Image_1_An Investigation of Compensation and Adaptation to Auditory Perturbations in Individuals With Acquired Apraxia of Speech.tiff

Two auditory perturbation experiments were used to investigate the integrity of neural circuits responsible for speech sensorimotor adaptation in acquired apraxia of speech (AOS). This has implications for understanding the nature of AOS as well as normal speech motor control. Two experiments were conducted. In Experiment 1, compensatory responses to unpredictable fundamental frequency (F0) perturbations during vocalization were investigated in healthy older adults and adults with acquired AOS plus aphasia. F0 perturbation involved upward and downward 100-cent shifts versus no shift, in equal proportion, during 2 s vocalizations of the vowel /a/. In Experiment 2, adaptive responses to sustained first formant (F1) perturbations during speech were investigated in healthy older adults, adults with AOS and adults with aphasia only (APH). The F1 protocol involved production of the vowel /ε/ in four consonant-vowel words of Australian English (pear, bear, care, dare), and one control word with a different vowel (paw). An unperturbed Baseline phase was followed by a gradual Ramp to a 30% upward F1 shift stimulating a compensatory response, a Hold phase where the perturbation was repeatedly presented with alternating blocks of masking trials to probe adaptation, and an End phase with masking trials only to measure persistence of any adaptation. AOS participants showed normal compensation to unexpected F0 perturbations, indicating that auditory feedback control of low-level, non-segmental parameters is intact. Furthermore, individuals with AOS displayed an adaptive response to sustained F1 perturbations, but age-matched controls and APH participants did not. These findings suggest that older healthy adults may have less plastic motor programs that resist modification based on sensory feedback, whereas individuals with AOS have less well-established and more malleable motor programs due to damage from stroke.