Dysfluency Characteristics in the Speech of Individuals with Parkinson's DiseaseBackground
A disorder in the fluency of speech typically is characterized by an interruption in the flow of speaking (e.g., atypical rate; rhythm; and repetitions in sounds, syllables, words, and phrases) and may be accompanied by excessive tension, struggle behavior, and secondary mannerisms (ASHA Ad Hoc Committee on Service Delivery in the Schools, 1993). The mechanisms behind the difficulties with speech initiation and speech disruptions remain unclear. Dysfluency can, however, have a neurogenic basis (Andy & Bhatnager, 1992; Van Borsel & Tailleu, 2001). The often dramatic improvements in fluency brought about by metronomic pacing, singing, choral speech, and delayed auditory feedback suggest that these dysfluencies are not the result of some general speech motor instability but instead a more specific disruption in the basal ganglia motor control circuits (Alm, 2004).
Disruptions of the basal ganglia motor control circuits, such as those seen in Parkinson’s disease (PD), can result in an acquired dysarthria (Jankovic, 1996). In the classic Mayo Clinic studies of Darley, Aronson, and Brown (1969a, 1969b), PD was associated with a specific form of dysarthria known as hypokinetic dysarthria. Disruption in speech prosody (rate, rhythm, fluency, intonation, and stress patterns) is common in hypokinetic dysarthria (Duffy, 2005) and often contributes to the listener’s perception of decreased speech naturalness.
There are only a few reports in the literature describing speech fluency in persons with PD (Benke, Hohenstein, Poewe, & Butterworth, 2000; Goberman & Blomgren, 2003; Koller, 1983; Lim, Wilder-Smith, Ong, & Seet, 2005). One of the most frequently cited studies describing dysfluent speech and Parkinson-like symptoms is that of Koller (1983), who describes adult-onset dysfluency as rare and as having evidence of multi-focal hemispheric damage. Transient acquired dysfluency is associated with unilateral foci, whereas, persistent acquired dysfluency is associated with bilateral lesions. Koller’s study was based on a patient who had acquired dysfluency and eventual signs of supranuclear palsy, prompting a review of patients with extrapyramidal disease and stuttering-like behaviors. Koller reports the case studies of 6 adult males ranging in age from 55 to 65 years (mean = 61.3 years, sd = 3.7 years) who presented with a variety of symptoms characteristic of Parkinson’s disease. Marked similarities existed in the speech characteristics of each patient. Repetitions on initial phonemes and words were common, irrespective of the part of speech. Disordered melody, rhythm, volume, rate, and tone were common. In every case, it was reported that dysfluencies occurred primarily on self-formulated speech. In none of the cases were secondary characteristics associated with dysfluencies reported. Eighty-three percent of participants reported an adaptation effect, meaning that dysfluencies decreased on successive oral readings of the same material (Koller). One-half of the patients in the study reported no behavioral impact, while one reported “slight annoyance,” another “mild frustration,” and one reported “mild annoyance.” While behavioral responses to stuttering by children and adults are variable, often, persons who stutter display severe anxiety and are very distressed by their abnormal speech (Bloodstein, 1969). Alternatively, the patients in this study showed mild or slight annoyance or frustration or no reaction at all to stuttering. One-half of the participants reported dysfluencies while singing, while the other half did not. With regard to the effects of L-dopa on dysfluencies, 67% reported no change with L-dopa treatment, with the other 33% reporting both worse “on” and worse “off” the medication.
Benke et al. (2000) investigated 53 patients with PD and described two variants of repetitive speech: (1) hyperfluency—poorly articulated iterations, mostly uttered with increasing speech rate and decreasing loudness, closely resembling palilalia; and (2) dysfluency—non-fluent, well-articulated iterations, pronounced with constant loudness and rate, produced in a staccato, stuttering-like manner. Patients iterated phonemes, syllables, words, and utterances, but most often single syllables and words. Both forms were present in each patient with repetitive speech, confirming that both are present in one disease, as well as the variability of speech rate, articulatory clearness, and loudness. Repetitive speech was observed in 28.3% of patients, with a prevalence of 54.3% in the advanced-stage, and 6.9% in stable patients. The numbers of iterations found disproves the notion that repetitive speech phenomena are rare in PD. Goberman and Blomgren (2003) examined dysfluencies in persons with PD to investigate the role of dopamine in speech dysfluencies. In their study, nine persons with PD were age-matched with eight control subjects. Participants completed a reading task and a speaking task. Participants with PD were found to be more dysfluent than the control participants in the “off” state, and there were no group differences from the “off” to the “on” state. The authors suggest that any change in dopamine levels may lead to increases or decreases in dysfluencies.
Two hypotheses regarding generation of the iterations were formulated in this study: (1) the motor hypothesis, and (2) the cognitive hypothesis. The motor hypothesis states that repetitive speech phenomena are the result of a malfunction at the level of motor speech, resulting from a disintegration of subcortical interplay, which causes the basal ganglia to stimulate speech activity in the cortex in an uncontrolled manner. Alternatively, defective execution of preprogrammed motor sequences may result in an impairment of the duration and fluency of speech events—that is, freezing or motor block. Motor speech can be paced by released tremor oscillations, described as the hastening phenomenon.
