 42% (51/122) were MH without aura (MO) and 58% (71/122) were MH with aura (MA); MH improved in 10% (16/153), resolved in 24% (37/153) but persisted beyond final follow-up in 76% (116/153). Antiplatelet agents were effective modulators of MH in 44% (11/25) studies. Possible adverse MH-predisposing traits were scarce: larger ASD size reported in ~2% (39/1,646) of patients experiencing de novo MH or preexisting MH exacerbation; short aortic rim reported in three de novo MH patients; allergic response to occluder nickel alloy in four patients with MH status change from baseline (de novo or preexisting MH change not specified). Early intensification of MH status change but later amelioration (virtually paralleling stages of endothelialization), relatively high efficacy of antiplatelet agents, and the emergence of MA as the dominant de novo MH type favor proinflammatory triggers of MH status change after pASDC.
Highlights
Migraine pathogenesis is a contentious, unresolved issue with rival theories implicating various neurovascular and biochemical mechanisms
Two of the articles were not included because they did not report on migraine headache (MH) in the context of atrial septal defect (ASD) [74, 87]; these two articles were used for additional background information
10 and 18% of patients experienced de novo MH and 72% of patients with preexisting MH experienced a change in MH status after percutaneous ASD closure (pASDC)
Summary
Migraine pathogenesis is a contentious, unresolved issue with rival theories implicating various neurovascular and biochemical mechanisms. In a much simplified description of the trigeminal pain pathway [for an elaboration, see Noseda and Burstein [9]], trigeminal axons projecting from the meninges and associated blood vessel nociceptors (the peripheral trigeminovascular system) carry pain signals to the brainstem trigeminocervical complex comprised of the caudal trigeminal nucleus and spinal cord dorsal horns C1 and C2. Projections from this complex ascend and connect with other brainstem nuclei (e.g., the ventrolateral periaqueductal gray) before connecting with the more dorsal hypothalamic and thalamic nuclei. Efferent fibers from the VPM, for example, project to the face area of the primary somatosensory cortex [9, 10]
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