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The role of CSD in migraine is actually generally accepted as one of the pathophysiological process. In fact several novel CGRP targeted migraine medications are showing that CGRP-mAb can prevent the activation and sensitization of high-threshold (central) trigeminovascular neurons by cortical spreading depression. Some of them are currently under review by FDA and expect to be on the market in late 2018. The research in rodents may not always be applicable to human with migraine and this theory has been in existence for over a decade. On your view of posterior cerebral circulation vulnerability to stroke, that was not quite relevant to the theme of current paper, which was about the association of migraine and stroke, not why stroke occurs more in posterior circulation. One fact of interest is that migraine sequelae related white matter changes would involve the entire brain, not limited to posterior circulation.
I read with interest the article by Zhang et al., (SVN, 2017, 2: e000077)  about "Migraine and stroke". At a time when the pathophysiology of migraine is poorly understood and the pathogenetic role of cortical spreading depression (CSD) is far from being generally accepted (Gupta, 2009) , Zhang et al. underscore the link between migraine with aura and ischemic stroke. With nosological splitting having been taken to the extreme end of the spectrum, Zhang et al., believe that migraine with aura (MwA) and migraine without aura (MwoA) are distinct entities.1 With the same epidemiology, the same clinical features (except the aura), and the same migraine preventive agents like propranolol, we have split wide the classification of the primary headache disorders, and maintain the belief-in-belief strategy at the cost of remaining confused at several levels, including the pathophysiology of primary headache disorders.
The concept of CSD is maintained by key omissions and assumptions (see Box 1, p. 1601, reference No. 2). The fact that atenolol, a hydrophilic pharmacologic agent, that does not cross the blood-brain barrier and does not influence any brain neuronal function including the CSD in unconscious experimental animals and prevents both MwA and MwoA equally efficiently is a pharmacologic absolute known since 1980, [3,4,] that is by itself sufficient to eliminate the concept of CSD from migraine pathophysiology.
The rodent model of...
The rodent model of migraine does not mimic migraine closely as we do not know whether rodents suffer aura or headache. What we do know is that rodents (rats and mice) cannot vomit.  Nausea and/or vomiting is a pathognomonic feature of migraine (both MwA and MwoA) that can remit the headache attack -- a fact that even struck Hippocrates. Nausea and /or vomiting have a distinct brain pathophysiology that is adaptive in migraine (but is unavailable to the rodent). [6, 7, 8]
Migraine is a lateralizing disorder, with the headache typically presenting as a unllateral, bilateral, side-locked or side-shifting feature.  No feature of CSD permits to rationalize lateralization of headache of migraine.
The rarity of stroke complicating migraine, does not allow the hypercoagulability or the endothelial dysfunction to be the final or common arbiter for development of stroke. A shift of focus to thrombophilia and hypercoagulation, as suggested by Zhang et al.,  would be far less productive than a re-focus of the optimal prevention of migraine attacks as well as the determination of the optimal blood pressure for migraine patients (as migraine patients generally maintain a low systemic blood pressure , and, migraine prophylactic agents like propranolol, atenolol, nadolol, metoprolol, flunarizine, verapamil, and clonidine commonly lower the systemic blood pressure.
Zhang et al,,  do not consider the particular anatomical vulnerability of the posterior cerebral circulation. 
1. Zhang Y, Parikh A, Qian S. Migraine and stroke. Stroke and Vascular Neurology 2017;2: e000077.
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5. Horn CC, Kimball BA, Wang H, Kaus J, Dienel S, Nagy A, Gathright GR, Yates BJ, Andrews PLR. Why can’t rodents vomit? A comparative behavioral, anatomical, and physiological Study. PLOS One Published: April 10, 2013 http://dx.doi.org/10.1371/journal.pone.0060537
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