Abstract
We congratulate Dilli et al. (1) on their efforts to clarify the relevance of the greater occipital nerve (GON) block in the prevention of both episodic and chronic migraine. In 2001, our group carried out a similar study on episodic migraine patients (2). The methodology was also double-blind and included an active group (bupivacaine 0.5%) and a placebo group (saline 0.9%). After a 30-day baseline period, a first GON block and second GON block were performed 30 days apart. For both groups, there were no differences in the frequency and duration of migraine attacks, but in the active group, the migraine intensity worsened, possibly reflecting an antinociceptive role of the GON circuitry in migraine pathophysiology. The role of the GON in migraine pathophysiology is ambiguous. While anesthetic blockade of the GON is claimed to control migraine, stimulation of the GON is also reported to have the same effect (3,4). During a local anesthetic blockade of the GON, two opposite effects may occur: a) initially, there may be a nociceptive effect related to the puncture procedure and distension of the nerve endings (3); and b) an antinociceptive (anesthetic) effect may occur over the GON territory. The initial nociceptive input probably reaches the diffuse nociceptive inhibitory control (5) and may, in a manner akin to that observed with acupuncture and electrical stimulation of the GON, lead to migraine control (3,4). However, anesthetic block may lessen the GON tone over the nucleus trigeminalis caudalis, leading to an increase in the intensity of migraine attacks, as seen in our study (2).
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