经典高分文献阅读·局部鼻内应用利多卡因不是蝶腭神经节阻滞

There is renewed interest in the central role of the sphenopalatine ganglion (SPG) in cerebrovascular（脑血管的） autonomic（自主的，不受意志支配的） physiology and the pathophysiology of different primary and secondary headache disorders. There are diverse neural structures (parasympathetic（副交感神经）, sympathetic（交感神经） and trigeminal sensory（三叉神经的感觉神经）) that convene into the SPG which is located within the pterygopalatine fossa (PPF). This makes the PPF an attractive target to neuromodulatory interventions of these different neural structures. Some experts advocate for the nasal（鼻的） application of local anesthetics as an effective route for SPG block with the belief that the local anesthetic can freely access the PPF . It is time to challenge this historical concept from the early 1900s. In this daring discourse, I will review anatomical（解剖的） studies, CT and MRI reports to debunk this old myth. Will provide anatomical evidence to explain that all these assumptions are untrue and the local anesthetic has to magically ’travel’ a distance of 4–12 mm of adipose（脂肪的） and connective tissue（结缔组织） to reach the SPG in sufficient concentration and volume to effectively induce SPG blockade. Future research should focus on assessing a clinical biomarker to confirm SPG blockade. It could be regional cerebral blood flow or lacrimal gland（泪腺） secretion.

蝶腭神经节(SPG)在脑血管自主生理和不同的原发性和继发性头痛的病理生理中的中心作用重新引起了人们的注意。不同的神经结构(副交感神经、交感神经和三叉神经的感觉神经)聚集在位于翼腭窝(PPF)的SPG。这使得PPF成为对这些不同神经结构进行神经调节干预的一个有吸引力的目标。一些专家认为局麻药可以自由进入PPF，主张经鼻使用局麻药作为SPG阻滞的有效方法。是时候挑战这一20世纪初的历史观念了。在这篇大胆的文章中，我将回顾解剖学研究、CT和MRI报告，以揭穿这个古老的神话。我将提供解剖学证据来解释所有这些假设都是不正确的，并且局麻药必须神奇地“透过”4 - 12mm的脂肪和结缔组织，以足够的浓度和容量到达SPG，从而有效地引起SPG阻滞。未来的研究应该集中在通过评估一种临床生物标志物来确认SPG阻滞。这种临床生物标志物可能是局部脑血流或泪腺分泌。

Conclusion:In conclusion, intranasal LA application is not a true SPG block and the reported In headache relief could be explained by systemic absorption of LA or a placebo effect. I propose another theory that nasal mucosal（黏膜的） irritation may lead to reflex cerebral vasoconstriction. However, this needs to be explored, investigated and validated.

总之，在鼻内应用局部麻醉药并不是真正的SPG阻滞，报道的头痛缓解可以解释为局部麻醉药的全身吸收或安慰剂效应。我提出另一种理论，鼻粘膜刺激可能导致反射性脑血管收缩。然而，这需要探索、调查和验证。