Speech Intensity Response to Altered Intensity Feedback in Individuals With Parkinson's Disease

Author(s):  
Anita Senthinathan ◽  
Scott Adams ◽  
Allyson D. Page ◽  
Mandar Jog

Purpose Hypophonia (low speech intensity) is the most common speech symptom experienced by individuals with Parkinson's disease (IWPD). Previous research suggests that, in IWPD, there may be abnormal integration of sensory information for motor production of speech intensity. In the current study, intensity of auditory feedback was systematically manipulated (altered in both positive and negative directions) during sensorimotor conditions that are known to modulate speech intensity in everyday contexts in order to better understand the role of auditory feedback for speech intensity regulation. Method Twenty-six IWPD and 24 neurologically healthy controls were asked to complete the following tasks: converse with the experimenter, start vowel production, and read sentences at a comfortable loudness, while hearing their own speech intensity randomly altered. Altered intensity feedback conditions included 5-, 10-, and 15-dB reductions and increases in the feedback intensity. Speech tasks were completed in no noise and in background noise. Results IWPD displayed a reduced response to the altered intensity feedback compared to control participants. This reduced response was most apparent when participants were speaking in background noise. Specific task-based differences in responses were observed such that the reduced response by IWPD was most pronounced during the conversation task. Conclusions The current study suggests that IWPD have abnormal processing of auditory information for speech intensity regulation, and this disruption particularly impacts their ability to regulate speech intensity in the context of speech tasks with clear communicative goals (i.e., conversational speech) and speaking in background noise.

2011 ◽  
Vol 42 (01) ◽  
Author(s):  
J. Pohlmann ◽  
A. Sprenger ◽  
C. Helmchen

2016 ◽  
Vol 23 (24) ◽  
pp. 2666-2679 ◽  
Author(s):  
Félix Jiménez-Jiménez ◽  
Hortensia Alonso-Navarro ◽  
María Herrero ◽  
Elena García-Martín ◽  
José Agúndez

2019 ◽  
Vol 26 (20) ◽  
pp. 3719-3753 ◽  
Author(s):  
Natasa Kustrimovic ◽  
Franca Marino ◽  
Marco Cosentino

:Parkinson’s disease (PD) is the second most common neurodegenerative disorder among elderly population, characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, exact cause remains unknown and the mechanism of neurons death uncertain. It is typically considered as a disease of central nervous system (CNS). Nevertheless, numerous evidence has been accumulated in several past years testifying undoubtedly about the principal role of neuroinflammation in progression of PD. Neuroinflammation is mainly associated with presence of activated microglia in brain and elevated levels of cytokine levels in CNS. Nevertheless, active participation of immune system as well has been noted, such as, elevated levels of cytokine levels in blood, the presence of auto antibodies, and the infiltration of T cell in CNS. Moreover, infiltration and reactivation of those T cells could exacerbate neuroinflammation to greater neurotoxic levels. Hence, peripheral inflammation is able to prime microglia into pro-inflammatory phenotype, which can trigger stronger response in CNS further perpetuating the on-going neurodegenerative process.:In the present review, the interplay between neuroinflammation and the peripheral immune response in the pathobiology of PD will be discussed. First of all, an overview of regulation of microglial activation and neuroinflammation is summarized and discussed. Afterwards, we try to collectively analyze changes that occurs in peripheral immune system of PD patients, suggesting that these peripheral immune challenges can exacerbate the process of neuroinflammation and hence the symptoms of the disease. In the end, we summarize some of proposed immunotherapies for treatment of PD.


2020 ◽  
Vol 25 (42) ◽  
pp. 4510-4522 ◽  
Author(s):  
Biancamaria Longoni ◽  
Irene Fasciani ◽  
Shivakumar Kolachalam ◽  
Ilaria Pietrantoni ◽  
Francesco Marampon ◽  
...  

: Exosomes are extracellular vesicles produced by eukaryotic cells that are also found in most biological fluids and tissues. While they were initially thought to act as compartments for removal of cellular debris, they are now recognized as important tools for cell-to-cell communication and for the transfer of pathogens between the cells. They have attracted particular interest in neurodegenerative diseases for their potential role in transferring prion-like proteins between neurons, and in Parkinson’s disease (PD), they have been shown to spread oligomers of α-synuclein in the brain accelerating the progression of this pathology. A potential neuroprotective role of exosomes has also been equally proposed in PD as they could limit the toxicity of α-synuclein by clearing them out of the cells. Exosomes have also attracted considerable attention for use as drug vehicles. Being nonimmunogenic in nature, they provide an unprecedented opportunity to enhance the delivery of incorporated drugs to target cells. In this review, we discuss current knowledge about the potential neurotoxic and neuroprotective role of exosomes and their potential application as drug delivery systems in PD.


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