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环杓关节关节炎中喉麻痹的证据。

Evidence for laryngeal paralysis in cricoarytenoid joint arthritis.

作者信息

Gacek R R, Gacek M R, Montgomery W W

机构信息

Department of Otolaryngology, SUNY Health Sciences Center, Syracuse, New York 13210, USA.

出版信息

Laryngoscope. 1999 Feb;109(2 Pt 1):279-83. doi: 10.1097/00005537-199902000-00019.

DOI:10.1097/00005537-199902000-00019
PMID:10890779
Abstract

OBJECTIVE/HYPOTHESIS: To demonstrate denervation atrophy of laryngeal muscles in a case of gout involving the cricoarytenoid joint.

METHODS

The posterior cricoarytenoid (PCA) and arytenoideus (A) muscles from a 72-year-old man with extensive gout were compared with those from a normal adult larynx (age and sex unknown) using stereologic techniques for changes in muscle composition and fiber diameter.

RESULTS

The PCA and A muscles in the gout specimen contained changes Indicative of muscle degeneration. In the PCA the volume fraction (VF) of intact muscle was 0.30, of degenerating muscle 0.13, and of fat 0.16. A normal PCA had a VF for intact muscle of 0.64 and 0 for degenerating muscle and fat. Similar changes were seen in the gout A muscle but were not measured. Muscle fiber diameters in the gout PCA (1,024 fibers) showed a significantly higher atrophy and hypertrophy factor than the normal PCA (1,255 fibers). The variability coefficient in the gout PCA (487) was almost double that in the normal PCA (290). Although muscle fiber diameters were not measured in the A muscle in gout, variability in fiber size was seen.

CONCLUSIONS

The pattern and magnitude of muscle fiber degeneration in the PCA and A muscles from a larynx with gout fixation of the cricoarytenoid joint indicate neural degeneration. Since similar changes were not found in the thyroarytenoid (TA) and lateral cricoarytenoid (LCA), the neuropathy is selective for the posterior branch of the recurrent laryngeal nerve. This neuropathy is likely responsible for vocal cord adduction (stridor) and incomplete closure of the posterior commissure (aspiration) associated with acute cricoarytenoid arthritis. In chronic cricoarytenoid joint arthritis, ankylosis of the joint space maintains the adducted cord position.

摘要

目的/假设:在一例痛风累及环杓关节的病例中证实喉肌失神经萎缩。

方法

运用体视学技术,比较一名72岁广泛痛风患者的后环杓肌(PCA)和杓肌(A)与一名正常成人喉部(年龄和性别未知)的相应肌肉,观察肌肉组成和纤维直径的变化。

结果

痛风标本中的PCA和A肌出现了提示肌肉变性的改变。在PCA中,完整肌肉的体积分数(VF)为0.30,变性肌肉为0.13,脂肪为0.16。正常PCA中完整肌肉的VF为0.64,变性肌肉和脂肪的VF为0。痛风A肌也出现了类似变化,但未进行测量。痛风PCA(1024根纤维)的肌纤维直径显示出比正常PCA(1255根纤维)显著更高的萎缩和肥大因子。痛风PCA的变异系数(487)几乎是正常PCA(290)的两倍。虽然痛风A肌未测量肌纤维直径,但可见纤维大小的变异性。

结论

环杓关节痛风固定的喉部PCA和A肌中肌纤维变性的模式和程度表明神经变性。由于在甲杓肌(TA)和环杓侧肌(LCA)中未发现类似变化,这种神经病变对喉返神经后支具有选择性。这种神经病变可能是与急性环杓关节炎相关的声带内收(喘鸣)和后联合不完全闭合(误吸)的原因。在慢性环杓关节炎中,关节间隙的强直维持了内收声带的位置。

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