Prosodic stress: Acoustic, aphasic, aprosodic and neuroanatomic interactions

Abstract

Abstract The neuroacoustic basis of prosodic (emphatic or contrastive) stress production was assessed in normals and patients with left and right brain damage (LBD, RBD). The results indicated that 1) pitch obtrusions are not an invariant acoustic signature of prosodic stress in normals, 2) LBD and RBD condition the acoustic signaling of prosodic stress, 3) LBD and RBD equally impair the production of prosodic stress, 4) left basal ganglia lesions are highly predictive of prosodic stress deficits whereas lesion location in RBD is not predictive of deficits, 5) aphasic non-fluency in LBD is highly correlated to prosodic stress deficits whereas loss of affective prosody in RBD is not predictive of deficits and 6) affective-prosodic deficits in LBD and RBD condition differentially and very robustly the acoustic signaling of prosodic stress. The results were interpreted as supporting the task-dependent but not the cue-dependent theory of prosodic lateralization in the brain.