Aronson, Arnold

Rate and regularity of diadochokinetic syllable repetitions of /pΛ/, /tΛ/, and /kΛ/ in 30 normal subjects, 30 subjects with spastic dysarthria, and 30 subjects with ataxic dysarthria were measured by computer. Normal subjects had rates (syllables per second) of 6.4, 6.1, and 5.7; spastic dysarthric subjects, 4.6, 4.2, and 3.5; and ataxic dysarthric subjects, 3.8, 3.9, and 3.4 for /pΛ/, /tΛ/, and /kΛ/, respectively. Spastic and ataxic subjects were significantly slower and more variable than normal subjects and ataxic subjects were significantly more variable than spastic subjects. The significantly slower than normal rate of repetition in the ataxic subjects and the significantly more variable than normal rhythm of repetition in the spastic subjects were unexpected findings and are in contrast with results from perceptually based investigations of dysarthria. The study demonstrates that slowness of syllable repetition is not restricted to spastic dysarthria and that dysrhythmia of syllable repetition is not restricted to ataxic dysarthria, thus suggesting the need for additional quantitative measurements of acoustic features on which certain notions about the dysarthrias are currently based.

This is a study of a 20-year-old girl who developed mild, breathy dysphonia which, because of its nonspecificity, had been previously diagnosed as psychogenic; in actuality her voice change was a sign of early myasthenia gravis. The case is presented to alert the clinician to the fact that voice changes can be one of the first and only signs of early neurologic disease. Differential diagnosis requires careful laryngologic, psychiatric, speech, and neurologic examinations. In this instance, the laryngologic and psychiatric examinations were nonproductive, but the speech examination elicited a marked increase in breathiness, hypernasality, and articulatory imprecision as the consequence of prolonged, effortful speaking. This finding, along with the neurologist’s demonstration of an increase in muscular strength by means of injecting edrophonium chloride (Tensilon) led to the diagnosis of myasthenia gravis. A summary of the incidence, clinical features, methods of examination, and treatment of this disease follow the case presentation.

This article presents retrospective longitudinal perceptual and acoustic analyses of the recovery of motor speech control in a right-handed 5-year-old male in the 46 weeks following acquired brain damage. The primary lesion site involved the left fronto-parietal cortex. Correlative descriptions of some aspects of linguistic recovery up to 29 months post-onset are also presented. A mute period of 8 days followed a 2-day comatose period. Spontaneous undifferentiated central vowel-like utterances emerged at 11 days post-injury. Intelligible purposeful utterances emerged at 26 weeks post-onset with the motor speech impairment resolving almost completely within the first year post-onset. The motor speech deficit following the mute period was more consistent with the diagnosis of apraxia of speech than dysarthria. Further, the seemingly lateralized damage associated with the communication disorder may indicate that lateralized hemispheric control of motor speech occurs in early childhood. Finally, the redevelopment of motor speech abilities indicates that the young child’s brain is able to reestablish parameters of motor control underlying speech following acquired brain damage.

Adductor spastic dysphonia may not be one disorder but a voice sign of several different neurologic and psychiatric syndromes. This study evaluates whether rhythmic voice arrests, often components of "spastic dysphonia," are signs of essential tremor, a neurologic disorder. Data on 22 patients originally diagnosed as having spastic dysphonia, who had tremor-like or rhythmic voice arrests, were compared with data on two groups of patients who had essential (voice) tremor. The frequency of voice arrests on vowel prolongation in the group labeled spastic dysphonia was compared with the frequency of voice tremor in the groups with essential tremor. The median frequencies of 5.7, 5.0, and 5.5 Hz were not significantly different among the three groups. Patients in all three groups had tremor in other parts of the body, other scattered neurologic signs, and histories of life stress associated with the onset of their voice disorders. Although the results do not prove conclusively that the patients diagnosed as having spastic dysphonia in this study actually had essential tremor, the similarities to that disorder strongly suggest a linkage.

Case history and voice data for 17 patients who presented with intermittent moments of breathy dysphonia (IBD) in contextual speech were analyzed. From recorded samples of vowel prolongation four variants of phonation were identified. Of 13 patients examined neurologically, 10 (77%) had positive neurologic signs. Psychiatric and physical illnesses were often associated with onset of the voice disorder. Sex ratio of the patients in this study was nearly the same as that for adductor spastic dysphonia. Age at onset was similar to that which has been described for "functional" voice disorders. Different therapies were generally ineffective in alleviating the disorder. Although not conclusive, patients presenting with IBD in connected speech may have an underlying neurologic or psychologic disorders.

Twelve patients (6 men and 6 women), ages 21–79 years, who, as far as it could be determined from their case histories, began to stutter for the first time in adulthood were classified by examining physicians and speech-language pathologists as having psychogenic stuttering. The case histories of these patients were examined to determine the details of their speech and allied complaints, the course and duration of stuttering, and if any psychologically stressful events surrounded the onset and development of the disorder. Minnesota Multiphasic Personality Inventory (MMPI) data on 10 of the 12 patients were analyzed independently. The main findings were (a) stuttering was the chief complaint of 11 patients; (b) all 12 patients had additional neurologic-like complaints that turned out to be nonorganic; (c) duration of stuttering from onset to examination ranged from 4 hr to 1.5 years; (d) the stuttering of most patients was variable in severity and returned to normal either spontaneously or as a result of speech therapy or psychotherapy; (e) psychologic stress was associated with the onset in 10 patients: the stress was chronic in 4 patients and acute in 6; (t) MMPI profiles of 9 of 1O patients were abnormal, with four profiles reflective of a conversion reaction; (g) differentiating neurologic from psychogenic stuttering and the need for interdisciplinary collaboration were essential in all 12 cases; and (h) speech therapy and psychotherapy are justified when psychogenic stuttering is diagnosed.