Hemifacial spasm (HFS) is a movement disorder characterized by involuntary, paroxysmal contractions of the facial muscles, typically caused by compression or demyelination of the facial nerve. It is often associated with facial distortion and twitching, significantly affecting the patient's quality of life. Traditional pharmacological treatments, such as anticonvulsants, benzodiazepines, and muscle relaxants, can provide some symptom relief, but their efficacy is limited, and side effects are prominent. In recent years, botulinum toxin type A (BTX-A) has emerged as the first-line clinical treatment for HFS. BTX-A works by inhibiting acetylcholine release at the nerve terminal, blocking the signal transmission at the neuromuscular junction, and reducing muscle overactivity. Additionally, it modulates the excitability of the central nervous system and improves neural plasticity, facilitating the recovery of facial nerve function and further alleviating HFS symptoms. This article systematically reviews the mechanism of action and clinical research of BTX-A in the treatment of HFS, analyzes current challenges in its use, and explores its future prospects in the treatment of HFS, aiming to provide safer, more effective, and personalized treatment options for HFS patients.