Raynaud’s phenomenon (RP) is a three-phase color change in the fingers and/or toes caused by vasospasm under cold or stress conditions and is often accompanied by pain, numbness, stiffness and even ulcers. The pathogenesis of RP is currently unclear, and specific treatments are still being explored. Botulinum neurotoxin type A (BoNT/A) is a polypeptide produced by Clostridium botulinum that can enter the presynaptic membrane of nerves to inhibit the release of neurotransmitters and exert chemical denervation. BoNT/A treatment has been shown to reduce pain, improve blood flow, increase skin temperature, and improve ulcer healing in RP patients. Therefore, BoNT/A has become a new therapeutic measure for relieving severe vasospasm in RP. However, the specific mechanisms by which BoNT/A antagonizes the abnormal contraction of small arteries are still unclear. This review is aimed to provide a summary of the current understanding of RP pathogenesis and the mechanism of action of BoNT/A in order to provide theoretical support for the use of BoNT/A as RP treatment.