- Association between Olfactory Deficit and Motor and Cognitive Function in Parkinson’s Disease
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Han Soo Yoo, Seok Jong Chung, Yang Hyun Lee, Byoung Seok Ye, Young H. Sohn, Phil Hyu Lee
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J Mov Disord. 2020;13(2):133-141. Published online April 6, 2020
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DOI: https://doi.org/10.14802/jmd.19082
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Abstract
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- Objective
To investigate whether baseline olfactory dysfunction in Parkinson’s disease (PD) patients is associated with baseline and longitudinal motor and cognitive function.
Methods We recruited 228 drug-naïve PD patients who were followed for a mean of 6 years. Patients underwent the Cross-Cultural Smell Identification Test (CCSIT), a neuropsychological test, and N-(3-[18F]fluoropropyl)-2β-carbomethoxy-3β-(4-iodophenyl) nortropane positron emission tomography within 6 months of the baseline evaluation. Olfactory dysfunction was categorized as normosmia (CCSIT score ≥ 9), hyposmia (CCSIT score 5–8), and anosmia (CCSIT score ≤ 4). During the follow-up period, we investigated changes in the levodopa-equivalent dose (LED) and the occurrence of wearing-off, levodopa-induced dyskinesia, and dementia.
Results Among the PD patients, 80.7% were hyposmic at the time of diagnosis, and 26.1% were anosmic. Baseline olfactory dysfunction was not associated with either initial parkinsonian motor symptoms or with the longitudinal LED increment and motor complications. Meanwhile, the anosmic group had lower baseline scores on the Korea version of the Boston Naming Test and Stroop color reading test than the normosmic and hyposmic groups. The anosmic group exhibited a higher rate of conversion to dementia than the normosmic [adjusted hazard ratio (HR) 3.99, 95% confidence interval (CI) 1.08–14.72] and hyposmic (adjusted HR 2.48, 95% CI 1.15–5.32) PD groups, regardless of baseline motor deficits and cognitive status.
Conclusion Baseline olfactory dysfunction was not associated with motor deficits and complications, but it was associated with cognitive dysfunction and prognosis, suggesting that severe olfactory impairment may reflect early cortical involvement, probably in the frontotemporal region, and rapid spreading of Lewy body pathology.
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- Olfactory Dysfunction in Parkinson’s Disease, Its Functional and Neuroanatomical Correlates
Gabriel Torres-Pasillas, Donají Chi-Castañeda, Porfirio Carrillo-Castilla, Gerardo Marín, María Elena Hernández-Aguilar, Gonzalo Emiliano Aranda-Abreu, Jorge Manzo, Luis I. García NeuroSci.2023; 4(2): 134. CrossRef - Impact of deep brain stimulation (DBS) on olfaction in Parkinson's disease: Clinical features and functional hypotheses
G. Brand, C. Bontempi, L. Jacquot Revue Neurologique.2023;[Epub] CrossRef - Sequential change in olfaction and (non) motor symptoms: the difference between anosmia and non-anosmia in Parkinson’s disease
Ting-Chun Fang, Yu-Shan Tsai, Ming-Hong Chang Frontiers in Aging Neuroscience.2023;[Epub] CrossRef - Traumatic brain injury-induced inflammatory changes in the olfactory bulb disrupt neuronal networks leading to olfactory dysfunction
Xiang Liu, Zhuofan Lei, Dylan Gilhooly, Junyun He, Yun Li, Rodney M. Ritzel, Hui Li, Long-Jun Wu, Shaolin Liu, Junfang Wu Brain, Behavior, and Immunity.2023; 114: 22. CrossRef - Olfactory dysfunction is associated with motor function only in tremor-dominant Parkinson’s disease
Fardin Nabizadeh, Kasra Pirahesh, Elham Khalili Neurological Sciences.2022; 43(7): 4193. CrossRef - Novel diagnostic tools for identifying cognitive impairment using olfactory-stimulated functional near-infrared spectroscopy: patient-level, single-group, diagnostic trial
Jaewon Kim, Dong Keon Yon, Kyu Yeong Choi, Jang Jae Lee, Namwoo Kim, Kun Ho Lee, Jae Gwan Kim Alzheimer's Research & Therapy.2022;[Epub] CrossRef - The Role of Olfactory System in the Etiogenesis of Parkinson’s Diseases: An Overview
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Zara M. Patel, Eric H. Holbrook, Justin H. Turner, Nithin D. Adappa, Mark W. Albers, Aytug Altundag, Simone Appenzeller, Richard M. Costanzo, Ilona Croy, Greg E. Davis, Puya Dehgani‐Mobaraki, Richard L. Doty, Valerie B. Duffy, Bradley J. Goldstein, David International Forum of Allergy & Rhinology.2022; 12(4): 327. CrossRef - Does Olfactory Dysfunction Correlate with Disease Progression in Parkinson’s Disease? A Systematic Review of the Current Literature
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- Heterogeneous Patterns of Striatal Dopamine Loss in Patients with Young- versus Old-Onset Parkinson’s Disease: Impact on Clinical Features
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Seok Jong Chung, Han Soo Yoo, Yang Hyun Lee, Phil Hyu Lee, Young H. Sohn
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J Mov Disord. 2019;12(2):113-119. Published online May 30, 2019
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DOI: https://doi.org/10.14802/jmd.18064
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6,768
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- Objective
Ample evidence has suggested that age at onset of Parkinson’s disease (PD) is associated with heterogeneous clinical features in individuals. We hypothesized that this may be attributed to different patterns of nigrostriatal dopamine loss.
Methods A total of 205 consecutive patients with de novo PD who underwent 18F-FP-CIT PET scans (mean follow-up duration, 6.31 years) were divided into three tertile groups according to their age at onset of parkinsonian motor symptoms. Striatal dopamine transporter (DAT) availability was compared between the old- (n = 73) and young-onset (n = 66) groups. In addition, the risk of developing freezing of gait (FOG) and longitudinal requirements for dopaminergic medications were examined.
Results The old-onset PD group (mean age at onset, 72.66 years) exhibited more severe parkinsonian motor signs than the young-onset group (52.58 years), despite comparable DAT availability in the posterior putamen; moreover, the old-onset group exhibited more severely decreased DAT availability in the caudate than the young-onset group. A Cox regression model revealed that the old-onset PD group had a higher risk for developing FOG than the young-onset group [hazard ratio 2.523, 95% confidence interval (1.239–5.140)]. The old-onset group required higher doses of dopaminergic medications for symptom control than the young-onset group over time.
Conclusion The present study demonstrated that the old-onset PD group exhibited more severe dopamine loss in the caudate and were more likely to develop gait freezing, suggesting that age at onset may be one of the major determinants of the pattern of striatal dopamine depletion and progression of gait disturbance in PD.
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