Abstract

Background and rationaleHistopathological studies revealed degeneration of the dorsal motor nucleus of the vagus nerve (VN) early in the course of idiopathic Parkinson’s disease (IPD). Degeneration of VN axons should be detectable by high-resolution ultrasound (HRUS) as a thinning of the nerve trunk. In order to establish if the VN exhibits sonographic signs of atrophy in IPD, we examined patients with IPD compared with age-matched controls.Material and methodsWe measured the caliber (cross-sectional area, CSA) and perimeter of the VN in 20 outpatients with IPD (8 females and 12 males; mean age 73.0 + 8.6 years) and in age-matched controls using HRUS. Evaluation was performed by blinded raters using an Esaote MyLab Gamma device in conventional B-Mode with an 8–19 MHz probe.ResultsIn both sides, the VN CSA was significantly smaller in IPD outpatients than in controls (right 2.37 + 0.91, left 1.87 + 1.35 mm2 versus 6.0 + 1.33, 5.6 + 1.26 mm2; p <0.001), as well as the perimeter (right 5.06 + 0.85, left 4.78 + 1.74 mm versus 8.87 + 0.86, 8.58 + 0.97 mm; p <0.001). There were no significant correlations between VN CSA and age, the Hoehn and Yahr scale, L-dopa therapy, and disease duration.ConclusionOur findings provide evidence of atrophy of the VNs in IPD patients by HRUS. Moreover, HRUS of the VN represent a non-invasive easy imaging modality of screening in IPD patients independent of disease stage and duration and an interesting possible additional index of disease.

Highlights

  • Idiopathic Parkinson’s disease (IPD) is known to be pathologically characterized by a progressive neuronal loss in the substantia nigra (SN) and pars compacta and aggregation of the α-synuclein protein that accumulates in Lewy bodies (LB) [1]

  • The vagus nerve (VN) cross-sectional area (CSA) was significantly smaller in idiopathic Parkinson’s disease (IPD) outpatients than in controls (6.0 + 1.33 mm2, 5.6 + 1.26 mm2; p

  • No significant differences in the right or left were detected in our sample

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Summary

Introduction

Idiopathic Parkinson’s disease (IPD) is known to be pathologically characterized by a progressive neuronal loss in the substantia nigra (SN) and pars compacta and aggregation of the α-synuclein protein that accumulates in Lewy bodies (LB) [1]. The accumulation of α-synuclein aggregates in some vagus nerve (VN) nuclei can be present even at earliest stages of IPD [4,5,6]. Autonomic dysfunction is present in the disease [14] and may precede the occurrence of the cardinal motor symptoms by many years [8, 15]. It involves the gastrointestinal tracts, which receive parasympathetic input via VN, and is responsible of constipation, gastroparesis, or nausea [8, 16]. Histopathological studies revealed degeneration of the dorsal motor nucleus of the vagus nerve (VN) early in the course of idiopathic Parkinson’s disease (IPD). There were no significant correlations between VN CSA and age, the Hoehn and Yahr scale, Ldopa therapy, and disease duration

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