Objectives: The physiological manifestations of Parkinson disease are heterogeneous, as evidenced by disease subtypes. Dysphonia has been well documented as an early and progressively significant impairment associated with the disease. The purpose of this study was to investigate how acoustic and aerodynamic measures of vocal function were affected by Parkinson tremor subtype (phenotype) in an effort to better understand the heterogeneity of voice impairment severity in Parkinson disease.
Study Design: This is a prospective case-control study.
Methods: Thirty-two speakers with Parkinson disease assigned to tremor and nontremor phenotypes and 10 healthy controls were recruited. Sustained vowels and connected speech were recorded from each speaker. Acoustic measures of cepstral peak prominence (CPP) and aerodynamic measures of transglottal airflow (TAF) were calculated from the recorded acoustic and aerodynamic waveforms.
Results: Speakers with a nontremor dominant phenotype exhibited significantly (P < 0.05) lower CPP and higher TAF in vowels compared with the tremor dominant phenotype and control speakers, who were not different from each other. No significant group differences were observed for CPP or TAF in connected speech.
Conclusions: When producing vowels, participants with nontremor dominant phenotype exhibited reduced phonation periodicity and elevated TAF compared with tremor dominant and control participants. This finding is consistent with differential limb-motor and cognitive impairments between tremor and nontremor phenotypes reported in the extant literature. Results suggest that sustained vowel production may be sensitive to phonatory control as a function of Parkinson tremor phenotype in mild to moderate stages of the disease.
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http://dx.doi.org/10.1016/j.jvoice.2018.01.016 | DOI Listing |
Rev Neurol (Paris)
December 2024
Department of Neurology, Inselspital, University Hospital Bern, University of Bern, Bern, Switzerland.
Introduction: Neuropsychiatric symptoms are highly prevalent in Parkinson's disease (PD) and significantly affect the quality of life of patients and their significant others. The aim of this work is to describe typical neuropsychiatric symptoms and their treatment.
Methods: This is a narrative opinion paper, illustrated by a fictional case report.
Neurobiol Dis
December 2024
Department of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine Hannover, Bünteweg 17, 30559 Hannover, Germany. Electronic address:
Increasing evidence points to infectious diseases as contributor to the pathogenesis of neurodegeneration in Parkinson's disease (PD), probably driven by a peripheral and CNS inflammatory response together with alpha-synuclein (aSyn) pathology. Pro-inflammatory lipopolysaccharide (LPS) endotoxin is suggested as a risk factor, and LPS shedding gram-negative bacteria are more prevalent in the gut-microbiome of PD patients. Here, we investigated whether LPS could contribute to the neurodegenerative disease progression via neuroinflammation, especially under conditions of aSyn pathology.
View Article and Find Full Text PDFBrain Res
December 2024
Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, São Paulo, Brazil.
Numerous studies have explored the role of cannabinoids in neurological conditions, chronic pain and neurodegenerative diseases. Restoring autophagy has been proposed as a potential target for the treatment of neurodegenerative diseases. In our study, we used a neuroblastoma cell line that overexpresses wild-type α-synuclein to investigate the effects of cannabidiol on autophagy modulation and reduction in the level of cytosolic α-synuclein.
View Article and Find Full Text PDFComput Biol Med
December 2024
School of Engineering, RMIT University, Victoria, Australia. Electronic address:
Background: Changes in voice are a symptom of Parkinson's disease and used to assess the progression of the condition. However, natural differences in the voices of people can make this challenging. Computerized binary speech classification can identify people with PD (PwPD), but its multiclass application to detect the severity of the disease remains difficult.
View Article and Find Full Text PDFActa Neuropathol Commun
December 2024
Department of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.
Mitochondrial dysfunction and α-synuclein (αSyn) aggregation are key contributors to Parkinson's Disease (PD). While genetic and environmental risk factors, including mutations in mitochondrial-associated genes, are implicated in PD, the precise mechanisms linking mitochondrial defects to αSyn pathology remain incompletely understood, hindering the development of effective therapeutic interventions. Here, we identify the loss of branched chain ketoacid dehydrogenase kinase (BCKDK) as a mitochondrial risk factor that exacerbates αSyn pathology by disrupting Complex I function.
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