A model for the assessment of eating problems in patients with Parkinson's disease

1987 ◽  
Vol 12 (4) ◽  
pp. 473-481 ◽  
Author(s):  
Astrid Norberg ◽  
Elsy Athlin ◽  
Bengt Winblad
Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2109
Author(s):  
Petter Fagerberg ◽  
Lisa Klingelhoefer ◽  
Matteo Bottai ◽  
Billy Langlet ◽  
Konstantinos Kyritsis ◽  
...  

Unintentional weight loss has been observed among Parkinson’s disease (PD) patients. Changes in energy intake (EI) and eating behavior, potentially caused by fine motor dysfunction and eating-related symptoms, might contribute to this. The primary aim of this study was to investigate differences in objectively measured EI between groups of healthy controls (HC), early (ESPD) and advanced stage PD patients (ASPD) during a standardized lunch in a clinical setting. The secondary aim was to identify clinical features and eating behavior abnormalities that explain EI differences. All participants (n = 23 HC, n = 20 ESPD, and n = 21 ASPD) went through clinical evaluations and were eating a standardized meal (200 g sausages, 400 g potato salad, 200 g apple purée and 500 mL water) in front of two video cameras. Participants ate freely, and the food was weighed pre- and post-meal to calculate EI (kcal). Multiple linear regression was used to explain group differences in EI. ASPD had a significantly lower EI vs. HC (−162 kcal, p < 0.05) and vs. ESPD (−203 kcal, p < 0.01) when controlling for sex. The number of spoonfuls, eating problems, dysphagia and upper extremity tremor could explain most (86%) of the lower EI vs. HC, while the first three could explain ~50% vs. ESPD. Food component intake analysis revealed significantly lower potato salad and sausage intakes among ASPD vs. both HC and ESPD, while water intake was lower vs. HC. EI is an important clinical target for PD patients with an increased risk of weight loss. Our results suggest that interventions targeting upper extremity tremor, spoonfuls, dysphagia and eating problems might be clinically useful in the prevention of unintentional weight loss in PD. Since EI was lower in ASPD, EI might be a useful marker of disease progression in PD.


Author(s):  
Nuriye Yıldırım Gökay ◽  
Bülent Gündüz ◽  
Fatih Söke ◽  
Recep Karamert

Purpose The effects of neurological diseases on the auditory system have been a notable issue for investigators because the auditory pathway is closely associated with neural systems. The purposes of this study are to evaluate the efferent auditory system function and hearing quality in Parkinson's disease (PD) and to compare the findings with age-matched individuals without PD to present a perspective on aging. Method The study included 35 individuals with PD (mean age of 48.50 ± 8.00 years) and 35 normal-hearing peers (mean age of 49 ± 10 years). The following tests were administered for all participants: the first section of the Speech, Spatial and Qualities of Hearing Scale; pure-tone audiometry, speech audiometry, tympanometry, and acoustic reflexes; and distortion product otoacoustic emissions (DPOAEs) and contralateral suppression of DPOAEs. SPSS Version 25 was used for statistical analyses, and values of p < .05 were considered statistically significant. Results There were no statistically significant differences in the pure-tone audiometry thresholds and DPOAE responses between the individuals with PD and their normal-hearing peers ( p = .732). However, statistically significant differences were found between the groups in suppression levels of DPOAEs and hearing quality ( p < .05). In addition, a statistically significant and positive correlation was found between the amount of suppression at some frequencies and the Speech, Spatial and Qualities of Hearing Scale scores. Conclusions This study indicates that medial olivocochlear efferent system function and the hearing quality of individuals with PD were affected adversely due to the results of PD pathophysiology on the hearing system. For optimal intervention and follow-up, tasks related to hearing quality in daily life can also be added to therapies for PD.


2004 ◽  
Vol 9 (2) ◽  
pp. 10-13
Author(s):  
Linda Worrall ◽  
Jennifer Egan ◽  
Dorothea Oxenham ◽  
Felicity Stewart

2007 ◽  
Vol 12 (1) ◽  
pp. 2-11
Author(s):  
Lorraine Ramig ◽  
Cynthia Fox

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