Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Spasticity

  • Author: Zeba F Vanek, MD, MBBS, DCN; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
 
Updated: Feb 04, 2016
 

Practice Essentials

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.

Signs and symptoms

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 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

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 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

See Clinical Presentation for more detail.

Diagnosis

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 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,[2] 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.

Management

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) [3, 4]
  • Positioning/orthotics (including taping, dynamic and static splints, wheelchairs, and standers)
  • Oral medications (such as baclofen and dantrolene) [5]
  • 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.

Next

Background

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.

Previous
Next

Pathophysiology

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.[6]

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[7] and F-wave amplitudes.[8] 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.

Previous
Next

Etiology

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

  • Tethered spinal cord
  • 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)
  • Noxious stimulus (eg, ingrown toenail, ill-fitting orthotics, occult fracture)
  • Bladder distention
  • Bowel impaction
  • Cold weather
  • Fatigue
  • Seizure activity
  • Stress
  • Malpositioning
Previous
Next

Prognosis

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[9] :

  • 15.7% had no spasticity
  • 50.3% had minimal to mild spasticity
  • 17.2% had moderate spasticity
  • 16.8% had severe spasticity

Stroke

A review of spasticity after stroke showed that it affects less than one quarter of stroke victims. Ninety-five patients were studied immediately after and 3 months after a first-time stroke. Seventy-seven (81%) were initially hemiparetic, of whom 20 had spasticity. Modified Ashworth score was grade 1 in 10 patients, grade 1+ in 7 patients, and grade 2 in 3 patients. At 3 months, 64 patients (67%) were hemiparetic and 18 were spastic, reflecting 5 whose tone normalized and 3 who became spastic in the interim.[10]

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
Previous
Next

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

Email: info@biausa.org

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: webmaster@mymsaa.org (general information) or MSquestions@mymsaa.org (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

Email: support@msfocus.org

National Multiple Sclerosis Society

733 3rd Avenue, 6th Floor

New York, NY 10017-3288, USA

TEL: (800) FIGHT MS (344-4867) or (212) 986-3240

FAX: (212) 986-7981

Email: info@nmss.org

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

Email: strokeclub@aol.com

United Cerebral Palsy

1825 K Street NW

Suite 600

Washington, DC 20006, USA

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

Previous
 
 
Contributor Information and Disclosures
Author

Zeba F Vanek, MD, MBBS, DCN Associate Professor of Neurology, University of California, Los Angeles, David Geffen School of Medicine

Zeba F Vanek, MD, MBBS, DCN is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Chief Editor

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Acknowledgements

Joseph Carcione Jr, DO, MBA Consultant in Neurology and Medical Acupuncture, Medical Management and Organizational Consulting, Central Westchester Neuromuscular Care, PC; Medical Director, Oxford Health Plans

Joseph Carcione Jr, DO, MBA is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

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

Glenn Lopate, MD Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University School of Medicine; Director of Neurology Clinic, St Louis ConnectCare; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital

Glenn Lopate, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and Phi Beta Kappa

Disclosure: Baxter Grant/research funds Other; Amgen Grant/research funds None

Consuelo T Lorenzo, MD Executive Health Resources

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Elizabeth A Moberg-Wolff, MD Medical Director, Pediatric Rehabilitation Medicine Associates

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: Merz None Speaking and teaching

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.

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

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. 2011 Dec. 34(4):349-56. [Medline].

  2. Burridge JH, Wood DE, Hermens HJ, Voerman GE, Johnson GR, van Wijck F, et al. Theoretical and methodological considerations in the measurement of spasticity. Disabil Rehabil. 2005 Jan 7-21. 27(1-2):69-80. [Medline].

  3. Beaulieu LD, Schneider C. Effects of repetitive peripheral magnetic stimulation on normal or impaired motor control. A review. Neurophysiol Clin. 2013 Oct. 43(4):251-60. [Medline].

  4. 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].

  5. Lubsch L, Habersang R, Haase M, Luedtke S. Oral baclofen and clonidine for treatment of spasticity in children. J Child Neurol. 2006 Dec. 21(12):1090-2. [Medline].

  6. Kheder A, Nair KP. Spasticity: pathophysiology, evaluation and management. Pract Neurol. 2012 Oct. 12(5):289-98. [Medline].

  7. Angel RW, Hoffman WW. The H reflex in rigid, spastic and normal subjects. Arch Neurol. 1983. 8:591-596.

  8. Eisen A, Odusote K. Amplitude of the F wave: a potential means of documenting spasticity. Neurology. 1979 Sep. 29(9 Pt 1):1306-9. [Medline].

  9. Rizzo MA, Hadjimichael OC, Preiningerova J, Vollmer TL. Prevalence and treatment of spasticity reported by multiple sclerosis patients. Mult Scler. 2004 Oct. 10(5):589-95. [Medline].

  10. Sommerfeld DK, Eek EU, Svensson AK, Holmqvist LW, von Arbin MH. Spasticity after stroke: its occurrence and association with motor impairments and activity limitations. Stroke. 2004 Jan. 35(1):134-9. [Medline].

  11. Chrysagis N, Skordilis EK, Tsiganos G, Koutsouki D. Validity evidence of the Lateral Step Up (LSU) test for adolescents with spastic cerebral palsy. Disabil Rehabil. 2013 Jun. 35(11):875-80. [Medline].

  12. Ansari NN, Naghdi S, Mashayekhi M, Hasson S, Fakhari Z, Jalaie S. Intra-rater reliability of the Modified Modified Ashworth Scale (MMAS) in the assessment of upper-limb muscle spasticity. NeuroRehabilitation. 2012. 31(2):215-22. [Medline].

  13. Tizard JP. Cerebral palsies: treatment and prevention. The Croonian lecture 1978. J R Coll Physicians Lond. 1980 Apr. 14(2):72-7, 80. [Medline].

  14. Ammar A, Ughratdar I, Sivakumar G, Vloeberghs MH. Intrathecal baclofen therapy--how we do it. J Neurosurg Pediatr. 2012 Nov. 10(5):439-44. [Medline].

  15. Katrak PH, Cole AM, Poulos CJ, McCauley JC. Objective assessment of spasticity, strength, and function with early exhibition of dantrolene sodium after cerebrovascular accident: a randomized double-blind study. Arch Phys Med Rehabil. 1992 Jan. 73(1):4-9. [Medline].

  16. Collin C, Davies P, Mutiboko IK, Ratcliffe S. Randomized controlled trial of cannabis-based medicine in spasticity caused by multiple sclerosis. Eur J Neurol. 2007 Mar. 14(3):290-6. [Medline].

  17. Lakhan SE, Rowland M. Whole plant cannabis extracts in the treatment of spasticity in multiple sclerosis: a systematic review. BMC Neurol. 2009 Dec 4. 9:59. [Medline]. [Full Text].

  18. Jarrett L, Nandi P, Thompson AJ. Managing severe lower limb spasticity in multiple sclerosis: does intrathecal phenol have a role?. J Neurol Neurosurg Psychiatry. 2002 Dec. 73(6):705-9. [Medline]. [Full Text].

  19. [Guideline] American Academy of Neurology. Assessment: botulinum neurotoxin for the treatment of spasticity (an evidence-based review). Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. National Guideline Clearinghouse. Available at http://guideline.gov/content.aspx?id=12942. Accessed: February 4, 2014.

  20. U.S. Food and Drug Administration. Available at . Accessed December 31, 2009. FDA Requires Boxed Warning for All Botulinum Toxin Products. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm149574.htm. Accessed: February 4, 2014.

  21. 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. 2012 Mar. 48(1):47-55. [Medline].

  22. Demetrios M, Khan F, Turner-Stokes L, Brand C, McSweeney S. Multidisciplinary rehabilitation following botulinum toxin and other focal intramuscular treatment for post-stroke spasticity. Cochrane Database Syst Rev. 2013 Jun 5. 6:CD009689. [Medline].

  23. Gooch JL, Patton CP. Combining botulinum toxin and phenol to manage spasticity in children. Arch Phys Med Rehabil. 2004 Jul. 85(7):1121-4. [Medline].

  24. Intiso D, Simone V, Di Rienzo F, Iarossi A, Pazienza L, Santamato A, et al. High doses of a new botulinum toxin type A (NT-201) in adult patients with severe spasticity following brain injury and cerebral palsy. NeuroRehabilitation. 2014 Jan 28. [Medline].

  25. Wang YJ, Gao BQ. Efficacy and safety of serial injections of botulinum toxin A in children with spastic cerebral palsy. World J Pediatr. 2013 Nov. 9(4):342-5. [Medline].

  26. Simpson DM. Clinical trials of botulinum toxin in the treatment of spasticity. Muscle Nerve Suppl. 1997. 6:S169-75. [Medline].

  27. Rosales RL, Chua-Yap AS. Evidence-based systematic review on the efficacy and safety of botulinum toxin-A therapy in post-stroke spasticity. J Neural Transm. 2008. 115(4):617-23. [Medline].

  28. Fehlings D, Rang M, Glazier J, Steele C. An evaluation of botulinum-A toxin injections to improve upper extremity function in children with hemiplegic cerebral palsy. J Pediatr. 2000 Sep. 137(3):331-7. [Medline].

  29. Jost WH, Hefter H, Reissig A, Kollewe K, Wissel J. Efficacy and safety of botulinum toxin type A (Dysport) for the treatment of post-stroke arm spasticity: Results of the German-Austrian open-label post-marketing surveillance prospective study. J Neurol Sci. 2013 Nov 22. [Medline].

  30. Snow BJ, Tsui JK, Bhatt MH, Varelas M, Hashimoto SA, Calne DB. Treatment of spasticity with botulinum toxin: a double-blind study. Ann Neurol. 1990 Oct. 28(4):512-5. [Medline].

  31. Dykstra DD, Sidi AA. Treatment of detrusor-sphincter dyssynergia with botulinum A toxin: a double-blind study. Arch Phys Med Rehabil. 1990 Jan. 71(1):24-6. [Medline].

  32. Koman LA, Mooney JF, Smith BP. Botulinum toxin: potential role in the management of cerebral palsy during childhood. Jankovic J, Hallett M, eds. Therapy with Botulinum Toxin. NY: Marcel Dekker; 1994. 511-522.

  33. Simpson DM, Alexander DN, O'Brien CF, Tagliati M, Aswad AS, Leon JM, et al. Botulinum toxin type A in the treatment of upper extremity spasticity: a randomized, double-blind, placebo-controlled trial. Neurology. 1996 May. 46(5):1306-10. [Medline].

  34. Molenaers G, Fagard K, Van Campenhout A, Desloovere K. Botulinum toxin A treatment of the lower extremities in children with cerebral palsy. J Child Orthop. 2013 Nov. 7(5):383-387. [Medline]. [Full Text].

  35. Schwerin A, Berweck S, Fietzek UM, Heinen F. Botulinum toxin B treatment in children with spastic movement disorders: a pilot study. Pediatr Neurol. 2004 Aug. 31(2):109-13. [Medline].

  36. Francisco GE, Yablon SA, Schiess MC, Wiggs L, Cavalier S, Grissom S. Consensus panel guidelines for the use of intrathecal baclofen therapy in poststroke spastic hypertonia. Top Stroke Rehabil. 2006 Fall. 13(4):74-85. [Medline].

  37. Krach LE, Nettleton A, Klempka B. Satisfaction of individuals treated long-term with continuous infusion of intrathecal baclofen by implanted programmable pump. Pediatr Rehabil. 2006 Jul-Sep. 9(3):210-8. [Medline].

  38. Zahavi A, Geertzen JH, Middel B, Staal M, Rietman JS. Long term effect (more than five years) of intrathecal baclofen on impairment, disability, and quality of life in patients with severe spasticity of spinal origin. J Neurol Neurosurg Psychiatry. 2004 Nov. 75(11):1553-7. [Medline]. [Full Text].

  39. Borowski A, Littleton AG, Borkhuu B, Presedo A, Shah S, Dabney KW, et al. Complications of intrathecal baclofen pump therapy in pediatric patients. J Pediatr Orthop. 2010 Jan-Feb. 30(1):76-81. [Medline].

  40. Centonze D, Koch G, Versace V, Mori F, Rossi S, Brusa L, et al. Repetitive transcranial magnetic stimulation of the motor cortex ameliorates spasticity in multiple sclerosis. Neurology. 2007 Mar 27. 68(13):1045-50. [Medline].

  41. Buckon CE, Thomas S, Pierce R, Piatt JH Jr, Aiona MD. Developmental skills of children with spastic diplegia: functional and qualitative changes after selective dorsal rhizotomy. Arch Phys Med Rehabil. 1997 Sep. 78(9):946-51. [Medline].

  42. Cole GF, Farmer SE, Roberts A, Stewart C, Patrick JH. Selective dorsal rhizotomy for children with cerebral palsy: the Oswestry experience. Arch Dis Child. 2007 Sep. 92(9):781-5. [Medline]. [Full Text].

  43. 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. 2013 May. 22(4):364-70. [Medline].

  44. 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. 2011 Oct 24. 504(2):112-4. [Medline].

  45. 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].

  46. 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. 2011 Aug. 53(8):742-50. [Medline].

  47. Negahban H, Rezaie S, Goharpey S. Massage therapy and exercise therapy in patients with multiple sclerosis: a randomized controlled pilot study. Clin Rehabil. 2013 Dec. 27(12):1126-36. [Medline].

  48. Warnink-Kavelaars J, Vermeulen RJ, Becher JG. Study protocol: precision of a protocol for manual intramuscular needle placement checked by passive stretching and relaxing of the target muscle in the lower extremity during BTX-A treatment in children with spastic cerebral palsy, as verified by means of electrical stimulation. BMC Pediatr. 2013 Aug 22. 13:129. [Medline]. [Full Text].

  49. Kubota S, Tanabe S, Sugawara K, Muraoka Y, Itoh N, Kanada Y. Stimulus point distribution in deep or superficial peroneal nerve for treatment of ankle spasticity. Neuromodulation. 2013 May-Jun. 16(3):251-5; discussion 255. [Medline].

  50. Pierson SH. Outcome measures in spasticity management. Muscle Nerve Suppl. 1997. 6:S36-60. [Medline].

  51. 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]. [Full Text].

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.