Reliability of rating synthesized hypernasal speech signals in connected speech and vowels

A dissertation submitted in partial fulfilment of the requirements for the Bachelor of Science (Speech and Hearing Sciences), The University of Hong Kong, June 30, 2007.Also available in print.Thesis (B.Sc)--University of Hong Kong, 2007.published_or_final_versionSpeech and Hearing SciencesBachelorBachelor of Science in Speech and Hearing Science

Nasalance and nasality in children with cochlear implants and children with hearing aids

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Simulating dysarthric speech for training data augmentation in clinical speech applications

Training machine learning algorithms for speech applications requires large, labeled training data sets. This is problematic for clinical applications where obtaining such data is prohibitively expensive because of privacy concerns or lack of access. As a result, clinical speech applications are typically developed using small data sets with only tens of speakers. In this paper, we propose a method for simulating training data for clinical applications by transforming healthy speech to dysarthric speech using adversarial training. We evaluate the efficacy of our approach using both objective and subjective criteria. We present the transformed samples to five experienced speech-language pathologists (SLPs) and ask them to identify the samples as healthy or dysarthric. The results reveal that the SLPs identify the transformed speech as dysarthric 65% of the time. In a pilot classification experiment, we show that by using the simulated speech samples to balance an existing dataset, the classification accuracy improves by about 10% after data augmentation.Comment: Will appear in Proc. of ICASSP 201

Modeling of oropharyngeal articulatory adaptation to compensate for the acoustic effects of nasalization

Hypernasality is one of the most detrimental speech disturbances that lead to declines of speech intelligibility. Velopharyngeal inadequacy, which is associated with anatomic defects such as cleft palate or neuromuscular disorders that affect velopharygneal function, is the primary cause of hypernasality. A simulation study by Rong and Kuehn [J. Speech Lang. Hear. Res. 55(5), 1438–1448 (2012)] demonstrated that properly adjusted oropharyngeal articulation can reduce nasality for vowels synthesized with an articulatory model [Mermelstein, J. Acoust. Soc. Am. 53(4), 1070–1082 (1973)]. In this study, a speaker-adaptive articulatory model was developed to simulate speaker-customized oropharyngeal articulatory adaptation to compensate for the acoustic effects of nasalization on /a/, /i/, and /u/. The results demonstrated that (1) the oropharyngeal articulatory adaptation effectively counteracted the effects of nasalization on the second lowest formant frequency (F2) and partially compensated for the effects of nasalization on vowel space (e.g., shifting and constriction of vowel space) and (2) the articulatory adaptation strategies generated by the speaker-adaptive model might be more efficacious for counteracting the acoustic effects of nasalization compared to the adaptation strategies generated by the standard articulatory model in Rong and Kuehn. The findings of this study indicated the potential of using oropharyngeal articulatory adaptation as a means to correct maladaptive articulatory behaviors and to reduce nasalit

Clinical and molecular investigation of rare congenital defects of the palate

Cleft palate (CP) affects around 1/1500 live births and, along with cleft lip, is one of the most common forms of birth defect. The studies presented here focus on unusual defects of the palate, especially to understand better the rarely reported but surprisingly common condition called submucous cleft palate (SMCP). The frequency and consequences of SMCP from a surgical perspective were first investigated based on the caseload of the North Thames Cleft Service at Great Ormond Street Hospital and St Andrew's Centre, Broomfield Hospital, Mid Essex Hospitals Trust. It was previously reported that up to 80% of individuals with unrepaired SMCP experience speech difficulties as a consequence of velopharyngeal insufficiency (VPI). Attempted repair of the palatal defect can sometimes give poor results, so controversies still exist about the correct choice of surgical technique to use. Over 23 years, 222 patients at The North Thames Cleft Service underwent operations to manage SMCP. Nearly half of them (42.8%) were diagnosed with 22q11.2 deletion syndrome (22q11.2 DS). The first operation was palate repair, with an exception of one case, followed by a second surgical intervention required in approximately half of the patients. A third procedure to manage VPI was carried out in 6% of patients. To better understand the histological anatomy of the palatal muscles in cleft patients, biopsies were taken from levator veli palatini (LVP) and/or palatopharyngeus (PP) muscles during surgical correction of CP. Muscles were compared from patients with SMCP to those with overt CP and also to controls. The controls consisted of descending PP muscle fibres from healthy children who underwent a tonsillectomy operation for obstructive sleep apnoea or recurrent chronic tonsillitis. Fifty-seven biopsy samples were available from children between 10 months to 9 years of age. Individual biopsy samples were also available from patients with achondroplasia, Apert, Cornelia de Lange and Kabuki syndromes. The study showed a prevalence of fast fibres in both muscles in all CP types. However, in both SMCP LVP and SMCP 22q11.2 DS LVP, this trend was reversed in favour of slow fibres. Single cases with syndromes did not reveal any obvious differences compared to more common cleft types. Mutations in TBX22 are a frequent genetic cause of cleft palate and SMCP. The functional role of the encoded TBX22 transcription factor was investigated in a mouse model with SMCP. Cell lineage-specific fluorescence activated cell sorting of a conditional allele of Tbx22, was used to look at the RNA-Seq transcriptome in developing palatal shelves, with a view to identify downstream target genes. Eleven up regulated genes reached statistical significance after multiple testing correction in cranial mesoderm (CM) derived cells when comparing Tbx22null/Y and WT samples (Cspg4, Foxp2, Reln, Bmpr1b, Adgrb3, Sox6, Zim1, Scarna13, Fat1, Notch3, Peg3). Eleven genes were down regulated in the same comparison (Nr2f2, Lars2, Ahr, Aplnr, Emcn, Npnt, Apln, Ccr2, Tll1, Snord34, Snord99). Comparing Tbx22null/Y and WT in cranial neural crest (CNC) derived cells, only Cxcl14 was up regulated, while Tbx22 was down regulated. Osteoclast differentiation, calcium signalling, focal adhesion, Wnt signalling and cell adhesion molecule pathways were the most enriched pathways in functional annotation of significantly differentially expressed genes analysis. Finally, a family with an unusual velopharyngeal anatomy was investigated in order to determine the likely genetic cause. This involved the implementation of genetic technologies in an autosomal dominant multigeneration Egyptian family with 8 affected individuals who presented with absent uvula, short posterior border of the soft palate and abnormal pillars of the fauces. Using a combination of cytogenetic, linkage analysis and exome sequencing, followed by more detailed segregation and functional analysis, a dominantly acting missense mutation in the activation domain of FOXF2 was revealed. This variant was found to co-segregate with a copy number variant of unknown significance that could not at this stage be causally distinguished from the point mutation

Beyond motor neurons: expanding the clinical spectrum in Kennedy's disease

Kennedy's disease, or spinal and bulbar muscular atrophy (SBMA), is an X-linked neuromuscular condition clinically characterised by weakness, atrophy and fasciculations of the limb and bulbar muscles, as a result of lower motor neuron degeneration. The disease is caused by an abnormally expanded triplet repeat expansions in the ubiquitously expressed androgen receptor gene, through mechanisms which are not entirely elucidated. Over the years studies from both humans and animal models have highlighted the involvement of cell populations other than motor neurons in SBMA, widening the disease phenotype. The most compelling aspect of these findings is their potential for therapeutic impact: muscle, for example, which is primarily affected in the disease, has been recently shown to represent a valid alternative target for therapy to motor neurons. In this review, we discuss the emerging study of the extra-motor neuron involvement in SBMA, which, besides increasingly pointing towards a multidisciplinary approach for affected patients, deepens our understanding of the pathogenic mechanisms and holds potential for providing new therapeutic targets for this disease

A feasibility study of visual feedback speech therapy for nasal speech associated with velopharyngeal dysfunction

Nasal speech associated with velopharyngeal dysfunction (VPD) is seen in children and adults with cleft palate and other conditions that affect soft palate function, with negative effects on quality of life. Treatment options include surgery and prosthetics depending on the nature of the problem. Speech therapy is rarely offered as an alternative treatment as evidence from previous studies is weak. However there is evidence that visual biofeedback approaches are beneficial in other speech disorders and that this approach could benefit individuals with nasal speech who demonstrate potential for improved speech. Theories of learning and feedback also lend support to the view that a combined feedback approach would be most suitable. This feasibility study therefore aimed to develop and evaluate Visual Feedback Therapy (VFTh), a new behavioural speech therapy intervention, incorporating speech activities supported by visual biofeedback and performance feedback, for individuals with mild to moderate nasal speech. Evaluation included perceptual, instrumental and quality of life measures. Eighteen individuals with nasal speech were recruited from a regional cleft palate centre and twelve completed the study, six female and six male, eleven children (7 to 13 years) and one adult, (43 years). Six participants had repaired cleft palate and six had VPD but no cleft. Participants received 8 sessions of VFTh from one therapist. The findings suggest that that the intervention is feasible but some changes are required, including participant screening for adverse response and minimising disruptions to intervention scheduling. In blinded evaluation there was considerable variation in individual results but positive changes occurred in at least one speech symptom between pre and post-intervention assessment for eight participants. Seven participants also showed improved nasalance scores and seven had improved quality of life scores. This small study has provided important information about the feasibility of delivering and evaluating VFTh. It suggests that VFTh shows promise as an alternative treatment option for nasal speech but that further preliminary development and evaluation is required before larger scale research is indicated