# Longitudinal Evaluation of Polyneuropathy in Atypical Parkinsonian Syndromes

## TL;DR

This study examines how polyneuropathy progresses in patients with atypical parkinsonian syndromes and finds it may reflect disease progression, especially in multiple system atrophy.

## Contribution

The first longitudinal evaluation of polyneuropathy progression in multiple system atrophy and progressive supranuclear palsy.

## Key findings

- Polyneuropathy was present in over 50% of patients with multiple system atrophy and progressive supranuclear palsy at baseline.
- Patients with polyneuropathy showed greater motor and cognitive impairments compared to those without.
- Tibial nerve amplitude decreased significantly over two years in multiple system atrophy patients, correlating with disease progression.

## Abstract

Background: In Parkinson’s disease (PD), a higher prevalence of polyneuropathy (PNP) is increasingly recognized, although the causal association is still under debate. In contrast, PNP in atypical parkinsonian syndromes (APS) has been insufficiently addressed, despite preliminary evidence suggesting elevated prevalence. Methods: Nerve conduction studies were performed on 13 patients with multiple system atrophy (MSA) and 9 patients with progressive supranuclear palsy (PSP) at baseline. PNP was diagnosed according to standard electrophysiological criteria after exclusion of common secondary causes. Comprehensive clinical evaluation included motor and non-motor assessments over two years of follow-up. Results: At baseline, PNP was present in 53.8% of MSA patients and 66.7% of PSP patients. MSA patients with PNP showed greater motor symptom severity (UPDRS III score; p = 0.046) and worse cognitive performance (MoCA; p = 0.044) compared to those without PNP. Over two years, a significant reduction in the tibial nerve amplitude was observed exclusively in MSA patients (p = 0.039), paralleling disease progression. Conclusions: This study provides the first longitudinal evaluation of clinical and electrophysiological PNP progression in MSA and PSP. A high comorbidity of PNP in patients with APS could contribute to motor and sensory impairments in these patients. Our findings indicate that PNP progression may reflect disease progression in MSA. Given the limited sample size, larger-scale longitudinal studies are needed to further investigate biomarker potential of PNP in APS and to clarify differences in peripheral nerve involvement between synucleinopathies and tauopathies.