Wu et al. presented increased microscopic brain permeability during the acute stage of reversible cerebral vasoconstriction syndrome (RCVS) as a marker of putatively pathogenetic blood-brain barrier disruption.1 Despite emphasis on a uniphasic course,2 there is a striking temporal gap between a key clinical feature of thunderclap headache (TCH) (peaking in <1 minute) and MRA-detected maximum vasoconstriction of branches of middle cerebral arteries, occurring a mean of 16 days after clinical onset. Delayed segmental cerebrovascular vasoconstriction, enhanced resistance, or enhanced microvascular brain permeability are highly unlikely to reflect primary pathogenetic aberration(s) of RCVS. Similarly, white matter hyperintensities1 are epiphenomenal, having no role in the genesis of nociceptive ophthalmic nerve traffic underlying TCH3—the truly acute phenomenon of RCVS. Generalization is essential to maintain hypothetical beliefs.3
Tae‐Jin Song, Keum Hwa Lee, Han Li, Jungyoon Kim, Kathleen Chang, Seong Heon Kim, Kyoung Hee Han, Bo Yi Kim, Andreas Kronbichler, Anne Ducros, Ai Koyanagi, Louis Jacob, Min Seo Kim, Dong Keon Yon, Seung Won Lee, Jee Myung Yang, Sung Hwi Hong, Ramy Abou Ghayda, Joon Won Kang, Jae Il Shin, Lee Smith
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