# What is new in Freezing of Gait?

**Authors:** Eileen Gülke, Simon J. G. Lewis

PMC · DOI: 10.1007/s00415-026-13765-6 · Journal of Neurology · 2026-03-21

## TL;DR

This paper reviews recent advancements in understanding and managing freezing of gait in Parkinson's disease.

## Contribution

The paper highlights new clinical definitions, outcome measures, and technological approaches for freezing of gait.

## Key findings

- The ICFOG introduced updated definitions and a standardized testing protocol for FOG.
- New ClinRO and PRO outcome measures are being developed for FOG assessment.
- Technological advances are enabling personalized treatment strategies for FOG.

## Abstract

Freezing of Gait (FOG) research is entering a rapidly evolving phase. Published in early 2026, the International Consortium for FOG (ICFOG) released updated clinical and technical definitions of FOG and introduced a consensus-based standardized testing protocol, the Giladi protocol (GP-FOG), which is currently still under evaluation in an ongoing study. Complementing these advances, two new outcome measures, the clinician-reported outcome (ClinRO) and the patient-reported outcome (PRO), are highlighted in this review. Recent technological developments in both detection and potential prevention of FOG are moving the field toward individualized, biomarker-based, on-demand treatment strategies. In addition, emerging insights into the pathophysiological mechanisms of FOG, particularly nondopaminergic contributions, are discussed. Together, these developments provide a contemporary framework for improving the assessment, understanding, and personalized management of FOG in Parkinson’s disease.

## Linked entities

- **Diseases:** Parkinson’s disease (MONDO:0005180)

## Full-text entities

- **Genes:** HTR2A (5-hydroxytryptamine receptor 2A) [NCBI Gene 3356] {aka 5-HT2A, HTR2}, SNCA (synuclein alpha) [NCBI Gene 6622] {aka NACP, PARK1, PARK4, PD1}, ACHE (acetylcholinesterase (Yt blood group)) [NCBI Gene 43] {aka ACEE, ARACHE, N-ACHE, YT}, SLC18A3 (solute carrier family 18 member A3) [NCBI Gene 6572] {aka CMS21, VACHT}, SLC6A2 (solute carrier family 6 member 2) [NCBI Gene 6530] {aka NAT1, NET, NET1, SLC6A5}
- **Diseases:** tremor (MESH:D014202), ADHD (MESH:D001289), dysarthria (MESH:D004401), FOG (MESH:D020234), neurodegeneration (MESH:D019636), fractures (MESH:D050723), Akinetic (MESH:D018476), anxiety (MESH:D001007), motor impairment (MESH:D000068079), PD (MESH:D010300), cognitive impairment (MESH:D003072), loss of independence (MESH:D064129), neuropsychiatric adverse effects (MESH:D064420), fall (MESH:C537863), gait disorders (MESH:D020233), depression (MESH:D003866), dyskinesia (MESH:D004409)
- **Chemicals:** paroxetine (MESH:D017374), noradrenaline (MESH:D009638), dopaminergic (MESH:D004298), water (MESH:D014867), Levodopa (MESH:D007980), ritanserin (MESH:D016713), FOG (-), Atomoxetine (MESH:D000069445), serotonin (MESH:D012701), rivastigmine (MESH:D000068836)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13005827/full.md

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13005827/full.md

---
Source: https://tomesphere.com/paper/PMC13005827