Physical Medicine and Rehabilitation for Spasticity

Author: Elizabeth A Moberg-Wolff, MD; Chief Editor: Consuelo T Lorenzo, MD more...

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Overview Clinical Symptoms And Patterns Differential Diagnosis on Initial Evaluation Considerations in Patient Evaluation/Workup Treatment of Spasticity Ongoing Management/Follow-up Care Miscellaneous Caveats: Functional Considerations for Present and Future Show All

References

Overview
Background
Spasticity (meaning to draw or tug) is involuntary, velocity-dependent, increased muscle tone that results in resistance to movement. The condition may occur secondary to a disorder or trauma, such as a spinal cord injury (SCI), a brain injury, a tumor, a stroke, multiple sclerosis (MS), or a peripheral nerve injury. A lag time may exist between injury and spasticity onset, and severity may wax and wane over time. Spasticity may be static or dynamic in nature. Although many therapeutic and medical interventions can attenuate its effects, spasticity can be severely debilitating. In spite of the fact that spasticity may coexist with other conditions, it should not be confused with any of the following:

Rigidity - Involuntary, bidirectional, non velocity-dependent resistance to movement Clonus - Self-sustaining, oscillating movements secondary to hypertonicity Dystonia - Involuntary, sustained contractions resulting in twisting, abnormal postures Athetoid movement - Involuntary, irregular, confluent writhing movements Chorea - Involuntary, abrupt, rapid, irregular, and unsustained movements

Ballisms - Involuntary flinging movements of the limbs or body Tremor - Involuntary, rhythmic, repetitive oscillations that are not self-sustaining

Pathophysiology
First described by Little in 1843, spasticity has many postulated causes, most of which revolve around altered afferent and efferent input to the alpha motor neuron. Spinal, peripheral nerve, or cortical injury can alter inhibitory and excitatory messages to the motor neuron. Alternatively, these injuries might result in denervation supersensitivity, deafferentation, central collateral sprouting, or disinhibition of the nerves. Polysynaptic responses may be involved in spinal cord mediated spasticity, while enhanced excitability of monosynaptic pathways is involved in cortically mediated spasticity. (Also, see the eMedicine Neurology article Spasticity.)

Frequency
Spasticity is present to some degree in most patients with MS, SCI, cerebral palsy (CP), and traumatic brain injury (TBI).

Advantages of spasticity

Substitutes for strength, allowing standing, walking, gripping May improve circulation and prevent deep venous thrombosis and edema May reduce the risk of osteoporosis

Morbidity/disadvantages of spasticity

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

Sex/age
Spasticity is not affected by sex, race, or age group, nor is it more prevalent in any of those groups.

Measurement
Spasticity is difficult to quantify, 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 Tardieu scale, surface electromyography, isokinetic dynamometry, the H reflex, the tonic vibration reflex, the F-wave response, the flexor reflex response, and transcranial electrical/magnetic stimulation.

Clinical Symptoms And Patterns

Clinical caveats
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 predict future functional status in addition to cosmetic or orthopedic deformities that may occur, helping to guide treatment decisions.

Cerebral palsy
Children with CP 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. (See also the Medscape CME entry Exercise Training Program Benefits Children With Cerebral Palsy.)

Spinal cord injury/multiple sclerosis

Spasticity in patients with incomplete or complete SCI and MS can vary greatly in both 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. (See also the Multiple Sclerosis Resource Center, on Medscape, as well as the Medscape CME entries Advances in Multiple Sclerosis and ECTRIMS 2007: Understanding MS: Pathogenesis, Neuroinflammation, and Degeneration.)

What to treat
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.

Upper extremity flexor patterns

The following patterns often are seen in patients with CP, stroke, or 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

The following muscles typically are involved and are targeted for treatment:

Pectoralis major Latissimus dorsi Teres major Biceps Brachioradialis Brachialis Pronator teres and quadratus Flexor carpi radialis or ulnaris Flexor digitorum profundus and superficialis Adductor pollicis

Lower extremity flexor patterns

The following flexor patterns often are seen in patients with CP, MS, or TBI or who have suffered a stroke: o Hip adduction and flexion o Knee flexion o Ankle plantar flexion or equinovarus positioning The following muscles typically are involved 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: o Knee extension or flexion o Equinus and/or valgus ankle o Great toe dorsiflexion or excessive toe flexion The following muscles typically are involved and are targeted for treatment: o Quadriceps femoris o Medial hamstrings o Gastrocnemius o Tibialis posterior o Extensor hallucis longus o Toe flexors o Peroneus longus

o o o o o o

Differential Diagnosis on Initial Evaluation

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

Tethered spinal cord Spinal cord tumor Nerve impingement peripherally or centrally Hydrocephalus Intracranial, epidural, or subdural bleeding

Factors that can exacerbate pre-existing spasticity from spinal injury, brain tumor/injury, cerebral palsy, or multiple sclerosis may include the following:

Infection (eg, otitis, urinary tract, 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 may be mistaken for seizure activity, but it (1) is not followed by a postictal period and (2) is typically not as rhythmic or symmetrical as seizure activity.

Considerations in Patient Evaluation/Workup

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.[1] In patients with a previous neurologic insult, a thorough history and physical examination is necessary to rule out any factors that exacerbate spasticity (eg, medication changes, noxious stimuli, increased intracranial pressure). Laboratory studies (eg, complete blood count [CBC], culture of urine, blood, cerebrospinal fluid) also may help to rule out infection. Radiographs also may be helpful to rule out problems, such as bowel impaction or occult fractures, that are especially important in the insensate patient with SCI or the cognitively impaired patient with TBI.

Consultations

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.[2] 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 the team by reinforcing the role of function in guiding treatment decisions and by implementing those medical interventions that may be helpful.

Treatment of Spasticity
Goals of spasticity management

To improve function related to the activities of daily living, mobility, the ease of care by caregivers, sleep, cosmesis, and overall functional independence To prevent orthopedic deformity, the development of pressure areas, and the need for corrective surgery To reduce pain To allow the stretching of shortened muscles, the strengthening of antagonistic muscles, and the appropriate orthotic fit

Considerations that impact treatment

Duration of spasticity and the 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

Treatment interventions
Interventions 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, and should not simply be used in a stepladder approach. Current spasticity management options include the following:

Preventative measures Therapeutic interventions (physical therapy, occupational therapy, hippotherapy, aquatics) and physical modalities (ultrasonography, e-stim, biofeedback)[3] Positioning/orthotics - Including taping, dynamic and static splints, wheelchairs, and standers Oral medications - Such as baclofen and dantrolene[4] Injectable medications - Botulinum toxins and phenol Surgical intervention

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

Pressure areas Infections - Such as bladder, toenail, ear, or skin infections Deep venous thrombosis Constipation Bladder distention Fatigue Cold

Therapeutic interventions and physical modalities

Physical, occupational, speech, and recreational therapists often are involved in providing the following[5, 6, 7, 8] :

Sustained stretching Massage

Vibration Heat modalities Cryotherapy Functional electrical stimulation/biofeedback Strengthening of antagonistic muscle groups Hippotherapy Hydrotherapy

Orthotics/positioning

Serial or inhibitive casting of the ankles, knees, fingers, wrists, and elbows Splinting/orthotics - Upper and lower extremities, soft or hard, custom or prefabricated; an orthosis may help to hold a limb in a functional position, reduce pain, and prevent deformity. Positioning to reduce synergy patterns - For example, wheelchair seating and bed positioning

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.

Common oral medications

Baclofen (Lioresal)[4] Diazepam (Valium) Dantrolene (Dantrium) Tizanidine (Zanaflex) Clonidine (Catapres)[4]

See the section Common Oral Medications for more detailed information.

Injectable medications/nerve blocks

Phenol
o o o o o o

Phenol 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. Phenol is inexpensive, easily compounded, and has an immediate onset of action.

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. o If lengthening of a shortened muscle is desired, serial casting following injections may enhance effectiveness. Botulinum toxin type A or B[9] o Injections of these substances block presynaptic release of acetylcholine at the neuromuscular junction. o Collateral sprouting of the axon occurs in about 3 months, eliminating any permanent effect. o These medications are expensive, but they are also simple and fairly painless to inject. o Onset of action is usually 3-5 days after injection. o Dosage is flexible, being based on the patient's weight, muscle size, and level of spasticity, as well as on treatment goals and the effect of prior injections. o Because of potential antibody formation, injections of the smallest effective amount at greater than 3-month intervals are encouraged. o Serial casting to improve length in shorted muscles may enhance the effect of injections. Combination therapy [10] o Botulinum toxin and phenol may effectively be used together. For instance, gait problems related to diplegic CP may involve the hip adductors, knee flexors, and ankle plantar flexors. o Treatment of all muscle groups may not be possible with just 1 medication because of dosage guidelines or adverse effects. o If phenol and botulinum toxin are used together, all muscle groups can be treated, leading to a more functional outcome.

Surgical/intrathecal interventions

Tenotomy/tendon transfer/osteotomy o Orthopedic interventions release muscle contractures, lengthen shortened tendons, protect against or reduce bony deformities, and may reduce the strength of a spastic muscle group. o The timing of procedures is critical. If the procedures 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. o Orthopedic interventions do not inherently alter the spasticity of muscle groups but instead alter the effects of spasticity. Myelotomy/cordectomy o Transection or resection of portions of the spinal cord result in reduced spasticity but potentially cause loss of bowel and bladder function, as well as loss of strength, pain, and temperature sensation. o These procedures rarely are performed. Selective dorsal rhizotomy[11]

Selective transection of the posterior spinal nerve roots from L2-S1 results in reduced lower extremity spasticity. Nerve roots are selected for ablation by evaluating the peripheral muscle and electromyographic activity that occurs during intraoperative stimulation. o Reduction in overflow tone from the lower extremities may alter the function and strength of the trunk and upper extremities. Sensation may be altered as well; patients with significant sensory integrative issues are not good candidates for selective dorsal rhizotomy (SDR). o SDR appears to be most effective in a select group of young diplegic children with CP who have strength underlying their spasticity, good cognition, cooperation, and motivation.[12] o Physical and occupational therapy are important postsurgical interventions to achieve the best outcome. Most often, therapy is recommended 5 times per week for 6 months after SDR. Spinal cord stimulator - 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. Stereotactic neurosurgery and cerebellar stimulation - These procedures have been used to reduce spasticity in some patient populations, but widespread benefits have not been noted. They may be more appropriate for subcategories of dystonia. Intrathecal baclofen therapy[13, 14, 15, 16] o Baclofen can be delivered intrathecally via an implantable pump placed under the skin or fascia of the abdomen. A catheter is attached and then tunneled into the intrathecal space, where it drips baclofen at a variable or continuous rate for 24 hours per day. o The level of optimum catheter placement is determined clinically by the level of the muscle groups in which relaxation is desired. o Because only a small intrathecal dose is needed for effectiveness, the sedation that often is seen with oral baclofen administration is eliminated. o A small dose of baclofen, given by lumbar puncture, usually is injected prior to pump implantation as a test dose. Its effect lasts approximately 6-8 hours and predicts quantitatively, but not qualitatively, whether the medication will be effective. After the implant, the dosage of baclofen gradually is titrated until the desired effect is obtained. o The pump reservoir is refilled every 1-6 months via injection into a refill port. An office procedure, this is simple and fairly painless. o Potential problems include catheter kinks or disconnection, which are diagnosed by clinical symptoms and radiographic studies. Surgery typically is needed to correct these problems. o Batteries within the pump need replacement approximately every 7 years. o Patients as small as 25 lb (11.5 kg) have successfully undergone this implant procedure. o The procedure is reversible.

Ongoing Management/Follow-up Care

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 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. The ability of muscles to function after spasticity reduction varies. Treating spasticity does not always facilitate the acquisition of previously undeveloped skills. The importance of physical and occupational therapy intervention for achieving functional goals cannot be overemphasized.

Miscellaneous Caveats: Functional Considerations for Present and Future

It is important to weigh the benefits of spasticity to the patient with regard to present function against the disadvantages of it that may alter future medical condition or function.

Contributor Information and Disclosures Author Elizabeth A Moberg-Wolff, MD Associate Professor, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin, Medical College of Wisconsin Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation Disclosure: Medtronic Neurological Grant/research funds Speaking and teaching Specialty Editor Board Martin K Childers, DO, PhD Professor, Department of Neurology, Wake Forest University School of Medicine; Professor, Rehabilitation Program, Institute for Regenerative Medicine, Wake Forest Baptist Medical Center Martin K Childers, DO, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Congress of Rehabilitation Medicine, American Osteopathic Association, Christian Medical & Dental Society, and Federation of American Societies for Experimental Biology Disclosure: Allergan pharma Consulting fee Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society Disclosure: Nothing to disclose. Kelly L Allen, MD Medical Director, Medevals Disclosure: Nothing to disclose. Chief Editor Consuelo T Lorenzo, MD Physiatrist, Department of Physical Medicine and Rehabilitation, Alegent Health, Immanuel Rehabilitation Center Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation Disclosure: Nothing to disclose. References 1. Wei XJ, Tong KY, Hu XL. The responsiveness and correlation between Fugl-Meyer Assessment, Motor Status Scale, and the Action Research Arm Test in chronic stroke with upper-extremity rehabilitation robotic training. Int J Rehabil Res. Dec 2011;34(4):349-56. [Medline]. 2. Peng Q, Park HS, Shah P, Wilson N, Ren Y, Wu YN, et al. Quantitative evaluations of ankle spasticity and stiffness in neurological disorders using manual spasticity evaluator. J Rehabil Res Dev. 2011;48(4):473-81. [Medline]. 3. Sahin N, Ugurlu H, Karahan AY. Efficacy of therapeutic ultrasound in the treatment of spasticity: a randomized controlled study. NeuroRehabilitation. 2011;29(1):61-6. [Medline]. 4. Lubsch L, Habersang R, Haase M, et al. Oral baclofen and clonidine for treatment of spasticity in children. J Child Neurol. Dec 2006;21(12):1090-2. [Medline]. 5. Kagawa S, Koyama T, Hosomi M, Takebayashi T, Hanada K, Hashimoto F, et al. Effects of Constraint-induced Movement Therapy on Spasticity in Patients with Hemiparesis after Stroke. J Stroke Cerebrovasc Dis. Nov 10 2011;[Medline]. 6. Hoseini N, Koceja DM, Riley ZA. The effect of operant-conditioning balance training on the down-regulation of spinal H-reflexes in a spastic patient. Neurosci Lett. Oct 24 2011;504(2):112-4. [Medline]. 7. Rayegani SM, Shojaee H, Sedighipour L, Soroush MR, Baghbani M, Amirani OB. The effect of electrical passive cycling on spasticity in war veterans with spinal cord injury. Front Neurol. 2011;2:39. [Medline]. [Full Text].

8. Johnston TE, Watson KE, Ross SA, Gates PE, Gaughan JP, Lauer RT, et al. Effects of a supported speed treadmill training exercise program on impairment and function for children with cerebral palsy. Dev Med Child Neurol. Aug 2011;53(8):742-50. [Medline]. 9. Kakuda W, Abo M, Momosaki R, Yokoi A, Fukuda A, Ito H, et al. Combined therapeutic application of botulinum toxin type A, low-frequency rTMS, and intensive occupational therapy for post-stroke spastic upper limb hemiparesis. Eur J Phys Rehabil Med. Nov 9 2011;[Medline]. 10. Gooch JL, Patton CP. Combining botulinum toxin and phenol to manage spasticity in children. Arch Phys Med Rehabil. Jul 2004;85(7):1121-4. [Medline]. 11. Buckon CE, Thomas S, Pierce R, et al. Developmental skills of children with spastic diplegia: functional and qualitative changes after selective dorsal rhizotomy. Arch Phys Med Rehabil. Sep 1997;78(9):946-51. [Medline]. 12. McLaughlin JF, Bjornson KF, Astley SJ, et al. Selective dorsal rhizotomy: efficacy and safety in an investigator-masked randomized clinical trial. Dev Med Child Neurol. Apr 1998;40(4):220-32. [Medline]. 13. Albright AL, Barron WB, Fasick MP, et al. Continuous intrathecal baclofen infusion for spasticity of cerebral origin. JAMA. Nov 24 1993;270(20):2475-7. [Medline]. 14. Coffey JR, Cahill D, Steers W, et al. Intrathecal baclofen for intractable spasticity of spinal origin: results of a long-term multicenter study. J Neurosurg. Feb 1993;78(2):22632. [Medline]. 15. Francisco GE, Yablon SA, Schiess MC, et al. Consensus panel guidelines for the use of intrathecal baclofen therapy in poststroke spastic hypertonia. Top Stroke Rehabil. 2006;13(4):74-85. [Medline]. 16. Krach LE, Nettleton A, Klempka B. Satisfaction of individuals treated long-term with continuous infusion of intrathecal baclofen by implanted programmable pump. Pediatr Rehabil. Jul-Sep 2006;9(3):210-8. [Medline]. 17. Albright AL, Awaad Y, Muhonen M, et al. Performance and complications associated with the synchromed 10-ml infusion pump for intrathecal baclofen administration in children. J Neurosurg. Aug 2004;101(1 Suppl):64-8. [Medline]. 18. Kato M, Ohkuma S, Kataoka K, et al. Release of digestive enzymes from isolated rat pancreatic acini following muscarinic stimulation: a comparative study with enzyme release and receptor binding. Jpn J Pharmacol. Jul 1991;56(3):311-25. [Medline]. [Full Text]. 19. Katz RT, Campagnolo DE. Pharmacologic management of spasticity. In: Katz RT, ed. Spasticity: State of the Art Review. vol 8. Philadelphia, Pa: Hanley & Belfus; 1994:47380. 20. Molnar GE. Cerebral palsy. In: Pediatric Rehabilitation. 2nd ed. Baltimore, Md: Lippincott Williams & Wilkins; 1992:481-523. 21. Peacock WJ, Arens LJ, Berman B. Cerebral palsy spasticity. Selective posterior rhizotomy. Pediatr Neurosci. 1987;13(2):61-6. [Medline]. 22. Zafonte RD, Elovic E, Grabois M, eds. Spasticity and abnormalities of muscle tone. In: Garrison SJ, Grabois M, Hart KA, et al, eds. Physical Medicine and Rehabilitation: The Complete Approach. London, England: Blackwell Science; 2000:848-56.

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