# Role of prefrontal cortex in freezing of gait in Parkinson’s disease: mechanisms and neuroimaging evidence

## TL;DR

This paper reviews how the prefrontal cortex contributes to freezing of gait in Parkinson’s disease, combining neuroimaging evidence and non-motor factors.

## Contribution

The paper highlights the prefrontal cortex's role in freezing of gait beyond traditional motor pathways, emphasizing non-motor influences.

## Key findings

- Structural and functional prefrontal cortex abnormalities are linked to freezing of gait in Parkinson’s disease.
- The dorsolateral and medial prefrontal cortex are specifically implicated in freezing episodes.
- Frontal lobe dysfunction may inform new therapeutic strategies targeting frontostriatal circuits.

## Abstract

Freezing of gait (FOG) is a complex and highly disabling motor symptom that frequently affects patients with Parkinson’s disease (PD), especially in the middle and late stages. Although traditionally associated with motor deficits, accumulating evidence suggests that FOG is also strongly influenced by non-motor domains, including cognitive dysfunction and emotional disturbances. The prefrontal cortex (PFC), a key hub for executive functions, attention, and emotional regulation, has been increasingly implicated in the pathophysiology of FOG. Structural and functional abnormalities in the PFC, particularly in the dorsolateral prefrontal cortex (DLPFC) and medial prefrontal cortex (MPFC), have been reported in PD patients with FOG. This narrative review aims to summarize current evidence on the role of the prefrontal cortex in the development and modulation of freezing episodes, focusing on neuroimaging findings. Clarifying the contribution of frontal lobe dysfunction to FOG may inform therapeutic strategies targeting frontostriatal circuits to improve mobility and quality of life in PD patients. This is a narrative review and does not employ formal systematic review methodology.