Pharmacologic treatment of spasticity in children and adolescents with cerebral palsy (an evidence-based review)

NEUROLOGY 2010;74:336-343
© 2010 American Academy of Neurology

Special Article

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
M. R. Delgado, MD, FRCPC, FAAN, D. Hirtz, MD, FAAN, M. Aisen, MD, FAAN, S. Ashwal, MD, FAAN, D. L. Fehlings, MD, MSc, FRCPC, J. McLaughlin, MD, L. A. Morrison, MD, M. W. Shrader, MD, A. Tilton, MD, FAAN and J. Vargus-Adams, MD, MS

From the University of Texas Southwestern Medical Center (M.R.D.), Dallas; National Institute of Neurological Disorders and Stroke (D.H.), Bethesda, MD; United Cerebral Palsy Research Foundation (M.A.); Loma Linda University (S.A.), Loma Linda, CA; Bloorview Kids Rehab (D.L.F.), Toronto, Canada; University of Washington (J.M.), Seattle; University of New Mexico (L.A.M.), Albuquerque; The Core Institute (M.W.S.), Sun City West, AZ; Louisiana State University (A.T.), New Orleans; and Cincinnati Children's Hospital (J.V.-A.), Cincinnati, OH.

Address correspondence and reprint requests to American Academy of Neurology, 1080 Montreal Avenue, St. Paul, MN 55116 guidelines@aan.com

Objective: To evaluate published evidence of efficacy and safety of pharmacologic treatments for childhood spasticity due to cerebral palsy.

Methods: A multidisciplinary panel systematically reviewed relevant literature from 1966 to July 2008.

Results: For localized/segmental spasticity, botulinum toxin type A is established as an effective treatment to reduce spasticity in the upper and lower extremities. There is conflicting evidence regarding functional improvement. Botulinum toxin type A was found to be generally safe in children with cerebral palsy; however, the Food and Drug Administration is presently investigating isolated cases of generalized weakness resulting in poor outcomes. No studies that met criteria are available on the use of phenol, alcohol, or botulinum toxin type B injections. For generalized spasticity, diazepam is probably effective in reducing spasticity, but there are insufficient data on its effect on motor function and its side-effect profile. Tizanidine is possibly effective, but there are insufficient data on its effect on function and its side-effect profile. There were insufficient data on the use of dantrolene, oral baclofen, and intrathecal baclofen, and toxicity was frequently reported.

Recommendations: For localized/segmental spasticity that warrants treatment, botulinum toxin type A should be offered as an effective and generally safe treatment (Level A). There are insufficient data to support or refute the use of phenol, alcohol, or botulinum toxin type B (Level U). For generalized spasticity that warrants treatment, diazepam should be considered for short-term treatment, with caution regarding toxicity (Level B), and tizanidine may be considered (Level C). There are insufficient data to support or refute use of dantrolene, oral baclofen, or continuous intrathecal baclofen (Level U).


Abbreviations: AAN = American Academy of Neurology; AE = adverse event; AS = Ashworth scale; BoNT-A = botulinum toxin type A; BoNT-B = botulinum toxin type B; CP = cerebral palsy; FDA = Food and Drug Administration; GAS = Goal Attainment Scale; GMFM = Gross Motor Function Measure; ITB = intrathecal baclofen; MAS = Modified Ashworth scale; OT = occupational therapy; PT = physiotherapy; QUEST = Quality of Upper Extremity Skills Test; TS = Tardieu scale.

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The prevalence of cerebral palsy (CP) was recently reported to be 3.6 cases per 1,000 in 8-year-old children,1 with very little variation among Western nations.2 More than 10,000 babies born in the United States each year will be affected by CP.3 CP is the most common cause of spasticity in children, and the majority of children with CP are affected by spasticity.4 The Taskforce on Childhood Motor Disorders defines spasticity as "hypertonia in which one or both of the following signs are present: 1) resistance to externally imposed movement increases with increasing speed of stretch and varies with the direction of joint movement; 2) resistance to externally imposed movement rises rapidly above a threshold speed of joint angle."5
Spasticity is one component of the multifaceted motor disability of CP and may not be the main factor interfering with function, participation, or activity.6 Alleviation of spasticity may not always be desirable; some patients may experience a decline in function with spasticity reduction.7 The decision to use antispasticity medications requires careful assessment of the patient's other impairments (e.g., weakness, movement disorders) and proper selection and use of the treatment. Reasons to treat spasticity include reducing pain and muscle spasms, facilitating brace use, improving posture, minimizing contractures and deformity, facilitating mobility and dexterity, and improving patient ease of care as well as hygiene/self-care.8

Several tools such as the Ashworth scale (AS)9 and the Modified Ashworth scale (MAS)10 have been used in clinical trials, with the assumption that they measure spasticity. These scales measure a broader set of neural and musculoskeletal factors of non-velocity-dependent hypertonia in addition to spasticity itself.11 A tool that is more consistent with the proposed definition of spasticity above is the Tardieu scale (TS).12 The TS accounts for the joint angle measure of the spastic phenomenon at different velocities of joint movement.

Over the last 20 years, several pharmacologic antispasticity treatments have been adapted for use in patients with CP. These include oral medications like benzodiazepines, dantrolene, baclofen, and tizanidine; neuromuscular blocking agents such as botulinum toxins A and B (BoNT-A and BoNT-B); chemical denervation using phenol and alcohol; and intrathecal baclofen (ITB).13 Oral medications and ITB are used when a generalized antispasticity effect is desired. Chemical denervation agents are used to treat localized (one extremity) or segmental (lower body, hemibody) spasticity. The mechanisms of action and pharmacology of these drugs are described in other publications.14,15

This article reviews and evaluates published evidence of the efficacy and safety of these medications in children and adolescents affected by spasticity due to CP.

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