Among the sequelae of certain types of brain damage are impairments in the production and perception of speech prosody. Prosody serves numerous functions in language, including signaling lexical differences when used phonemically in tone languages, providing cues to stress, sentence type or modality, and syntactic boundaries, and conveying a speaker's emotions. Any or all of these functions of prosody may be impaired subsequent to brain damage. The hemispheric lateralization of the brain lesion seems to play an important role in the nature of the ensuing deficits; however, the neural substrates for prosody are still far from clear (see Baum and Pell, 1999, for a review). Historically, clinical impressions led to the contention that subsequent to right hemisphere damage (RHD), patients would present with flat affect and monotonous speech, whereas patients with left hemisphere damage (LHD) would maintain normal speech prosody. As research progressed, several alternative theories concerning the control of speech prosody were posited. Among these are the hypothesis that affective or emotional prosody is controlled within the right hemisphere, and thus RHD would yield emotional prosodic deficits, whereas linguistic prosody is controlled within the left hemisphere, yielding linguistic prosodic deficits when damage is confined to the left hemisphere (e.g., Van Lancker, 1980; Ross, 1981). A second hypothesis proposes that prosody is principally controlled in subcortical regions and via cortical-subcortical connections (e.g., Cancelliere and Kertesz, 1990); evidence of prosodic deficits in individuals with Parkinson's disease supports this view. A third alternative contends that the individual acoustic cues to prosody (i.e., duration, amplitude, and fundamental frequency) are differentially lateralized to the right and left hemispheres, with temporal properties processed by the left hemisphere and spectral properties by the right hemisphere (e.g., Van Lancker and Sidtis, 1992). Whereas several recent investigations have utilized functional neuroimaging techniques in normal individuals to address these hypotheses (e.g., Gandour et al., 2000), by far the most data have been gathered in studies of individuals who have suffered brain damage. These investigations allow us to characterize the nature of prosodic deficits that may emerge in neurologically impaired populations. The discussion is divided into affective and linguistic prosodic impairments.

Beginning with deficits in the production and perception of affective prosody, one of the salient speech characteristics of individuals who have suffered RHD is a flat affect. That is, in conjunction with a reduction in emotional expression as reflected in facial expressions, clinical impressions suggest that individuals with RHD tend to produce speech that is reduced, if not devoid, of affect. In fact, based on clinical judgments of the speech of RHD patients with varying sites of lesion, Ross (1981) proposed a classification system for affective impairments, or aprosodias, that paralleled the popular aphasia syndrome classification system of Goodglass and Kaplan (1983). Ross's 1981 classification scheme sparked a good deal of research on affective prosodic deficits that ultimately resulted in its abandonment by the majority of investigators. However, the investigations it catalyzed contributed significantly to our understanding of prosodic impairments; much of the work inspired by Ross's proposal took advantage of increasingly reliable methods such as acoustic analysis of speech. When studying RHD patients in an acute stage, results seemed to support impairments in patients' ability to accurately signal emotions such as happiness, sadness, and anger. However, the majority of investigations of patients who had reached a more chronic stage (i.e., at least 3 months post onset) reported few differences between RHD patients and normal controls in signaling various emotions, as reflected in acoustic measures as well as perceptual judgments. Occasionally, studies have reported affective prosodic impairments in speech production subsequent to LHD (e.g., Cancelliere and Kertesz, 1990), although such findings are far less frequent.

With respect to the perception of affective prosody, early studies again suggested deficits in the processing of emotions cued by vocal signals subsequent to RHD (see Baum and Pell, 1999). Additional investigations have also indicated that LHD patients may exhibit deficits in the perception of affective prosody, particularly when the processing load is heavy (e.g., Tompkins and Flowers, 1985). The finding that both LHD and RHD may yield impairments in prosodic processing led to the proposal that the individual acoustic properties that serve as prosodic cues (i.e., duration, F0, and amplitude) may be processed independently in the two cerebral hemispheres and that patients with RHD and LHD may rely to different degrees on multiple cues (e.g., Van Lancker and Sidtis, 1992).

With regard to linguistic prosody, in keeping with the hypothesized functional lateralization of prosody described earlier (Van Lancker, 1980), numerous investigations have demonstrated that individuals with LHD exhibit impairments in the production of linguistic prosody, particularly at the phonemic level (i.e., in tone languages such as Mandarin, Norwegian, or Thai; e.g., Gandour et al., 1992). Deficits in the ability to signal emphatic stress contrasts, declarative versus interrogative sentence types, and syntactic clause boundaries have also been shown subsequent to LHD (e.g., Danly and Shapiro, 1982), but some studies have shown similar impairments in RHD patients (e.g., Pell, 1999) or have demonstrated that the production of only certain acoustic cues, primarily temporal parameters, is affected in LHD patients (e.g., Baum et al., 1997). The clearest evidence for the role of the left hemisphere in the production of linguistic prosody comes from studies of the phonemic use of tone; while this is arguably the “most linguistic” of the functions of prosody, it is also the smallest unit (i.e., a single syllable) in which prosodic cues may be manifest. It has therefore been suggested that the size or domain of the production unit may play a role in the brain regions implicated in prosodic processing. As an obvious corollary, patients with LHD and RHD may display impairments limited to different domains of prosodic processing.

Impairments in the perception or comprehension of linguistic prosody have also been found in both LHD and RHD patient groups, with varying results depending on the nature of the stimuli or the task. Investigations focusing on the perception of stress cues have mainly reported reduced performance relative to normal by individuals with LHD. For instance, several studies have shown that LHD patients are impaired in the ability to identify phonemic (lexical) and emphatic stress (e.g., Emmorey, 1987). With regard to the perception of linguistic prosodic cues at the phrase or sentence level, both individuals with RHD and LHD have difficulty identifying declarative, interrogative, and imperative sentence types on the basis of prosodic cues alone. LHD but not RHD patients tend to be relatively more impaired in linguistic than affective prosodic perception when direct comparisons are made within a single study (Heilman et al., 1984). Baum and colleagues (1997) have also noted impairments in the perception of phrase boundaries by both LHD and RHD patients. Investigations of individuals with basal ganglia disease due to Parkinson's or Huntington's disease have also reported deficits in the comprehension of prosody (e.g., Blonder, Gur, and Gur, 1989), suggesting that subcortical structures or cortical-subcortical connections are important in prosodic processing. Due to its multiple functions in language, understanding prosodic deficits and the neural substrates implicated in the processing of prosody is clearly a complex task.

Although this article has considered affective and linguistic prosody separately, this represents a somewhat artificial distinction, as they are integrated in natural speech production and perception. A handful of recent investigations have begun to address this integration, with mixed results appearing even in normal individuals (e.g., Pell, 1999). Exploring the integration of affective and linguistic prosody in individuals who have suffered brain damage only compounds the problem and the inconsistencies.

In summary, impairments in the production and perception of speech prosody may emerge subsequent to focal brain damage to numerous cortical and subcortical regions. The precise nature of the deficit may depend in part on the site of the lesion, but it seems to vary along the dimensions of the prosodic functional load (from affective to linguistic), the size or domain of the production or processing unit, and the specific acoustic parameters contributing to the prosodic signal. Prosodic deficits clearly interact with other communicative impairments, including disorders of linguistic and pragmatic processing, contributing to the symptom complexes associated with the aphasias, motor speech disorders, and right hemisphere communication deficits.

See also right hemisphere language and communication functions in adults; right hemisphere language disorders.