• Vol. 34 No. 9, 579–581
  • 15 October 2005

Adult-onset Re-emergent Stuttering as a Presentation of Parkinson’s Disease



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Introduction: The basal ganglia-thalamocortical motor circuits are postulated to play a key role in the aetiopathogenesis of stuttering. The main dysfunction is thought to be an impairment in the ability of the basal ganglia to produce timing cues for the initiation of the next motor segment of speech, explaining the association of acquired and re-emergent stuttering with diseases such as dystonia and Parkinson’s disease. Clinical Picture: We describe a 61-year-old man presenting with re-emergent stuttering and mild hypomimia, only to develop unilateral rest tremors, hypo- and bradykinesia, rigidity and gait difficulties one year later. Treatment and Outcome: His parkinsonism responded well to treatment with bromocriptine, but he continued to stutter. Discussion: This case illustrates the association between acquired or re-emergent stuttering and basal ganglia disorders, and highlights the need to assess such patients for an underlying aetiology.

A 61-year-old right-handed man with no past medical history presented to our movement disorders clinic with a history of stuttering which had begun 5 years earlier, and appeared to worsen in the preceding year. He had stuttered briefly in childhood, from the age of 5 to 11, but had been able to speak fluently thereafter, until the age of 56, when he suddenly found himself once again having difficulty with fluent speech. He noticed that the stuttering was worse when he was stressed or anxious, and when he spoke on the telephone. He stuttered less when speaking to close friends or family, but fared badly when speaking to a stranger. He had no family history of tremors or Parkinson’s disease (PD), had no exposure to neuroleptic medications, and denied brady- or hypokinesia, postural difficulties, tremors, autonomic symptomatology such as orthostasis, erectile impotence or constipation, change in handwriting, sialorrhoea or limb stiffness. He denied cognitive or bulbar dysfunction, and had no postural difficulties. Clinical examination was unremarkable, except for a barely discernible hypomimia, which could have passed for normal, and a tendency to stutter, in that he demonstrated repetitions and prolongations on initial syllables. This occurred mainly in self-formulated speech. He had less difficulty speaking when he read from a prepared text or when he quoted a well-remembered speech, such as the pledge of allegiance. He had no hypophonia, brady- or hypokinesia, tremors or cogwheel rigidity, and was scored at 1 (for hypomimia) on the motor scale of the Unified Parkinson’s Disease Rating Scale (UPDRS). He walked with normal stride length, had good armswing and did not retropulse on the pull test. Cognition was assessed with the abbreviated mini-mental examination, and was within normal limits. Neuroimaging with computed tomography scan of the brain and the electroencephalographic examination were within normal limits. Thyroid dysfunction and Wilson’s disease were excluded, and he had no acanthocytosis. He was referred to a speech therapist and underwent intensive smooth speech therapy, but defaulted in view of his perceived poor response. He felt that his stuttering was less marked when he spoke slowly, and when he chorus-spoke. He was reviewed on a six-monthly basis in view of the mild hypomimia.

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