Washington, D.C.; and Dallas, Texas From the Department of Plastic Surgery, Peripheral Nerve Surgery Institute, Georgetown University Hospital, and the Department of Plastic Surgery, University of Texas Southwestern Medical Center.
Plast Reconstr Surg. 2011 Oct;128(4):908-912. doi: 10.1097/PRS.0b013e3182174229.
Recent evidence has shown that some cases of occipital neuralgia are attributable to musculofascial compression of the greater occipital nerve and improve with neurolysis. A mechanical interaction at the intersection of the nerve and the occipital artery may also be capable of producing neuralgia, although that mechanism remains one theoretical possibility among several. The authors evaluated the possibility of unrecognized vasculitis of the occipital artery as a potential mechanism of occipital neuralgia arising from the occipital artery/greater occipital nerve junction.
Twenty-five patients with preoperatively documented bilateral occipital neuralgia-related chronic headaches underwent peripheral nerve surgery with decompression of the greater occipital nerve bilaterally, including the area of its intersection with the occipital artery. In 15 patients, a 2-cm segment of the occipital artery was excised and submitted for pathologic evaluation. All patients were evaluated intraoperatively for evidence of arterially mediated greater occipital nerve compression, and the configuration of the nerve-vessel intersection was noted.
None of the 15 specimens submitted for pathologic evaluation showed vasculitis. Intraoperatively, all 50 sites examined showed an intimate physical association between the occipital artery and greater occipital nerve.
Surgical specimens from this first in vivo study provided no histologic evidence of vasculitis as a cause of greater occipital nerve irritation at the occipital artery/greater occipital nerve junction in patients with chronic headaches caused by occipital neuralgia. Based on these findings, mechanical (and not primary inflammatory) irritation of the nerve by the occipital artery remains an important theoretical cause for otherwise idiopathic cases. The authors have adopted an operative technique that includes physical separation of the nerve-artery intersection (in addition to musculofascial neurolysis) for a more thorough surgical treatment of occipital neuralgia.
CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.
最近的证据表明，一些枕神经痛病例是由于枕大神经的肌筋膜压迫引起的，并通过神经松解术得到改善。神经和枕动脉的交叉处的机械相互作用也可能导致神经痛，尽管这种机制仍然是几种理论可能性之一。作者评估了枕动脉未被识别的血管炎作为枕动脉/枕大神经交界处引起枕神经痛的潜在机制的可能性。
25 例术前确诊为双侧枕神经相关慢性头痛的患者接受了外周神经手术，双侧枕大神经减压，包括与枕动脉交叉的区域。在 15 例患者中，切除了 2 厘米长的枕动脉段并进行病理评估。所有患者均在术中评估是否存在动脉介导的枕大神经压迫，并注意神经-血管交叉的形态。
15 个送检标本中均未发现血管炎。术中，检查的 50 个部位均显示枕动脉与枕大神经之间存在密切的物理联系。
这项首次在体内进行的研究的手术标本未提供组织学证据表明血管炎是引起慢性头痛患者枕大神经在枕动脉/枕大神经交界处受刺激的原因。基于这些发现，动脉对神经的机械性（而非原发性炎症性）刺激仍然是其他特发性病例的一个重要理论原因。作者采用了一种手术技术，包括神经-动脉交叉处的物理分离（除了肌筋膜神经松解术），以更彻底地治疗枕神经痛。
临床问题/证据水平：治疗，IV 级。
