In the frontal group (n = 19), 1 subject had persistent forehead numbness (1 year

postoperatively), 1 subject had asymmetric eyebrow elevation, and 1 subject appreciated residual function of the corrugator supercilii. In the temporal group (n = 19), 10 subjects experienced temporal hollowing, 2 subjects experienced intense pruritis, and 1 subject experienced temporal hair loss/thinning. In the occipital group (n = 11), 1 patient experienced neck stiffness (1 year postoperatively). Interestingly, only 2 of the adverse events were specifically cited to last for greater than 1 year, which would lead some readers to assume that the other events lasted for less than 1 year and resolved when in fact some of these adverse events may actually be ongoing. Other complications of the intervention noted in the literature include cutaneous hypersensitivity, neck

weakness, and facial nerve injury.[6] Midostaurin mw LY294002 molecular weight The author attributes some of the improvement in the sham surgery group at 1 year after surgery to the placebo effect. To expand on the power of sham procedures, the author references a sham intervention placebo effect noted in an acupuncture trial involving 37 subjects who received either 16 real or sham acupuncture treatments over 3 months. These subjects experienced similar reductions in migraine frequency regardless of receiving sham or actual acupuncture.[26] It is interesting that the author references

a sham procedure placebo effect for acupuncture, which has weak evidence for migraine prevention, to support the high placebo effect for another procedure with weak evidence such as surgical deactivation Glutathione peroxidase of migraine headache trigger sites. The author also suggests that the subjects in the sham surgery group provided exaggerated preoperative data to increase their chance of selection, which would also improve outcomes in the placebo group. This is a great argument to nullify any control group in any study if there is gain to be made by promoting the actual intervention. The author then attempts to oversimplify and discredit the trigeminovascular theory of migraine by claiming that the literature is unclear whether migraines are caused by cortical neuronal hyperexcitability, cortical spreading depression, peripheral activation/sensitization, central activation/sensitization, abnormal modulation of brain nociceptive systems due to dysfunction of the periaqueductal gray matter, or changes in the meningeal vasculature.[7] The reality is that these different mechanisms that the author attempts to single out as a potential cause of migraine are likely different events that occur in sequence leading up to a migraine. Migraine is a complex genetic disorder with susceptibility likely arising from one or more variants in the genetic code.