青少年特发性脊柱侧凸患者体感诱发电位的特点及与Cobb角的关系

Characteristic of somatosensory evoked potentials in adolescent idiopathic scofiosis and relationship with Cobb angle

目的分析不同Cobb角青少年特发性脊柱侧凸（AIS）体感诱发电位（SEP）的异常模式，探讨其在AIS发病机制中的作用。方法回顾性分析2001年9月至2007年9月治疗的489例AIS患者（AIS组）的术前SEP的峰潜伏期及左、右侧峰潜伏期差值，并与45例年龄匹配的健康青少年（对照组）的SEP相比较。SEP波形消失、峰潜伏期延长及峰潜伏期不对称定义为SEP异常的标准。计算AIS组SEP异常发生率，并分析SEP异常与侧凸严重程度的相关性。结果AIS组峰潜伏期（身高校正）较对照组略高，但无统计学意义。AIS组左右侧峰潜伏期差值显著高于对照组。489例AIS中SEP异常者共有166例，其中波形单侧或双侧消失17例（10．2％），单侧潜伏期延长50例（30．1％），两侧均延长38例（22．9％），两侧不对称120例（72．3％）。根据不同侧凸严重程度分组分析，结果提示SEP异常与侧凸严重程度无关。结论部分AIS患者存在体感传导通路异常，其可能为AIS的原发性因素，可能在AIS的发病机制中起着重要的作用。

Objective To investigate the abnormality of somatosensory evoked potentials （SEPs） in adolescent idiopathic scoliosis （AIS） with different curve magnitudes, and to explore its effect on the etiopathogenesis of AIS. Methods Posterior tibial nerve SEPs were evaluated on 489 young operative treated AIS patients with a Cobb angle 〉 40° and 45 age-matched healthy control individuals. Absence of SEPs waveforms, prolongation of peek latency or asymmetrical peek latency were defined as pathological change. Base on the control reference, the incidence of pathological SEPs was determined in AIS group. The association of abnormal SEPs and curve severity for AIS patients was also assessed. Results Peek latency corrected for body height was slightly longer in AIS patients than in controls, however, with no significant difference. Interside difference of latency was significantly larger in AIS patients. Abnormal SEPs were found in 166 of 489 AIS patients. Among these, 17 （ 10. 2% ） showed absent waveforms, 50 （30. 1% ） had unilateral latency prolongation, 38 （22. 9% ） had bilateral latency prolongation, and 120 （72. 3% ） showed significant interside difference. Statistical analysis failed to show a correlation between abnormal SEPs and the curve severity of spinal deformity. Conclusion Disorder of somatosensory pathways does exist in a subgroup of AIS patients, and it might be a primary factor other than secondary change, and could play an import role in the etiopathogenesis of AIS.