Different mechanism of vocal cord paralysis between spinocerebellar ataxia (SCA 1 and SCA 3) and multiple system atrophy

Different mechanism of vocal cord paralysis between spinocerebellar ataxia (SCA 1 and SCA 3) and multiple system atrophy
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DOI:
10.1016/s0022-510x(02)00046-1
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发表时间:
2002-05-15
影响因子:
4.4
通讯作者:
Hirai, S
Hirai, S
中科院分区:
医学3区
文献类型:
--
作者:
Isozaki, E;Naito, R;Hirai, S

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虽然多系统萎缩(MSA)经常与导致严重呼吸衰竭的声带麻痹(VCP)相关,但遗传性脊髓小脑变性是否会出现类似的喉麻痹仍不清楚。我们从纤维喉镜和喉肌病理学的角度分析了喉功能,然后试图阐明脊髓小脑共济失调 I 型(SCA 1)、3 型(SCA 3)和 MSA 患者 VCP 机制的差异。研究人员对 7 名 SCA 1 患者、19 名 SCA 3 患者和 11 名 MSA 患者进行了研究。通过纤维喉镜在清醒和地西泮诱导的睡眠(睡眠负荷测试)期间分析声带运动。对 5 例尸检病例(1 例 SCA I,4 例 SCA 3)的喉固有肌石蜡包埋切片或冷冻切片进行组织学检查。在 7 名 SCA I 患者中的 2 名 (29%)、19 名 SCA 3 患者中的 3 名 (16%) 以及 11 名 MSA 患者中的 9 名 (82%) 中发现了 VCP。在 SCA I 和 SCA 3 中观察到的 VCP 严重程度各不相同,除了一名 SCA 3 患者外,所有 8 名患者的睡眠负荷测试均未显示恶化。在该患者中,纤维喉镜检查的结果与 MSA 中发现的结果非常相似。在尸检的 1 名 SCA I 和 4 名 SCA 3 患者中,所有喉固有肌,包括环甲肌 (CT)、杓间肌 (IA) 和环杓后肌 (PCA) 均显示神经源性萎缩。我们的结论是,SCA I 和 SCA 3 中的 VCP 在其发生、对睡眠负荷测试的反应以及喉内肌中神经源性异常的分布方面与 MSA 中的 VCP 形成鲜明对比。 (C) 2002 Elsevier Science B.V. 保留所有权利。
While multiple system atrophy (MSA) is frequently associated with vocal cord paralysis (VCP) causing severe respiratory failure, it is still unknown whether hereditary types of spinocerebellar degeneration develop similar laryngeal paralysis. We analyzed the laryngeal function from the viewpoints of fiberoptic laryngoscopy and laryngeal myopathology and then attempted to clarify the difference of the mechanism of VCP among the patients with spinocerebellar ataxia type I (SCA 1), type 3 (SCA 3), and MSA. Seven patients with SCA 1, nineteen with SCA 3, and eleven with MSA were studied. Vocal cord movement was analyzed by fiberoptic laryngoscopy during wakefulness and diazepam-induced sleep (sleep load test). Paraffin-embedded sections or cryosections of the intrinsic laryngeal muscles from five autopsied cases (one with SCA I and four with SCA 3) were histologically examined. VCP was found in two of the seven SCA I patients (29%), three of the nineteen SCA 3 patients (16%), and in nine of the eleven MSA patients (82%). VCP observed in SCA I and SCA 3 was various in the severity and showed no exacerbation on sleep load test in all of the eight patients but one SCA 3 patient. In this patient, the findings of fiberoptic laryngoscopy were quite similar to those found in MSA. All the intrinsic laryngeal muscles including cricothyroid (CT), interarytenoid (IA), and posterior cricoarytenoid (PCA) muscles showed neurogenic atrophy in one autopsied SCA I and four SCA 3 patients. Our conclusion is that VCP in SCA I and SCA 3 contrasts with that in MSA in its occurrence, response to the sleep load test, and the distribution of the neurogenic abnormalities among the intrinsic laryngeal muscles. (C) 2002 Elsevier Science B.V. All rights reserved.