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Cerebral Palsy Medication

  • Author: Hoda Z Abdel-Hamid, MD; Chief Editor: Amy Kao, MD  more...
Updated: Dec 23, 2015

Medication Summary

The goal of pharmacotherapy in patients with cerebral palsy is to reduce symptoms (eg, spasticity) and prevent complications (eg, contractures). Most of the medications used for this disorder in children are off label for age and indication and should be used only by physicians experienced in their use and familiar with their adverse effects.

Note that the indications and doses listed in this section are from a general formulary. A wide range of dosing can be encountered in clinical practice, because information in the literature regarding medication for cerebral palsy in children is scant.


Neuromuscular Blocker Agent, Toxins

Class Summary

Botulinum toxin type A is the drug of choice. This agent causes presynaptic paralysis of myoneural junctions and reduces abnormal contractions. The therapeutic effects may last 3-6 months.

OnabotulinumtoxinA (BOTOX)


OnabotulinumtoxinA treats excessive, abnormal contractions associated with blepharospasm, hemifacial spasm, and cervical dystonia. This drug binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which, in turn, inhibits transmission of impulses in neuromuscular tissue.

Reexamine patients 7-14 days after the initial dose to assess for a treatment response. Increase the doses 2-fold over the previous doses for patients experiencing incomplete paralysis of the target muscle. The procedure needs to be repeated every 3-6 months depending on the response.


Muscle relaxants

Class Summary

The muscle-relaxing effects of muscle-relaxant agents may come from inhibition of the transmission of monosynaptic and polysynaptic reflexes at the spinal cord level. These are thought to work centrally by suppressing conduction in the vestibular cerebellar pathways. They may have an inhibitory effect on the parasympathetic nervous system.

Baclofen (Lioresal, Gablofen)


Baclofen is a gamma-aminobutyric acid (GABA) analogue that inhibits calcium influx into presynaptic terminals and suppresses the release of excitatory neurotransmitters.

Baclofen may induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at the spinal level. This agent undergoes rapid gastrointestinal absorption, which peaks in 1-2 hours. It is primarily excreted renally and is partially metabolized by the liver. Baclofen works better in the treatment of spinal spasticity than it does against cerebral spasticity, but the drug should be tried in both conditions.

This drug's use is often limited by central nervous system (CNS) adverse effects, and thus, an effective dose is usually not obtainable with oral dosing. Intrathecal baclofen is available for use with a surgically implanted pump, which may improve the effectiveness of dosing.

Dantrolene (Dantrium, Revonto)


Dantrolene inhibits the release of calcium into the sarcoplasmic reticulum. This agent may weaken even nonspastic muscles and is generally used only in patients with severe hypertonicity.



Class Summary

Benzodiazepines are used in the acute management of seizures that may accompany cerebral palsy. By binding to specific receptor sites, these agents appear to potentiate the effects of gamma-aminobutyric acid (GABA) and facilitate neurotransmission of GABA and other inhibitory transmitters. Benzodiazepines may act in the spinal cord to induce muscle relaxation.

Diazepam (Valium, Diastat)


Diazepam is effective in treating seizures by depressing all levels of the central nervous system (CNS) (eg, limbic and reticular formation), possibly by increasing the activity of GABA at the spinal and supraspinal sites. Individualize the dosage, and increase cautiously to avoid adverse effects. Diazepam undergoes rapid gastrointestinal absorption; renal excretion and hepatic metabolism occur.

Sedation is common. Diazepam may worsen swallowing problems. This drug is generally used only in patients in whom severe hypertonicity is compromising care.


Anticholinergic Agents

Class Summary

Anticholinergic agents provide benefit for tremor in approximately 50% of Parkinson's disease patients, but they do not improve bradykinesia or rigidity. If 1 anticholinergic does not work, try another. Adverse effects include dry mouth and dry eyes, memory difficulty, confusion, and rare urinary retention.



Trihexyphenidyl is a synthetic tertiary amine anticholinergic agent that reduces the incidence and severity (by 20%) of akinesia, rigidity, tremor, and secondary symptoms such as drooling. Besides suppressing central cholinergic activity, these agents may inhibit reuptake and storage of dopamine at central dopamine receptors, thereby prolonging the action of dopamine.


Dopamine Prodrugs

Class Summary

Dopamine does not the cross blood-brain barrier, but levodopa (L-dopa) (the metabolic precursor of dopamine) does. L-dopa is decarboxylated to dopamine in the brain and in the periphery. The formation of dopamine in the blood causes many of the adverse effects associated with L-dopa. When administered alone, levodopa induces a high incidence of nausea and vomiting.

A peripheral decarboxylase inhibitor such as carbidopa is combined with levodopa to reduce the incidence of nausea and vomiting by inhibiting the peripheral conversion of levodopa to dopamine. Levodopa/peripheral decarboxylase inhibitor is the criterion standard of symptomatic treatment for Parkinson disease; it provides the greatest antiparkinsonian efficacy in moderate to advanced disease with the fewest acute adverse effects.

Because dopaminergic drugs block cholinergic nerve impulses that affect the muscles in the arms, legs, and other parts of the body, these agents may help patients with cerebral palsy. These medications help regulate muscle movement and motor function.

Levodopa/carbidopa (Sinemet, Sinemet CR, Parcopa)


Levodopa/carbidopa is a large, neutral amino acid absorbed in the proximal small intestine by a saturable carrier-mediated transport system. Absorption of this drug is decreased by meals that include other large, neutral amino acids. Only patients with meaningful motor fluctuations need to consider a low-protein or protein-redistributed diet.


Anticonvulsant Agents

Class Summary

Anticonvulsant drugs are used to terminate clinical and electrical seizure activity as rapidly as possible and to prevent seizure recurrence.

Levetiracetam (Keppra)


Levetiracetam is used as adjunct therapy for partial seizures and myoclonic seizures. This agent is also indicated for primary generalized tonic-clonic seizures. The mechanism of action of levetiracetam is unknown.

Oxcarbazepine (Trileptal)


The pharmacologic activity of oxcarbazepine is primarily by the 10-monohydroxy metabolite (MHD) of oxcarbazepine. This agent may block voltage-sensitive sodium channels, inhibit repetitive neuronal firing, and impair synaptic impulse propagation. The anticonvulsant effect of oxcarbazepine may also occur by affecting potassium conductance and high-voltage activated calcium channels.

The drug pharmacokinetics of oxcarbazepine are similar in older children (>8 y) and adults. Young children (< 8 y) have a 30-40% increased clearance compared with older children and adults. Children younger than 2 years have not been studied in controlled clinical trials.

Valproic acid (Depakote, Depakene, Depacon)


Valproic acid is chemically unrelated to other drugs used to treat seizure disorders. Although its mechanism of action is not established, the activity of valproic acid may be related to increased brain levels of gamma-aminobutyric acid (GABA) or enhanced GABA action; it may also potentiate postsynaptic GABA responses, affect potassium channels, or have a direct membrane-stabilizing effect.



Phenobarbital exhibits anticonvulsant activity in anesthetic doses and can be administered orally; in status epilepticus, it is important to achieve therapeutic levels as quickly as possible. The intravenous (IV) dose may require approximately 15 minutes to attain peak levels in the brain. If injected continuously until convulsions stop, brain concentrations may continue to rise and can exceed that which is required to control seizures. It is important to use the minimal amount required and to wait for an anticonvulsant effect to develop before giving a second dose.

Restrict IV use to conditions in which other routes are not possible, either because the patient is unconscious or because prompt action is required.

If an intramuscular (IM) route is chosen, administer phenobarbital into areas with little risk of encountering a nerve trunk or major artery, such as a large muscle (eg, gluteus maximus, vastus lateralis). A permanent neurologic deficit may result from injecting into or near peripheral nerves.


Alpha2 Adrenergic Agonist Agents

Class Summary

These agents are used for their antispasticity effects.

Tizanidine (Zanaflex)


Tizanidine is an imidazoline derivative and a central alpha2 noradrenergic agonist. The antispasticity effects are the probable result H-reflex inhibition. The drug may facilitate the inhibitory actions of glycine, reduce the release of excitatory amino acids and substance P, and produce analgesic effects. Tizanidine is a centrally acting muscle relaxant that is metabolized in the liver and excreted in the urine and feces.

Contributor Information and Disclosures

Hoda Z Abdel-Hamid, MD Assistant Professor, Department of Pediatrics, University of Pittsburgh School of Medicine; Director of EMG Laboratory and Neuromuscular Program, Director of Pediatric MDA Clinic, Division of Child Neurology, Children’s Hospital of Pittsburgh, University of Pittsburgh Medical Center

Hoda Z Abdel-Hamid, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, Child Neurology Society

Disclosure: Nothing to disclose.


Boosara Ratanawongsa, MD Clinical Assistant Professor of Pediatrics, Pennsylvania State University College of Medicine; Pediatric Neurologist, Pediatric Specialists of Lehigh Valley, Lehigh Valley Physician Group

Boosara Ratanawongsa, MD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society

Disclosure: Nothing to disclose.

Ari S Zeldin, MD, FAAP, FAAN Staff Pediatric Neurologist, Naval Medical Center San Diego

Ari S Zeldin, MD, FAAP, FAAN is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, Child Neurology Society

Disclosure: Nothing to disclose.

Alicia T F Bazzano, MD, PhD, MPH Clinical Faculty, Division of Pediatric Emergency Medicine, Harbor/UCLA Medical Center; Chief Physician, Westside Regional Center

Alicia T F Bazzano, MD, PhD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Public Health Association, American Society for Bioethics and Humanities

Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Have stock from Cellectar Biosciences; have stock from Varian medical systems; have stock from Express Scripts.


Ann M Neumeyer, MD Medical Director, Lurie Family Autism Center/LADDERS; Assistant Professor of Neurology, Harvard Medical School

Ann M Neumeyer, MD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

  1. Simpson DM, Gracies JM, Graham HK, Miyasaki JM, Naumann M, Russman B, et al. Assessment: Botulinum neurotoxin for the treatment of spasticity (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2008 May 6. 70(19):1691-8. [Medline].

  2. Scholtes VA, Dallmeijer AJ, Knol DL, Speth LA, Maathuis CG, Jongerius PH, et al. The combined effect of lower-limb multilevel botulinum toxin type a and comprehensive rehabilitation on mobility in children with cerebral palsy: a randomized clinical trial. Arch Phys Med Rehabil. 2006 Dec. 87(12):1551-8. [Medline].

  3. Dai AI, Wasay M, Awan S. Botulinum toxin type A with oral baclofen versus oral tizanidine: a nonrandomized pilot comparison in patients with cerebral palsy and spastic equinus foot deformity. J Child Neurol. 2008 Dec. 23(12):1464-6. [Medline].

  4. Yang EJ, Rha DW, Kim HW, Park ES. Comparison of botulinum toxin type A injection and soft-tissue surgery to treat hip subluxation in children with cerebral palsy. Arch Phys Med Rehabil. 2008 Nov. 89(11):2108-13. [Medline].

  5. Pascual-Pascual SI, Pascual-Castroviejo I. Safety of botulinum toxin type A in children younger than 2 years. Eur J Paediatr Neurol. 2009 Nov. 13(6):511-5. [Medline].

  6. Hoving MA, van Raak EP, Spincemaille GH, Palmans LJ, Becher JG, Vles JS. Efficacy of intrathecal baclofen therapy in children with intractable spastic cerebral palsy: a randomised controlled trial. Eur J Paediatr Neurol. 2009 May. 13(3):240-6. [Medline].

  7. Trost JP, Schwartz MH, Krach LE, Dunn ME, Novacheck TF. Comprehensive short-term outcome assessment of selective dorsal rhizotomy. Dev Med Child Neurol. 2008 Oct. 50(10):765-71. [Medline].

  8. Nordmark E, Josenby AL, Lagergren J, Andersson G, Strömblad LG, Westbom L. Long-term outcomes five years after selective dorsal rhizotomy. BMC Pediatr. 2008 Dec 14. 8:54. [Medline]. [Full Text].

  9. Mutch L, Alberman E, Hagberg B, Kodama K, Perat MV. Cerebral palsy epidemiology: where are we now and where are we going?. Dev Med Child Neurol. 1992 Jun. 34(6):547-51. [Medline].

  10. Bax M, Goldstein M, Rosenbaum P, Leviton A, Paneth N, Dan B, et al. Proposed definition and classification of cerebral palsy, April 2005. Dev Med Child Neurol. 2005 Aug. 47(8):571-6. [Medline].

  11. Shevell MI, Bodensteiner JB. Cerebral palsy: defining the problem. Semin Pediatr Neurol. 2004 Mar. 11(1):2-4. [Medline].

  12. Stanley F, Blair E, Alberman E. Cerebal Palsies: Epidemiology and Causal Pathways. London, United Kingdom: MacKeith Press; 2000.

  13. Jacobsson B, Hagberg G. Antenatal risk factors for cerebral palsy. Best Pract Res Clin Obstet Gynaecol. 2004 Jun. 18(3):425-36. [Medline].

  14. Odding E, Roebroeck ME, Stam HJ. The epidemiology of cerebral palsy: incidence, impairments and risk factors. Disabil Rehabil. 2006 Feb 28. 28(4):183-91. [Medline].

  15. Russman BS, Ashwal S. Evaluation of the child with cerebral palsy. Semin Pediatr Neurol. 2004 Mar. 11(1):47-57. [Medline].

  16. Doyle LW, Crowther CA, Middleton P, Marret S, Rouse D. Magnesium sulphate for women at risk of preterm birth for neuroprotection of the fetus. Cochrane Database Syst Rev. 2009 Jan 21. CD004661. [Medline].

  17. Rouse DJ, Hirtz DG, Thom E, Varner MW, Spong CY, Mercer BM, et al. A randomized, controlled trial of magnesium sulfate for the prevention of cerebral palsy. N Engl J Med. 2008 Aug 28. 359(9):895-905. [Medline]. [Full Text].

  18. Conde-Agudelo A, Romero R. Antenatal magnesium sulfate for the prevention of cerebral palsy in preterm infants less than 34 weeks' gestation: a systematic review and metaanalysis. Am J Obstet Gynecol. 2009 Jun. 200(6):595-609. [Medline].

  19. Volpe JJ. Neurology of the Newborn. 4th ed. Philadelphia, Pa: WB Saunders; 2001. 4.

  20. Moster D, Wilcox AJ, Vollset SE, Markestad T, Lie RT. Cerebral palsy among term and postterm births. JAMA. 2010 Sep 1. 304(9):976-82. [Medline].

  21. Papile LA, Burstein J, Burstein R, Koffler H. Incidence and evolution of subependymal and intraventricular hemorrhage: a study of infants with birth weights less than 1,500 gm. J Pediatr. 1978 Apr. 92(4):529-34. [Medline].

  22. Nelson KB. Can we prevent cerebral palsy?. N Engl J Med. 2003 Oct 30. 349(18):1765-9. [Medline].

  23. Lie KK, Grøholt EK, Eskild A. Association of cerebral palsy with Apgar score in low and normal birthweight infants: population based cohort study. BMJ. 2010 Oct 6. 341:c4990. [Medline]. [Full Text].

  24. American College of Obstetricians and Gynecologists, American Academy of Pediatrics. Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology. Washington, DC: American College of Obstetricians and Gynecologists; 2003. [Full Text].

  25. Capute AJ, Accardo PJ, eds. Developmental Disabilities in infancy and Childhood. 2nd ed. Baltimore, Md: Brookes Publishing; 2001. Vol 2.:

  26. Majnemer A, Mazer B. New directions in the outcome evaluation of children with cerebral palsy. Semin Pediatr Neurol. 2004 Mar. 11(1):11-7. [Medline].

  27. Vincer MJ, Allen AC, Joseph KS, Stinson DA, Scott H, Wood E. Increasing prevalence of cerebral palsy among very preterm infants: a population-based study. Pediatrics. 2006 Dec. 118(6):e1621-6. [Medline].

  28. Ancel PY, Livinec F, Larroque B, Marret S, Arnaud C, Pierrat V, et al. Cerebral palsy among very preterm children in relation to gestational age and neonatal ultrasound abnormalities: the EPIPAGE cohort study. Pediatrics. 2006 Mar. 117(3):828-35. [Medline].

  29. Dolk H, Pattenden S, Johnson A. Cerebral palsy, low birthweight and socio-economic deprivation: inequalities in a major cause of childhood disability. Paediatr Perinat Epidemiol. 2001 Oct. 15(4):359-63. [Medline].

  30. Strauss D, Shavelle R, Reynolds R, Rosenbloom L, Day S. Survival in cerebral palsy in the last 20 years: signs of improvement?. Dev Med Child Neurol. 2007 Feb. 49(2):86-92. [Medline].

  31. Hemming K, Hutton JL, Colver A, Platt MJ. Regional variation in survival of people with cerebral palsy in the United Kingdom. Pediatrics. 2005 Dec. 116(6):1383-90. [Medline].

  32. Hemming K, Hutton JL, Pharoah PO. Long-term survival for a cohort of adults with cerebral palsy. Dev Med Child Neurol. 2006 Feb. 48(2):90-5. [Medline].

  33. Hutton JL, Pharoah PO. Life expectancy in severe cerebral palsy. Arch Dis Child. 2006 Mar. 91(3):254-8. [Medline]. [Full Text].

  34. Verrall TC, Berenbaum S, Chad KE, Nanson JL, Zello GA. Children with Cerebral Palsy: Caregivers' Nutrition Knowledge, Attitudes and Beliefs. Can J Diet Pract Res. 2000 Autumn. 61(3):128-134. [Medline].

  35. Bax M, Tydeman C, Flodmark O. Clinical and MRI correlates of cerebral palsy: the European Cerebral Palsy Study. JAMA. 2006 Oct 4. 296(13):1602-8. [Medline].

  36. Woodward LJ, Anderson PJ, Austin NC, Howard K, Inder TE. Neonatal MRI to predict neurodevelopmental outcomes in preterm infants. N Engl J Med. 2006 Aug 17. 355(7):685-94. [Medline].

  37. Wyatt K, Edwards V, Franck L, Britten N, Creanor S, Maddick A, et al. Cranial osteopathy for children with cerebral palsy: a randomised controlled trial. Arch Dis Child. 2011 Jun. 96(6):505-12. [Medline].

  38. Edwards P, Sakzewski L, Copeland L, Gascoigne-Pees L, McLennan K, Thorley M, et al. Safety of Botulinum Toxin Type A for Children With Nonambulatory Cerebral Palsy. Pediatrics. 2015 Nov. 136 (5):895-904. [Medline].

  39. Blackmore AM, Boettcher-Hunt E, Jordan M, Chan MD. A systematic review of the effects of casting on equinus in children with cerebral palsy: an evidence report of the AACPDM. Dev Med Child Neurol. 2007 Oct. 49(10):781-90. [Medline].

  40. Delgado MR, Hirtz D, Aisen M, et al. Practice parameter: pharmacologic treatment of spasticity in children and adolescents with cerebral palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2010 Jan 26. 74(4):336-43. [Medline].

  41. Muthusamy K, Recktenwall SM, Friesen RM, Zuk J, Gralla J, Miller NH, et al. Effectiveness of an anesthetic continuous-infusion device in children with cerebral palsy undergoing orthopaedic surgery. J Pediatr Orthop. 2010 Dec. 30(8):840-5. [Medline].

  42. Perlman JM. Intrapartum hypoxic-ischemic cerebral injury and subsequent cerebral palsy: medicolegal issues. Pediatrics. 1997 Jun. 99(6):851-9. [Medline]. [Full Text].

  43. Du RY, McGrath CP, Yiu CK, King NM. Oral health behaviors of preschool children with cerebral palsy: a case-control community-based study. Spec Care Dentist. 2014 Nov-Dec. 34 (6):298-302. [Medline].

  44. Anderson P. FDA Clears Stimulation System for Foot Drop in Children. Medscape Medical News. Jan 25 2013. Available at Accessed: February 5, 2013.

  45. Dabney KW, Lipton GE, Miller F. Cerebral palsy. Curr Opin Pediatr. 1997 Feb. 9(1):81-8. [Medline].

  46. Girard S, Kadhim H, Roy M, Lavoie K, Brochu ME, Larouche A, et al. Role of perinatal inflammation in cerebral palsy. Pediatr Neurol. 2009 Mar. 40(3):168-74. [Medline].

  47. Jones MW, Morgan E, Shelton JE, Thorogood C. Cerebral palsy: introduction and diagnosis (part I). J Pediatr Health Care. 2007 May-Jun. 21(3):146-52. [Medline].

  48. Mattern-Baxter K. Effects of partial body weight supported treadmill training on children with cerebral palsy. Pediatr Phys Ther. 2009 Spring. 21(1):12-22. [Medline].

Magnetic resonance image (MRI) of a 1-year-old boy who was born at gestational week 27. The clinical examination was consistent with spastic diplegic cerebral palsy. Pseudocolpocephaly and decreased volume of the white matter posteriorly were consistent with periventricular leukomalacia. Evidence of diffuse polymicrogyria and thinning of the corpus callosum is noted in this image.
Magnetic resonance image (MRI) of a 16-month-old boy who was born at term but had an anoxic event at delivery. Examination findings were consistent with a spastic quadriplegic cerebral palsy with asymmetry (more prominent right-sided deficits). Cystic encephalomalacia in the left temporal and parietal regions, delayed myelination, decreased white matter volume, and enlarged ventricles can be seen in this image. These findings are most likely the sequelae of a neonatal insult (eg, periventricular leukomalacia with a superimposed left-sided cerebral infarct).
Magnetic resonance image (MRI) of a 9-day-old girl who was born at full term and had a perinatal hypoxic-ischemic event. Examination of the patient at 1 year revealed findings consistent with a mixed quadriparetic cerebral palsy notable for dystonia and spasticity. Severe hypoxic-ischemic injury to the medial aspect of the cerebellar hemispheres, medial temporal lobes, bilateral thalami, and bilateral corona radiata is observed in this image.
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