内收型痉挛性发声障碍的诊断

目的梳理内收型痉挛性发声障碍（ADSD）的主要诊断方法，对ADSD及其他相关疾病的嗓音听感特征进行描述、比较及分析；归纳出ADSD的鉴别诊断要点。诊断ADSD主要依据嗓音的听感特征，但还需结合病史、症状变化及体征等信息进行综合判断。     

痉挛性发音障碍的喉功能特点

目的 为了探讨痉挛性发音障碍的喉功能特点及其发音障碍的表现形式。方法 对24例痉挛性发音障碍患者（男4例,女18例）的发病诱因、发音障碍特征、喉镜所见、喉肌电及喉空气动力学改变进行了分析。结果 痉挛性发音障碍主要表现为音韵及声音的流畅性障碍,主观听觉上以紧张性发音障碍为特点;喉镜检查可看到痉挛性发音时声带过度内收,室带不同程度的内收超越,重者声带强烈内收,会厌、室带以及整个喉呈闭锁状态;典型的喉肌电图所见为束发性放电;喉呼气流率明显减少。结论 痉挛性发音障碍伴随着紧张性发音的同时声带或整个喉强烈内收痉挛,同时伴有呼气流率下降,典型病例可看到喉肌电的改变。     

痉挛性发音障碍诊断及治疗的研究

目的对痉挛性发音障碍患者临床特点,喉肌电图表现,疗效进行分析,探讨痉挛性发音障碍诊断及治疗特点。方法对22例痉挛性发音障碍患者治疗前后症状、嗓音声学特征,频闪喉镜下声带状态,喉肌电图特征进行分析;根据不同分型,应用肉毒素A行特定肌肉注射并观察疗效。结果22例痉挛性发音障碍患者中,内收肌型18例(81 8% ),外展肌型4例(18 2% )。内收肌型患者发音嘶哑,音质紧张、言语中断,发音时声带过度内收,杓间区明显,伴局部震颤; 2例患者发音时还同时伴有舌及软腭震颤;肌电图甲杓肌运动单位电位(motorunitpotential,MUP)振幅明显增加(P<0 01),干扰相呈密集束状放电,募集活动异常活跃,幅度明显增大(700~2500μV)。4例外展肌型患者发音低哑、震颤,气息声明显,发音时声门闭合不良;环杓后肌MUP振幅明显增加,在374~538μV间,募集活动异常活跃,幅度增大(3000~5000μV)。内收肌型患者应用肉毒素A进行甲杓肌注射,单侧剂量大于2 5U疗效明显。症状开始改善时间为注射后6h~2d,平均( x±s,下同)为( 1 4±0 8)d, 2周时最为明显,肌电图及喉肌诱发电位显示药物作用完全,注射肌肉失神经支配。疗效维持8~24周,平均维持(15 2±4 9)周,副作用包括不同程度的发音气息声,声门闭合不良,吞咽不适,饮水呛咳。外展肌型患者采用环杓后肌     

内收型痉挛性发音障碍的语音特征

目的 探讨内收型痉挛性发音障碍的语音特征.方法 采用嗓音和语音的声信号和三维语图分析及主观评价的方法对1O例内收型痉挛性发音障碍患者(女7例,男3例)的语音特征与10例健康志愿者(男5例,女5例)进行对比.结果 内收型痉挛性发音障碍主要表现为音质、音韵及语音的流畅性改变,在朗读文章时出现紧张性发音困难,语音颤抖,频率及响度瞬间起伏,嗓音挤卡、中断,语音延长,失去正常韵律.10例患者中表现为轻度障碍者(异常音节数<25%)1例,中度障碍(异常音节数占25%～49%)6例,重度(异常音节数占50%～74%)1例,极重度(异常音节数≥75%)2例.10例患者朗读时间中位数为49 S,声信号中间断出现无音区,无音比率中位数为42%;而健康对照组朗读时间中位数为30 S,无声音中断.在三维语图中不同的患者在各自症状音节中可以看到嗓音起始时间延长,元音共振峰不规则、断裂甚至消失,症状音节的辅音缺失,或塞擦音的擦音成分延长等.结论 内收型痉挛性发音障碍语音特征为音质、音韵及语音的流畅性改变,在症状音节的三维语图中可以看到相应的元音或辅音音素的特征性改变.     

内收型痉挛性发声障碍患者的喉空气动力学特征分析

目的 分析内收型痉挛性发声障碍(adductor spasmodic dysphonia, ADSD)患者的喉空气动力学特征。方法 选取临床诊断为ADSD的患者18例为ADSD组，募集健康受试者30例为正常组。采用言语发声空气动力学测试系统(PAS)对受试者进行喉空气动力学评估，记录以下指标：声门下压(subglottal pressure, SGP)、发声阈压(phonation threshold pressure, PTP)、发声阈能(phonation threshold power, PTW)、声门阻力(glottal resistance, GR)及发声效率(vocal efficiency, VE)。对ADSD患者的嗓音进行主观听感知评估(consensus auditory perceptual evaluation of voice, CAPE-V),比较两组结果。结果 ADSD组的SGP、GR、VE、PTP大于正常组，差异有统计学意义(P<0.05);ADSD组的PTW与正常组间差异无统计学意义(P>0.05)。受试者工作特征曲线(receiver op...     

痉挛性发音障碍与声带麻痹的关系

目的探索痉挛性发音障碍（ｓｐａｓｍｏｄｉｃｄｙｓｐｈｏｎｉａ）与声带麻痹发病关系。方法用肌电图仪测定喉内肌电位，用电视闪光放大喉镜录像观察声带运动状态，将声带麻痹程度分为轻、中、重三度。结果１９８３～１９９４年１２年中遇到轻、中、重声带麻痹１３００例，在１３００例中伴有痉挛性发音障碍者５例；其中重度和中度声带麻痹者各１例，轻度者３例。结论通过５例的观察，发现声带麻痹的进行或治愈过程中皆可出现痉挛性发音障碍，考虑此５例为喉周围神经器质性病变所引起。     

痉挛性发音障碍患者发病危险因素调查分析

痉挛性发音障碍常分为功能性、心因性和原因不明的运动失调。为了探讨痉挛性发音障碍患者的有关发病危险因素,作者对168例诊断明确的痉挛性发音障碍患者进行回顾性研究。168例患者中男性34例,女性134例,发病年龄为13-71岁,平均发病年龄45岁;对照组186例,男性89例,女性97例。患者均为诊断明确后,在肉毒杆菌毒素注射治疗期间完成有关调查内容,调查主要包括:受教育水平,工作生活史,重大生活事件经历,既往患病史,家族史等。调查结果与对照组或本地区同年龄的相关平均水平值比较,进行统     

喉发音钮术后痉挛性发音障碍

喉发音钮术后痉挛性发音障碍丁浩，刘清明，韩在文，赵立民喉全切除术后用发音赝复物重建发音具有发育清晰、易懂、应用范围广、安装成功率高及使用方便等优点，但亦可见并发症或痉挛性发音障碍。我科于１９９０年用自行研制新型硅橡胶发音钮用于全喉切除患者，发现８例痉...     

痉挛性发声障碍发病机制研究及治疗新进展

痉挛性发声障碍(spamodic dysphonia,SD)是一种散发的、罕见的、发病机制不清的神经障碍类疾病,主要累及喉内肌,导致患者出现显著的言语性发声中断和震颤症状,影响言语性发声活动,好发于中     

痉挛性发音障碍与声带麻痹的关系

目的 探索痉挛性发音障碍与声带麻痹发病关系。方法 用肌电图仪测定喉内肌电位，用电视闪光放大喉镜录像观察声带运动状态，将声带麻痹程度分为轻、中、重三度。结果１９８３￣１９９４年１２月中遇到轻、中、重声带麻醉１３００例，在１３００例中伴有痉挛性发音障碍者５例；其中重度和中度声带麻痹者各１例，轻度者３例。结论 通过５例的观察，发现声带麻痹的进行或治愈过程中皆可出现痉挛性发音障碍，考虑此５例为喉周围神经器     

Spasmodic dysphonia

Few speech disorders have been more controversial as to etiology and treatment as spasmodic dysphonia. This article reviews the historical background and origins of spasmodic dysphonia theories and the legacy of their implications on the current treatment of afflicted patients. The evolution and impact of "organic theories" is discussed and a personal perspective on the central nervous system investigations performed by the authors is briefly elucidated and their practical experience in managing spasmodic dysphonia patients is offered for the reader's consideration.     

Functional dysphonia

Functional dysphonia-a voice disturbance in the absence of structural or neurologic laryngeal pathology-is an enigmatic and controversial voice disorder that is frequently encountered in multidisciplinary voice clinics. Poorly regulated activity of the intrinsic and extrinsic laryngeal muscles is cited as the proximal cause of functional dysphonia, but the origin of this dyregulated laryngeal muscle activity has not been fully elucidated. Several causes have been cited as contributing to this imbalanced muscle tension; however, recent research evidence points to specific personality traits as important contributors to its development and maintenance. Voice therapy by an experienced speech-language pathologist remains an effective short-term treatment for functional dysphonia in the majority of cases, but less is known regarding the long-term fate of such intervention. Further research is needed to better understand the pathogenesis of functional dysphonia, and factors contributing to its successful management.     

Task specificity in adductor spasmodic dysphonia versus muscle tension dysphonia

OBJECTIVES: Adductor spasmodic dysphonia (ADSD) has been characterized as a "task specific" laryngeal dystonia, meaning that the severity of dysphonia varies depending on the demands of the vocal task. Voice produced in connected speech as compared with sustained vowels is said to provoke more frequent and severe laryngeal spasms. This study examined the diagnostic value of "task specificity" as a marker of ADSD and its potential to differentiate ADSD from muscle tension dysphonia (MTD), a functional voice disorder that can often masquerade as ADSD. STUDY DESIGN: Case-control study. METHODS: Five listeners, blinded to the purpose of the study, used a 10 cm visual analogue scale to rate dysphonia severity of subjects with ADSD (n = 36) and MTD (n = 45) producing either connected speech or a sustained vowel "ah."RESULTS: In ADSD, dysphonia severity for connected speech (M = 6.22 cm, SD = 2.56) was rated significantly more severe than sustained vowel productions (M = 4.8 cm, SD = 2.8 [t (35) = 3.67, P < .001]). In MTD, however, no significant difference in severity was observed for the connected speech sample (M = 5.98 cm, SD = 2.83 versus the sustained vowel M = 5.86 cm, SD = 2.87 [t (44) = 0.378, P = .707]). The receiver operating characteristic (ROC) curve, an index of the accuracy of task specificity as a diagnostic marker, revealed that a 1 cm difference criterion correctly identified 53% of ADSD cases (sensitivity) and 76% of MTD cases (specificity) (chi2 (1) = 6.88, P = .0087). CONCLUSIONS: Reduced dysphonia severity during sustained vowels supports task specificity in ADSD but not MTD and highlights a valuable diagnostic marker whose recognition should contribute to improved diagnostic precision.     

Late diagnosis of dysphonia

The authors report on an observation of left-hand recurrent palarysis revealed by a sudden onset of dysphonia. The negative endoscopic findings led to a diagnosis of idiopathic recurrent paralysis. The biopsy of a right-hand sub-costsal subcutaneous tumefaction appeared three months later, leading to the diagnosis of mediastinal and hepatic metastasis following an epidermoid carcinoma of the right auricular pavilion, operated upon 5 years earlier.     

Neuropathology of spasmodic dysphonia

Spasmodic dysphonia is a devastating voice disorder of unknown etiology, with a variable clinical presentation and response to treatment. Three independent evaluations of brain stem function were performed on spasmodic dysphonic patients, and age and sex-matched controls. Statistically significant (p less than 0.01 approximately 0.05) differences were noted between these groups, and the findings were consistent with impairment of somatic and visceral brain stem pathways. A significant correlation (p less than 0.05) was found between the severity of tested central nervous system impairment and vocal tremor, number of associated neurologic signs and duration of illness. Possible etiologies (viral or traumatic), age, and sex, did not correlate with the severity of brain stem impairment. Clinical signs and the brain stem findings appeared to stabilize 3 to 5 years after onset of dysphonia. The investigation of other spasmodic cranial nerve disorders afforded insight into the etiology and therapy for spasmodic dysphonia. Drawing upon previous observations and the results of the brain stem tests, two models are proposed for neuronal processing in spasmodic dysphonia, and future strategies are discussed. The evidence cited in this research project are consistent with spasmodic dysphonia being one of several spasmodic brain stem disorders with variable presentation which are known by the cranial nerve nuclei or pathways of major clinical involvement.