Multiple sclerosis (MS) is a progressive neurodegenerative and autoimmune disease associated with the immune-mediated destruction of myelin (the protective layer of nerves) in the central nervous system.– The prevalence of MS in Canada (based on survey data from 2010 to 2011) was 290 per 100,000. Multiple sclerosis is the leading cause of disability in young adults; for instance, self-reported data from a survey distributed to Canadian household residents aged 15 or older (i.e., individuals not living in a long-term care institution) reported that 82% were diagnosed between the ages of 20 to 49 (95% confidence interval, 75.9 to 86.5). Of note, pediatric MS (onset before 18 years of age) is considered a rare disease; data from 1965 to 2018 of individuals aged 19 and younger reported an overall incidence of 0.05 to 2.85 per 100,000 and an overall prevalence of 0.7 to 26.9 per 100,000. Spasticity affects 40% to 80% of patients with MS and may present differently; however, muscle pain, spasms, weakness, stiffness, and loss of active function and voluntary movement are common manifestations.– Additionally, spasticity may result in poor body image and low self-esteem potentially causing social isolation. Spasticity impacts a patient’s ability and independence to complete daily activities through worsening fatigue and impairing ambulation; thus, reducing one’s quality of life and increasing the burden on caregivers and the need for health care resources and utilization. Spasticity management aims to reduce muscle tone to a degree that facilitates active function without eliminating all muscle tone. Pharmacological interventions for spasticity in patients with MS include baclofen (oral or intrathecal administration), tizanidine, dantrolene, and benzodiazepines (e.g., clonazepam and diazepam). Non-pharmacological interventions include physiotherapy, transcutaneous electrical nerve stimulation, transcranial magnetic stimulation, electromagnetic therapy, and whole body vibration. Botulinum neurotoxins are produced by the bacteria and there are various subtypes (A to G) that may have different formulations. Botulinum toxin type A products may be used to treat focal spasticity in patients with MS. To treat spasticity, botulinum toxin type A is administered through intramuscular injections temporarily causing local muscle paresis (i.e., partial paralysis) and may also elicit an analgesic effect lasting for 3 to 4 months. The pharmacological activity of botulinum toxin type A is the inhibition of the pre-synaptic transmission of acetylcholine at the neuromuscular junction. There are 3 licensed formulations of botulinum toxin type A available for multiple indications, not exclusive to spasticity, on the North American market: onabotulinum toxin A (Botox), abobotulinum toxin A (Dysport), and incobotulinum toxin A (Xeomin).– These formulations have different manufacturing processes and vary in pharmacological activity and intracellular targets; therefore, they are not interchangeable. This report focuses on onabotulinum toxin A, which will be referred to herein as Botox — its brand name. In Canada, Botox was first approved by Health Canada in 1999 for the treatment of spasticity in pediatric patients with cerebral palsy. Treatments to alleviate spasticity in MS have not been well-studied; further, there are limited data on the effectiveness of Botox to treat spasticity and the majority of published data focuses on spasticity due to stroke. Accordingly, there is uncertainty regarding the clinical effectiveness and safety of Botox as a treatment for MS-related spasticity. The purpose of this rapid review is to evaluate recent evidence regarding the clinical effectiveness (including safety), cost-effectiveness, and evidence-based guidelines regarding the use of Botox for the treatment of spasticity associated with MS.