A POSSIBLE FELINE MODEL FOR HUMAN BLEPHAROSPASM
A POSSIBLE FELINE MODEL FOR HUMAN BLEPHAROSPASM
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DOI：
10.1080/01616412.1993.11740105
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发表时间：
1993-02-01
影响因子：
1.9
通讯作者：
DZIEZYC, J
中科院分区：
文献类型：
--
作者：
KLEMM, WR;BRATTON, GR;DZIEZYC, J
“良性原发性眼睑痉挛”是一种病因不明的人类眼睑疾病，其特征是眼轮匝肌的不自主、双侧和致残性痉挛性挛缩。治疗往往令人失望。在这里，我们报告了可能是开发动物模型以探索疾病机制和潜在治疗的第一步。我们通过外科手术将刺激电极植入到已知的面神经核外侧分支输入的大脑区域，以通过电刺激诱导眨眼。在面部核、臂旁核、红核和间质核或其附近的单脉冲刺激产生一致的刺激诱导的眼睑收缩。除了对侧反应发生的间质核外，刺激的反应是同侧的。在眨眼阈值电压下，面部、头部或身体的其他运动很少或没有发生。当这些部位受到脉冲序列的刺激时，眼睑会随着刺激频率而闭合，并倾向于融合成持续闭合。在三天的测试中，每个刺激部位的阈值保持不变。药物治疗对任何刺激部位的眨眼阈值都没有一致的影响，即使一般行为受到影响。我们得出结论，这些面神经核的输入通路可能导致眼睑痉挛，未来对这些通路的神经化学和电生理研究可能会产生一个合适的动物模型来理解这种疾病。
'Benign essential blepharospasm' is a human eyelid disorder of unknown aetiology characterized by involuntary, bilateral, and disabling spasmodic contracture of the orbicularis oculi muscle. Treatments are frequently disappointing. Here we report what might be a first step toward developing an-animal model for exploring mechanisms of the disorder and potential treatments. We surgically implanted stimulating electrodes into brain areas known to supply input to the lateral division of the facial nerve nucleus to induce blinking by electrical stimulation. Single-pulse stimuli at or near the facial, parabrachial, red, and interstitial nuclei produced consistent stimulus-induced eyelid contractions. Responses were ipsilateral to stimulation, except for the interstitial nucleus where contralateral responses occurred. Little or no other movements of the face, head, or body occurred at eye-blink threshold voltages. When these sites were stimulated with pulse trains, eyelid closures followed stimulus frequency and tended to fuse into constant closure. Thresholds at each stimulus site remained constant during three days of testing. Drug treatments produced no consistent effect on eyeblink threshold from any stimulation site, even when general behaviour was affected. We conclude that these input pathways to the facial nucleus may contribute to blepharospasm and that future neurochemical and electrophysiological study of these pathways may produce a suitable animal model for understanding this disorder.