Freezing of gait (FoG) is a disabling clinical phenomenon characterized by brief episodes of inability to step or extremely short steps, often occurring when initiating gait or turning while walking. It is a common feature of parkinsonian syndromes and significantly impairs mobility, increases fall risk, and reduces quality of life. The pathogenesis of FoG is not fully understood, and while treatments like medications, deep brain stimulation, and rehabilitation can alleviate symptoms in some patients, they are ineffective in advanced cases. Understanding FoG is crucial for developing effective therapeutic strategies. FoG is episodic and involves transient disruptions in locomotor circuitry. It is associated with abnormalities in frontal cortical regions, the basal ganglia, and the midbrain locomotor region. Clinical features include difficulty in initiating gait, shuffling steps, and a subjective feeling of feet being glued to the floor. FoG can be triggered by various cues and is often asymmetrical. It is also linked to other midline signs, speech disturbances, and postural instability. Physiological studies show that FoG is associated with increased variability in step timing, disordered bilateral coordination, and reduced stride amplitude. Continuous gait and turning deficits are unrelated to disease severity but are related to postural instability. FoG is more pronounced in patients with Parkinson's disease (PD) when dopaminergic drug effects are at their nadir, suggesting a dopaminergic contribution to FoG. Episodic abnormalities during FoG include a profound decrease in stride length, reduced joint ranges, disordered temporal control of gait cycles, and high-frequency leg movements. These abnormalities are not solely due to tremor or increased co-contraction of lower-limb muscles. FoG is often accompanied by other motor disturbances, such as freezing in other motor tasks like finger movements and speech. Neuroimaging studies have identified brain areas involved in FoG, including the frontal cortex, basal ganglia, and midbrain. These areas are crucial for locomotion and postural control. Hypotheses for the pathogenesis of FoG include abnormalities in gait pattern generation, problems with central drive and automaticity of movement, and issues with coupling posture with gait. Executive dysfunction, particularly set-shifting and conflict resolution, is also implicated in FoG. Assessment of FoG is challenging due to its episodic nature, and validated questionnaires like the FOG-Q are used. Treatments include levodopa, dopamine agonists, and deep brain stimulation, but their efficacy varies. Rehabilitation strategies, such as attentional strategies and cueing, can help manage FoG. Despite advances, the exact mechanisms of FoG remain unclear, and further research is needed to develop more effective treatments.Freezing of gait (FoG) is a disabling clinical phenomenon characterized by brief episodes of inability to step or extremely short steps, often occurring when initiating gait or turning while walking. It is a common feature of parkinsonian syndromes and significantly impairs mobility, increases fall risk, and reduces quality of life. The pathogenesis of FoG is not fully understood, and while treatments like medications, deep brain stimulation, and rehabilitation can alleviate symptoms in some patients, they are ineffective in advanced cases. Understanding FoG is crucial for developing effective therapeutic strategies. FoG is episodic and involves transient disruptions in locomotor circuitry. It is associated with abnormalities in frontal cortical regions, the basal ganglia, and the midbrain locomotor region. Clinical features include difficulty in initiating gait, shuffling steps, and a subjective feeling of feet being glued to the floor. FoG can be triggered by various cues and is often asymmetrical. It is also linked to other midline signs, speech disturbances, and postural instability. Physiological studies show that FoG is associated with increased variability in step timing, disordered bilateral coordination, and reduced stride amplitude. Continuous gait and turning deficits are unrelated to disease severity but are related to postural instability. FoG is more pronounced in patients with Parkinson's disease (PD) when dopaminergic drug effects are at their nadir, suggesting a dopaminergic contribution to FoG. Episodic abnormalities during FoG include a profound decrease in stride length, reduced joint ranges, disordered temporal control of gait cycles, and high-frequency leg movements. These abnormalities are not solely due to tremor or increased co-contraction of lower-limb muscles. FoG is often accompanied by other motor disturbances, such as freezing in other motor tasks like finger movements and speech. Neuroimaging studies have identified brain areas involved in FoG, including the frontal cortex, basal ganglia, and midbrain. These areas are crucial for locomotion and postural control. Hypotheses for the pathogenesis of FoG include abnormalities in gait pattern generation, problems with central drive and automaticity of movement, and issues with coupling posture with gait. Executive dysfunction, particularly set-shifting and conflict resolution, is also implicated in FoG. Assessment of FoG is challenging due to its episodic nature, and validated questionnaires like the FOG-Q are used. Treatments include levodopa, dopamine agonists, and deep brain stimulation, but their efficacy varies. Rehabilitation strategies, such as attentional strategies and cueing, can help manage FoG. Despite advances, the exact mechanisms of FoG remain unclear, and further research is needed to develop more effective treatments.