Abstract

A key issue for the study of language and the brain in the twenty-first century is the delineation of the neural substrate underlying the perception and production of prosody in relation to linguistic and affective components of the speech signal. The notion of speech prosody dates back to MonradKrohn’s (1947) case study of a woman who was unable to produce the phonemic tone contrasts in her native Norwegian dialect even though she retained considerable musical ability. Because of its multiple functions (e.g., linguistic, attitudinal, affective) and its multiple phonetic cues (e.g., pitch, duration, loudness), the neural substrate of speech prosody remains elusive and controversial to the present day (Baum & Pell, in press). During the second half of the twentieth century, two major, competing lines of investigation have emerged concerning hemispheric specialization for speech prosody. One emphasizes task-dependent or domain-specific effects (e.g., Van Lancker, 1980; Ross & Mesulam, 1979), and the other cuedependent effects that cut across task domains (e.g., Robin, Tranel, & Damasio, 1990; Ivry & Robertson, 1998). In speech perception, for example, task-specific hypotheses assume that unique, neural mechanisms are recruited for the speech domain, whereas cue-dependent hypotheses claim that speech processing is subserved by neurobiological mechanisms specialized for particular aspects of the acoustic signal, irrespective of communicative or linguistic relevance. Evidence for or against these hypotheses has been drawn primarily from neurologically impaired populations with unilateral lesions to the left (LH) or right hemisphere (RH) as well as from studies using dichotic listening procedures or the Wada technique. Within the past decade, empirical evidence has also begun to appear from functional neuroimaging studies.

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