The prevalence of major psychiatric pathologies in patients with voice disorders

We conducted a study of 47 patients with various voice disorders to determine the prevalence of concomitant psychopathology. The prevalence of psychiatric symptoms varied considerably among patients with the three most common voice disorders: 63.6% among patients with vocal fold paralysis, 29.4% among those with functional dysphonia, and 7.1% among those with spasmodic dysphonia. Levels of anxiety and depression correlated moderately with the severity of voice symptoms in patients with vocal fold paralysis, but not in those with functional or spasmodic dysphonia. Certain abnormal personality traits--including interpersonal sensitivity and distrust of others--were more common among patients with functional dysphonia. The low rate of psychopathology among patients with spasmodic dysphonia is consistent with rates reported in previous investigations. Our findings suggest that the prevalence of psychopathology in patients with voice disorders varies according to the specific voice diagnosis, as does the relationship between specific psychiatric and voice symptoms.     

Laryngeal long latency response conditioning in abductor spasmodic dysphonia.

Previously, we demonstrated that patients with adductor spasmodic dysphonia (ADSD) have a disinhibition of laryngeal responses to sensory input. In this study, sensorimotor responses to stimulation of the superior laryngeal nerve were compared between 10 subjects with abductor spasmodic dysphonia (ABSD) and 15 normal volunteers. The groups had similar latency and frequency characteristics of their unconditioned adductor responses (p>.05). The conditioned R1 (early) responses of the subjects with ABSD were greater and more variable in amplitude than those of the normal volunteers (p< or =.008). Similar R2 (late) conditioning effects were found in both groups, with a nonsignificant trend toward reduced inhibition of contralateral R2 responses at lower interstimulus intervals (p = .01) in the patient group. Thus, inhibitory mechanisms that modulate the R1 laryngeal sensorimotor pathway in the brain stem may be abnormal in subjects with ABSD. Abnormal modulation of laryngeal sensorimotor responses seems present in both types of spasmodic dysphonia.     

Recurrent laryngeal nerve pathology in spasmodic dysphonia.

Since it was first described in 1871, spasmodic (spastic) dysphonia has been considered a disease of psychogenic origin. Unsupported theories of possible organic etiology have appeared sporadically in the literature. In 1976 sectioning of the recurrent laryngeal nerve for patients with this disease was reported with resultant improvement in voice production. This was attempted because the spasmodic dysphonic has, in effect, already compensated vocal cords bilaterally. It was reasoned, therefore, that if one of these was paralyzed the patient would immediately be converted to a state approximating that of a well-compensated unilateral vocal cord paralysis which situation, as is well known, usually carries with it a fairly good voice. A controlled study to evaluate the efficacy of this surgical approach has been undertaken at the Cleveland Clinic during the past year. In an attempt to elucidate the possible organic etiology of spasmodic dysphonia, a section of nerve was removed in every case and examined by both light and electron microscopy. Special stains for myelin were also used on the light microscopy specimens. Demyelinization has been found in most of the cases examined by electron microscopy. Possible correlation between this disease entity and other cranial nerve syndromes of unknown etiology is noted. Such conditions as trigeminal neuralgia, glossopharyngeal neuralgia, blepharospasm, hemifacial spasm, and even possibly Bell's palsy may exhibit a similar etiology.     

Risk factors and demographics in patients with spasmodic dysphonia

OBJECTIVES: Spasmodic dysphonia has been characterized as a functional, psychogenic, or movement disorder with no known etiology or cure. In the present study, risk factors associated with other movement disorders were evaluated in patients with spasmodic dysphonia. STUDY DESIGN: Retrospective patient survey of 168 patients with a known diagnosis of spasmodic dysphonia who completed questionnaires at the time of interval botulinum toxin injection. METHODS: Patients completed questionnaires on demographics, education level, work history, significant life events, medical, social, and family history. The results were compared with those of first-degree relatives as a control group with similar demographics. Data were analyzed using percentages calculated on the total number of responses and distribution of frequency of each. Statistical significance was estimated on t tests of chi2 values. RESULTS: In the series of 168 patients, there was a female predominance of 79%. Age range at onset was 13 to 71 years with an average of age of 45 years. Sixty-five percent of patients had previously had the measles or mumps compared with the national average of 15% in a similar age group (P =.0001). Thirty percent of patients directly associated onset of spasmodic dysphonia symptoms to an upper respiratory tract infection, and 21% to a major life stress. There was no significant incidence of any other medical or neurological condition or symptomatology. There was no family history of spasmodic dysphonia. Twenty-six percent of patients had an essential tremor compared with 4% of first-degree relatives (P =.0001), and 11% had associated writer's cramp compared with 2% of relatives (P =.02). Less than 1% of patients described a history of toxic exposure or electrical injury. CONCLUSIONS: The majority of patients with spasmodic dysphonia are girls and women. A significantly higher incidence of childhood viral illness was found in the patients with spasmodic dysphonia. Patients with spasmodic dysphonia had a significant incidence of both essential tremor and writer's cramp but no history of major illness or other neurological disorder. There appear to be no significant environmental or hereditary patterns in the etiology of spasmodic dysphonia. Stress or viral infection may induce the onset of symptoms of spasmodic dysphonia. Many features of the disorder are common to other movement disorders, and this knowledge may direct future research efforts.     

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.     

Histology of nerves and muscles in adductor spasmodic dysphonia

To elucidate the etiology and pathophysiology of spasmodic dysphonia, we examined the adductor branch of the recurrent laryngeal nerve and the lateral cricoarytenoid muscle from 9 consecutive patients with this disorder who were previously treated with botulinum toxin. Histologic examination revealed average muscle fiber diameters ranging from 21 to 57 microm. Botulinum toxin treatment-related muscle atrophy was observed up to 5 months after injection. Endomysial fibrosis was present in all samples. Histochemical analysis in 8 patients revealed type 2 fiber predominance in 7 patients and fiber type grouping in 2. Type-specific muscle fiber size changes were not present. Nerve samples were examined in plastic sections. In 8 patients the nerves contained homogeneous, large-diameter myelinated nerve fibers and sparse small fibers. One patient had a relatively increased proportion of small myelinated nerve fibers. Overall, the nerve fiber diameter was slightly larger in patients than in controls. These findings may implicate the central nervous system in the pathophysiology of adductor spasmodic dysphonia.     

Safety and tolerability of the implantable recurrent laryngeal nerve stimulator

The recurrent laryngeal nerve (RLN) stimulator has been implanted on a limited basis since 1988 for control of spasmodic dysphonia. A similar vagus nerve stimulator has been implanted in a larger series of patients to control epilepsy. The safety and tolerability of these two stimulators were evaluated. In 113 patients implanted with the vagus nerve stimulator, the complication rate was 0.9%. All patients were monitored for vital signs, electrocardiographic changes, and adverse effects. The absence of changes in vital signs and electrocardiograms during vagal stimulation establishes the safety of this treatment. Since placement of the electrode around the vagus nerve is an easier surgical technique than placement deep to the RLN, it seems reasonable to change the technique to implant the stimulator on the vagus in patients with spasmodic dysphonia.     

Botulinum toxin management of adductor spasmodic dysphonia after failed recurrent laryngeal nerve section

This study examined botulinum toxin type A (BTX-A) treatment of adductor spasmodic dysphonia patients who had previously undergone recurrent laryngeal nerve section that failed to control symptoms. Information was retrieved from records of patients treated by our group between 1984 and 1999. Complete records with standardized outcome measurements were available for 181 BTX-A injection sessions in 16 patients who had had nerve section. These were compared to previously published information regarding 4,621 sessions in 639 adductor spasmodic dysphonia patients also treated by our group. Treatment with BTX-A resulted in significant improvement in voice function in the studied patients (change, 38.2% +/- 24.5%; p < .0001). The onset of effect took place approximately 2.3 days after treatment, and the peak effect about 10.0 days after treatment. The therapeutic effect lasted 14.1 weeks on the average. These features were not significantly different from those observed in adductor spasmodic dysphonia patients as a whole. The incidence of complications was also comparable. However, lower baseline and peak posttreatment perceptions of voice function in the nerve section group were statistically significant (baseline, 45.6% +/- 23.0% versus 52.4% +/- 22.0%; peak, 83.8% +/- 16.4% versus 89.7% +/- 13.0%; both p < .001). We conclude that BTX-A is effective in the treatment of adductor spasmodic dysphonia in patients who have had recurrent nerve section. However, nerve section may adversely affect perceived voice function and may make botulinum toxin therapy less satisfactory. Because of this finding, and because of the unusual pathological features of the focal dystonias, irreversible means of treating adductor spasmodic dysphonia should be approached with caution.     

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。     

Neurologic aspects of spasmodic dysphonia

We discuss the etiology of 100 spasmodic dysphonia patients. Seventy-one patients had underlying essential tremor, 25 had Meige's syndrome, 12 were hypothyroid, and 27 had either a functional disturbance or focal dystonia. Six patients had intermittent breathy dysphonia. A large corpus of spasmodic dysphonia patients have organic neurolaryngeal disease.     

Singer's dystonia: first report of a variant of spasmodic dysphonia

OBJECTIVES: We discuss the phonatory characteristics of a previously undescribed focal laryngeal dystonia present in the singing voice. METHODS: We performed a retrospective chart review of 5 patients with singer's dystonia at a neurolaryngology referral center. RESULTS: Four patients reviewed demonstrated phonatory characteristics consistent with adductor spasmodic dysphonia present in their singing voice. One patient demonstrated abductor spasmodic dysphonia in the singing voice. Each patient initially exhibited normal connected speech in conversational voicing. The treatment protocol and outcome are discussed, including the use of botulinum toxin. CONCLUSIONS: Singer's dystonia is a previously undescribed neurologic disorder that should be understood by those who treat voice performers and voice disorders.     

Findings of multiple muscle involvement in a study of 214 patients with laryngeal dystonia using fine-wire electromyography

Although perceptual and stroboscopic data help in diagnosing and classifying laryngeal dystonia, these measures do not aid the voice clinician in targeting which specific muscles to treat with botulinum toxin. Most patients achieve smoother, less effortful voicing with standard injection regimens. However, there is a notable failure rate. We performed fine-wire electromyography on 214 consecutive patients with laryngeal dystonia. We correlated voice ratings, stroboscopy data, and fine-wire electromyography data. Videostroboscopy was successful in visually demonstrating most of the audible findings in isolated vocal tremor, but it was much less successful in identifying breaks alone or a combination of breaks and tremor. Fine-wire electromyography revealed that the thyroarytenoid muscle was significantly more likely than the lateral cricoarytenoid muscle to be the predominant muscle associated with adductor spasmodic dysphonia, and that the thyroarytenoid and lateral cricoarytenoid muscles were equally likely to be predominantly involved in tremor spasmodic dysphonia. In addition, several patients in both the adductor spasmodic dysphonia and the tremor spasmodic dysphonia groups presented with interarytenoid muscle predominance. All of the intrinsic laryngeal muscles are capable of being the predominant muscle in laryngeal dystonia, and there are patterns of muscle abnormalities that differ between adductor spasmodic dysphonia and tremor spasmodic dysphonia. Some of the failures in treating adductor spasmodic dysphonia with botulinum toxin, and the greater difficulty with success in treating patients with tremor spasmodic dysphonia, are due to failure to deliver toxin to the appropriate muscles.     

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.     

Adductor spasmodic dysphonia versus muscle tension dysphonia: examining the diagnostic value of recurrent laryngeal nerve lidocaine block

OBJECTIVES: Differentiating adductor spasmodic dysphonia (ADSD) from muscle tension dysphonia (MTD) can be difficult. This investigation examined the precision of response to unilateral lidocaine block of the recurrent laryngeal nerve (RLN block) as a potential diagnostic test to discriminate ADSD from MTD. METHODS: Patients with ADSD (n = 23) and MTD (n = 20) were audio-recorded before and during RLN block. The patients completed self-ratings of dysphonia severity, vocal effort, and laryngeal tightness, and blinded listeners completed auditory-perceptual ratings of overall severity, breathiness, and strain of voice samples before and during the block. RESULTS: Repeated-measures analysis of variance, with "group" (ADSD/MTD) as the between-subjects variable and "time" (before block/during block) as the within-subjects variable, confirmed significant "time" effects, but no significant "group-by-time" interaction effects, indicating that both disorder groups responded favorably to RLN block, according to patient- and listener-based ratings. Furthermore, low estimates of sensitivity and specificity and weak receiver operating characteristic curves confirmed that a positive response to the RLN block test did not distinguish ADSD from MTD. CONCLUSIONS: We conclude that RLN block offers little discriminatory value in the differential diagnosis of ADSD versus MTD, and a positive response to RLN block should not be considered confirmatory of ADSD.     

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。     

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。     

Evaluation of brainstem function in patients with spasmodic dysphonia using vestibular evoked myogenic potentials and auditory brainstem responses

CONCLUSION: The vestibular area is closer than the auditory region to nucleus ambiguus. If a 'shared' lesion involves regions of adjacent nuclei of the brainstem in patients with spasmodic dysphonia then vestibular area involvement is more possible than that of the auditory region. OBJECTIVES: The authors hypothesize that lower brainstem lesions and involvement of descending pathways of the spinal tract may be the site of lesion in patients with spasmodic dysphonia. PATIENTS AND METHODS: Ten patients with spasmodic dysphonia were tested using the auditory brainstem response (ABR) and vestibular evoked myogenic potentials (VEMPs). RESULTS: No ABR abnormalities were found in right ears. Results of ABR on the left ear showed that one patient had abnormal ABR. This patient had severe sensorineural hearing loss on the left side. VEMPs displayed normal response in two patients bilaterally. First positive (p13) and second negative (n23) waves of VEMP could not be recorded in three cases unilaterally and in five patients bilaterally.     

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     

Botulinum toxin injection of the vocal fold for spasmodic dysphonia. A preliminary report

A number of different therapies have been used in the management of spasmodic dysphonia. None are curative, and the results of the most widely used surgical procedure (resection of the recurrent laryngeal nerve) are not universally good, with a high recurrence rate in some series. Furthermore, the procedure is not reversible. Using a special electromyographic hypodermic needle, we injected botulinum A toxin into one of the vocal folds of two patients with severe spasmodic dysphonia. Both had significant improvement without any complications. Although the resultant paresis is not permanent, the injection can be repeated as needed as an outpatient procedure.     

Selective laryngeal adductor denervation-reinnervation: a new surgical treatment for adductor spasmodic dysphonia

During the past decade, botulinum toxin (Botox) has emerged as the accepted treatment for adductor spasmodic dysphonia (ASD). This therapy, which produces bilateral weakness of the thyroarytenoid muscle, undoubtedly produces physiologic effects that are beneficial to patients with ASD. However, it also has important limitations, including the need for repeated injections, the unpredictable relationship between dosage and response, and the possibility of short-term swallowing and voice problems. In this study, we will report our preliminary experience with a new surgical treatment for ASD. In this new procedure, the adductor branch of the recurrent laryngeal nerve is selectively denervated bilaterally, and its distal nerve stumps are reinnervated with branches of the ansa cervicalis nerve. Each of the patients was followed for at least 12 months; the median follow-up is 36 months. The outcome of the operation in 21 consecutive patients is reported. Nineteen of the 21 patients were judged to have an overall severity of dysphonia that was "absent to mild" following the procedure. Only 1 patient underwent further treatment with Botox postoperatively. The implications of this new procedure for ASD are discussed.