Sensory problems in PD have been recognized for years (66), and these problems may underlie some of the disorders of the speech system. Sensorimotor deficits in the orofacial system (62,63,67) and abnormal auditory, temporal, and perceptual processing of voice and speech (26,27,53,68) have been documented in PD (28,63) and have been implicated as important etiologic factors in hypokinetic dysarthria secondary to PD (69). Schneider et al. (63) found marked sensorimotor deficits in the orofacial and limb systems of individuals with PD. They observed that individuals with PD, compared with age-matched controls, showed greater deficits in tests of sensory function and sensorimotor integration. They suggested that PD patients might have complex deficits in the utilization of specific sensory inputs to organize and guide movements due to abnormal sensory gating or filtering associated with basal ganglia motor dysfunction. Caliguiri and Abbs (62) described abnormal orofacial reflexes in some but not all individuals with PD. Problems in sensory perception of effort have been identified as an important focus of successful speech and voice treatment for individuals with PD (70). It has been observed (33) that when individuals with PD are asked to produce loud speech, they increased their otherwise underscaled soft speech to a level within normal limits but felt they were talking too loud. Thus, it appears that sensory kinesthesia problems may be a factor in the speech and voice disorder observed in individuals with PD.
Ho et al. (27) compared voice loudness perception in individuals with PD and hypophonic dysarthria with that of neurologically normal speakers. They found that unlike the normal speakers, the patients overestimated the loudness of their speech during both reading and conversation. They interpreted these findings to suggest that either impaired speech production is driven by a basic perceptual fault or that abnormal speech perception is a consequence of impaired mechanisms involved in the generation of soft speech. The latter explanation may be related to the phenomenon of central inhibitory influences of the vocal motor system, via feed-forward mechanisms, on auditory cortical activity during self-produced vocalization.
This phenomenon has been demonstrated in humans and animals (71-73) and has been argued to be defective in PD, thus interfering with self-monitoring and self-regulation of vocal loudness and effort (28).
Ho et al. (26) also examined the ability of individuals with PD and neurologi-cally normal individuals to adjust their voice volume in response to two types of implicit cues, background noise and instantaneous auditory feedback. Control subjects demonstrated the Lombard effect by automatically speaking louder in the presence of background noise. They also decreased speech loudness in the presence of increasing levels of facilitative instantaneous auditory feedback. Subjects with PD demonstrated a decreased overall speech loudness; they were less able than controls to appropriately increase loudness as background noise increased and to decrease volume as auditory feedback increased. However, under explicit loudness instructions, the ability of subjects with PD to regulate loudness was similar to that of the normal controls, suggesting that individuals with PD have the capacity to speak with normal loudness, provided that they consciously attend to speaking loudly. The subjects with PD had overall speech loudness that was always lower than for control subjects, suggesting either a reduction of cortical motor input to the speech subsystems, or abnormal perception of their own voice via motor-to-sensory inhibitory mechanisms.
It has been suggested that the main function of the basal ganglia is to serve as an amplifier, by controlling the gain, through gating and scaling, of cortically generated movement patterns (74). Penny et al. (75,76) suggested that basal ganglia excitatory circuits inadequately activate cortical motor centers, and as a result, motor-neuron pools are not provided with adequate facilitation, thus movements are small and slow. Berardelli et al. (77) suggested that the defect in motor cortex activation is due to a perceptual failure to select the muscle commands to match the external force and speed requirements. Maschke et al. (78) referred to this as a problem with kinesthesia and stated that when individuals with PD match their effort to their kinesthetic feedback, they will constantly underscale their movement. In sum, the neurophysiologic mechanisms underlying hypokinetic dysarthria in PD are poorly understood; however, speech motor abnormalities are at least partially secondary to sensorimotor gating abnormalities and poor perception of one's own voice.
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