Clinical findings of hyperechoic substantia nigra in patients with Parkinson's disease

Author:

Fan Yongyan12,Ma Jianjun123ORCID,Yang Dawei12,Li Xiaohuan12,Liang Keke23,She Zonghan12,Qi Xuelin12,Shi Xiaoxue123,Gu Qi123,Zheng Jinhua123,Li Dongsheng123

Affiliation:

1. Department of Neurology Zhengzhou University People's Hospital Zhengzhou China

2. Department of Neurology Henan Provincial People's Hospital Zhengzhou China

3. Department of Neurology Henan University People's Hospital Zhengzhou China

Abstract

AbstractThis study aims to analyse hyperechoic substantia nigra (HSN) characteristics and the correlation of HSN with clinical features and blood biomarkers in patients with Parkinson's disease (PD). Transcranial sonography (TCS) evaluations of the substantia nigra (SN) were performed in 40 healthy controls and 71 patients with PD, including patients with SN hyperechogenicity (SN+) and those with normal SN echogenicity (SN−). Evaluation of motor and non‐motor symptoms was assessed by a series of rating scales. The uricase method was used to determine serum uric acid (UA) levels, and enzyme‐linked immunosorbent assay (ELISA) was used to measure plasma interleukin (IL)‐1β levels. TCS showed 92.50% specificity and 61.97% sensitivity in differentiating PD patients from controls. The area of SN+ contralateral to the side of initial motor symptoms (SNcontra) was larger than that ipsilateral to the side of initial motor symptoms (SNipsi). The PDSN+ group had lower Argentine Hyposmia Rating Scale (AHRS) scores and UA levels than the PDSN− group. Binary logistic regression analysis revealed that AHRS scores and UA levels could be independent predictors for HSN. The larger SN echogenic area (SNL) sizes positively correlated with plasma IL‐1β levels in PD patients with SN+. The present study provides further evidence of the potential of SN echogenicity as an imaging biomarker for PD diagnosis. PD patients with HSN have more severe non‐motor symptoms of hyposmia. HSN in PD patients is related to the mechanism of abnormal iron metabolism and microglial activation.

Publisher

Wiley

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