Understanding Botox Treatment for Cerebral Palsy

Author: Anna Rose Diel, PharmD Candidate

“Cerebral”: having to do with the brain 
“Palsy”: weakness in or muscle functioning issues 

Cerebral Palsy (CP), a group of disorders affecting movement, posture, and balance, is caused by non-progressive disturbances to the developing brain or abnormal brain development. Though classified as non-progressive, this refers to the brain insult and neurological involvement; however, the musculoskeletal aspect remains dynamic with time and growth of the child. The majority of CP causes are congenital (85-90%), and the lesser percentage is considered acquired CP as the abnormal brain development/damage (likely from infection or head injury) may happen within 28 days of birth.[1][2] 

CP is the most common childhood motor disability and affects a person’s ability to control muscles, resulting in activity limitations. Symptoms of CP vary depending on severity. Those with severe CP may need to use special orthotics or have surgical intervention to walk. In other severe cases of CP, the individuals may not be ambulatory and require life long care. On the other hand, those with mild or moderate CP may encounter mobility issues and require less extensive care with physical therapy or orthotics.[1][2] 

Understanding plegia versus paresis is crucial to comprehend more about the CP classifications. Plegia is the complete loss of voluntary motor function while paresis is a partial loss of motor function, seen as muscle weakness in an affected region of the body. 

Three major types of CP: 

Spastic CP: Affecting about 80% of those with CP, spastic CP represents the most common type. An increased muscle tone and stiffness are seen and further classified based on which body regions are affected. Spastic diplegia/diparesis is when muscle stiffness is observed in the lower limbs, creating a scissoring gait due to tightness in hips and leg muscles. Spastic hemiplegia/hemiparesis is when one side of a person’s body is affected, typically upper extremities are more susceptible to this. Lastly, spastic quadraplegia/quadrparesis is the most severe form of spastic CP, affecting all four limbs, the trunk, and face. Individuals with this type of spastic CP may not be able to walk and may have other developmental disabilities such as but not limited to epilepsy or vision, speech, and hearing challenges.[2] 

Dyskinetic CP: Dyskinetic CP affects movement control of the person’s hands, arms, feet, and legs, creating difficulty in walking or sitting. This term also includes athetoid, choreoathetoid, and dystonic CPs. With uncontrolled movements, patients may experience slow and contorting motions while others may experience rapid and abrupt movements. The muscle tone in dyskinetic CP can change daily or within the same day from too tight to too loose, creating challenges for the individual.[2] 

Ataxic CP: Ataxic CP affects coordination and balance wherein walking can be unsteady and difficult with quick movements. Additionally, higher fine motor skills like writing that require controlled motions may be demanding.[2] 

To note, there can be cases of mixed CP with the most common being spastic-dyskinetic CP. 

Is there a cure? What are the treatment options? 

While there is no cure for CP, there are many treatment options such as orthotics, surgery, and physical, occupational, and speech therapies. As there are different types and severity levels of CP, there are no standard treatments best for all children.[2] In recent years, the mention of botulinum toxin type A (BoNT-A) has become an option of medical intervention for children with CP. BoNT-A use is “off-label” for CP treatment efforts.[1] Like all other medications, BoNT-A does not come without adverse effects. It is important to understand and evaluate the benefits and risks to determine if BoNT-A is the right treatment for the individual with CP. 

What are Botulinum Neurotoxins? 

Botulinum neurotoxins (BoNT) are large proteins produced by bacteria from the Clostridia Botulinum family. BoNT acts to inhibit the release of acetylcholine from the presynaptic motor nerve terminals, creating a temporary weakening or relaxation of the muscles. The overall effect of this is a neuro paralysis or chemical denervation of muscle. BoNT types A and B have been used in patients with CP although BoNT-B is only indicated in cases with resistance to BoNT-A by neutralizing antibodies because of the greater adverse event profile and shorter duration with BoNT-B.[1] Clinical studies have used different preparations of BoNT-A like onabotulinumtoxinA (Botox®), abobotulinumtoxinA (Dysport®), and incobotulinumtoxinA. While all three are within the BoNT-A class, the products are not interchangeable due to the biological activity of the various toxins and neurotoxin load. OnabotulinumtoxinA has the greatest neurotoxin load at 0.73ng/100U, followed by abobotulinumtoxinA at 0.65ng/100U, leaving incobotulinumtoxinA with the smallest neurotoxin load at 0.44ng/100U. This correlates to the relative potency in which incobotulinumtoxinA was the least potent and onabotulinumtoxinA was the most potent. These BoNT-A injections are dose dependent with partially reversible chemo denervation of the injected muscle(s) through acetylcholine blockade at the presynaptic neuromuscular junction.[1][6] 

BoNT-A Usage in CP 

While the FDA has not approved BoNT-A for children with limb spasticity, it is used “off-label” for just that. Children and parents have seen better range of motion, better positioning of limbs and more fluid joint movement, fewer spastic movements, decreased pain, and improved gait.[3] The most common indications for BoNT-A treatment are in unilateral CP, bilateral ambulant CP, and bilateral non ambulant CP for upper limbs, lower limbs, and the spine. The study found that for upper limbs BoNT-A improved function and appearance for unilateral CP as well as pain management, easier care, and functional/cosmetic improvements of hand positioning. For the lower limbs, there was improved gait observed for unilateral and bilateral ambulant CP with pain management, easier care, improvement of weight bearing, and hip dislocation prevention in bilateral non ambulant CP patients. For the spine, it was noted that BoNT-A only displayed effects of postural management, care, and pain management for bilateral non ambulant CP patients.[4] 

The goal is to improve function and support motor development as well as delay corrective surgeries until the child is older or to reach a stage in function which surgery is no longer necessary.[3][4] The best age range for children to receive BoNT-A therapy (as decided by a multi disciplinary team for effectiveness and consent obtained) is between the ages 2 and 12 because of the quick development during these stages of childhood.[1] Studies have found these injections demonstrate therapeutic effects up to 3 to 6 months (depending on site of injection and amount used).[8] It is important to discuss with a trusted team of healthcare workers to determine if BoNT-A is the right therapy intervention for each child. 

Understanding the Risks 

BoNT-A is a botulinum neurotoxin, which is within the most potent biological toxins in the natural world. Ingesting BoNT-A is highly toxic and deadly. BoNT-A is to be administered through injection for medical and therapeutic purposes only.[3] Deaths from ingested botulinum toxin, in the form of food poisoning, still occur as well as deaths from botulinum toxin injected for medical and therapeutic purposes. Botulism is a rare but serious potential effect when the botulinum toxin attacks the body’s nerves, causing muscle paralysis, difficulty breathing, and in some cases, death.[7] If the botulinum toxin spreads from the area of injection, serious side effects may occur such as asthenia, generalized muscle weakness, diplopia, ptosis, dysphagia, dysphonia, dysarthria, urinary incontinence, and breathing issues.[6] It is important to weigh the risks and benefits of BoNT-A before use, especially in children prior to initiation for CP related spasticity. 

Author Bio:

References:

1. Multani I, Manji J, Hastings-Ison T, Khot A, Graham K. Botulinum Toxin in the Management of Children with Cerebral Palsy. Paediatr Drugs. 2019 Aug;21(4):261-281. doi: 10.1007/s40272-019-00344-8. PMID: 31257556; PMCID: PMC6682585. 
2. About Cerebral Palsy | cerebral palsy (CP) | CDC. Accessed June 29, 2026. https://www.cdc.gov/cerebral-palsy/about/index.html. 
3. Cerebral Palsy and botox treatment | cerebral palsy guidance. Accessed June 30, 2026. https://cerebralpalsyguidance.com/cerebral-palsy/treatment/botox/. 
4. Strobl W, Theologis T, Brunner R, Kocer S, Viehweger E, Pascual-Pascual I, Placzek R. Best clinical practice in botulinum toxin treatment for children with cerebral palsy. Toxins (Basel). 2015 May 11;7(5):1629-48. doi: 10.3390/toxins7051629. PMID: 25969944; PMCID: PMC4448165. 
5. Pharmacological differences and clinical implications of various botulinum toxin preparations: A critical appraisal - PMC. Accessed July 3, 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC5901944/. 
6. How to stay safe when getting botulinum toxin injections | botulism | CDC. Accessed July 3, 2026. https://www.cdc.gov/botulism/prevention/botulinum-toxin-injections.html. 
7. Mirska A, Kułak W, Okurowska-Zawada B, Dmitruk E. Effectiveness of multiple botulinum toxin sessions and the duration of effects in spasticity therapy in children with cerebral palsy. Childs Nerv Syst. 2019 Jan;35(1):141-147. doi: 10.1007/s00381-018-3923-6. Epub 2018 Jul 30. PMID: 30058050; PMCID: PMC6341047.