I read with interest the article by Akram et al.1 The investigators accepted that the pathophysiology of cluster headache (CH) is not fully understood, that evidence for primary involvement of the hypothalamus is suggestive, and that primary activation of trigeminoparasympathetic brainstem reflex is uncertain. An unresolved discrepancy exists between posterior hypothalamus and the ventral tegmental area as the key pathophysiologic focus.1–3 The investigators also accepted that the mode of action of deep brain stimulation (DBS), the optimal stimulation site, and the neural networks involved remain poorly understood.1 CH is not a pan-trigeminal disorder, but dominantly involves the ophthalmic division. It is unclear whether DBS selectively affected the ophthalmic trigeminal nerve in this study or how intrinsic trigeminohypothalamic activation can generate unilateral CH.
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