Freezing of gait (FOG) is defined as a “brief, episodic absence or marked reduction of forward progression of the feet despite the intention to walk.” [[1], [2], [3]], which is a common and disabling gait difficulty in Parkinson's disease (PD) [4]. As the disease duration increases, the risk of the development of FOG increases [5], which impairs the individual's life quality and brings a heavy burden to the family and society [4]. To date, the structures responsible for triggering FOG remain elusive.

FOG is more common in late-stage PD, but not all patients will develop FOG [6]. In the past several years, many researchers have sought to determine the mechanism behind this common and disabling symptom using several imaging techniques including structural and functional imaging. For instance, voxel-based morphometry (VBM) analyses [[7], [8], [9], [10]], diffusion fiber tract imaging [[11], [12], [13]], resting and task functional magnetic resonance imaging (fMRI) [[14], [15], [16]], and positron emission tomography or single photon emission computed tomography (PET/SPECT) [17,18] have all been used to study this symptom. It has been reported that various brain regions are involved in the generation of this symptom, such as cortical areas including the supplementary motor area and sensorimotor area, as well as subcortical regions including the mesencephalic locomotor region (MLR), the cerebellar locomotor region, and the basal ganglia [[19], [20], [21], [22], [23]]. It seems that the widespread structural and functional impairments in cortical and subcortical brain regions are associated with the pathophysiology of FOG.

Quantitative susceptibility mapping (QSM) [24] and neuromelanin-sensitive magnetic resonance imaging (NM-MRI) [25] are emerging imaging techniques that make it possible to quantitatively measure iron content in the brain and neuromelanin (NM) contrast in the substantia nigra pars compacta (SNpc). Some studies recently found that iron deposition in the DGM and decreased NM in the SNpc play a crucial role in PD-FOG taking advantage of QSM and NM-MRI, respectively [26,27]. However, there is no study yet that explores the iron deposition and NM changes in PD patients with FOG simultaneously. Moreover, a longitudinal study found both the PD-FOG-converters and non-converters showed atrophy in the basal ganglia relative to controls [28].

We hypothesized that structural changes of the DGM in the basal ganglia pathways will contribute to FOG in PD patients. In this study, we performed a region-of-interest analysis to compare DGM volume and susceptibility on QSM and investigated the volume and relative contrast of the SNpc on NM-MRI, further exploring the associations of FOG severity with MRI measurements and disease stage using multiple linear regression analysis.