Relation between speech perception and speech production impairment in children with developmental dysphasia

Contralateral masking of transient-evoked otoacoustic emissions is a phenomenon that suggests an inhibitory effect of the olivocochlear efferent auditory pathway. Many studies have been inconclusive in demonstrating a clear connection between this system and a behavioral speech-in-noise listening skill. The purpose of this study was to investigate the activation of a medial olivocochlear (MOC) efferent in children with poor speech-in-noise (PSIN) performance and children with language impairment and PSIN (SLI + PSIN).

Transient evoked otoacoustic emissions (TEOAEs) with and without contralateral white noise were tested in 52 children (between 6 and 12 years). These children were arranged in three groups: typical development (TD) (n = 25), PSIN (n = 14) and SLI + PSI (n = 13).

PSIN and SLI + PSI groups presented reduced otoacoustic emission suppression in comparison with the TD group.

Our finding suggests differences in MOC function among children with typical development and children with poor SIN and language problems.

McArthur and Bishop (2004) found that people with specific language impairment (SLI) up to 14 years of age have poor behavioural frequency discrimination (FD) thresholds for 25-ms pure tones, while people with SLI upto 20 years of age have abnormal auditory N1–P2–N2 event-related potential (ERP) responses to the same tones. In the present study, we extended these findings to more complex non-speech and speech sounds by comparing younger (around 13 years) and older (around 17 years) teenagers with SLI and controls for their behavioural FD thresholds and N1–P2 ERPs to 25 and 250-ms pure tones, vowels, and non-harmonic complex tones. We found that a subgroup of people with SLI had abnormal responses to tones and vowels at the level of behaviour and the brain, and that poor processing was associated with the spectral complexity of auditory stimuli rather than their phonetic significance. We suggest that both the age of listeners and the sensitivity of psychoacoustic tasks to age-related changes in auditory skills may be crucial factors in studies of sound processing in SLI.

Specific Language Impairment (SLI) has been explained by two broad classes of hypotheses, which posit either a deficit specific to grammar, or a non-linguistic processing impairment. Here we advance an alternative perspective. According to the Procedural Deficit Hypothesis (PDH), SLI can be largely explained by the abnormal development of brain structures that constitute the procedural memory system. This system, which is composed of a network of interconnected structures rooted in frontal/basal-ganglia circuits, subserves the learning and execution of motor and cognitive skills. Crucially, recent evidence also implicates this system in important aspects of grammar. The PDH posits that a significant proportion of individuals with SLI suffer from abnormalities of this brain network, leading to impairments of the linguistic and non-linguistic functions that depend on it. In contrast, functions such as lexical and declarative memory, which depend on other brain structures, are expected to remain largely spared. Evidence from an in-depth retrospective examination of the literature is presented. It is argued that the data support the predictions of the PDH, and particularly implicate Broca's area within frontal cortex, and the caudate nucleus within the basal ganglia. Finally, broader implications are discussed, and predictions for future research are presented. It is argued that the PDH forms the basis of a novel and potentially productive perspective on SLI.

Research is reviewed concerning the performance of several neurological groups on the perception and production of voicing contrasts in speech. Patients with cerebellar damage, Parkinson's disease, specific language impairment, Broca's aphasia, apraxia, and Wernicke's aphasia have been reported to be impaired in the perception and articulation of voicing. The types of deficits manifested by these neurologically impaired groups in creating and discriminating voicing contrasts are discussed and the respective contributions of separate neural areas are identified. A model is presented specifying the level of phonemic processing thought to be impaired for each patient group and critical tests of the model's predictions are identified.

This article offers a developmental theory of language and the neural systems that lead to and subserve linguistic capabilities. Early perceptual experience and discontinuities in linguistic development suggest that language develops in four phases that occur in a fixed, interdependent sequence. In each phase of language, a unique ontogenetic function is accomplished. These functions have proprietary neural systems that vary in their degree of specialization. Of particular interest is an analytical mechanism that is responsible for linguistic grammar. This mechanism is time-locked and can only be turned on in the third phase. Confirming evidence is provided by children who are delayed in the second phase of the language learning process. These children store insufficient lexical material to activate their analytic mechanism. Inactivation behaves like damage, shifting language functions to homologous mechanisms in the nondominant hemisphere, thereby increasing functional and anatomical symmetry across the hemispheres. This atypical assembly of neurolinguistic resources produces functional but imperfect command of spoken language and may complicate learning of written language. The theory thus offers a different role for genetics and early experience, and a different interpretation of neuroanatomic findings, from those entertained in most other proposals on developmental language disorders.