A number of studies have provided evidence, through various aerodynamic measurements, for disordered respiratory function in individuals with PD. These disorders include reduced vital capacity, reduced total amount of air expended during maximum phonation tasks, reduced intraoral air pressure during consonant/vowel productions, and abnormal airflow patterns (48-50). The origins of these airflow abnormalities are not clear but they may be related to variations in airflow resistance due to abnormal movements of the vocal folds and supralaryngeal area (50) or abnormal chest wall movements and respiratory muscle activation patterns (23,48,51).
Articulatory and Velopharyngeal Disorders: Acoustic and Kinematic Correlates of Articulatory Abnormalities in Parkinson's Disease
Imprecise consonants and vowels may be present in 45% of PD patients with dysarthria (2,28). Logemann et al. (2) reported articulation problems in 45% of 200 unmedicated patients. They suggested that inadequate narrowing of the vocal tract due to hypokinetic articulatory movements may underlie problems with stops /p/, /b/, affricates/ sh/, /ch/, and fricatives /s/, /f/.
Acoustic correlates of disordered articulation include problems with timing of vocal onsets and offsets (voicing during normally voiceless closure intervals of voiceless stops) (24) and spirantization (presence of fricative-like, aperiodic noise during stop closures), as well as problems with articulatory undershoot, reflected in vowel formant frequencies (28). Dysarthric speakers with PD showed longer voice onset times (VOTs) than normal (52). Such abnormal VOTs may reflect a problem with movement initiation (52), which may be related to deficits in internal cueing, timing, and/or sensory gating (4,53). Sapir et al. (4) reported abnormal articulation in 50% of 42 medicated patients with PD. In another study, Sapir et al. (28) analyzed acoustic parameters of vowel articulation in individuals with and without PD reading sentences aloud. They found abnormally high second formant (F2) during the production of the vowel /u/, and abnormally low ratio of F2 of the vowel /i/ and the vowel /u/ (F2i/F2u) in the speech of individuals with PD compared with the speech of the neurologically normal age-matched controls. These acoustic abnormalities most likely reflect reduced range of articulatory movements during vowel production.
Kinematic analyses of jaw movements demonstrated disordered articulatory movements in individuals with PD (52,54-57). These individuals show a significant reduction in the size and peak velocity of jaw movements during speech when compared with neurologically healthy individuals without speech problems (52,57-59). Also, jaw movement of individuals with PD is approximately half the size of the jaw movements observed in nondisordered speakers. Although the reduction in range of movement has been attributed to rigidity of the articulatory muscles (60), it is more likely that these movement abnormalities are related to problems with sensorimotor gating, perception, and/or amplitude scaling of speech and nonspeech movements (1,26,27,53). In contrast to range of movements, durations of movements in individuals with PD have been reported to be similar to those of healthy individuals (52).
EMG studies of the lip and jaw muscles in individuals with and without PD have provided some evidence for increased levels of tonic resting and background activity (19,20,61), as well as loss of reciprocity between agonist and antagonistic muscle groups in these individuals (19,20). These findings are consistent with evidence for abnormal sensorimotor gating in the orofacial and limb systems, which are presumably related to basal ganglia dysfunction (62,63). Whether these abnormal sensorimotor findings are indicative of excess rigidity in the speech musculature is not clear (56,57,64). Hunker et al. (58) found evidence to suggest a positive correlation between muscle stiffness and decrements in the range of lip movement. However, Conner et al. (56,57) found no evidence for excess rigidity in jaw muscles during speech movements, but they did find some abnormalities during nonspeech, visually guided movements. They concluded that motor impairment in PD may be task-dependent. Caliguiri (64) obtained measures of labial muscle rigidity and movement for 12 parkinsonian and 9 age-matched control subjects. Displacement amplitude, peak instantaneous velocity, and movement time were evaluated during repetitive syllable productions. He reported that although mean displacement amplitudes and velocities were lower for the subjects with PD compared with the normal controls, there was no statistical relationship between labial rigidity and the degree of movement abnormality. He concluded that although rigidity may play a part in the overall disability, it does not sufficiently explain the labial articulatory difficulties associated with PD. He further argued that rigidity and bradykinesia probably represent independent pathophysiologic phenomena.
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