Sensory regeneration following intraoperatively verified trigeminal nerve injury
Sensory regeneration following intraoperatively verified trigeminal nerve injury
复制标题
DOI：
10.1212/01.wnl.0000129490.67954.c2
复制
发表时间：
2004-06-08
期刊：
影响因子：
9.9
通讯作者：
Forsell, H
中科院分区：
文献类型：
--
作者：
Jääskeläinen, SK;Teerijoki-Oksa, T;Forsell, H
目的：观察下牙槽神经损伤后有髓和无髓轴突介导的感觉功能恢复情况。研究方法：作者使用神经生理学（IAN的精神神经眨眼反射、感觉神经传导[NCS]）和定量感觉测试（QST;冷、暖、热疼痛和触觉模式）评估了IAN的传入Abeta、Adelta和C纤维的功能。在术后2周、1个月、3个月、6个月和12个月进行测试，并与20例接受下颌双侧矢状劈开截骨术的患者的术前基线进行比较。19例患者接受术中监测。结果如下：在原发性脱髓鞘损伤（21/40神经），感觉改变和所有测试正常化组水平的前3个月内。部分轴突病变后（15/40神经），神经生理学和热QST结果保持异常，在1年的控制在一个高比例的IAN分布（高达67%）。1年时，40%的触觉QST异常，但87%的症状性IAN分布的NCS异常。神经病理性疼痛发生在5%的患者，只有严重的轴突损伤后。结论：感觉神经传导和热定量感觉测试显示轴突三叉神经损伤后1年感觉再生不完全。在感觉恢复的随访中，触觉定量感觉测试的临床检查不太可靠。感觉Abeta-、Adelta-和C-纤维以相似的速率恢复功能。三叉神经对神经性疼痛的易感性与其他外周神经没有区别。
Objective: To follow recovery of sensory function mediated by both myelinated and unmyelinated axons in relation to the type of inferior alveolar nerve (IAN) injury. Methods: The authors assessed the function of afferent Abeta-, Adelta-, and C-fibers of the IAN using neurophysiologic ( mental nerve blink reflex, sensory nerve conduction [NCS] of the IAN) and quantitative sensory tests (QST; cold, warm, heat pain, and tactile modalities). The tests were done 2 weeks, 1, 3, 6, and 12 months postoperatively and compared to the preoperative baseline in 20 patients undergoing mandibular bilateral sagittal split osteotomy. Nineteen patients underwent intraoperative monitoring. Results: In primarily demyelinating injuries (21/40 nerves), the sensory alteration and all tests normalized on the group level within the first 3 months. After partial axonal lesions (15/40 nerves), neurophysiologic and thermal QST results remained abnormal at 1-year control in a high proportion of the IAN distributions (up to 67%). At 1 year, the tactile QST was abnormal in 40%, but the NCS in 87% of the symptomatic IAN distributions. Neuropathic pain occurred in 5% of the patients, only after severe axonal damage. Conclusions: Sensory nerve conduction and thermal quantitative sensory testing showed incomplete sensory regeneration at 1 year after axonal trigeminal nerve damage. Clinical examination with tactile quantitative sensory testing was less reliable in the follow-up of sensory recovery. Sensory Abeta-, Adelta-, and C-fibers recovered function at similar rates. The trigeminal nerve does not differ from other peripheral nerves as regards susceptibility to neuropathic pain.