Abstract
As an example of complex auditory signal processing, the analysis of accented speech is potentially vulnerable in the progressive aphasias. However, the brain basis of accent processing and the effects of neurodegenerative disease on this processing are not well understood. Here we undertook a detailed neuropsychological study of a patient, AA with progressive nonfluent aphasia, in whom agnosia for accents was a prominent clinical feature. We designed a battery to assess AA's ability to process accents in relation to other complex auditory signals. AA's performance was compared with a cohort of 12 healthy age and gender matched control participants and with a second patient, PA, who had semantic dementia with phonagnosia and prosopagnosia but no reported difficulties with accent processing. Relative to healthy controls, the patients showed distinct profiles of accent agnosia. AA showed markedly impaired ability to distinguish change in an individual's accent despite being able to discriminate phonemes and voices (apperceptive accent agnosia); and in addition, a severe deficit of accent identification. In contrast, PA was able to perceive changes in accents, phonemes and voices normally, but showed a relatively mild deficit of accent identification (associative accent agnosia). Both patients showed deficits of voice and environmental sound identification, however PA showed an additional deficit of face identification whereas AA was able to identify (though not name) faces normally. These profiles suggest that AA has conjoint (or interacting) deficits involving both apperceptive and semantic processing of accents, while PA has a primary semantic (associative) deficit affecting accents along with other kinds of auditory objects and extending beyond the auditory modality. Brain MRI revealed left peri-Sylvian atrophy in case AA and relatively focal asymmetric (predominantly right sided) temporal lobe atrophy in case PA. These cases provide further evidence for the fractionation of brain mechanisms for complex sound analysis, and for the stratification of progressive aphasia syndromes according to the signature of nonverbal auditory deficits they produce.
Highlights
The progressive aphasias (PPA) are a diverse group of neurodegenerative syndromes with characteristic clinico-anatomical signatures and heterogeneous histopathology (Mesulam, 1982; GornoTempini et al, 2008, 2011)
AA showed markedly impaired perception of changes in accents despite intact perception of changes in phonemes and voices; in addition, she showed a severe deficit of accent identification
PA was able to perceive changes in accents, phonemes and voices normally, but showed a relatively mild deficit of accent identification; and while both patients showed deficits of voice and environmental sound identification, AA was able to identify faces normally, whereas PA showed an additional deficit of face identification
Summary
The progressive aphasias (PPA) are a diverse group of neurodegenerative syndromes with characteristic clinico-anatomical signatures and heterogeneous histopathology (Mesulam, 1982; GornoTempini et al, 2008, 2011). Accent modifies the acoustic properties of spoken phonemes, interacting with individual vocal characteristics and prosody (Boula de Mareuil & Vieru-Dimulescu, 2006; Clopper & Pisoni, 2004; Howell, Barry, & Vinson, 2006); if spoken phonemes are regarded as auditory objects (Griffiths & Warren, 2004), a phoneme spoken in a non-native accent could be considered as a non-canonical ‘view’ of the phoneme for a particular listener, and should engage auditory apperceptive processing Both recognition of non-native accents and comprehension of words spoken with less familiar accents have been shown to be impaired in patients with PNFA, in keeping with conjoint semantic and apperceptive deficits of accent processing in this PPA syndrome (Hailstone et al, 2012). AA's performance on apperceptive and semantic analysis of accents, voices, speech and environmental sounds was assessed using a novel neuropsychological battery and compared with the performance of healthy control participants and another patient, PA, with a syndrome of SD characterised by progressive anomia, prosopagnosia and phonagnosia, but no reported difficulties with accent processing
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