Parkinsonism & related disorders · 2014
Cognitive and cortical thinning patterns of subjective cognitive decline in patients with and without Parkinson's disease.
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Hong Jin Yong, Yun Hyuk Jin, Sunwoo Mun Kyung, Ham Jee Hyun, Lee Jong-Min, Sohn Young H, Lee Phil Hyu
Аннотация
BACKGROUND: Subjective cognitive decline (SCD) has gained attention as a predictor of future cognitive decline in neurodegenerative diseases. Based on the hypothesis that different pathologies may distinctly contribute to SCD, we investigated the cognitive profiles and cortical thickness of patients with SCD, with and without Parkinson's disease (PD).
METHODS: In total, 96 patients experiencing SCD were classified as having PD (SCD-PD(+), n = 49) or no neurological disease (SCD-PD(-), n = 47); cognitively normal subjects without SCD (n = 23) were included as controls. Neurocognitive profiles and cortical thickness were examined using standardized neuropsychological tests and magnetic resonance imaging-based analysis.
RESULTS: No significant differences in demographic characteristics were found among the three groups. Neuropsychological tests demonstrated that the SCD-PD(+) patients had lower semantic fluency than SCD-PD(-) patients and controls, and showed poorer performance in visual memory and confrontational naming than controls, whereas no significant difference in cognitive performance was observed between the SCD-PD(-) patients and controls. Cortical thickness analysis revealed that the SCD-PD(+) patients had focal cortical thinning in the dorsolateral prefrontal, orbitofrontal, parietal, and parahippocampal areas compared with controls. Compared with SCD-PD(-) patients, SCD-PD(+) patients had cortical thinning in the frontal, parahippocampal, and posterior cortical areas.
CONCLUSION: Our data show that cortical thinning and cognitive performance in patients with SCD may differ based on the presence of PD, suggesting that SCD in patients with PD reflects disease-related cortical thinning and cognitive dysfunctions more closely than SCD without PD.
METHODS: In total, 96 patients experiencing SCD were classified as having PD (SCD-PD(+), n = 49) or no neurological disease (SCD-PD(-), n = 47); cognitively normal subjects without SCD (n = 23) were included as controls. Neurocognitive profiles and cortical thickness were examined using standardized neuropsychological tests and magnetic resonance imaging-based analysis.
RESULTS: No significant differences in demographic characteristics were found among the three groups. Neuropsychological tests demonstrated that the SCD-PD(+) patients had lower semantic fluency than SCD-PD(-) patients and controls, and showed poorer performance in visual memory and confrontational naming than controls, whereas no significant difference in cognitive performance was observed between the SCD-PD(-) patients and controls. Cortical thickness analysis revealed that the SCD-PD(+) patients had focal cortical thinning in the dorsolateral prefrontal, orbitofrontal, parietal, and parahippocampal areas compared with controls. Compared with SCD-PD(-) patients, SCD-PD(+) patients had cortical thinning in the frontal, parahippocampal, and posterior cortical areas.
CONCLUSION: Our data show that cortical thinning and cognitive performance in patients with SCD may differ based on the presence of PD, suggesting that SCD in patients with PD reflects disease-related cortical thinning and cognitive dysfunctions more closely than SCD without PD.