Cerebellar degeneration (CD) has deleterious effects on speech motor behavior. Recently, a dissociation between feedback and feedforward control of speaking was observed in CD: Whereas CD patients exhibited reduced adaptation across trials to consistent formant feedback alterations, they showed enhanced within-trial compensation for unpredictable formant feedback perturbations. In this study, it was found that CD patients exhibit abnormally increased within-trial vocal compensation responses to unpredictable pitch feedback perturbations. Taken together with recent findings, the results indicate that CD is associated with a general hypersensitivity to auditory feedback during speaking.

Speakers respond automatically and rapidly to compensate for brief perturbations of pitch in their auditory feedback. The specific adjustments in vocal output require integration of brain regions involved in speech-motor-control in order to detect the sensory-feedback error and implement the motor correction. Cortical regions involved in the pitch reflex phenomenon are highly vulnerable targets of network disruption in Alzheimer's disease (AD). We examined the pitch reflex in AD patients (n = 19) compared to an age-matched control group (n = 16). We measured the degree of behavioral compensation (peak compensation) and the extent of the adaptive response (pitch-response persistence). Healthy-controls reached a peak compensation of 18.7 ± 0.8 cents, and demonstrated a sustained compensation at 8.9 ± 0.69 cents. AD patients, in contrast, demonstrated a significantly elevated peak compensation (22.4 ± 1.2 cents, p < 0.05), and a reduced sustained response (pitch-response persistence, 4.5 ± 0.88 cents, p < 0.001). The degree of increased peak compensation predicted executive dysfunction, while the degree of impaired pitch-response persistence predicted memory dysfunction, in AD patients. The current study demonstrates pitch reflex as a sensitive behavioral index of impaired prefrontal modulation of sensorimotor integration, and compromised plasticity mechanisms of memory, in AD.