Matsuo Kiyoshi, Ban Ryokuya, Ban Midori
Department of Plastic and Reconstructive Surgery, Shinshu University School of Medicine, Matsumoto, Japan.
Eplasty. 2014 Sep 12;14:e33. eCollection 2014.
Although the mixed orbicularis oculi muscle lacks the muscle spindles required to induce reflex contraction of its slow-twitch fibers, the mechanoreceptors in Müller's muscle function as extrinsic mechanoreceptors to induce reflex contraction. We hypothesize that strong stretching of these mechanoreceptors increases reflex contraction of the orbicularis oculi slow-twitch muscle fibers, resulting in blepharospasm.
We examined a 71-year-old man with right blepharospasm and bilateral aponeurosis-disinserted blepharoptosis to determine whether the patient's blepharospasm was worsened by increased trigeminal proprioceptive evocation via stretching of the mechanoreceptors in Müller's muscle owing to a 60° upward gaze and serrated eyelid closure, and whether local anesthesia of the mechanoreceptors via lidocaine administration to the upper fornix as well as surgical disinsertion of Müller's muscle from the tarsus and fixation of the disinserted aponeurosis to the tarsus decreased trigeminal proprioceptive evocation and improved patient's blepharospasm.
Before pharmacological desensitization, 60° upward gaze and serrated eyelid closure exacerbated the patient's blepharospasm. In contrast, these maneuvers did not worsen his blepharospasm following lidocaine administration. One year after surgical desensitization, the blepharospasm had disappeared and a 60° upward gaze did not induce blepharospasm.
Strong stretching of the mechanoreceptors in Müller's muscle appeared to increase reflex contraction of the orbicularis oculi slow-twitch muscle fibers, resulting in blepharospasm. In addition to botulinum neurotoxin injections into the involuntarily contracted orbicularis oculi muscle and myectomy, surgical desensitization of the mechanoreceptors in Müller's muscle may represent an additional procedure to reduce blepharospasm.
尽管眼轮匝肌混合肌缺乏诱导其慢肌纤维反射性收缩所需的肌梭，但米勒肌中的机械感受器作为外在机械感受器可诱导反射性收缩。我们假设这些机械感受器的强烈拉伸会增加眼轮匝肌慢肌纤维的反射性收缩，从而导致眼睑痉挛。
我们检查了一名71岁患有右侧眼睑痉挛和双侧腱膜分离性上睑下垂的男性患者，以确定通过60°向上注视和锯齿状眼睑闭合导致米勒肌中机械感受器拉伸，增加三叉神经本体感觉诱发是否会使患者的眼睑痉挛加重，以及通过在上穹窿注射利多卡因对机械感受器进行局部麻醉以及将米勒肌从睑板分离并将分离的腱膜固定到睑板是否会减少三叉神经本体感觉诱发并改善患者的眼睑痉挛。
在药物脱敏前，60°向上注视和锯齿状眼睑闭合会加重患者的眼睑痉挛。相比之下，在注射利多卡因后，这些动作并未使他的眼睑痉挛加重。手术脱敏一年后，眼睑痉挛消失，60°向上注视不会诱发眼睑痉挛。
米勒肌中机械感受器的强烈拉伸似乎会增加眼轮匝肌慢肌纤维的反射性收缩，从而导致眼睑痉挛。除了向不自主收缩的眼轮匝肌注射肉毒杆菌神经毒素和进行肌切除术外，对米勒肌中的机械感受器进行手术脱敏可能是一种减少眼睑痉挛的额外方法。
