Speech perception, rapid temporal processing, and the left hemisphere: A case study of unilateral pure word deafness☆

Abstract

The mechanisms and functional anatomy underlying the early stages of speech perception are still not well understood. One way to investigate the cognitive and neural underpinnings of speech perception is by investigating patients with speech perception deficits but with preserved ability in other domains of language. One such case is reported here: patient NL shows highly impaired speech perception despite normal hearing ability and preserved semantic knowledge, speaking, and reading ability, and is thus classified as a case of pure word deafness (PWD). NL has a left temporoparietal lesion without right hemisphere damage and DTI imaging suggests that he has preserved cross-hemispheric connectivity, arguing against an account of PWD as a disconnection of left lateralized language areas from auditory input. Two experiments investigated whether NL’s speech perception deficit could instead result from an underlying problem with rapid temporal processing. Experiment 1 showed that NL has particular difficulty discriminating sounds that differ in terms of rapid temporal changes, be they speech or non-speech sounds. Experiment 2 employed an intensive training program designed to improve rapid temporal processing in language impaired children (Fast ForWord; Scientific Learning Corporation, Oakland, CA) and found that NL was able to improve his ability to discriminate rapid temporal differences in non-speech sounds, but not in speech sounds. Overall, these data suggest that patients with unilateral PWD may, in fact, have a deficit in (left lateralized) temporal processing ability, however they also show that a rapid temporal processing deficit is, by itself, unable to account for this patient’s speech perception deficit.

Auditory agnosia

“…SHELL underlying problems with sound analysis (Goldstein, 1974;Buchtel and Stewart, 1989;Griffiths et al, 1999;Griffiths, 2002). Still, while considerable work argues that auditory agnosia (and its subtypes) may indeed reflect relatively basic problems perceiving and/or analyzing sound patterns (e.g., Albert and Bear, 1974;Buchtel and Stewart, 1989;Phillips and Farmer, 1990;Poeppel, 2001;Vignolo, 2003;Stefanatos, 2008;Slevc et al, 2011), there are cases that seem better characterized as associative deficits (e.g., Franklin et al, 1996;Saygin et al, 2010). This apperceptive/associative distinction might thus be expected to link different forms of auditory agnosia to different anatomic etiologies (e.g., Buchtel and Stewart, 1989;Goll et al, 2010b).…”

“…This is, critically, distinct from posterior (sensory) aphasia in that other domains of linguistic processing, including reading, writing, and speaking, are relatively intact, although agnosia is often still accompanied by some degree of aphasic symptoms (for reviews, see Goldstein, 1974;Buchman et al, 1986;Poeppel, 2001;Badecker, 2005;Stefanatos et al, 2005b). Verbal auditory agnosia often evolves from Wernicke's aphasia, in that paraphasias and reading and writing deficits resolve without corresponding improvement of speech perception and repetition (e.g., Albert and Bear, 1974;Slevc et al, 2011). The term pure word deafness is somewhat misleading as the syndrome does not typically seem to be an agnosia for words per se, but rather agnosia for speech sounds.…”

“…Indeed, verbal auditory agnosia typically results from bilateral temporal lesions in the superior temporal cortex (or subcortically, affecting the relevant projecting auditory radiations; see Chapter 1, Fig. 1.9): of 63 reports with sufficiently detailed lesion data (Wang et al, 2000;J€ orgens et al, 2008;Slevc et al, 2011; and earlier cases reviewed by Poeppel, 2001), 43, or almost 70%, involve bilateral lesions. Patients with verbal auditory agnosia are aware of speech but describe it as sounding like a foreign language (Albert and Bear, 1974), as distorted and cartoonlike (Wee and Menard, 1999), as rapidly fading (Klein and Harper, 1956), or with descriptions like "voice comes but no words" (Hemphill and Stengel, 1940).…”

“…Speech production in verbal auditory agnosia is relatively normal (Table 32.1), although in some cases production is overly loud and has abnormal prosody (e.g., Otsuki et al, 1998;J€ orgens et al, 2008). Speech perception is typically improved by relying on cross-modal information such as lip reading and from "top-down" contextual information (e.g., Saffran et al, 1976;Coslett et al, 1984;Buchtel and Stewart, 1989;Slevc et al, 2011;Robson et al, 2012). Perception is also sometimes improved by dramatically slowing the speech signal (Albert and Bear, 1974;Stefanatos et al, 2005a), perhaps by ameliorating some patients' particular difficulty with rapid temporal aspects of the speech signal (see below).…”

“…Whereas cortically deaf patients typically behave as if they were deaf (despite normal peripheral hearing and brainstem evoked potentials), patients with auditory agnosia are aware of sounds but have difficulty with sound identification. Auditory agnosia is also distinct from language perception deficits associated with the posterior (sensory) aphasias, although both cortical deafness and sensory aphasia can evolve into auditory agnosia (e.g., Mendez and Geehan, 1988;Slevc et al, 2011).…”