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多系统萎缩中的喉喘鸣:临床病理特征及病因假说

Laryngeal stridor in multiple system atrophy: Clinicopathological features and causal hypotheses.

作者信息

Ozawa Tetsutaro, Sekiya Kanako, Aizawa Naotaka, Terajima Kenshi, Nishizawa Masatoyo

机构信息

Department of Neurology, Uonuma Institute of Community Medicine, Niigata University Medical and Dental Hospital, 4132 Urasa, Minami Uonuma, Niigata 949-7302, Japan.

Department of Neurology, Brain Research Institute, Niigata University, 1 Asahimachi-dori Chuoku, Niigata 951-8585, Japan.

出版信息

J Neurol Sci. 2016 Feb 15;361:243-9. doi: 10.1016/j.jns.2016.01.007. Epub 2016 Jan 7.

Abstract

Laryngeal stridor is recognized as a characteristic clinical manifestation in patients with multiple system atrophy (MSA). However, the pathogenic mechanisms underlying this symptom are controversial. Neurogenic atrophy of the posterior cricoarytenoid muscle has been identified in cases of MSA, suggesting that laryngeal abductor weakness contributes to laryngeal stridor. However, dystonia in the laryngeal adductor muscles has also been reported to cause laryngeal stridor. Depletion of serotonergic neurons in the medullary raphe nuclei, which exert tonic drive to activate the posterior cricoarytenoid muscle, has recently been identified in MSA cases. This adds weight to the possibility that laryngeal abductor weakness underlies laryngeal stridor in MSA. Continuous positive airway pressure therapy is currently used in the treatment of laryngeal stridor, but should be used with caution in patients showing contraindications. Current knowledge of the clinical and neuropathological features of laryngeal stridor is summarized in this paper, and the hypothesized causes and possible therapeutic options for this symptom are discussed.

摘要

喉喘鸣被认为是多系统萎缩(MSA)患者的一种特征性临床表现。然而,这种症状背后的致病机制存在争议。在MSA病例中已发现环杓后肌的神经源性萎缩,这表明喉外展肌无力是导致喉喘鸣的原因。然而,也有报道称喉内收肌的肌张力障碍会引起喉喘鸣。最近在MSA病例中发现,延髓中缝核的5-羟色胺能神经元缺失,而这些神经元对激活环杓后肌有紧张性驱动作用。这进一步增加了MSA中喉喘鸣是由喉外展肌无力引起的可能性。持续气道正压通气疗法目前用于治疗喉喘鸣,但在有禁忌证的患者中应谨慎使用。本文总结了目前关于喉喘鸣的临床和神经病理学特征的知识,并讨论了该症状的假定病因和可能的治疗选择。

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