Updated: Jun 28, 2019
Author: Krupa Pandey, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA 


Practice Essentials

Spasticity is increased, involuntary, velocity-dependent muscle tone that causes resistance to movement. The condition is typically a result of insult to the central nervous system or motor neurons. It may occur as a primary condition such as in degenerative conditions or as a result of secondary causes such as spinal cord injury, trauma to the brain, or inflammatory conditions such as multiple sclerosis.

Signs and symptoms

Typically, the most common sign on exam is resistance to a passive change in a joint angle. It is most commonly noted in the flexor muscles of the upper extremities, the proximal extensor muscles of the lower extremities, and the distal flexor muscles of the lower extremities. As such, depending on the insult, specific patterns may arise that can aide in treatment.

Cerebral palsy

Children with cerebral palsy tend to exhibit one of the following spasticity patterns:

  • Diplegic pattern: Scissoring, crouching, and toe walking

  • Quadriplegic pattern: Diplegic patterning in addition to flexion of the elbow, flexion of the wrist and fingers, adduction of the thumb, and internal rotation, pronation, or adduction of the arms

  • Hemiplegic pattern: Plantar flexion of the ankle, flexion of the knee, adduction of the hip, flexion of the wrist and finger, adduction of the thumb, and flexion, internal rotation, pronation, or adduction of the arms

Equinovarus positioning of the foot is a common posture in the lower extremity, and it can be a major limitation to functional transfers or gait as a child grows older.

Spasticity of the upper extremities

The following patterns present in patients with cerebral palsy, stroke, or traumatic brain injury (TBI):[1]

  • Adduction and internal rotation of the shoulder

  • Flexion of the elbow and wrist

  • Pronation of the forearm

  • Flexion of the fingers and adduction of the thumb

The following flexor patterns can occur in patients with cerebral palsy, MS, or TBI or who have suffered a stroke:[1]

  • Hip adduction and flexion

  • Knee flexion

  • Ankle plantar flexion or equinovarus positioning

The following extensor patterns may be seen in patients following TBI:

  • Knee extension or flexion

  • Equinus and/or valgus ankle

  • Great toe dorsiflexion or excessive toe flexion

See Clinical Presentation for more detail.


In patients with new-onset spasticity, a thorough history, including family history, and physical examination are crucial. Additional tests such as electromyography for evaluation of motor neuron disease, determination of nerve conduction velocities, or imaging studies of the head, neck, and spine may be useful in eliminating treatable causes of increased tone.[2]

In patients with a previous neurologic insult, a thorough history and physical examination is necessary to rule out any factors that can exacerbate spasticity (eg, medication changes, noxious stimuli, increased intracranial pressure).

Laboratory studies (eg, complete blood count [CBC] and culturing of urine, blood, cerebrospinal fluid) may help to rule out infection.

Spasticity is difficult to quantify,[3] but clinically useful scales include the following:

  • Ashworth Scale/Modified Ashworth: From 0-4 (normal to rigid tone)

  • Physician's Rating Scale: Gait pattern and range of motion assessed

  • Spasm Scale: From 0-4 (no spasms to >10/h)

See Workup for more detail.


Interventions for spasticity may vary from conservative (therapy and splinting) to more aggressive (surgery); most often, a variety of treatments are used at the same time or are employed interchangeably. Treatment options do not need to be used in a stepladder approach and indeed should not be. Current spasticity management options include the following:

  • Preventative measures

  • Therapeutic interventions (physical therapy, occupational therapy, hippotherapy, aquatics) and physical modalities (ultrasonography, electrical stimulation, biofeedback)[4, 5]

  • Positioning/orthotics (including taping, dynamic and static splints, wheelchairs, and standers)

  • Oral medications (such as baclofen and dantrolene)[6]

  • Injectable neurolytic medications (botulinum toxins and phenol)

  • Intrathecal baclofen

  • Surgical intervention (including selective dorsal rhizotomy and orthopedic procedures)

See Treatment and Medication for more detail.


Spasticity is increased, involuntary, velocity-dependent muscle tone that causes resistance to movement. The condition may occur secondary to a disorder or trauma, such as a tumor, a stroke, multiple sclerosis (MS), cerebral palsy, or a spinal cord, brain, or peripheral nerve injury. (See Pathophysiology and Etiology.)

Spasticity usually is accompanied by paresis and other signs, such as increased stretch reflexes, which collectively are called upper motor neuron syndrome. Paresis particularly affects distal muscles, with loss of the ability to perform fractionated movements of the digits. (See Clinical Presentation.)

Upper motor neuron syndrome results from damage to descending motor pathways at the cortical, brainstem, or spinal cord levels. 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 the following (see Clinical Presentation):

  • Clonus

  • Clasp-knife phenomenon

  • Hyperreflexia

  • Babinski sign

  • Flexor reflexes

  • Flexor spasms

Spasticity can be severely debilitating, but with appropriate neurologic, surgical, rehabilitative, and psychosocial interventions, its manifestations can be treated, thus greatly improving the quality of life of affected individuals. (See Prognosis, Treatment, and Medication.)

While the incidence of spasticity is not known with certainty, the condition likely affects over half a million people in the United States and over 12 million people worldwide.


The pathophysiologic basis of spasticity is incompletely understood. Polysynaptic responses may be involved in spinal cord–mediated spasticity, while enhanced excitability of monosynaptic pathways is involved in cortically mediated spasticity.

Spasticity-related 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, along with 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.[7]

Cortical and spinal cord damage

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.

Physiologic evidence suggests that interruption of reticulospinal projections is important in the genesis of spasticity. 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 weakness of extensor muscles.

Mechanisms of spasticity

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.

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 H-M ratios[8] and F-wave amplitudes.[9] Judged by recordings from Ia spindle afferents, muscle spindle sensitivity is not increased in human spasticity.

Local anesthetic injections into spastic muscles in man can diminish spasticity through 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.

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. 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 central nervous system (CNS) is another theoretical explanation for some of the events in spasticity.


Treatable factors that may cause sudden onset of spasticity include the following:

  • Tethered spinal cord

  • Spinal cord tumor

  • Nerve impingement peripherally or centrally

  • Hydrocephalus

  • Intracranial, epidural, or subdural bleeding

Factors that can exacerbate preexisting spasticity from spinal injury, brain tumor/injury, cerebral palsy, or MS include the following:

  • Infection (eg, otitis, urinary tract infection, pneumonia)

  • Pressure sore

  • Noxious stimulus (eg, ingrown toenail, ill-fitting orthotics, occult fracture)

  • Deep venous thrombosis

  • Bladder distention

  • Bowel impaction

  • Cold weather

  • Fatigue

  • Seizure activity

  • Stress

  • Malpositioning


Spasticity can have a devastating effect 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 available.

Multiple sclerosis

Rizzo et al, in an analysis of a cross-sectional database of 17,501 patients with MS (NARCOMS registry), reported the following with regard to the prevalence of spasticity[10] :

  • 15.7% had no spasticity

  • 50.3% had minimal to mild spasticity

  • 17.2% had moderate spasticity

  • 16.8% had severe spasticity


In several studies examining patients at 12 months post-stroke, spasticity has been estimated to occur in up to 46% of patients 12 months after stroke.[11, 12, 13] Spasticity is associated with a negative impact on the health-related quality of life (HRQoL) of stroke survivors with statistically and clinically meaningful differences existing between stroke survivors with and without spasticity. These results suggest an opportunity to improve HRQoL among stroke survivors with spasticity.[1]

Disadvantages of spasticity

The negative impacts of spasticity on health and quality of life include the following:

  • Orthopedic deformity, such as hip dislocation, contractures, or scoliosis

  • Impairment of activities of daily living (eg, dressing, bathing, toileting)

  • Impairment of mobility (eg, inability to walk, roll, sit)

  • Skin breakdown secondary to positioning difficulties and shearing pressure

  • Pain or abnormal sensory feedback

  • Poor weight gain secondary to high caloric expenditure

  • Sleep disturbance

  • Depression secondary to lack of functional independence

Advantages of spasticity

Spasticity can confer certain benefits to the patient, including the following:

  • Substitutes for strength, allowing standing, walking, gripping

  • May improve circulation and prevent deep venous thrombosis and edema

  • May reduce the risk of osteoporosis

Patient Education

Resources and advocacy groups

Christopher & Dana Reeve Foundation

636 Morris Turnpike

Suite 3A

Short Hills, NJ 07078, USA

TEL: (800) 225-0292 or

(973) 379-2690 (outside the United States)

American Stroke Association, a division of the American Heart Association

7272 Greenville Avenue

Dallas, TX 75231, USA

TEL: (888) 478-7653

Brain Injury Association of America

1608 Spring Hill Road

Suite 110

Vienna, VA 22182, USA

TEL: (703) 761-0750


Multiple Sclerosis Association of America

706 Haddonfield Road

Cherry Hill, NJ 08002, USA

TEL: (800) 532-7667 or (856) 488-4500

FAX: (856) 661-9797

Email: (general information) or (MS questions)

Multiple Sclerosis Foundation

6520 N Andrews Avenue

Ft Lauderdale, FL 33309-2130, USA

TEL: (888) 673-6287 or (954) 776-6805

FAX: (954) 351-0630


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


National Spinal Cord Injury Association

A program of the United Spinal Association

75-20 Astoria Blvd

Jackson Heights, NY 11370, USA

TEL: (718) 803-3782

National Stroke Association

9707 East Easter Lane

Suite B

Centennial, CO 80112, USA

TEL: (800) 787-6537

FAX: (303) 649-1328

Stroke Clubs International

Contact: Ellis Williamson

805 12th Street

Galveston, TX 77550, USA

TEL: (409) 762-1022


United Cerebral Palsy

1825 K Street NW

Suite 600

Washington, DC 20006, USA

TEL: (800) 872-5827 or (202) 776-0406




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 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.

Studies have been made of assessment tools, such as the Lateral Step Up test for adolescents with cerebral palsy and the Modified Ashworth Scale for the assessment of upper-limb muscles.[14, 15]

In an infant, spasticity is generally manifested by increased muscle tone. Abnormalities of muscle tone are most readily documented by assessing tone of supination and pronation of the upper extremities and dorsiflexion and plantar flexion of the lower extremities. In newborns or small infants, spasticity of the lower extremities becomes evident when the examiner suspends the infant by the feet, upside down, and each lower extremity is released in turn. In spasticity, the released lower extremity remains “hung up.”

Spasticity can wax and wane, appearing at variable times relative to the date of injury or disease onset. Involved muscles may demonstrate spontaneous or elicited clonus, as well as increased deep tendon reflexes.

Spasticity can occur in any muscle, but common patterns exist, especially when associated with an upper motor neuron injury. Understanding these patterns helps to predict a patient’s future functional status, as well as cosmetic or orthopedic deformities that may occur, aiding in treatment decisions.

Cerebral palsy

Children with cerebral palsy tend to exhibit one of the following spasticity patterns:

  • Diplegic pattern: Scissoring, crouching, and toe walking

  • Quadriplegic pattern: Diplegic patterning in addition to flexion of the elbow, flexion of the wrist and fingers, adduction of the thumb, and internal rotation, pronation, or adduction of the arms

  • Hemiplegic pattern: Plantar flexion of the ankle, flexion of the knee, adduction of the hip, flexion of the wrist and finger, adduction of the thumb, and flexion, internal rotation, pronation, or adduction of the arms

Equinovarus positioning of the foot is a common posture in the lower extremity, and it can be a major limitation to functional transfers or gait as a child grows older.

While some muscles may maintain underlying volitional strength, others may not. Muscles crossing 2 joints most commonly are involved in contracture development. Spasticity often is worse when the patient awakens or at the end of a tiring day.

Spinal cord injury/multiple sclerosis

Spasticity in patients with incomplete or complete spinal cord injury (SCI) or multiple sclerosis (MS) can vary greatly in location and degree. Spasticity often is worse at night or with fatigue. Chronic compression of nerves secondary to spasticity may lead to problems such as carpal tunnel syndrome.

Spasticity of the upper extremities

The following patterns often are seen in patients with cerebral palsy, stroke, or traumatic brain injury (TBI):

  • Adduction and internal rotation of the shoulder

  • Flexion of the elbow and wrist

  • Pronation of the forearm

  • Flexion of the fingers and adduction of the thumb

Muscles that often contribute to spastic adduction/internal rotation dysfunction of the shoulder include the latissimus dorsi, the teres major, the clavicular and sternal heads of the pectoralis major, and the 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 metacarpophalangeal flexion and PIP extension also may occur. A patient may be spastic in only 1 or 2 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, the most common pathologic posture seen in the lower extremity, is a key deformity that can prevent even limited functional ambulation or unassisted transfers.

The following flexor patterns often are seen in patients with cerebral palsy, MS, or TBI or who have suffered a stroke:

  • Hip adduction and flexion

  • Knee flexion

  • Ankle plantar flexion or equinovarus positioning

The following muscles typically are involved in the flexor patterns and are targeted for treatment:

  • Adductor magnus

  • Iliopsoas

  • Hamstrings (medial more often than lateral)

  • Tibialis posterior

  • Soleus

  • Gastrocnemius

The following extensor patterns often are seen in patients following TBI:

  • Knee extension or flexion

  • Equinus and/or valgus ankle

  • Great toe dorsiflexion or excessive toe flexion

The following muscles typically are involved in the extensor patterns and are targeted for treatment:

  • Quadriceps femoris

  • Medial hamstrings

  • Gastrocnemius

  • Tibialis posterior

  • Extensor hallucis longus

  • Toe flexors

  • Peroneus longus

Physical Examination

In patients with new-onset spasticity, a thorough history and physical examination, as well as examination using electromyography, a determination of nerve conduction velocities, or imaging studies of the head, neck, and spine may be useful in eliminating treatable causes of increased tone.[2]

In patients with a previous neurologic insult, a thorough history and physical examination is necessary to rule out any factors that can exacerbate spasticity (eg, medication changes, noxious stimuli, increased intracranial pressure).

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.

Standardized assessments for motor control that can be tested for validity and reliability have yet to be devised for use in the patient with neurologic 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 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, and then 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.



Diagnostic Considerations

Spasticity may be mistaken for seizure activity, but differences are as follows:

  • Spasticity is not followed by a postictal period

  • Spasticity is typically not as rhythmic or symmetrical as seizure activity

Spasticity is associated with some very common neurologic disorders, including the following:

  • Multiple sclerosis (MS)

  • Stroke

  • Cerebral palsy

  • Spinal cord and brain injuries

  • Neurodegenerative diseases affecting the upper motor neuron, pyramidal, and extrapyramidal pathways



Approach Considerations

As previously stated, in patients with new onset spasticity, a thorough history and physical examination, as well as examination using electromyography, a determination of nerve conduction velocities, or imaging studies of the head, neck, and spine may be useful in eliminating treatable causes of increased tone.[2]

Radiographs are especially important in the insensate patient with spinal cord injury (SCI) or the cognitively impaired patient with traumatic brain injury (TBI) if occult fractures are present. Radiography can provide evidence of bowel impaction as well.

Laboratory studies (eg, complete blood count [CBC] and culturing of urine, blood, cerebrospinal fluid) may help to rule out infection.

Spasticity is difficult to quantify,[3] but clinically useful scales include the following:

  • Ashworth Scale/Modified Ashworth: From 0-4 (normal to rigid tone)

  • Physician's Rating Scale: Gait pattern and range of motion assessed

  • Spasm Scale: From 0-4 (no spasms to >10/h)

Functional scales such as the Functional Independence Measure or Gross Motor Function Measure also may be valuable, although they do not measure spasticity directly.

Research-oriented tools for measurement include the following:

  • Tardieu Scale

  • Surface electromyography

  • Isokinetic dynamometry

  • H reflex

  • Tonic vibration reflex

  • F-wave response

  • Flexor reflex response

  • Transcranial electrical/magnetic stimulation



Approach Considerations

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 and expectations for treatment. In a patient who can walk, for example, a reduction of leg muscle tone may worsen mobility if tone compensates for leg weakness, allowing the patient to stand. Manual dexterity and strength also do not improve by reducing muscle tone, which means that treatment of spasticity may not lead to an improvement in function.

Therefore, clearly identifying the goals of the patient and caregiver is vital and before treatment is initiated, the following should be considered[16] :

  • Does the patient need treatment?

  • What are the aims of treatment?

  • Do the patient and caregivers have the time required for treatment?

  • 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, activities of daily living (ADLs), pain, and ease of care; decreasing the frequency of spasm and related discomfort; and eliminating noxious stimuli.

The ability of muscles to function after spasticity reduction varies. Treating spasticity does not always facilitate the acquisition of previously undeveloped skills.

Agonist versus antagonist muscle groups

When deciding to treat a spastic muscle, it is important to assess the impact of its antagonistic muscle groups. While often weak, these muscle groups themselves may be spastic. Treatment of the agonist muscle without treatment of the antagonist muscle may create an additional problem instead of a solution. Additionally, careful assessment of the role spasticity plays in substituting for strength (specifically, to facilitate with transfers) is important to avoid decreasing, rather than increasing, function.

Types of therapy

Interventions for spasticity vary from conservative (therapy and splinting) to more aggressive (surgery); most often, a variety of treatments are used at the same time or are employed interchangeably. Treatment options do not need to be used in a stepladder approach and indeed should not be. Current spasticity management options include the following:

  • Preventative measures

  • Therapeutic interventions (physical therapy, occupational therapy, hippotherapy, aquatics) and physical modalities (ultrasonography, electrical stimulation, biofeedback)[4, 5]

  • Positioning/orthotics: Including taping, dynamic and static splints, wheelchairs, and standers

  • Oral medications: Such as baclofen and dantrolene[6]

  • Injectable neurolytic medications: Botulinum toxins and phenol

  • Surgical intervention

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.

Considerations that impact treatment

These include the following:

  • Duration of spasticity and likely duration of therapy

  • Severity of spasticity

  • Location of spasticity

  • Success of prior interventions

  • Current functional status and future goals

  • Underlying diagnosis and comorbidities

  • Ability to comply with treatment and therapy

  • Availability of support/caregivers and follow-up therapy

Pharmacologic Therapy

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, including sedation and 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.

Common oral medications include the following:

  • Diazepam (Valium)

  • Baclofen (Lioresal)[6]

  • Dantrolene (Dantrium)

  • Tizanidine (Zanaflex)

  • Clonidine (Catapres)[6]

Benzodiazepines (diazepam and clonazepam)

The benzodiazepines bind in the brainstem and at the spinal cord level and increase the affinity of gamma-aminobutyric acid (GABA) for 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 dosage can be increased slowly to 60 mg/day in divided doses. Clonazepam can be started at 0.5 mg at night and slowly increased to a maximum of 20 mg/day 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 that potentiate sedation and have central depressant properties (eg, baclofen or tizanidine) should be monitored carefully.


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.

Baclofen may be given orally or by intrathecal pump. An analysis by Rizzo et al of a database of 17,501 patients with multiple sclerosis found that the use of oral medication was proportional to the severity of spasticity, with 78% of patients who were severely affected using at least 1 drug and 46% using at least 2.[10] 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/day in divided amounts. Tolerance may develop, and the drug must be tapered slowly to prevent withdrawal effects. Withdrawal from baclofen can have clinical manifestations that include agitation, insomnia, confusion, delusions, hallucinations, seizures, visual changes, psychosis, dyskinesia, hyperthermia, and increased spasticity.[17, 18]

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.[19]

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 intrathecal dose. 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 (TBI); it acts by decreasing muscle tone, clonus, and muscle spasm. The drug acts at the level of the muscle fiber, reducing muscle contraction by affecting the release of calcium from the sarcoplasmic reticulum of skeletal muscle. 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/day in divided doses (in children, the dose range 0.5-3.0 mg/kg/day).

Adverse effects include drowsiness, dizziness, fatigue, diarrhea, and generalized weakness, including weakness of the respiratory muscles. Hepatotoxicity occurs in less than 1% of patients; elevation in liver function test results is seen particularly in adolescents and women who have been treated for more than 60 days and at dosages of greater than 300 mg/day.

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 doses, the medication should be discontinued.[20]


Data from approximately 50 clinical trials indicate that tizanidine (Zanaflex) is effective 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. The drug also may facilitate inhibitory actions of glycine and reduce release of excitatory amino acids and substance P; it may have analgesic effects as well. 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. In placebo-controlled studies, the efficacy of tizanidine in reducing muscle tone 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 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.

Tizanidine should be started at a low dose, 2-4 mg, preferably at bedtime. It should be titrated carefully to each patient, with the dosage increased slowly and gradually. The average maintenance dosage of tizanidine is 18-24 mg/day, with the maximum recommended dosage being 36 mg/day. 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.


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.

Other oral agents

Additional agents that may be beneficial in selected patients include the following:

  • Gabapentin: A GABA analogue that modulates enzymes that metabolize glutamate; it may be useful in some patients with spasticity, but sedation can be a bothersome adverse effect

  • Lamotrigine: Blocks sodium channels and reduces the release of glutamate and other excitatory amino acids

  • Cyproheptadine: A 5-HT antagonist that may neutralize serotonergic inputs; it is beneficial in some patients

  • Standardized oromucosal whole-plant cannabis-based medicine (CBM): Contains delta-9 tetrahydrocannabinol (THC) and cannabidiol (CBD); may represent a useful agent for the relief of spasticity in multiple sclerosis (MS)

In a double-blind study performed over 6 weeks, in which 189 subjects with MS and spasticity received daily active preparation of standardized oromucosal whole-plant CBM (n=124) or placebo (n=65), the daily subject-recorded Numerical Rating Scale of spasticity showed the active preparation to be significantly superior. Secondary efficacy measures (Ashworth Score and a subjective measure of spasm) also were in favor of active preparation but did not achieve statistical significance.[21]

Another study, a meta-analysis, suggested that combined THC and CBD extracts may provide therapeutic benefit for spasticity in MS patients, although only subjective relief attained statistical significance.[22]


Neurolysis with neurotoxins, chemodenervation, or local anesthetic (ie, injections of phenol, botulinum toxin, alcohol, or 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.


Phenol is inexpensive, easily compounded, and has an immediate onset of action. It is injected, usually in a 5% concentration, near motor points in the affected muscle. A neurostimulator with a Teflon-coated needle electrode is used for guidance.

Gamma fibers are demyelinated for about 6 months, resulting in a less irritable, weakened muscle that can more easily be stretched.

Because 5% phenol injections do not cause permanent reduction in spasticity, a focus on obtaining functional improvements after injections is important.

Injections can be uncomfortable for some patients, and children may need to be sedated before injection. Possible adverse effects include pain and swelling at the site of injection. In a very small number of patients, dysesthesias may occur if injections are done near sensory-rich nerve branches.

If lengthening of a shortened muscle is desired, serial casting following injections may enhance effectiveness.

Intrathecal bolus injection of phenol

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.[23]

Botulinum toxin

A guideline from the American Academy of Neurology recommends offering botulinum toxin as a treatment option to reduce muscle tone and improve passive function in adults with spasticity (level A recommendation). It also recommends considering botulinum toxin injection to improve active function (level B).[24] (Collateral sprouting of the axon occurs in about 3 months, eliminating any permanent neurologic effect.)

Patients with focal spasms are candidates for focal treatment with botulinum toxin A (BoNT-A). Patients with segmental or nongeneralized spasticity may be candidates for systemic or intrathecal baclofen treatment, with BoNT-A added for focal symptom relief.

In 2009, the US Food and Drug Administration (FDA) required a boxed warning for all botulinum toxin products—types A and B—because of reports that the effects of the botulinum toxin may spread from the area of injection to other areas of the body, causing effects similar to those of botulism. These effects have included life-threatening, and sometimes fatal, swallowing and breathing difficulties. Most of the reports involved children with cerebral palsy being treated for spasticity.[25, 26, 27]

After botulinum 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 improving functioning in activities of daily living (ADLs). Decreased spasticity and improvements in range of motion and strength have considerable implications for activities such as dressing, bathing, feeding, and grooming.

Combination therapy

Botulinum toxin and phenol may effectively be used together.[28] For instance, gait problems related to diplegic cerebral palsy may involve the hip adductors, knee flexors, and ankle plantar flexors.

Treatment of all muscle groups may not be possible with just 1 medication, because of dosage guidelines or adverse effects.

If phenol and botulinum toxin are used together, all muscle groups can be treated, leading to a more functional outcome.

Botulinum toxin type A

BoNT-A injections have been used as a safe and effective treatment for a variety of movement disorders, including muscle overactivity and spasticity. Controlled clinical trials of BoNT-A injections for focal muscle spasticity have demonstrated prolonged, yet reversible, clinical effects; few adverse effects; and minimal immunogenicity.[29, 30]

Botulinum toxin A products approved for spasticity include:

  • Botox (onabotulinumtoxinA): Upper and lower limbs (adults); upper limbs (children aged 2 y or older)
  • Dysport (abobotulinumtoxinA): Upper and lower limbs (adults and children aged 2 y or older)
  • Xeomin (incobotulinumtoxinA): Upper limbs (adults)

BoNT-A inhibits acetylcholine release at the neuromuscular junction. Once inside the cholinergic nerve terminal cell, BoNT-A inhibits the docking and fusion of acetylcholine vesicles at the presynaptic membrane. 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. Gradually, muscle function returns by the regeneration or sprouting of blocked nerves forming new neuromuscular junctions.

In pediatric patients, treatment should be initiated at a time when children still are developing their motor control apparatus. This may prevent them from entering a vicious cycle in which central nervous system (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.

Proficiency in dosing and injecting BoNT-A demands the development of considerable skill. Each patient's treatment must be individualized, and appropriate patient selection is important. BoNT-A injections are most effective in relieving focal spasticity around a joint or series of joints.

Clinical data

The results of clinical trials strongly support the efficacy and safety of BoNT-A for the treatment of spasticity caused by cerebral palsy, MS, stroke, spinal cord injury, brain injury, or neurodegenerative disease. Major benefits of BoNT-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, botulinum toxin was 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. Significant adverse effects were not reported in any of the studies.[31]

A systematic review of BoNT-A therapy in poststroke spasticity by Rosales et al found an odds ratio of 4.5 (95% confidence index 2.79-7.25) for an improvement of 1 or more points on the Modified Ashworth Scale at 4-6 weeks after BoNT-A treatment.[32]

Treatment objectives and effects

Even though BoNT-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, there is an inverse relationship between spasticity and voluntary motor control. 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 BoNT-A.

In the upper limb, patterns of spasticity that may improve specifically from botulinum toxin include an adducted and internally rotated shoulder, flexed elbow, pronated forearm, flexed wrist, thumb-in-palm, and clenched fist.[33, 34] In the lower extremity, botulinum toxin 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 crucial to gauge the response and to fine-tune muscle selection and dose as necessary.


BoNT-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 BoNT-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. Examples of doses of BoNT-A in clinical trials for spasticity from MS, cerebral palsy, TBI, spinal cord injury (SCI), and stroke are as follows:

  • In MS, injection of 400 U of BoNT-A into the thigh adductors resulted in significant improvement in spasticity and hygiene compared with placebo[35]

  • In SCI, injection of 20-80 U of BoNT-A into the rhabdosphincter resulted in decreased urethral pressure and postvoid residual volume[36]

  • In adults suffering from cerebral palsy, injection of 1 U/kg of BoNT-A into the medial and lateral gastrocnemius of each leg resulted in an improvement in gait pattern compared with placebo[37]

  • For children with cerebral palsy, the American Academy of Neurology recommends offering injection of the calf muscles as a treatment option for equinus varus deformity (level A), but does not specify dosage[24]

  • In stroke, injections of 75-300 U of BoNT-A into the elbow and wrist flexors resulted in significant improvement in results of the Ashworth Scale compared with placebo[38]

Future trials of BoNT-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.

Injection strategies

BoNT-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). Ultrasonography, fluoroscopy, or computed tomography (CT) scanning 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, BoNT-A injections usually are needed at 3- to 6-month intervals to maintain therapeutic benefit. Reinjections should not be given any sooner than 3 months after the last injections to decrease the possibility of antibody formation.

A study by Molenaers et al of 577 patients with cerebral palsy, all of whom were younger than 24 years at the time of treatment, found that Goal Attainment Scale scores were higher for patients who received multilevel injections of BoNT-A or injections of the drug only in the distal muscle groups than they were for patients who received the injections only in the proximal muscles of the lower limb.[39]

Complementary treatments and additional medications

When used in the management of spasticity, treatment with BoNT-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. For example, in a controlled study in 20 children with upper limb spastic cerebral palsy, Kanellopoulos et al found that use of a static night splint after of BoNT-A injection resulted in significantly better results after 6 months.[32]

The above-mentioned study by Molenaers and colleagues found that, in addition to the injection strategy, factors in achieving a successful outcome in BoNT-A therapy included the following[39] :

  • Amount of physical therapy per week

  • Postinjection casting

  • Frequency with which day and night orthoses were used after injection

Treatment with BoNT-A can be combined with various oral medications, the baclofen pump, and sometimes with phenol or alcohol neurolysis. The primary reason for combining BoNT-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 BoNT-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 BoNT-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 BoNT-A necessary to achieve therapeutic benefit should be used, the interval between treatments should be extended for as long as possible, and booster injections should be avoided. When the amount injected totals the maximum of 400 U, 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. Injecting 10-20 U into 1 corrugator/frontalis muscle and testing for the ability to elevate 1 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 BoNT-A resistance may benefit from injections with other serotypes such as botulinum toxin type B (BoNT-B). BoNT-B, which is now available commercially, and other serotypes, when they become available, may offer hope to patients with resistance to BoNT-A.

Botulinum toxin type B

Schwerin et al reported the following results of a pilot study in which 29 children with spasticity underwent 62 treatment sessions with BoNT-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 BoNT-A nonresponders, 11 attained therapy goals with BoNT-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 recommended a starting dose of BoNT-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.[40]

Intrathecal Baclofen

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.

ITB therapy 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 those patients whose conditions are not sufficiently relieved by oral baclofen and other oral medications.[41, 42]

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 to decrease and often discontinue other spasticity medications.

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.

In a study of the long-term effects (>5 y) of ITB on impairment, disability, and quality of life in patients with severe spasticity of spinal origin, Zahavi et al found 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.[43]

Of 21 patients treated in the study, 11 had MS, 6 had SCI, 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 and spasm score. The Expanded Disability Status Scale score worsened, as did the ambulation index and overall incapacity status scale score. 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 MS and those with static spinal disorders.

The most common complications were muscle weakness, somnolence, catheter malfunction, and surgery complications. The authors reported that all patients but 2 were satisfied with their treatment and would undergo treatment again.

A review of ITB therapy in 174 children with cerebral palsy by Borowski et al found that ITB therapy is safe and effective for severe spasticity in this population, and that patients and caregivers find it highly satisfactory, but that the technique does have a 31% rate of complications requiring surgical management over a 3-year treatment period.[44]

Treatment goals

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 physiologic 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 treatment begins. Thus, appropriately chosen patients with clearly defined and realistic treatment objectives benefit the most from this form of treatment.

Intrathecal pump technology

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 with less systemic side effects than oral baclofen.

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.

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 noninvasive and affords flexibility in individualizing doses.


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 life-threatening adverse effects.

The initial total daily dose of ITB after implantation may be up to double the screening dose that resulted in a beneficial response. Intrathecal doses are 100 times less than the oral dose required to produce similar side effects so caution should be exercised when adjusting the pump.

About 60 days following surgery or when a stable dose program has been established, dose delivery can start to be fine-tuned. Maintenance doses of ITB are as follows:

  • For spasticity of spinal cord origin, the dose ranges from 12-2000 mcg/day, with most patients requiring 300-800 mcg/day

  • Patients with spasticity of cerebral origin receive doses ranging from 22-1400 mcg/day; for most patients, doses of 90-703 mcg/day result in therapeutic benefits

  • For children younger than 12 years, the average daily dose is 274 mcg/day, with a range of 24-1199 mcg/day

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.

Adverse effects

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 lightheadedness can stem from the pump delivering an inappropriate dosage of baclofen.

The pump itself can malfunction, and 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.

Transcranial Magnetic Stimulation

Centonze et al reported that repetitive transcranial magnetic stimulation (rTMS) may improve spasticity in patients with MS. They used high-frequency (5 Hz) and low-frequency (1 Hz) rTMS protocols in 19 patients with relapsing-remitting MS and lower limb spasticity.[45]

In the study, rTMS was applied over the leg primary motor cortex, measuring the H/M amplitude ratio of the soleus H reflex, a reliable neurophysiologic measure of stretch reflex. A significant improvement of lower limb spasticity was observed when rTMS applications were repeated over 2 weeks, lasting at least 7 days after the end of treatment; no effect was obtained after a 2-week sham stimulation. These results, though promising, need to be verified by larger well-designed studies.

Neurosurgical Therapy

The surgical treatment of spasticity aims at 4 different levels: the brain, spinal cord, peripheral nerves, and muscle. Each approach has its strengths and weaknesses, but none of them completely eliminates spasticity.

Stereotactic brain surgery, whether involving the globus pallidum, ventrothalamic nuclei, or cerebellum, has had little success. Cerebellar pacemakers have been tried, but with mixed results that were not ultimately encouraging.

Selective dorsal rhizotomy

Selective dorsal rhizotomy (SDR) is performed under general anesthesia, involves the 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" indicates that the target nerve roots enter the posterior spinal cord. These fibers carry sensory information to the cord from muscle.[46]

Sensory nerves are targeted because of the probable role they play in generating spasticity. SDR is thought to improve spasticity by partially restoring the proper physiologic balance between the disinhibited sensory nerves and the resulting excess physiologic muscle tone.

The surgery is employed only when less-invasive procedures are unable to control spasticity adequately. 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.

SDR has been performed mostly on children with cerebral palsy and less often in adults with spasticity from cerebral palsy or other etiologies. Studies have shown that most children with cerebral palsy experience a reduction in spasticity and an increase in range of motion that occurs immediately after SDR and persists for at least a year.

Cole et al emphasized the importance of applying strict selection criteria when considering children for SDR, as this is more likely to result in encouraging results. Of 53 children referred for SDR, only 19 (35%) fulfilled their selection criteria. These children showed improvement in cosmesis of gait, clinical examination, and temporal, kinetic, and kinematic parameters of gait analysis.[47]

Physical and occupational therapy are important postsurgical interventions to achieve the best outcome in patients who have undergone SDR. Most often, therapy is recommended 5 times per week for 6 months after the operation.

The relatively few longer-term follow-up studies that have been done on SDR indicate that 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. 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. Rare, long-term complications include low back pain, scoliosis or kyphosis (ie, spinal curves), and hip displacement.

Spinal cord stimulation

Implanted percutaneously, stimulators currently are used more for pain reduction than for reduction of spasticity, but they may prove to be clinically effective in the future.

Orthopedic Surgery

These surgeries constitute the most frequently used procedures for spasticity. The following types of surgery are employed:

  • Lengthening or release of muscles and tendons

  • Procedures involving bones

These operations aim to reduce spasticity, increase range of motion, improve accessibility for hygiene, increase tolerance to braces, or reduce pain. The timing of the procedures is critical. If they are performed too early, repetitive procedures may be necessary or developmental milestones may be delayed. If the procedures are delayed too long, future pain or irreversible bone deformity may occur. The majority of these operations are performed in children aged 4-8 years.

Contracture release

Contracture release is the most commonly performed orthopedic procedure. The most 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; a cast is then 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.

Tendon transfer

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

Physical, occupational, speech, and recreational therapists often are involved in providing the following for patients with spasticity[48, 49, 50, 51] :

  • Sustained stretching

  • Massage[52]

  • Vibration

  • Heat modalities

  • Cryotherapy

  • Functional electrical stimulation/biofeedback[53]

  • Strengthening of antagonistic muscle groups

  • Hippotherapy

  • Hydrotherapy

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.


Stretching forms the basis of spasticity treatment, helping to prevent contracture and maintain the full range of motion of a joint.


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. However, no clear evidence exists yet that intensive physiotherapy (1 h/day, 5 days/wk) is more beneficial than routine physiotherapy (6-7 h over 3 mo).

Orthoses, casts, and braces

Application of these allows a spastic limb to be maintained in a more normal position. For instance, an ankle-foot orthosis can help to 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.

Children may require a new orthosis every few months because of growth. When a child is undergoing new casting, splinting, or positioning, his or her skin should be closely monitored for signs of breakdown.

Cold packs

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.

Electrical stimulation

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.[54]


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/herself to reduce muscle tone consciously, and this may play a modest role in reducing spasticity.

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.

However, the 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.[55]

Most spasticity rating scales are ordinal. Equal intervals between units on an ordinal scale cannot be assumed automatically. Noninterval 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 are as follows:

  • Spasm Frequency Scale

  • Medical Research Council Motor Testing Scale

  • Modified Ashworth Scale,

  • Adductor Tone Rating

  • Global Pain Scale


Prevention of spasticity consists of the alleviation or treatment of precipitating factors, such as the following:

  • Pressure areas

  • Infections (eg, bladder, toenail, ear, or skin infections)

  • Deep venous thrombosis

  • Constipation

  • Bladder distention

  • Fatigue

  • Cold


Plastic surgeons, orthopedic surgeons, and neurosurgeons can play an important role in managing spasticity and its sequelae; thus, their contributions to the spasticity management team may be beneficial.

Neurologists and urologists can assist with issues such as seizure control and neurogenic bladder, which may affect spasticity control.[56]

Physical, occupational, speech, and recreational therapists can assist with family/patient training and education, as well as with therapeutic interventions.

Physical medicine and rehabilitation physicians lead a patient’s spasticity management team by reinforcing the role of function in guiding treatment decisions and by implementing those medical interventions that may be helpful.

Long-Term Monitoring

Because tolerance can occur with medications, drug dosages should regularly be reviewed and implantable devices (pumps, stimulators) should be checked.

Ongoing documentation of compliance with therapeutic interventions and evaluation of orthotic or positioning devices is important.

Children with spasticity should be monitored regularly for onset of orthopedic or other abnormalities, because rapid growth may result in permanent contractures, scoliosis, or loss of function.

If spasticity worsens, caregivers may have difficulty transferring patients safely or providing adequate hygiene and general care. Recognizing caregiver difficulties and intervening to educate and help caregivers ensure that patients receive proper care.

Monitoring skin integrity is essential in patients with spasticity, because pressure ulcers can lead to sepsis and death.

Overly aggressive surgical lengthening of severe contractures should be avoided because compression or overstretch injuries to the nerves and arteries of the limb may occur.



Medication Summary

Medications used in the treatment of spasticity include the following:

  • Skeletal muscle relaxants (dantrolene sodium, baclofen)

  • Benzodiazepines (diazepam)

  • Alpha2-adrenergic agonists (clonidine, tizanidine)

  • Botulinum toxins (onabotulinumtoxinA, abobotulinumtoxinA, incobotulinumtoxinA)

Because tolerance can occur with medications, drug dosages should regularly be reviewed and implantable devices (pumps, stimulators) should be checked.

Gabapentin, clonazepam, progabide, piracetam, lamotrigine, and cyproheptadine are medications that potentially may affect spasticity. These agents are not indicated for spasticity and currently are under investigation, have undergone little clinical evaluation, or are not available in the United States.

Pharmaceutical cannabinoids and plant-based cannabinoids have been investigated for their therapeutic potential in treating spasticity. There is sufficient evidence that cannabinoids may be effective for symptoms of spasticity in MS but no strong evidence in other conditions.[57, 58]

Skeletal Muscle Relaxants

Class Summary

These agents may be helpful in the treatment of reversible and intractable spasticity

Dantrolene sodium (Dantrium, Revonto, Ryanodex)

This is a peripherally acting medication that prevents calcium release from the sarcoplasmic reticulum. It is particularly effective in cerebral-origin spasticity, such as that occurring in traumatic brain injury (TBI), stroke, or cerebral palsy.

Baclofen (Lioresal, Gablofen)

Baclofen presynaptically inhibits the nerve terminal. It is centrally acting and can be administered intrathecally or orally. Baclofen is the preferred drug for spasticity related to spinal cord injury (SCI) or multiple sclerosis (MS) and is useful in cerebral palsy. Tolerance can occur. Adverse effects are minimized if the drug is given intrathecally.


Class Summary

These agents are skeletal muscle relaxants that can treat convulsive disorders.

Diazepam (Valium, Diastat)

Diazepam acts presynaptically and is a gamma-aminobutyric acid A (GABA-A) agonist. It is centrally acting and is particularly effective in patients with SCI and MS. Tolerance and addiction can occur.

Alpha2-adrenergic Agonists

Class Summary

These agents may reduce sympathetic outflow from the central nervous system (CNS).

Clonidine (Catapres, Kapvay)

Clonidine stimulates alpha-2 adrenoreceptors in the brainstem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow. These effects cause a decrease in vasomotor tone and heart rate. Clonidine is effective in SCI-associated spasticity and possibly in TBI-associated spasticity as well.

Tizanidine (Zanaflex)

Tizanidine is a centrally acting muscle relaxant that is metabolized in the liver and excreted in urine and feces. It is used in patients with predominantly upper motor neuron involvement. It is not a DEA-controlled substance.

Botulinum Toxins

Class Summary

Treatment with botulinum toxins are used to reduce muscle tone and improve passive and/or active function in adults with spasticity. Botulinum toxins are a neurotoxin derived from Clostridium botulinum. Botulinum toxin prevents acetylcholine from the presynaptic membrane, causing temporary calming of muscle contractions by blocking the transmission of nerve impulses.

OnabotulinumtoxinA (Botox)

Binds to the motor nerve terminal. The binding domain of the type A molecule appears to be the heavy chain, which is selective for cholinergic nerve terminals. It is then internalized via receptor-mediated endocytosis, a process in which the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal. After internalization, the light chain of the toxin molecule, which has been demonstrated to contain the transmission-blocking domain, is released into the cytoplasm of the nerve terminal. Subsequently blocks acetylcholine release by cleaving SNAP-25, a cytoplasmic protein that is located on the cell membrane and that is required for the release of this transmitter. The affected terminals are inhibited from stimulating muscle contraction. The toxin does not affect the synthesis or storage of acetylcholine or the conduction of electrical signals along the nerve fiber.

It is approved for upper and lower limb spasticity in adults and children aged 2 years or older.

AbobotulinumtoxinA (Dysport)

Binds to receptor sites on the motor nerve terminals and, after uptake, inhibits release of acetylcholine, blocking transmission of impulses in neuromuscular tissue. At 7-14 days after administration of the initial dose, assess the patient for a satisfactory response. Increase the dose 2-fold over the previously administered dose in patients who experience incomplete paralysis of the target muscle.

It is indicated for treatment of upper and lower limb spasticity in adults. It is also indicated for lower limb spasticity in children aged 2 years or older.

IncobotulinumtoxinA (Xeomin)

IncobotulinumtoxinA is botulinum toxin type A that is free of complexing proteins found in the natural toxin from Clostridium botulinum. This drug inhibits acetylcholine release and elicits neuromuscular blockade. It is indicated for treatment of upper limb spasticity in adults.


Questions & Answers


How is spasticity characterized?

What are the patterns of spasticity in upper extremities?

What is the most common sign of spasticity?

What are the patterns of spasticity in children with cerebral palsy?

What are the patterns of spasticity in the lower extremities?

How is spasticity diagnosed?

What are the clinical scales for spasticity?

How is spasticity treated?

What is spasticity?

What are the signs and symptoms of spasticity?

What types of interventions are used in the treatment of spasticity?

What is the prevalence of spasticity?

What is the pathophysiology of spasticity?

What is the role of cortical and spinal cord damage in the pathogenesis of spasticity?

What are the pathophysiologic mechanisms of spasticity?

What causes the sudden onset of spasticity?

Which factors exacerbate preexisting spasticity?

What is the prognosis of spasticity?

What is the prevalence of spasticity in multiple sclerosis (MS)?

What is the prognosis of spasticity following stroke?

How does spasticity affect health and quality of life (QoL)?

What are the possible benefits of spasticity?

Which organizations offer resources and advocacy groups for patients with spasticity?


What are the initial steps in the assessment of spasticity?

What are the manifestations of spasticity in cerebral palsy?

Which clinical history findings are characteristic of spasticity in patients with spinal cord injury or multiple sclerosis (MS)?

Which clinical history findings are characteristic of spasticity in the upper extremities?

Which muscles contribute to spasticity of the shoulder?

Which muscles contribute to spasticity of the hand?

Which clinical history findings are characteristic of spasticity of the lower extremities?

Which muscles contribute to flexor patterns of spasticity in the lower extremities?

Which clinical history findings are characteristic of spasticity following traumatic brain injury (TBI)?

Which muscles contribute to extensor patterns of spasticity in the lower extremities?

What is included in the physical exam to evaluate spasticity?

When is a physical and occupational therapy evaluation of spasticity indicated?

How is a physical and occupational therapy evaluation of spasticity administered?


How is spasticity differentiated from seizure activity?

Which neurologic disorders are associated with spasticity?


Which studies are performed in the workup of spasticity?

What are the research-oriented tools used to measure spasticity?


What should be considered prior to spasticity treatment selection?

What types of therapy are used in the treatment of spasticity?

What is the role of surgery in the treatment of chronic spasticity?

Which factors have an effect on spasticity treatment selection?

What is the role of dantrolene sodium in the treatment of spasticity?

What is the role of phenol in the treatment of spasticity?

What is the role of oral medications in the treatment of spasticity?

Which oral medications are used in the treatment of spasticity?

What is the role of benzodiazepines in the treatment of spasticity?

What is the role of baclofen in the treatment of spasticity?

What is the role of tizanidine in the treatment of spasticity?

What is the role of clonidine in the treatment of spasticity?

What is the role of gabapentin in the treatment of spasticity?

What is the role of lamotrigine in the treatment of spasticity?

What is the role of cyproheptadine in the treatment of spasticity?

What is the role of cannabis-based medicine (CBM) in the treatment of spasticity?

What is the role of neurolysis in the treatment of spasticity?

What is the role of botulinum toxin in the treatment of spasticity?

What is the role of botulinum toxin and phenol combination therapy in the treatment of spasticity?

What is the role of BoNT-A in the treatment of spasticity?

What is the efficacy of BoNT-A in the treatment of spasticity?

What are the goals for BoNT-A treatment of spasticity?

How is BoNT-A dosed for the treatment of spasticity?

What are BoNT-A injection strategies for the treatment of spasticity?

Which complementary therapies are used in combination with BoNT-A for the treatment of spasticity?

What causes resistance to BoNT-A in the treatment of spasticity?

How is resistance to BoNT-A assessed in the treatment of spasticity?

What are spasticity treatment alternatives for patients with BoNT-A resistance?

What is the efficacy of BoNT-B in the treatment of spasticity?

What is the role of intrathecal baclofen (ITB) in the treatment of spasticity?

What is the goal of ITB therapy for spasticity?

What is the role of pump technology in ITB treatment of spasticity?

How is ITB dosed for the treatment of spasticity?

What is the dosing of ITB maintenance therapy for spasticity?

What are the possible adverse effects of ITB spasticity treatment?

What is the role of transcranial magnetic stimulation (TMS) in the treatment of spasticity?

What is the role neurosurgery in the treatment of spasticity?

What is the role of selective dorsal rhizotomy (SDR) in the treatment of spasticity?

What is the role of spinal cord stimulation in the treatment of spasticity?

What is the role of orthopedic surgery in the treatment of spasticity?

What is the role of contracture release in the treatment of spasticity?

What is the role of tendon transfer in the treatment of spasticity?

What is the role of osteotomy in the treatment of spasticity?

What is the role of electrical stimulation in the treatment of spasticity?

What is the role of physical and occupational therapy in the treatment of spasticity?

What is the role of stretching exercises in the treatment of spasticity?

What is the role of strengthening exercises in the treatment of spasticity?

What is the role of orthoses in the treatment of spasticity?

What is the role of cold packs in the treatment of spasticity?

What is the role of biofeedback in the treatment of spasticity?

What is the role of outcome measures in spasticity treatment?

What are the most commonly used spasticity rating scales?

How is spasticity prevented?

Which specialist consultations are beneficial to patients with spasticity?

What is included in the long-term monitoring of spasticity?


Which types of medications are used in the treatment of spasticity?

Which medications in the drug class Botulinum Toxins are used in the treatment of Spasticity?

Which medications in the drug class Alpha2-adrenergic Agonists are used in the treatment of Spasticity?

Which medications in the drug class Benzodiazepines are used in the treatment of Spasticity?

Which medications in the drug class Skeletal Muscle Relaxants are used in the treatment of Spasticity?