eMedicine Specialties > Neurology > Pediatric Neurology

Cerebral Palsy: Treatment & Medication

Author: Ari S Zeldin, MD, Fellow, Divison of Pediatric Neurology, Department of Neurosciences, University of California at San Diego School of Medicine
Coauthor(s): Boosara Ratanawongsa, MD, Associate in Neurology, Department of Pediatric Neurology, Children's Specialists, University of California at San Diego; Alicia T F Bazzano, MD, MPH, Fellow and Clinical Instructor in Pediatrics, University of California at Los Angeles; Consulting Staff, Division of Pediatric Emergency Medicine, Harbor/UCLA Medical Center, Children's Hospital Los Angeles
Contributor Information and Disclosures

Updated: Mar 30, 2007

Treatment

Medical Care

The physician's responsibility is to closely supervise and manage the multiple medical complications associated with CP (see Complications).

  • The 2004 AAN practice parameter suggests screening for the following potential CP-associated deficits at the initial assessment:
    • Mental retardation
    • Ophthalmologic and hearing impairments
    • Speech and language disorders
    • Oromotor dysfunction
  • Various medications may improve spasticity.
  • Numerous medications, although often used off label for age and indication, may relieve the movement difficulties associated with CP. These drugs target dystonia, myoclonus, chorea, athetosis, and spasticity.
  • While antiparkinsonian drugs (eg, anticholinergic and dopaminergic drugs) and antispasticity agents (eg, baclofen) have primarily been used in the management of dystonia, anticonvulsants, antidopaminergic drugs, and antidepressants have also been tried.
  • Anticonvulsants (including benzodiazepines such as diazepam, valproic acid, and barbiturates) have been useful in the management of myoclonus. Chorea and athetosis are often difficult to manage, although benzodiazepines, neuroleptics, and antiparkinsonian drugs (eg, levodopa) have been tried. Benzodiazepines and baclofen are commonly used to manage spasticity.
  • Neurologists and rehabilitation medicine specialists (physiatrists) play significant roles in the management of antispasticity medications.
  • Seizure disorders are common in persons with CP, and the clinician should be comfortable with the management of anticonvulsant medications (see Antiepileptic Drugs: An Overview).

Consultations

  • A rehabilitation medicine specialist (physiatrist) should be consulted for the evaluation and management of the rehabilitation program (eg, equipment, coordination of therapy, spasticity management). Phenol intramuscular neurolysis and botulinum A toxin (BOTOX®) intramuscular blocks may reduce spasticity for 3-6 months. This can allow for improved range of motion, reduced deformity, improved response to occupational and physical therapy, and delay in the need for surgical management of spasticity.
  • An orthopedist should be consulted for the surgical management of hip dislocation, scoliosis, and spasticity (eg, tenotomy, a tendon-lengthening procedure).
  • A geneticist should be consulted to evaluate for an underlying genetic syndrome, particularly in the setting of dysmorphic features, multiple organ abnormalities, or a family history of a similar neurological syndrome.
  • A neurosurgeon should be consulted for identifying and treating hydrocephalus, a tethered spinal cord, or spasticity.
    • By cutting I-a sensory fibers, selective dorsal rhizotomy decreases spasticity by decreasing reflexive motoneuron activation, which is thought to result from the lack of descending fiber input.
    • Intrathecal baclofen can be administered via a pump implanted by a neurosurgeon. The pump is placed in the anterior abdominal wall and connects to a catheter inserted in the subarachnoid space overlying the conus of the spinal cord. Intrathecal baclofen can allow more local presynaptic inhibition of I-a sensory afferents and has fewer adverse effects than oral baclofen.
    • Although data are limited in this population, stereotactic basal ganglia surgery may improve rigidity, choreoathetosis, and tremor.
    • Additionally, reconstructive surgery to the upper extremities can restore muscle balance, release contractures, and stabilize joints to improve placement of the hand in space, as well as voluntary grasp, release, and pinch functions.
  • A gastroenterologist, nutritionist, and a feeding and swallowing team should be consulted for management of feeding and swallowing difficulties and gastroesophageal reflux and for assessment of nutritional status.
  • A pulmonologist should be consulted for the management of chronic pulmonary disease due to bronchopulmonary dysplasia and frequent or recurrent aspiration.
  • A multidisciplinary learning disability team specializing in children with special needs should be consulted to identify specific learning disabilities, monitor cognitive progression, and guide services through early intervention and school. The child should be evaluated by a communication enhancement center to guide speech and language treatment and the use of communicative devices.

Diet

Oromotor dysfunction may require limitations in the texture of food and liquid, feeding only by gastrostomy or jejunostomy tube, supplemental feedings via gastrostomy or jejunostomy tube to increase energy intake, and aspiration precautions.

Activity

Regular physical therapy and occupational therapy are crucial. The goal should be to maximize the functional use of limbs and ambulation and to reduce the risk of contractures.

Medication

The goal of pharmacotherapy is to reduce symptoms (eg, spasticity) and prevent complications (eg, contractures). Most of the medications used for CP 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. The indications and doses listed are from a general formulary. A wide range of dosing can be encountered in clinical practice because information in the literature regarding medication for CP in children is scant.

Benzodiazepines

Used in the acute management of seizures that may accompany CP. By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate neurotransmission of GABA and other inhibitory transmitters.


Diazepam (Valium)

Effective in treating seizures; depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Individualize dosage and increase cautiously to avoid adverse effects.

Adult

5-10 mg PO/IV/IM q4-6h

Pediatric

<6 months: Not recommended
> 6 months: 0.05-0.3 mg/kg/dose IV/IM over 2-3 min; repeat in 2-4 h prn; alternatively, 0.12-0.8 mg/kg/24h PO divided q6-8h; not to exceed 10 mg/dose

Toxicity in CNS increased by phenothiazines, barbiturates, alcohols, or MAOIs; cisapride can increase toxicity significantly

Documented hypersensitivity, narrow-angle glaucoma

Pregnancy

D - Unsafe in pregnancy

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Anticonvulsants

Used to terminate clinical and electrical seizure activity as rapidly as possible and to prevent seizure recurrence.


Valproic acid (Depakote, Depakene, Depacon)

Chemically unrelated to other drugs used to treat seizure disorders. Although mechanism of action not established, activity may be related to increased brain levels of GABA or enhanced GABA action; also may potentiate postsynaptic GABA responses, affect potassium channels, or have direct membrane-stabilizing effect.
For conversion to monotherapy, concomitant antiepilepsy drug dosage ordinarily can be reduced by approximately 25% q2wk. Reduction may start at initiation of therapy or be delayed by 1-2 wk if concern that seizures may occur. Monitor patients closely during this period for increased seizure frequency.
As adjunctive therapy, divalproex sodium may be added to patient's regimen at 10-15 mg/kg/d. May increase by 5-10 mg/kg/wk to achieve optimal clinical response. Ordinarily, optimal clinical response achieved at daily doses <60 mg/kg/d.

Adult

Monotherapy: 10-15 mg/kg/d PO qd or divided bid/tid; if daily dose >250 mg, give in divided doses; increase by 5-10 mg/kg/wk until seizures are controlled or adverse effects prevent further increases; not to exceed 60 mg/kg/d

Pediatric

Administer as in adults

Coadministration with cimetidine, salicylates, felbamate, or erythromycin may increase toxicity; rifampin may significantly reduce levels; in pediatric patients, protein binding and metabolism decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations with possible loss of seizure control; may increase diazepam and ethosuximide toxicity (monitor closely); may increase phenobarbital and phenytoin levels, while either one may decrease valproic acid levels; may displace warfarin from protein-binding sites (monitor coagulation tests); may increase zidovudine levels in HIV-seropositive patients

Documented hypersensitivity, hepatic disease or dysfunction

Pregnancy

D - Unsafe in pregnancy

Precautions

Thrombocytopenia and abnormal coagulation parameters have occurred; risk of thrombocytopenia increases significantly at total trough plasma concentrations >110 mcg/mL in females and >135 mcg/mL in males; at periodic intervals and prior to surgery, determine platelet counts and bleeding time before initiating therapy; reduce dose or discontinue therapy if hemorrhage, bruising, or a hemostasis/coagulation disorder occurs; hyperammonemia may occur, resulting in hepatotoxicity; monitor patients closely for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness


Phenobarbital (Luminal, Barbita)

Exhibits anticonvulsant activity in anesthetic doses and can be administered orally; in status epilepticus, important to achieve therapeutic levels as quickly as possible. IV dose may require approximately 15 min to attain peak levels in brain. If injected continuously until convulsions stop, brain concentrations may continue to rise and can exceed that required to control seizures. Important to use minimal amount required and to wait for anticonvulsant effect to develop before giving second dose.
If IM route chosen, administer into areas with little risk of encountering nerve trunk or major artery, such as large muscle (eg, gluteus maximus, vastus lateralis). A permanent neurological deficit may result from injecting into or near peripheral nerves.
Restrict IV use to conditions in which other routes are not possible, either because patient is unconscious or because prompt action required.

Adult

60-100 mg/d PO; 200-320 mg IV/IM q6h prn

Pediatric

3-6 mg/kg/d PO; alternatively, 4-6 mg/kg/d IV/IM for 7-10 d to attain blood level of 10-15 mcg/mL or 10-15 mg/kg/d

Coadministration with alcohol may produce additive CNS effects and death; chloramphenicol and MAOIs may increase effects; may decrease chloramphenicol effects; MAOIs may enhance sedative effects of barbiturates; rifampin may decrease effects; valproic acid appears to decrease barbiturate metabolism and increase toxicity; barbiturates can decrease effects of anticoagulants, and patients stabilized on anticoagulants may require dosage adjustments if barbiturates added to or withdrawn from their regimen; may decrease serum carbamazepine levels; may decrease effects of contraceptives because of induction of microsomal enzymes; in women, menstrual irregularities and pregnancy may occur; barbiturates may decrease corticosteroid effects by inducing hepatic microsomal enzymes; barbiturates may increase digitoxin metabolism; may decrease antimicrobial effects of metronidazole; barbiturates decrease theophylline levels, possibly resulting in decreased effects; may decrease bioavailability of verapamil

Documented hypersensitivity, severe respiratory disease, marked impairment of liver function, nephritis

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; exercise caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; use caution in patients with myasthenia gravis or myxedema

Dopamine prodrugs

Dopamine does not 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.


Levodopa/carbidopa (Sinemet, Sinemet CR)

A large neutral amino acid absorbed in proximal small intestine by saturable carrier-mediated transport system; absorption decreased by meals that include other large neutral amino acids. Only patients with meaningful motor fluctuations need consider a low-protein or protein-redistributed diet. Greater consistency of absorption achieved when taken 1 h or more after meals. Nausea often reduced if taken immediately following meals. Some patients with nausea benefit from additional carbidopa in doses up to 200 mg/d. Half-life approximately 2 h.
Most common acute adverse effects are nausea, hypotension, and hallucinations. Long-term adverse effects include motor fluctuations and dyskinesia (chorea)
Provide at least 70-100 mg/d carbidopa. When more carbidopa required, substitute one 25/100 tab for each 10/100 tab. When more levodopa required, substitute 25/250 tab for 25/100 or 10/100 tab.
CR formulation more slowly absorbed and provides more sustained levodopa levels than IR form. CR form as effective as IR form when levodopa initially required and may be more convenient when fewer intakes are desired.
Patients with dissipating motor fluctuations (and no dyskinesia) often benefit from prolongation of short duration response when switched from IR to CR form. However, patients with meaningful fluctuations and dyskinesia often experience an increase in dyskinesia when switched to CR formulation.
Doses and dosing intervals of CR form may be increased or decreased based on response. Most patients have been treated adequately with 2-8 tab/d (divided doses) at intervals of 4-8 h while awake. Higher doses (>12 tab/d) and intervals <4 h have been used but usually are not recommended. If <4-h interval used or if divided doses are not equal, give smaller doses at end of day. Allow at least a 3-d interval between dosage adjustments. May administer as whole or half tab, which should not be crushed or chewed. Most patients are controlled on a levodopa dose of 300-600 mg for several years.

Adult

IR tab: 1 tab 25 mg carbidopa/100 mg levodopa PO tid or 10 mg carbidopa/100 mg levodopa tid/qid; may increase by 1 tab qd or qod prn; not to exceed 8 tab/d
Tab of 2 ratios (ie, 1:4, 25/100; 1:10, 10/100 and 25/250) may be given separately or combined prn to provide optimum dosage
CR tab: 1 tab PO bid; not more frequently than q6h

Pediatric

Not established

Hydantoins, pyridoxine, phenothiazine, and hypotensive agents may decrease effects; toxicity increases with antacids and MAOIs

Documented hypersensitivity, narrow-angle glaucoma, malignant melanoma, undiagnosed skin lesions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Certain adverse CNS effects (eg, dyskinesias) may occur at lower dosages and earlier in therapy with CR form; caution in patients with history of MI, arrhythmias, asthma, or peptic ulcer disease; sudden discontinuation may cause worsening of Parkinson disease; high-protein diets should be distributed throughout day to avoid fluctuations in levodopa absorption

Anticholinergics

Provide benefit for tremor in approximately 50% of patients but 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 (Artane, Trihexy)

A synthetic tertiary amine anticholinergic agent that reduces 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 action of dopamine.

Adult

1-2 mg/d PO; increase by 2 mg q3-5d
Maintenance dose: 4-15 mg/d PO divided tid/qid; young adults may tolerate 15-20 mg/d divided tid/qid; 4-8 mg/d for older individuals

Pediatric

Not established

Amantadine may increase anticholinergic adverse effects that disappear when dose is reduced; haloperidol may result in worsening of schizophrenic symptoms because of decreased haloperidol serum concentrations; pharmacologic/therapeutic actions of phenothiazines may be reduced by concurrent anticholinergics

Documented hypersensitivity, glaucoma, peptic ulcers, pyloric or duodenal obstruction, stenosing prostatic hypertrophy or bladder neck obstructions, achalasia, toxic megacolon

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Dose adjustment may be required in geriatric patients; caution in patients with tachycardia, cardiac hypotension, prostatic hypertrophy, arrhythmias, hypertension, or any tendency toward urinary retention, liver or kidney disorders, or obstructive disease of GI or GU tract; if dry mouth is severe and impairs swallowing or speaking or if loss of appetite and weight occurs, reduce dosage or temporarily discontinue medication

Toxins

Botulinum toxin type A is DOC. It causes presynaptic paralysis of myoneural junctions and reduces abnormal contractions. Therapeutic effects may last 3-6 months.


Botulinum toxin type A (BOTOX®)

Treats excessive, abnormal contractions associated with blepharospasm. Binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which, in turn, inhibits transmission of impulses in neuromuscular tissue.
Re-examine patients 7-14 d after initial dose to assess for response. Increase doses 2-fold over previous for patients experiencing incomplete paralysis of target muscle. Do not exceed 25 U when giving as single injection or 200 U as cumulative dose in 30-d period.

Adult

1.25-2.5 U (0.05-0.1 mL) injection into most active neck muscles; give q3-4mo; double next dose if paralysis of target muscle incomplete; not to exceed 25 U/single injection or 200 U/mo

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Aminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Do not exceed recommended dosages and frequencies of administration; presence of antibodies to botulinum toxin type A may reduce effects of therapy

Muscle relaxants

The muscle-relaxing effects may come from inhibition of the transmission of monosynaptic and polysynaptic reflexes at the spinal cord level.


Baclofen (Lioresal)

May induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at spinal level.

Adult

Initial dosing schedule: 5 mg PO tid for 3 d; 10 mg PO tid for 3 d; 15 mg PO tid for 3 d; 20 mg PO tid for 3 d; thereafter, additional increases prn; not to exceed 80 mg/d PO divided qid
Maintenance dose: 40-80 mg/d PO

Pediatric

Not established

Opiate analgesics, benzodiazepines, alcohol, TCAs, guanabenz, MAOIs, clindamycin, and hypertensive agents may increase effects

Pregnancy

D - Unsafe in pregnancy

Precautions

Caution in patients with history of autonomic dysreflexia and when spasticity is used to obtain increased function; autonomic dysreflexia can result from withdrawal

More on Cerebral Palsy

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Multimedia: Cerebral Palsy
References
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Further Reading

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Keywords

CP, MRCP, brain paralysis, static encephalopathy, periventricular leukomalacia, cerebral injury, premature birth, hypoperfusion, germinal matrix hemorrhage, spastic diplegia, periventricular hemorrhage, intraventricular hemorrhage, subependymal hemorrhage, germinal matrix hemorrhage, periventricular hemorrhagic venous infarction, intraparenchymal hemorrhage, ipsilateral germinal matrix hemorrhage, acute hyperbilirubin encephalopathy, chorionitis, spastic hemiplegia

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Contributor Information and Disclosures

Author

Ari S Zeldin, MD, Fellow, Divison of Pediatric Neurology, Department of Neurosciences, University of California at San Diego School of Medicine
Ari S Zeldin, MD is a member of the following medical societies: American Academy of Cerebral Palsy and Developmental Medicine and American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Boosara Ratanawongsa, MD, Associate in Neurology, Department of Pediatric Neurology, Children's Specialists, University of California at San Diego
Boosara Ratanawongsa, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, and Child Neurology Society
Disclosure: Nothing to disclose.

Alicia T F Bazzano, MD, MPH, Fellow and Clinical Instructor in Pediatrics, University of California at Los Angeles; Consulting Staff, Division of Pediatric Emergency Medicine, Harbor/UCLA Medical Center, Children's Hospital Los Angeles
Alicia T F Bazzano, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Public Health Association, and American Society for Bioethics and Humanities
Disclosure: Nothing to disclose.

Medical Editor

Ann M Neumeyer, MD, Clinic Director, Instructor, Departments of Neurology and Pediatrics, Massachusetts General Hospital, 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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Kenneth J Mack, MD, PhD, Senior Associate Consultant, Department of Child and Adolescent Neurology, Mayo Clinic
Kenneth J Mack, MD, PhD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society, Phi Beta Kappa, and Society for Neuroscience
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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