Freezing of gait (FoG) is a disabling clinical phenomenon characterized by brief episodes of inability to step or extremely short steps, commonly occurring in Parkinson’s disease and other parkinsonian syndromes. It significantly impairs mobility, increases fall risk, and reduces quality of life. The pathogenesis of FoG is not fully understood, and current treatments are limited in their effectiveness, especially in advanced cases. FoG is associated with disturbances in frontal cortical regions, the basal ganglia, and the midbrain locomotor region. Medications, deep brain stimulation, and rehabilitation techniques can alleviate symptoms in some patients, but are not universally effective. FoG is episodic and can be triggered by various situations, such as starting to walk, turning, or approaching a destination. It is often accompanied by leg trembling, reduced step length, and a subjective feeling of feet being glued to the floor. FoG can be asymmetrical and is influenced by environmental and emotional factors. It is also associated with other midline signs, speech disturbances, and postural instability. FoG is more common in patients with advanced Parkinson’s disease and is not always correlated with the cardinal features of parkinsonism. Physiological studies show that FoG is associated with impaired gait rhythm, coordination, and balance. Continuous gait abnormalities occur between freezing episodes, and FoG is linked to postural instability. The pathogenesis of FoG is thought to involve disruptions in the locomotor and postural circuits, including the brainstem reticular formation, the mesencephalic locomotor region (MLR), the basal ganglia, and frontal cortical regions. Neuroimaging studies suggest that FoG is associated with reduced activity in certain brain areas and increased activity in others. Several hypotheses have been proposed to explain the pathogenesis of FoG, including abnormalities in gait pattern generation, problems with central drive and automaticity of movement, impaired coupling of posture with gait, perceptual malfunction, and frontal executive dysfunction. These hypotheses suggest that FoG may result from disruptions in the coordination of rhythmic movement, impaired automaticity, or difficulties in coupling posture with gait. Assessment of FoG is challenging, and current tools such as the FOG-Q questionnaire are used to evaluate its severity. Treatment options include pharmacological interventions, deep brain stimulation, and rehabilitation strategies such as attentional strategies and cueing. Despite these approaches, FoG remains a significant clinical challenge, and further research is needed to develop more effective therapeutic strategies.Freezing of gait (FoG) is a disabling clinical phenomenon characterized by brief episodes of inability to step or extremely short steps, commonly occurring in Parkinson’s disease and other parkinsonian syndromes. It significantly impairs mobility, increases fall risk, and reduces quality of life. The pathogenesis of FoG is not fully understood, and current treatments are limited in their effectiveness, especially in advanced cases. FoG is associated with disturbances in frontal cortical regions, the basal ganglia, and the midbrain locomotor region. Medications, deep brain stimulation, and rehabilitation techniques can alleviate symptoms in some patients, but are not universally effective. FoG is episodic and can be triggered by various situations, such as starting to walk, turning, or approaching a destination. It is often accompanied by leg trembling, reduced step length, and a subjective feeling of feet being glued to the floor. FoG can be asymmetrical and is influenced by environmental and emotional factors. It is also associated with other midline signs, speech disturbances, and postural instability. FoG is more common in patients with advanced Parkinson’s disease and is not always correlated with the cardinal features of parkinsonism. Physiological studies show that FoG is associated with impaired gait rhythm, coordination, and balance. Continuous gait abnormalities occur between freezing episodes, and FoG is linked to postural instability. The pathogenesis of FoG is thought to involve disruptions in the locomotor and postural circuits, including the brainstem reticular formation, the mesencephalic locomotor region (MLR), the basal ganglia, and frontal cortical regions. Neuroimaging studies suggest that FoG is associated with reduced activity in certain brain areas and increased activity in others. Several hypotheses have been proposed to explain the pathogenesis of FoG, including abnormalities in gait pattern generation, problems with central drive and automaticity of movement, impaired coupling of posture with gait, perceptual malfunction, and frontal executive dysfunction. These hypotheses suggest that FoG may result from disruptions in the coordination of rhythmic movement, impaired automaticity, or difficulties in coupling posture with gait. Assessment of FoG is challenging, and current tools such as the FOG-Q questionnaire are used to evaluate its severity. Treatment options include pharmacological interventions, deep brain stimulation, and rehabilitation strategies such as attentional strategies and cueing. Despite these approaches, FoG remains a significant clinical challenge, and further research is needed to develop more effective therapeutic strategies.