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Spasticity
Last Updated: May 23, 2005
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Section 1 of 10
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other
Medical Treatments Surgical Treatments Physical And Occupational Therapy Summary Resources And
Advocacy Groups Bibliography
Author: Zeba F Vanek, MD, Clinical Director, Assistant Professor,
Department of Neurology, University of California at Los Angeles
Coauthor(s): John H Menkes, MD , Director Emeritus, Pediatric
Neurology, Cedars-Sinai Medical Center; Professor Emeritus,
Department of Neurology, University of California at Los Angeles
Zeba F Vanek, MD, is a member of the following medical societies:
Movement Disorders Society
Editor(s): Joseph R Carcione, Jr, DO, MBA , Consultant in Neurology
and Medical Acupuncture, Medical Management and Organizational
Consulting, Central Westchester Neuromuscular Care, PC; Medical
Director, Oxford Health Plans; Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor, eMedicine; Glenn Lopate, MD, Associate
Professor, Department of Neurology, Division of Neuromuscular
Diseases, Washington University School of Medicine; Chief of
Neurology, St Louis ConnectCare; Selim R Benbadis, MD, Director
of Comprehensive Epilepsy Program, Professor, Departments of
Neurology and Neurosurgery, University of South Florida, Tampa
General Hospital; and Nicholas Lorenzo, MD, Chief Editor,
eMedicine Neurology; Consulting Staff, Neurology Specialists and
Consultants
INTRODUCTION AND
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Synonyms and related keywords: increased muscular tone, increased muscle tone,
increased stretch reflexes, hyperexcitability of the stretch reflex, paresis, upper motor
neuron syndrome, spinal cord injury, multiple sclerosis, MS, botulinum toxin type A,
botulinum toxin type B, damage to motor pathways, hyporeflexia, clonus, clasp -knife
phenomenon, hyperreflexia, Babinski sign, flexor reflexes, flexor spasms
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Section 2 of 10
7/26/2005
eMedicine - Spasticity : Article by Zeba F Vanek, MD
Page 2 of 24
PATHOPHYSIOLOGY
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other
Medical Treatments Surgical Treatments Physical And Occupational Therapy Summary Resources And
Advocacy Groups Bibliography
Introduction
Spasticity has been defined as an increase in muscle tone due to
hyperexcitability of the stretch reflex and is characterized by a velocitydependent increase in tonic stretch reflexes (Lance, 1980).
Spasticity usually is accompanied by paresis and other signs, such as
increased stretch reflexes, collectively called the upper motor neuron
syndrome. Paresis particularly affects distal muscles, with loss of the
ability to perform fractionated movements of the digits. The upper
motor neuron syndrome results from damage to descending motor
pathways at cortical, brainstem, or spinal cord levels, and spasticity
evolves in the days and weeks after injury. When the injury that leads
to spasticity is acute, muscle tone is flaccid with hyporeflexia before
the appearance of spasticity. The interval between injury and the
appearance of spasticity varies from days to months according to the
level of the lesion. In addition to weakness and increased muscle tone,
the signs in spasticity include clonus, the clasp-knife phenomenon,
hyperreflexia, the Babinski sign, flexor reflexes, and flexor spasms.
Pathophysiology
The pathophysiologic basis of spasticity is incompletely understood.
The changes in muscle tone probably result from alterations in the
balance of inputs from reticulospinal and other descending pathways
to the motor and interneuronal circuits of the spinal cord, and the
absence of an intact corticospinal system. Loss of descending tonic or
phasic excitatory and inhibitory inputs to the spinal motor apparatus,
alterations in the segmental balance of excitatory and inhibitory
control, denervation supersensitivity, and neuronal sprouting may be
observed. Once spasticity is established, the chronically shortened
muscle may develop physical changes such as shortening and
contracture that further contribute to muscle stiffness (Dietz, 1981).
Selective damage to area 4 in the cerebral cortex of primates produces
paresis that improves with time, but increases in muscle tone are not a
prominent feature. Lesions involving area 6 cause impairment of
postural control in the contralateral limbs. Combined lesions of areas 4
and 6 cause both paresis and spasticity to develop (Tower, 1940).
Physiologic evidence suggests that interruption of reticulospinal
projections is important in the genesis of spasticity (Burke, 1972). In
spinal cord lesions, bilateral damage to the pyramidal and
reticulospinal pathways can produce severe spasticity and flexor
spasms, reflecting increased tone in flexor muscle groups and
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weakness of extensor muscles.
The pathophysiologic mechanisms causing the increase in stretch
reflexes in spasticity also are not well understood. Unlike healthy
subjects, in whom rapid muscle stretch does not elicit reflex muscle
activity beyond the normal short-latency tendon reflex, patients with
spasticity experience prolonged muscle contraction when spastic
muscles are stretched. After an acute injury, the ease with which
muscle activity is evoked by stretch increases in the first month of
spasticity; then, the threshold remains stable until declining after a year
(Thilmann, 1991).
During the development of spasticity, the spinal cord undergoes
neurophysiologic changes in the excitability of motor neurons,
interneuronal connections, and local reflex pathways. The excitability
of alpha motor neurons is increased, as is suggested by enhanced HM ratios (Angel and Hoffmann, 1983) and F-wave amplitudes (Eisen
and Odusote, 1979). Judged by recordings from Ia spindle afferents,
muscle spindle sensitivity is not increased in human spasticity
(Hagbarth, 1973).
Local anesthetic injections into spastic muscles in man can diminish
spasticity by an effect on gamma motor neurons. Renshaw cells
receive inputs from descending motor pathways, and recurrent
collateral axons from motor neurons activate Renshaw cells, which
inhibit gamma motor neurons. Renshaw cell activity is not reduced
significantly in spasticity (Katz and Pierrot-Deseilligny, 1982).
Reciprocal inhibition between antagonist muscles is mediated by the Ia
inhibitory interneuron, which also receives input from descending
pathways. Altered activity in Ia pathways has been shown in spasticity
(Nakashima, 1989). Inhibitory interneurons acting on primary afferent
terminals of the alpha motor neuron also influence the local circuitry.
Finally, plasticity and the formation of new aberrant connections in the
CNS is another theoretical explanation for some of the events in
spasticity.
CLINICAL CONSIDERATIONS
Section 3 of 10
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other
Medical Treatments Surgical Treatments Physical And Occupational Therapy Summary Resources And
Advocacy Groups Bibliography
Clinical considerations
Spasticity is associated with some very common neurological
disorders—multiple sclerosis, stroke, cerebral palsy, spinal cord and
brain injuries, and neurodegenerative diseases affecting the upper
motor neuron, pyramidal and extrapyramidal pathways. While the
incidence of spasticity is not known with certainty, it likely affects over
half a million people in the United States and over 12 million
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worldwide.
Rizzo et al have analyzed a cross-sectional database of 17,501
patients with multiple sclerosis (NARCOMS registry). Of these patients
with multiple sclerosis, 15.7% had no spasticity, 50.3% had minimal to
mild spasticity, 17.2% had moderate spasticity, and 16.8% had severe
spasticity (Rizzo, 2004).
A review of spasticity after stroke has shown that it affects less than
one quarter of stroke victims. Ninety-five patients were studied
immediately after and 3 months after a first-time stroke. Seventy-seven
(81%) were initially hemiparetic, of whom 20 had spasticity. Modified
Ashworth score was grade 1 in 10 patients, grade 1+ in 7 patients, and
grade 2 in 3 patients. At 3 months, 64 patients (67%) were hemiparetic
and 18 were spastic, reflecting 5 whose tone normalized and 3 who
became spastic in the interim (Sommerfeld, 2004). Spasticity can have
a devastating affect on function, comfort, and care delivery, and it also
may lead to musculoskeletal complications. Spasticity does not always
require treatment, but when it does, a wide range of effective
therapies—used alone or in combination—are now available.
Assessment
Assessment of spasticity includes identifying which muscles or muscle
groups are overactive and determining the effect of spasticity on all
aspects of patient function, including mobility, employment, and
activities of daily living (ADLs). Physical and occupational therapists
are vital members of the team called in to assess and treat the patient
with spasticity. Identification of the spastic muscles can be a complex
task, since many muscles may cross the joint involved, and not all
muscles with the potential to cause deformity will be spastic.
Electromyography and diagnostic blocks with local anesthetics can be
used to test hypotheses regarding the deformity and provide
information for long-term denervation treatments (Mayer, 1997).
Spasticity of the upper extremities
Muscles that often contribute to spastic adduction/internal rotation
dysfunction of the shoulder include latissimus dorsi, teres major, the
clavicular and sternal heads of pectoralis major, and subscapularis. In
the flexed elbow, the brachioradialis is spastic more often than the
biceps and brachialis. In the spastic flexed wrist, carpal tunnel
symptoms may develop. Flexion with radial deviation implicates flexor
carpi radialis.
In the clenched fist, if the proximal interphalangeal (PIP) joints flex
while the distal interphalangeal (DIP) joints remain extended, spasticity
of the flexor digitorum superficialis (FDS) rather than the flexor
digitorum profundus (FDP) may be suspected. A combined
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metacarpophalangeal flexion and PIP extension also may occur. A
patient may be spastic in only one or two muscle slips of either FDP or
FDS. Neurolysis with botulinum toxin is beneficial for spasticity of the
intrinsic hand muscles because of their size and accessibility.
Spasticity of the lower extremities
Spastic deformities of the lower limbs affect ambulation, bed
positioning, sitting, chair level activities, transfers, and standing up.
Equinovarus is the most common pathologic posture seen in the lower
extremity. Equinovarus is a key deformity that can prevent even limited
functional ambulation or unassisted transfers. Chemodenervation of
the extensor hallucis longus (EHL) for striatal toe (ie, hitchhiker's great
toe) may reveal co-contraction of the flexor hallucis longus (FHL),
which also requires treatment. Overactivity of the hamstrings may
indicate that knee stiffness is a defense against knee flexion collapse.
Diagnostic motor point block may reveal whether weakening strategies
are indicated for reducing knee stiffness. In the flexed knee,
overactivity in the hamstrings is more often medial than lateral.
Hamstring contracture is likely to occur from chronic overactivity.
Adductor and hip flexor spasticity often coexist and may lead to pelvic
obliquity. Complex hip and knee deformities may require a combination
of neurolytic and chemodenervation agents.
Physical and occupational therapy evaluation
Physical and occupational therapists play important roles in the
management of patients with spasticity. Patients who are candidates
for treatment with botulinum toxin injections need baseline evaluations
that include areas beyond the muscles being injected, since reduction
of local spasticity may lead to more widespread functional changes.
Assessments should include evaluation of tone, mobility, strength,
balance, endurance, and the need, if any, for assistive devices. A
videotape of the baseline examination is of considerable help.
After injection, therapeutic interventions have multiple aims, including
strengthening and facilitation, increasing range of motion, retraining of
ambulation and gait, improving the fit and tolerance of orthoses, and
improved functioning in ADLs (Albany, 1997). Decreased spasticity
and improvements in range of motion and strength have considerable
implications for activities such as dressing, bathing, feeding, and
grooming.
Standardized assessments for motor control that can be tested for
validity and reliability have yet to be devised for use in the patient with
neurological deficits. Because the assessment measures themselves
may influence tone, running the testing series in the same order each
time is important. Muscle tone should be assessed before any
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functional assessments. The upper extremity is evaluated in the sitting
position, and the shoulder rotators, pronators, supinators, wrist
flexors/extensors, and finger flexors are assessed with the elbow in
90° of flexion. Other muscle groups are assessed with the elbow
extended.
The patient is placed in the supine position for assessment of all
muscle groups of the lower extremity except the knee flexors. The
patient is then moved to the prone position for assessment of the right,
then the left, knee flexors. The Modified Ashworth Scale assessment
should be followed by the Bilateral Adductor Tone measure, if
required. Goniometric measurements for active and passive ranges of
movement follow muscle tone assessment.
Outcome measures
Measures designed to assess technical and functional outcomes,
patient satisfaction, and the cost-effectiveness of treatment can be
used to evaluate status and track changes in spasticity management.
While double -blind, placebo-controlled studies remain the standard for
clinical testing, the single-subject design is a useful alternative in many
treatment protocols. Development of validated and reliable outcome
measures for spasticity rehabilitation has been hampered by the
difficulty of quantifying functionally important parameters such as pain,
ease of care, and mobility. Because no single tool can measure the
many types of changes possible with treatment, the choice of
assessment tools must be based on the functional changes expected
from the treatment. A wide range of assessment tools have been
reviewed critically for their sensitivity, reliability, validity, and ease of
administration (Pierson, 1997).
Most spasticity rating scales are ordinal. Equal intervals between units
on an ordinal scale cannot be assumed automatically. Non-interval
scaling can be addressed using Rasch analysis, though care must be
taken to avoid inappropriate extrapolation. Ratio scales, such as
before/after measurements, are useful, reliable, and easy to
administer. A technical outcome is an expected change in a
measurable variable, based on the technical goals of a procedure. A
functional outcome is an expected change in a patient's ability to
perform a task. Patient satisfaction measures are concerned with both
the result and the process of care delivery. The choice of test must be
based on the change expected, and the sensitivity must match the
range of expected improvement. Otherwise, the results will be
meaningless. Changes in technical measures of spasticity may not
correlate well with clinical improvement.
Because agreement among clinical spasticity scales is poor, a
comprehensive set of tests is needed to evaluate the effects of
treatment. Some of the more commonly used spasticity rating scales
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are the Spasm Frequency Scale, the Medical Research Council Motor
Testing Scale, the Modified Ashworth Scale, the Adductor Tone
Rating, and the Global Pain Scale.
Burridge et al (2005) have recently discussed the theoretical and
methodological considerations in the measurement of spasticity. They
analyzed the measurement of spasticity in the clinical and research
environments; made recommendations based on the SPASM reviews
of biomechanical, neurophysiological, and clinical methods of
measuring spasticity; and indicated future developments of
measurement tools. They concluded that methods appropriate for use
in research, particularly into the mechanism of spasticity, do not often
satisfy the needs of the clinician and the need for an objective but
clinically applicable tool is still needed; therefore, standardized
protocols for ”best practice” in the application of spasticity
measurement tools and scales are needed.
Treatment overview
A variety of strategies are available for the management of spasticity.
The treatment of children with spasticity has been the subject of
innumerable publications, most of them surprisingly uncritical and
devoid of controls. A vital preliminary consideration is the indication for
treatment and the expectations from such treatments. For example, in
a patient who can walk, a reduction of leg muscle tone may worsen
mobility if tone compensates for leg weakness, allowing the patient to
stand. Loss of manual dexterity or weakness also does not improve by
reducing muscle tone, and therefore treatment of spasticity may not
lead to an improvement in function.
Therefore, clearly identifying the goals of the patient and caregiver is
vital. Tizard (1980) proposes that before treatment is initiated, the
following should be considered: (1) does the patient need treatment?,
(2) what are the aims of treatment?, (3) does the patient and
caregivers have the time required for treatment?, and (4) will treatment
disrupt the life of the patient and caregivers? Specific functional
objectives in the management of spasticity include strategies aimed at
improving gait, hygiene, ADLs, pain, and ease of care; decreasing the
frequency of spasm and related discomfort; and eliminating noxious
stimuli.
Various means are available for the treatment of spasticity.
Physiotherapy is the most traditional form of treatment and is the
principal nonsurgical treatment of spasticity in children. A variety of
oral medications have been proposed. Other treatments include
neurolysis with the neurotoxins phenol and alcohol, intrathecal
baclofen, intramuscular botulinum injection and surgical treatments,
along with appropriate physical and occupational therapies. In the
following sections, these treatment options are discussed in depth.
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ORAL MEDICATIONS
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Section 4 of 10
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other
Medical Treatments Surgical Treatments Physical And Occupational Therapy Summary Resources And
Advocacy Groups Bibliography
The use of oral medications for the treatment of spasticity may be very
effective. At high dosages, however, oral medications can cause
unwanted adverse effects that include sedation as well as changes in
mood and cognition. These adverse effects preclude their extensive
use in children, since the intellectual function of the majority of children
with spasticity is at best precarious, and sedation inevitably results in
some degree of impaired learning or school performance.
Benzodiazepines - Diazepam and clonazepam
The benzodiazepines bind in the brain stem and at the spinal cord
level and increase the affinity of GABA to the GABA -A receptor
complex. This results in an increase in presynaptic inhibition and then
reduction of monosynaptic and polysynaptic reflexes. These drugs
may improve passive range of motion and reduce hyperreflexia, painful
spasms, and anxiety. Diazepam has a half-life of 20-80 hours and
forms active metabolites that prolong its effectiveness. The half-life of
clonazepam ranges from 18-28 hours. Benzodiazepines should be
started at low dosages and increased slowly. In adults, diazepam can
be started at 5 mg at bedtime, and if daytime therapy is indicated, the
drug can be increased slowly to 60 mg/d given in divided doses.
Clonazepam can be started at 0.5 mg at night and slowly increased to
a maximum of 20 mg/d in 3 divided doses.
Sedation, weakness, hypotension, adverse gastrointestinal effects,
memory impairment, incoordination, confusion, depression, and ataxia
may occur. Tolerance and dependency can occur, and withdrawal
phenomena, notably seizures, have been associated with abrupt
cessation of therapy. Patients who are taking benzodiazepines with
agents such as baclofen or tizanidine that potentiate sedation and
have central depressant properties should be monitored carefully
(Gracies, 1997).
Baclofen - Oral and intrathecal pump
Baclofen is a GABA agonist, and its primary site of action is the spinal
cord, where it reduces the release of excitatory neurotransmitters and
substance P by binding to the GABA-B receptor. Studies show that
baclofen improves clonus, flexor spasm frequency, and joint range of
motion, resulting in improved functional status.
In the analysis of the database of 17,501 patients with multiple
sclerosis, Rizzo et al found that the use of oral medication was
proportional to the severity of spasticity, with 78% of patients who were
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severely affected using at least one drug and 46% using at least two.
Baclofen was the most commonly used agent, followed by gabapentin,
tizanidine, and diazepam. Comparison of 198 patients who used
intrathecal baclofen (ITB) and 315 who used oral medications showed
that those who used ITB had lower levels of spasticity, less leg
stiffness, less pain, and fewer spasms.
The oral dose of baclofen used to treat spasticity ranges from 30-100
mg/d in divided amounts. Tolerance may develop, and the drug must
be tapered slowly to prevent withdrawal effects such as seizures,
hallucinations, and increased spasticity. Baclofen must be used with
care in patients with renal insufficiency, as its clearance is primarily
renal. Adverse effects include sedation, ataxia, weakness, and fatigue.
When used in combination with tizanidine or benzodiazepines, the
patient should be monitored for unwanted depressant effects (Gracies,
1997).
Adverse effects of baclofen can be minimized by intrathecal infusion of
the drug, because the concentration gradient favors higher levels at
the spinal cord versus the brain. Intrathecal baclofen is approved in the
United States for the treatment of spasticity of spinal or cerebral origin.
In children, intrathecal baclofen is particularly effective for the
treatment of spasticity of the lower extremities in a selected group of
patients who have responded favorably to a trial dose of intrathecal
baclofen. Complications of the procedure are relatively few and usually
are limited to mechanical failures of the pump or the catheter. Adverse
drug effects are usually temporary and can be managed by reducing
the rate of infusion.
Dantrolene sodium
Dantrolene sodium is useful for spasticity of supraspinal origin,
particularly in patients with cerebral palsy or traumatic brain injury. It
decreases muscle tone, clonus, and muscle spasm. It acts at the level
of the muscle fiber, affecting the release of calcium from the
sarcoplasmic reticulum of skeletal muscle and thus reducing muscle
contraction. It is, therefore, less likely than the other agents to cause
adverse cognitive effects. Its peak effect is at 4 -6 hours, with a half-life
of 6-9 hours. The dose range is 25-400 mg/d in divided doses
(children, dose range 0.5-3.0 mg/kg/d).
Adverse effects include generalized weakness, including weakness of
the respiratory muscles, drowsiness, dizziness, weakness, fatigue, and
diarrhea. Hepatotoxicity occurs in fewer than 1% of patients; this
elevation in liver function test results is seen particularly in adolescents
and women who have been treated for greater than 60 days and at
dosages greater than 300 mg/d. Dantrolene should not be used with
other agents known to cause hepatotoxicity, including tizanidine. If no
benefit is seen after 4-6 weeks of treatment at maximal therapeutic
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doses, the medication should be discontinued (Katrak, 1992).
Tizanidine
Data from approximately 50 clinical trials indicate that tizanidine
(Zanaflex) is a new and effective therapeutic option for the
management of spasticity due to cerebral or spinal damage. Tizanidine
is an imidazoline derivative and a central alpha2-noradrenergic
agonist. The antispasticity effects of tizanidine are the probable result
of inhibition of the H-reflex. It also may facilitate inhibitory actions of
glycine and reduce release of excitatory amino acids and substance P,
and may have analgesic effects. While spasms and clonus are
reduced in patients using tizanidine, the Ashworth Scale does not
reveal significant differences from placebo groups. In the long term,
however, tizanidine does improve spasms and clonus.
Patients report less muscle weakness from tizanidine than from
baclofen or diazepam. The efficacy of tizanidine in reducing muscle
tone defined by various placebo-controlled studies is comparable to
that of baclofen and better than that of diazepam. When combined with
baclofen, tizanidine presents the opportunity to maximize therapeutic
effects and minimize adverse effects by reducing the dosages of both
drugs. If tizanidine is prescribed in conjunction with baclofen or
benzodiazepines, the patient should be advised of possible potential
additive effects, including sedation. In addition, when tizanidine is
prescribed with benzodiazepines, liver enzymes should be monitored
closely since the combination increases the likelihood of liver toxicity.
Tizanidine hydrochloride is a short-acting drug with extensive first -pass
hepatic metabolism to inactive compounds following an oral dose. The
half-life is 2.5 hours with peak plasma level at 1-2 hours, and
therapeutic and side effects dissipate within 3-6 hours. Therefore, use
must be directed to those activities and times when relief of spasticity
is most important and titrated to avoid intolerance. It should be started
at a low dose, 2-4 mg, preferably at bedtime. It should be titrated
carefully to each patient, increasing the dosage slowly and gradually.
The average maintenance dosage of tizanidine is 18-24 mg/d. The
maximum recommended dose is 36 mg/d. Patients with impaired
kidney function also require gradual titration, since they show a 2-fold
increase in plasma concentration.
Dry mouth, somnolence, asthenia, and dizziness are the most
common adverse events associated with tizanidine. Liver function
problems (5%), orthostasis, and hallucinations (3%) are rare
tizanidine-related adverse events (Delwaide and Pennisi, 1994).
Other oral agents
Other agents that may be beneficial in selected patients include the
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following:
l
Clonidine has shown efficacy for spasticity in open-label studies.
It is a selective alpha2-receptor agonist and may inhibit
presynaptic sensory afferents. Hypotension is the main adverse
effect.
l
Gabapentin is a GABA analogue that modulates enzymes that
metabolize glutamate. It may be useful in some patients with
spasticity. Sedation can be a bothersome adverse effect.
l
Lamotrigine blocks sodium channels and reduces the release of
glutamate and other excitatory amino acids.
l
Cyproheptadine is a 5 -HT antagonist that may neutralize
serotonergic inputs. It is beneficial in some patients.
l
Cannabinoid -like compounds (dronabinol, nabilone) that act on
the cannabinoid receptors (CB1 and CB2) may be useful in
muscle spasms and spasticity (Gracies, 1997).
Neurolysis with neurotoxins, chemodenervation, and local
anesthetics
Injections of botulinum toxin, phenol, alcohol, and lidocaine can offer
significant benefits to the appropriately selected patient as part of a
comprehensive spasticity management plan. Many clinicians use
various combinations of treatments. The distribution of spasticity is
vital in determining whether to use focal or global treatment, and in
deciding which measures should be used. Patients with focal spasms
are candidates for focal treatment with botulinum toxin A (BTX-A),
described in the next section. Patients with segmental or
nongeneralized spasticity may be candidates for systemic or ITB
treatment, with BTX -A added for focal symptom relief.
OTHER MEDICAL TREATMENTS
Section 5 of 10
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other Medical Treatments Surgical
Treatments Physical And Occupational Therapy Summary Resources And Advocacy Groups Bibliography
Botulinum toxin type A
BTX-A injections have been used as a safe and effective treatment for a variety of
movement disorders, including muscle overactivity and spasticity. BTX-A therapy was
approved by the US Food and Drug Administration (FDA) in 1989 for strabismus,
blepharospasm, and hemifacial spasm in patients older than 12 years. The use of BTX-A to
treat spasticity in adults and children is therefore off-label. Controlled clinical trials of BTX-A
injections for focal muscle spasticity have demonstrated prolonged yet reversible clinical
effects, few adverse effects, and minimal immunogenicity.
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BTX-A inhibits acetylcholine release at the neuromuscular junction. Once inside the
cholinergic nerve terminal cell, BTX-A inhibits the docking and fusion of acetylcholine
vesicles at the presynaptic membrane (Ahnert-Hilger and Bigalke, 1995). The effect of the
toxin becomes evident within 12 hours to 7 days, and the duration of effect is usually 3-4
months, but can be longer or shorter (Wong, 1998). Gradually, muscle function returns by
the regeneration or sprouting of blocked nerves forming new neuromuscular junctions.
The results of clinical trials strongly support the efficacy and safety of BTX-A for the
treatment of spasticity caused by cerebral palsy, multiple sclerosis, stroke, spinal cord injury,
brain injury, or neurodegenerative disease. Major benefits of BTX-A therapy for spasticity
include improved function, increased ease of care and comfort, prevention or treatment of
musculoskeletal complications such as contractures and pain, and cosmesis. In a review of
18 open -label or double-blind, placebo-controlled trials by Simpson et al (1997), botulinum
toxin has been shown to be an effective measure for reduction of focal spasticity.
Improvements were documented in tone reduction, range of motion, hygiene, autonomic
dysreflexia, gait pattern, positioning, and other criteria, though not all criteria tested showed
improvement in all studies. In none of the studies were significant adverse effects reported.
Proficiency in dosing and injecting BTX-A demands the development of considerable skill.
Each patient's treatment must be individualized, and appropriate patient selection is
important. BTX-A injections are most effective in relieving focal spasticity around a joint or
series of joints. Even though BTX -A is a focal treatment, untreated muscles may benefit from
the disruption of the synergy patterns that often replace isolated muscle control. Increased
range of motion, reduction in spasms, ease of caregiving, and reduced pain are primary
goals leading to improved function and quality of life. Treatment begins with mutually agreed
upon goals and expectations, a treatment plan that addresses all the clinical issues.
Generally, the relationship between spasticity and voluntary motor control is inverse.
Patients with severe spasticity often have less voluntary movement than patients with mild
spasticity. Underlying motor control, strength, and coordination should be assessed to
project the functional results of reducing spasticity. Since reduction of spasticity in patients
with poor selective motor control may not provide mobility, treatment goals of improving
positioning, caregiving, or comfort may be more appropriate. Patients with cognitive deficits
may not be able to take full advantage of their reduced spasticity; treatment aimed at easing
their care or pain may be more beneficial. Patients with painful spasms or contracture often
experience significant pain relief after treatment with BTX-A.
In the upper limb, patterns of spasticity that may improve specifically from BTX include an
adducted and internally rotated shoulder, flexed elbow, pronated forearm, flexed wrist,
thumb-in-palm, and clenched fist (Fehlings, 2000). In the lower extremity, BTX injections
may particularly improve spasticity causing flexed hip, flexed knee, adducted thighs, stiff (ie,
extended) knee, equinovarus foot, and striatal toe. Outcomes should be evaluated by
subjective and objective clinical measures including rating scales and videotape recordings
that clearly reflect defined goals and objectives.
In summary, common functional goals with neurolysis using the botulinum toxins (or phenol
or alcohol) include improving gait, hygiene, and ADLs; easing pain and care; and decreasing
spasm frequency. Technical objectives are to promote tone reduction and to improve range
of motion and joint position. Once begun, treatment is evaluated constantly; follow-up is
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crucial to gauge the response and to fine-tune muscle selection and dose as necessary.
When used in the management of spasticity, treatment with BTX-A is almost never used as
monotherapy. Complementary therapies, such as physical and occupational therapy,
frequently are utilized to maximize anticipated outcomes. These therapies usually are
instituted or modified after injection. In children, treatment should be initiated at a time when
they still are developing their motor control apparatus. This might prevent them from entering
a vicious cycle in which CNS lesions affect the musculoskeletal system, thereby preventing
the development of motor functions. In addition, experimental data on the formation of a
cortical somatotopic map during early life indicate that the periphery plays an instructional
role on the formation of central neuronal structures.
BTX-A dosing has to be individualized and is dependent upon muscles involved, prior
response, and functional goals. Adverse effects are minimal; however, conditions requiring
caution include patients who are hypersensitive to any ingredient in BTX -A, those using
aminoglycoside antibiotics, those with neuromuscular disease, and women who are
pregnant or potentially lactating.
A consensus on the dosage has been recommended by the Spasticity Study Group (Mayer,
1997). Examples of doses of BTX-A, in clinical trials for spasticity from multiple sclerosis,
cerebral palsy, traumatic brain injury, spinal cord injury, and stroke are as follows:
l
In multiple sclerosis, injection of 400 U of BTX -A into the thigh adductors resulted in
significant improvement in spasticity and hygiene compared to placebo (Snow, 1990).
l
In spinal cord injury, injection of 20-80 U of BTX-A into the rhabdosphincter resulted in
decreased urethral pressure and postvoid residual volume (Dykstra and Sidi, 1990).
l
In adults suffering from cerebral palsy, injection of 1 U/kg of BTX-A into the medial and
lateral gastrocnemius of each leg resulted in an improvement in gait pattern compared
to placebo (Koman, 1994). For children, no firm recommendations exist as to dosage
and optimal sites of injection.
l
In stroke, injections of 75-300 U of BTX-A into the elbow and wrist flexors resulted in
significant improvement in results of the Ashworth Scale compared to placebo
(Simpson, 1996).
Future trials of BTX-A may be improved by attention to dose-effect response, dose
escalation, broader randomization, and more uniform timing of injection in relation to the
onset of neurologic deficit.
BTX-A is injected using a 23- to 27-gauge needle. Larger and superficial muscles are
identified by palpation, while small or deep muscle groups are identified by
electromyography (EMG) or electrical stimulation (ES). Ultrasound, fluoroscopy, or CT also
may be used. Local anesthetic cream, general anesthesia, or sedation may be necessary,
particularly for some children. Depending on the location and severity of spasticity, BTX-A
injections usually are needed at 3 - to 6-month intervals to maintain therapeutic benefit. Re injections should not be given any sooner than 3 months after the last injections to decrease
the possibility of antibody formation.
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Treatment with BTX-A can be combined with various oral medications, the baclofen pump,
and sometimes with phenol or alcohol neurolysis. The primary reason for combining BTX-A
with phenol or alcohol neurolysis would be to avoid loss of responsiveness by remaining
under the maximum dose per visit. The decision to combine therapies usually depends on
the location and number of target muscles involved. If both lower and upper extremities are
to be injected, the combination of BTX-A and phenol may be warranted. Although using
phenol or alcohol neurolysis is associated with certain difficulties, they provide inexpensive,
long-term chemodenervation for some patients, mainly adults.
Antibody formation
Resistance to BTX -A is characterized by absence of any beneficial effect and by lack of
muscle atrophy following the injection. Antibodies against the toxin are presumed to be
responsible for most cases of resistance. Resistance has been reported to occur in 3 -10% of
people.
Repeated, high-dose injections are far more likely to result in antibody formation than are
less frequently repeated, low-dose injections. The smallest amount of BTX-A necessary to
achieve therapeutic benefit should be used, and the interval between treatments should be
extended as long as possible. Booster injections also should be avoided. When the amount
injected totals the maximum of 400 units, further injections should not be given before 3
months after the last treatment.
Several types of assays are available to detect the presence of antibody in serum. The most
widely used is the in vivo mouse neutralization assay, available through Northview Pacific
Laboratories (Berkeley, Calif) at (510) 548-8440. Injecting 10-20 units into one
corrugator/frontalis muscle and testing for the ability to elevate one eyebrow and frown 2 -3
weeks later is a simple clinical way to check for resistance. Checking for a marked decrease
in compound motor action potential (CMAP) amplitude in an injected muscle may be helpful.
This would indicate that resistance has not developed and that the dose or injection site may
have been suboptimal.
A number of studies have confirmed that patients with BTX-A resistance may benefit from
injections with other serotypes such as botulinum toxin type B (BTX-B). BTX-B, which is now
available commercially, and other serotypes, when they become available, may offer hope to
patients with resistance to BTX-A.
Botulinum toxin type B
Schwerin et al have reported the results of a pilot study using BTX-B in children with spastic
movement disorders. Twenty-nine children with spasticity underwent 62 treatment sessions
with BTX-B. Motor function improvement goals were attained or surpassed in 28 of 46
sessions and partially attained in 12. Care, hygiene, or orthotic management goals were
attained in 5 of 12 sessions and partially attained in 6. Correction of limb position goals were
attained in 3 of 4 sessions. Of 17 BTX-A nonresponders, 11 attained therapy goals with
BTX-B. Side effects included dry mouth (9.7% of sessions), diarrhea (6.5%), and swallowing
difficulties (6.5%). Systemic side effects were more likely when the dose surpassed 400
U/kg. The authors recommend a starting dose of BTX-B not to exceed 400 U/kg for children
up to 25 kg and a total dose for older children and adults of not more than 10,000 U
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(Schwerin, 2004).
Intrathecal baclofen
ITB consists of long-term delivery of baclofen to the intrathecal space. This treatment can be
helpful for patients with severe spasticity affecting the lower extremities, particularly for those
patients whose conditions are not sufficiently relieved by oral baclofen and other oral
medications. Lack of substantial therapeutic benefit from oral baclofen, a mainstay of drug
therapy, can result from an inadequate penetration of the blood-brain barrier by the drug.
Since unacceptable CNS effects often occur when high doses of baclofen are taken orally,
the therapeutic effect usually cannot be improved by increasing the dose. Sedation,
somnolence, ataxia, and respiratory and cardiovascular depression are the drug's CNS
depressant properties.
Zahavi et al have reported on the long-term effect (>5 y) of ITB on impairment, disability, and
quality of life in patients with severe spasticity of spinal origin. Of 21 patients treated, 11 had
multiple sclerosis, 6 had spinal cord injury, and the rest had a variety of nonprogressive
spinal disorders. The mean length of treatment was 6.5 years. Significant sustained
improvement was seen for spasticity (2.82 at baseline, 0.91 at follow-up, p= 0.0) and spasm
score (1.79, 0.67, p=0.001). Expanded Disability Status Scale score worsened (7.71, 7.88,
p=0.023), as did ambulation index (7.74, 8.05, p=0.027) and overall incapacity status scale
score (25.74, 28.76, p=0.011). No significant changes were seen on the Sickness Impact
Profile or the Hopkins Symptom Checklist. No significant differences were found for any
measure between patients with multiple sclerosis and those with static spinal disorders.
The most common complications were muscle weakness, somnolence, catheter
malfunction, and surgery complications. The authors report that all patients but two were
satisfied with their treatment and would undergo treatment again. Zahavi and coworkers
concluded that the most prominent improvements reported by the patients were increased
ease of transfer, better seating posture, ease of care in ADLs (passive), and decrease in
pain (Zahavi, 2004).
ITB (SynchroMed Infusion System) provides direct, pattern-controlled delivery of baclofen to
its target via an implanted, programmable pump. This precise delivery yields better spasticity
reduction at lower doses: doses 100 times the intrathecal dose are needed to produce
similar benefits if baclofen is taken orally. Thus, adverse effects associated with high
dosages of oral baclofen are minimized.
The pump is a small titanium disk that is about 3 inches in diameter and 1 inch thick. It
contains a refillable reservoir for the liquid baclofen as well as a computer chip that regulates
the battery-operated pump. A telemetric wand programs the dose of baclofen to be received.
A flexible silicone catheter serves as the pathway through which the baclofen flows to the
intrathecal space. To prevent accidental depletion of baclofen, the pump contains a
programmable alarm that sounds when the reservoir needs to be refilled, the battery is low,
or the pump is not delivering the baclofen.
ITB can be used to treat severe spasticity from various causes. Benefits of ITB typically
include reduced tone, spasms, and pain, and increased mobility. Other benefits may include
improved sleep quality, bladder control, self-care, and self-image. It also may allow patients
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to decrease and often discontinue other spasticity medications.
Patient selection, screening, pump implantation, and dosage
ITB should be considered in patients who have disabling spasticity unresponsive to
conservative pharmacotherapy or in whom therapeutic doses induce intolerable side effects.
Pharmacotherapy should include, but need not be limited to, a trial of oral baclofen. The
Ashworth Scale and Spasm Frequency Scale appear to be clinically useful measures of
spasticity; a severity of 3 on the Ashworth and 2 on the Spasm Frequency for at least 12
months are considered reasonable criteria for ITB therapy consideration.
The screening process requires the administration of an intrathecal test dose of baclofen
(typically 50 mcg, usually not to exceed 100 mcg) via lumbar puncture. Peak effect of the
drug usually occurs within 4 hours. Patients who respond positively to the test dose can be
considered for long-term ITB therapy. The test dose must be monitored closely in a fully
equipped and staffed setting because of the rare risk of respiratory arrest and other lifethreatening adverse effects.
The ITB pump generally is implanted near the waistline. The tip of a catheter rests between
the first and second lumbar vertebrae in the intrathecal space. The distal end of the catheter
loops around the torso and connects to the pump. The dose delivered by the pump is
adjusted using the programmer and telemetry wand. This system is non-invasive and affords
flexibility in individualizing doses. The initial total daily dose of ITB after implantation may be
up to double the screening dose that resulted in a beneficial response. The initial doses
should be adjusted and increased carefully and have to be individualized.
About 60 days following surgery or when a stable dose program has been established, the
fine-tuning of the dose delivery may begin. Maintenance doses of ITB are as follows:
l
For spasticity of spinal cord origin, the dose ranges from 12 -2000 mcg/d, with most
patients requiring 300-800 mcg/d.
l
Patients with spasticity of cerebral origin receive doses ranging from 22-1400 mcg/d.
For most patients, doses of 90-703 mcg/d result in therapeutic benefits.
l
For children younger than 12 years, the average daily dose is 274 mcg/d, with a range
of 24-1199 mcg/d.
The dose may be increased if greater therapeutic benefits are needed, or reduced to
alleviate adverse effects. Dose should always be reduced in a stepwise fashion. Sudden
withdrawal of ITB can result in cardiovascular instability, fever, and rash, and requires
emergency treatment. The pump's reservoir must be refilled every 4 -12 weeks, depending
on the daily dose. The pump hardware can last 4-6 years, depending upon the battery life,
and generally is replaced within 4 -5 years.
As with any surgical procedure, the implantation of the pump exposes a patient to risks of
infection and spinal fluid leakage, as well as the general risks of general anesthesia.
Drowsiness, nausea, headache, muscle weakness, and light-headedness can stem from the
pump delivering an inappropriate dosage of baclofen. The pump itself can malfunction, and
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the catheter can become kinked or fractured. A large and sudden escalation in dose
requirement, for example, suggests a catheter complication. In cases such as these, surgical
intervention may be necessary. In cases in which overdose is possible, the patient should be
brought immediately to the hospital for evaluation.
As some degree of muscle tone may be required to assist in the support of circulatory
function, prevent deep vein thrombosis, and optimize ADLs and ease of care, optimizing the
change of tone with ITB requires striking a balance between the patient's condition,
functional goals, and physiological demands. Since ITB may be appropriate for a broad
range of disabilities, from ambulatory to vegetative states, treatment and functional goals
must be individualized, clearly understood, and agreed upon by the patient, family,
caregivers, and care-provider team before starting treatment. Thus, in summary,
appropriately chosen patients with clearly defined and realistic treatment objectives benefit
the most from this form of treatment.
Other Treatments
Jarret et al have reported that intrathecal bolus injection of phenol can reduce lower-limb
spasticity. Twenty-five patients with advanced multiple sclerosis received 1.5-2.5 mL 5%
phenol in glycerol at L2/3 or L2/4, and improvements were seen in the Ashworth score,
spasm frequency, and pain, although the duration of the beneficial effect was not indicated.
No serious adverse effects were reported (Jarret, 2002).
SURGICAL TREATMENTS
Section 6 of 10
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Treatments Physical And Occupational Therapy Summary Resources And Advocacy Groups Bibliography
Surgery can play a very important role in the treatment of chronic spasticity. In most cases,
complementary neurosurgical and functional orthopedic approaches are used. Children with
spasticity represent a different challenge because their spasticity may change as they grow
and develop so that, at times, surgery may be undertaken to allow more normal bone and
muscle growth. While each surgical approach has certain strengths and weaknesses, none
of them completely eliminate spasticity.
Neurosurgical treatments
The surgical treatment of spasticity has been aimed at 4 different levels: brain, spinal cord,
peripheral nerves, and muscle. Each approach has its strengths and weaknesses; none of
them completely eliminates spasticity. Stereotactic brain surgery, whether involving the
globus pallidum, ventrothalamic nuclei, or the cerebellum, has had little success. Cerebellar
pacemakers have been tried; results have been mixed but not ultimately encouraging.
Selective dorsal rhizotomy (SDR) is currently the most widely used and effective CNS
procedure.
Selective dorsal rhizotomy
Also known as selective posterior rhizotomy, this procedure involves cutting of selective
nerve roots between the levels of L2 and S1 or S2, the fibers lying just outside the vertebral
column that transmit nerve impulses to and from the spinal cord. "Dorsal" or "posterior"
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indicates that the target nerve roots enter the posterior spinal cord. These fibers carry
sensory information to the cord from muscle.
Sensory nerves are targeted because of the probable role they play in generating spasticity.
Under normal physiologic conditions, excitatory signals from these sensory nerves are
counterbalanced by inhibitory signals from the brain, maintaining normal muscle tone. In
simplistic terms, when brain or spinal cord damage upsets this balance, excess sensory
signaling can lead to spasticity. SDR is thought to improve spasticity by partially restoring
the proper physiologic balance between these circuits.
SDR is used to treat severe spasticity of the lower extremities that interferes with mobility or
positioning. It has been performed mostly on children with cerebral palsy and less often in
adults with spasticity from cerebral palsy or other etiologies. The best candidate for SDR is a
person with good strength and balance, little or no fixed contractures in the lower limbs, and
strong motivation and support. This procedure is used only when less-invasive procedures
are unable to control spasticity adequately. SDR is performed under general anesthesia.
The candidate nerve rootlets are stimulated electrically and those that lead to abnormal
responses are cut; usually 25-50% of all tested rootlets are cut.
Studies of SDR in children with cerebral palsy have shown that most patients experience a
reduction in spasticity and an increase in range of motion immediately after surgery, which
persists for at least a year. Relatively few longer-term follow-up studies have been done, and
these indicate tone reduction may last for a number of years. Reduction of spasticity can in
some instances improve function, with most studies showing some benefit in mobility for
subjects with spastic diplegia, but less for those with spastic quadriplegia. The extent of
functional improvement after SDR therefore varies, and positive prognostic factors include
the extent of mobility before the operation, underlying strength and balance, availability of
regular physical therapy after SDR, and the patient's motivation and ability to undertake the
rehabilitation process. The possible complications from the surgery include those involving
general anesthesia. Pain, altered sensation, and fatigue may continue for a number of
weeks after the operation, as may changes in sleep and bladder or bowel function. Other
rare long-term complications include low back pain, scoliosis or kyphosis (ie, spinal curves),
and hip displacement.
Other surgical procedures targeting the brain or the peripheral nerves (neurectomy) or
involving cerebellar stimulation of the brain have been used in the past with limited success
and currently are not recommended for the treatment of spasticity as they are often not
successful and produce complications. Musculoskeletal surgery, however, does remain an
important procedure for treatment of contractures secondary to spasticity.
Orthopedic surgery
These surgeries constitute the most frequently used procedures for spasticity. Two
categories of surgical procedures are used: lengthening or release of muscles and tendons,
and procedures involving bones. These procedures aim to reduce spasticity, increase range
of motion, improve accessibility for hygiene, increase tolerance to braces, or reduce pain.
The majority of such operations are performed in children aged 4-8 years.
Contracture release is the most commonly performed orthopedic procedure. The most
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common site for contracture release is the Achilles tendon. The tendon is lengthened to
correct "equinus" deformity. Other common targets are contractures involving muscles of the
knees, hips, shoulders, elbows, and wrists. The tendon of a contractured muscle is cut and
the joint is then positioned at a more normal angle, and a cast is applied. Regrowth of the
tendon to this new length occurs over several weeks, and serial casting may be used to
gradually extend the joint. Following cast removal, physical therapy is used to strengthen the
muscles and improve range of motion.
In a tendon transfer, the attachment point of a spastic muscle is moved. The muscle can no
longer pull the joint into a deformed position and, in some situations, the transfer allows
improved function. In others, the joint retains passive but not active function. Ankle -bracing
procedures that follow surgery are among the most effective interventions.
Osteotomy also can be used to correct a deformity. A small wedge is removed from a bone
to allow it to be repositioned or reshaped. A cast is applied while the bone heals in a more
natural position. This procedure is used most commonly to correct hip displacements and
foot deformities. Arthrodesis is performed most commonly on the bones in the ankle and
foot. It is a fusing together of bones that normally move independently, and this limits the
ability of a spastic muscle to pull the joint into an abnormal position. Osteotomy and
arthrodesis usually are accompanied by contracture release surgery for fuller correction of
the joint deformity.
PHYSICAL AND OCCUPATIONAL THERAPY
Section 7 of 10
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other Medical Treatments Surgical
Treatments Physical And Occupational Therapy Summary Resources And Advocacy Groups Bibliography
These treatments are designed to reduce muscle tone, maintain or improve range of motion
and mobility, increase strength and coordination, and improve comfort. The choice of
treatments is individualized to meet the needs of the person with spasticity. Treatments may
include any of the following:
l
Stretching forms the basis of spasticity treatment. Stretching helps to maintain the full
range of motion of a joint and helps prevent contracture.
l
Strengthening exercises are aimed at restoring the proper level of strength to affected
muscles, so that as tone is reduced through other treatments, the affected limb can be
used to its fullest potential. As yet no clear evidence exists that intensive physiotherapy
(1 h a day, 5 days a wk) is more beneficial than routine physiotherapy (6-7 h over 3
mo) (Bower, 2001).
l
Application of orthoses, casts, and braces allows a spastic limb to be maintained in a
more normal position. For instance, an ankle -foot orthosis can help keep the foot
flexed and reduce contracture of the calf muscles. A cast is a temporary brace, and
serial casting gradually stretches out a contractured limb through the application of
successive casts. Proper limb positioning improves comfort and reduces spasticity.
l
Brief application of cold packs to spastic muscles may be used to improve tone and
function for a short period of time or to ease pain.
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l
Electrical stimulation may be used to stimulate a weak muscle to oppose the activity of
a stronger, spastic one. It also may reduce spasticity for short periods of time.
Electrical stimulation is used most often to help flex the ankle for walking, and to help
extend spastic fingers.
l
Biofeedback is the use of an electrical monitor that creates a signal, usually a sound,
as a spastic muscle relaxes. In this way, the person with spasticity may be able to train
himself to reduce muscle tone consciously, and this may play a modest role in
reducing spasticity.
SUMMARY
Section 8 of 10
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other Medical Treatments Surgical
Treatments Physical And Occupational Therapy Summary Resources And Advocacy Groups Bibliography
Spasticity is a chronic disorder of muscle stiffness, control, and function resulting from a
variety of insults to the CNS, including injury, stroke, multiple sclerosis, and cerebral palsy.
With appropriate neurologic, surgical, rehabilitative, and psychosocial interventions, the
many debilitating manifestations of spasticity can be treated, thus greatly improving the
quality of life of the affected individual.
RESOURCES AND ADVOCACY GROUPS
Section 9 of 10
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other Medical Treatments Surgical
Treatments Physical And Occupational Therapy Summary Resources And Advocacy Groups Bibliography
Christopher Reeve Paralysis Foundation
500 Morris Avenue
Springfield, NJ 07081, USA
TEL: (800) 225-0290 or (973) 379-2690
American Stroke Association, A Division of American Heart Association
7272 Greenville Avenue
Dallas, TX 75231, USA
TEL: (888) 4 STROKE
FAX: (800) 787-8985
Email: [email protected]
Brain Injury Association of America
8201 Greensboro Drive, Suite 311
McLean, VA 22102
TEL: (703) 761-0750 or Family Helpline (800) 444-6443
Email: [email protected]
Multiple Sclerosis Association of America
706 Haddonfield Road
Cherry Hill, NJ 08002, USA
TEL: (800) 532-7667
FAX: (856) 661-9797
Email: [email protected]
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Multiple Sclerosis Foundation
6350 N Andrews Avenue
Ft Lauderdale, FL 33309, USA
TEL: (800) 441-7055 or (954) 776-6805
FAX: (954) 938-8708
Email: [email protected]
National Multiple Sclerosis Society
733 3rd Avenue, 6th Floor
New York, NY 10017-3288, USA
TEL: (800) FIGHT MS (344-4867) or (212) 986-3240
FAX: (212) 986-7981
Email: [email protected]
National Spinal Cord Injury Association
6701 Democracy Blvd, Suite 300-9
Bethesda, MD 20817
TEL: (800) 962-9629
National Stroke Association
9707 East Easter Lane
Englewood, CO 80112
TEL: (800) STROKES or (303) 649-9299
FAX: (303) 649-1328
Stroke Clubs International
Contact: Ellis Williamson
805 12th Street
Galveston, TX 77550, USA
TEL: (409) 762-1022
Email: [email protected]
United Cerebral Palsy Associations
1660 L Street NW, Suite 700
Washington, DC 20036, USA
TEL: (800) 872-5827 or (202) 776-0406
FAX: (202) 776-0414
BIBLIOGRAPHY
Section 10 of 10
Author Information Introduction And Pathophysiology Clinical Considerations Oral Medications Other Medical Treatments Surgical
Treatments Physical And Occupational Therapy Summary Resources And Advocacy Groups Bibliography
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