Objective:

To evaluate whether the presence of ideomotor apraxia (IMA) is associated with increased risk of developing freezing of gait (FOG) in patients with Parkinson’s disease (PD), using cross-sectional, longitudinal, and survival analyses.

Background:

IMA and FOG may share overlapping pathophysiological mechanisms involving disrupted fronto-parieto-striato-mesencephalic circuits. Both reflect failures to translate motor intention into automatic execution, interfering with the integration of goal-directed and habitual control, contributing to impaired movement initiation and sequencing in PD.

Design/Methods:

A cross-sectional and longitudinal study was conducted using data from the Parkinson’s Progression Markers Initiative (PPMI; www.ppmi-info.org). Approximately 3,596 PD patients with serial clinical records were included. Gait apraxia was defined as a binary variable (APRAXIA_BIN), and FOG was assessed using three outcomes: FOG_BIN, FOG_UPDRS-II, and FOG_UPDRS-III. Cross-sectional analyses included 2×2 contingency tables, χ²/Fisher’s tests, and odds ratios (OR) with 95% confidence intervals. Mixed-effects logistic models with random intercepts per patient were fitted, accounting for time since baseline. Kaplan–Meier and Cox survival analyses evaluated FOG onset. Models were adjusted for age, sex, and follow-up duration.

Results:

Among 3,596 patients, ideomotor apraxia was observed in ~40% during follow-up. In cross-sectional analyses, apraxia was consistently associated with greater FOG prevalence across all definitions subjective (FRZGT12M), UPDRS-II, and UPDRS-III with ORs ranging from 3.49 to 8.04 (all p < 0.000001), strongest with clinician-rated measures (UPDRS-III). In longitudinal models, apraxia remained a significant predictor of FOG via UPDRS-III (OR = 4.57; 95% CI: 2.58–8.10), while time also increased risk (OR per year = 1.33; 95% CI: 1.23–1.44). Kaplan–Meier curves showed significantly reduced FOG-free survival in patients with apraxia (log-rank p < 0.0001).

Conclusions:

IMA is associated with an approximately fivefold increased risk of developing FOG in PD. These findings suggest that apraxia may serve as an early clinical marker of fronto-subcortical dysfunction, highlighting its prognostic utility in clinical settings.