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  • Title: [Prosodic disorders in neurologic diseases--a review of the literature].
    Author: Ackermann H, Hertrich I, Ziegler W.
    Journal: Fortschr Neurol Psychiatr; 1993 Jul; 61(7):241-53. PubMed ID: 7690005.
    Abstract:
    The prosodic quality of speech comprises intonation, accent pattern, and rhythm. Among others, these dimensions contribute to the linguistic structure of an utterance and subserve emotional behaviour. Both cortical and subcortical dysfunctions can give rise to impaired speech prosody. The present paper reviews the clinical and linguistic features of the various dys- and aprosodic syndromes as well as their neuroanatomic substrates. 1. Sporadically, lesions of the left hemisphere present with dysprosody in terms of a "foreign accent". In most instances this syndrome seems to be due to apraxia of speech. 2. Some authors consider dysprosodic speech a characteristic feature of Broca's aphasia. The dysprosody of these patients predominantly reflects disturbed temporal organisation of speech utterances. Altered intonation contours, presumably, result from disordered sentence planning rather than from deficits of pitch processing. Wernicke aphasics may show increased variability of intonational patterns. 3. Impaired discrimination and identification of affective prosody has been observed in patients with temporoparietal lesion of the right hemisphere ("auditory affective agnosia"). With respect to linguistic prosody, controversial findings are reported on. Besides pitch extraction from acoustic signals the right hemisphere seems to provide categorical representations of emotional behaviour required for the "interpretation" of perceived intonation. 4. Damage to the right hemisphere can give rise to monotonous speech devoid of affective modulation ("motor aprosodia"). It is unsettled to which extent linguistic suprasegmental features are also distorted. The available data indicate an underlying dysfunction of basal ganglia loops and/or transcallosal projections. 5. Both Parkinson's and Huntington's disease may present with reduced prosodic modulation of speech. Probably, these deficits reflect disordered motor control of articulatory and phonatory functions. At least with respect to Parkinsonian patients perceptual and acoustic studies have so far failed to provide sufficient evidence of impaired prosodic planning.
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