eMedicine Specialties > Physical Medicine and Rehabilitation > Disorders of the Motor Unit

Kugelberg Welander Spinal Muscular Atrophy

Joyce L Oleszek, MD, Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Colorado at Denver Health Sciences Center, The Children's Hospital of Denver
Stephanie E Vallee, MS, Certified Genetic Counselor, Dartmouth-Hitchcock Medical Center, Children's Hospital at Dartmouth; Michael Dichiaro, MD, Chief Resident, Department of Physical Medicine and Rehabilitation, University of Colorado at Denver Health Sciences Center; Mary Louise Caire, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Wise Regional Medical Center; Stephen Kishner, MD, Residency Program Director, Professor of Clinical Medicine, Department of Medicine, Section of Physical Medicine and Rehabilitation, Louisiana State University School of Medicine

Updated: Jul 29, 2008

Introduction

Background

Spinal muscular atrophies (SMAs) represent a rare group of inherited disorders that cause progressive degeneration of the anterior horn cells of the spinal cord. The exact cause of the degeneration is unknown. Loss of these cells results in a progressive lower motor neuron disease that has no sensory involvement and that is manifested as hypotonia, weakness, and progressive paralysis. Kugelberg Welander spinal muscular atrophy (also known as Wohlfart-Kugelberg-Welander syndrome or mild SMA) is a milder form of SMA, with symptoms typically presenting after age 18 months.^1,2,3

SMAs were first described in the 1890s, by Guido Werdnig, a physician from the University of Vienna, in his lecture "On a Case of Muscular Dystrophy with Positive Spinal Cord Findings." Soon after, Professor Johann Hoffmann from Heidelberg University presented a paper describing a syndrome of progressive atrophy, weakness, and death during the early childhood period of siblings with genetically normal parents. Both physicians conducted autopsies on their patients and found severe atrophy of the ventral roots of the spinal cord. They also found histologic evidence of loss of motor neurons in the anterior horn cells of this region. Hoffmann called the syndrome spinale muskelatrophie (spinal muscular atrophy).

In the early 1960s, Byers and Banker classified SMA into categories based on the severity and age of onset of the symptoms, in an effort to predict prognosis. Their system, summarized below, became the basis for the most widely recognized system now used for the classification of SMA.

• Type I
  • Onset of symptoms before age 6 months
  • Also known as infantile onset SMA, or Werdnig-Hoffmann disease
• Type II⁴
  • Onset of symptoms at age 6-18 months
  • Also known as chronic SMA, juvenile SMA, or intermediate SMA
• Type III⁴
  • Onset of symptoms after age 18 months, usually in late childhood or adolescence
  • Also known as Kugelberg Welander SMA, or mild SMA

Although Byers and Banker's classification system focuses on only the above 3 categories, many sources refer to a fourth type of SMA.

• Type IV
  • This category is reserved for onset of symptoms during early adulthood.
  • This disorder usually carries a much more favorable prognosis than do the other types of SMA.

This article focuses only on SMA types III and IV.

Related eMedicine topics:
Focal Muscular Atrophies
Spinal Muscle Atrophy
Spinal Muscular Atrophy

Related Medscape topic:
Resource Center Spinal Disorders

Pathophysiology

Spinal muscular atrophy (SMA) is caused by successive motor unit degeneration. Muscle atrophy, caused by a progressive loss of the anterior horn cells in the spinal cord, is universal. The motor nuclei in the lower brainstem, usually those of cranial nerves V-XII (V, VII, IX, XII), also may be involved. Various stages of degeneration can be observed histologically at these sites. As the nerve cells decrease in number, replacement gliosis, pyknosis, and secondary Wallerian degeneration in the roots and peripheral nerves are observed. These processes generally begin at the caudal end of the cord and typically are symmetrical. The lower limbs usually are affected sooner and more profoundly than are the upper limbs. This degeneration most often affects the proximal musculature before it impacts the distal. Note that, unlike in amyotrophic lateral sclerosis (ALS), no corticospinal tract involvement is seen in SMA.

Frequency

United States

Spinal muscular atrophy has an estimated incidence of 1 case per 15,000 live births. The genetic carrier prevalence is 1:80.

International

Spinal muscular atrophy has an estimated incidence of 1 case per 15,000-20,000 live births worldwide.

Mortality/Morbidity

Spinal muscular atrophy (SMA) types III and IV, unlike types I and II, are consistent with survival well into adulthood.⁵ Significant morbidity occurs from progressive weakness, and patients may frequently fall or may have difficulty with stairs. Most patients use wheelchair mobility by their fourth decade of life. Scoliosis and joint contractures are also extremely common. Morbidity associated with these conditions often can be minimized with spinal surgery, as well as with aggressive physical therapy. Respiratory failure in SMA types III and IV is not as common as in types I and II. Respiratory complaints usually can be managed medically, and mechanical ventilation seldom is necessary.^6,7,8

Race

Spinal muscular atrophy (SMA) affects all races equally.

Sex

Spinal muscular atrophy affects males and females at the same rate; however, disease progression is more severe in males.

Age

The age of onset for spinal muscular atrophy is discussed above in the Background section.

Clinical

History

• Patients with spinal muscular atrophy types III and IV usually present with an insidious onset of weakness, often following a brief period of illness, such as with influenza. The illness may have required a short period of bed rest.
• Patients most often report symptoms associated with weakness of the hip extensor and hip abductor muscles and describe difficulty climbing stairs or getting up from a seated position on the floor.
• Some patients also may report a mild tremor and occasional, painful muscle cramps.
• Difficulty walking or running also is reported by the patient.
• Parents of younger patients may report delayed developmental milestones or decreased athletic abilities in their children.
• A family history of such disorders also may be elicited.

Physical

• Proximal muscle weakness is seen in spinal muscular atrophy, with the pelvic girdle being more affected than the shoulder girdle.⁹
• Patients have decreased muscle tone.
• Patients have diminished deep tendon reflexes. Ankle reflexes, however, may be preserved until very late in the disease's progress.
• Fasciculations may be present in the tongue or shoulder girdle muscles (especially after manual muscle testing).
• Minipolymyoclonus, a fine, irregular tremor of the outstretched fingers, may be seen. This is the result of denervation followed by reinnervation and the asynchronous firing of restructured and enlarged motor units.
• Calf pseudohypertrophy has occasionally been noted, but muscle wasting of affected musculature is more prominent.
• Patients may have a positive Gower sign and a waddling gait.
• Approximately one third of patients have facial and masseter muscle weakness.
• Sensory examination findings are normal.

Causes

The exact etiology of spinal muscular atrophy (SMA) is unknown. SMA is an inherited disorder that almost always occurs in an autosomal recessive pattern. A few cases of autosomal dominant and X-linked recessive patterns have been reported.

All forms of SMA have been linked to a gene deletion on the long arm of chromosome 5, at band 5q13. The 2 genes associated with SMA are SMN1 (survival motor neuron 1) and SMN2, which are adjacent to each other on band 5q. SMN1 is believed to be the primary disease-causing gene.¹⁰ SMN2 differs from it by 1 C-T transition in exon 7, leading to alternate splicing and a nonfunctional protein for 70-90% of the protein produced.¹¹ An attenuated disease severity and a milder phenotype appears to be correlated with the presence of 3 or more copies of SMN2.

Several mechanisms have been proposed for the relationship between the SMN genes and the natural history of SMA. The SMN1 protein has been associated with the assembly of spliceosomal ribonucleoproteins, which are critical to messenger RNA processing. The SMN1 protein has also been associated with the NAIP (neuronal apoptosis inhibitory protein) gene, a gene that helps to regulate programmed cell death. Some authors have hypothesized that a deletion of the SMN gene may be related to disturbances in the metabolism of 3',5'-adenosine monophosphate. Whether or not these disturbances contribute to neuronal degeneration in SMA remains to be seen.

Differential Diagnoses

Other Problems to Be Considered

Duchenne muscular dystrophy
Glycolytic or lipid storage myopathy
Polyneuritis
Endocrine-related myopathy
Muscular hypotonia secondary to Marfan syndrome or Prader-Willi syndrome
Malnutrition
Metabolic disorders (eg, organic aciduria) and mitochondrial disorders
Leukodystrophy
Peripheral neuropathies
Transverse myelitis
Arthrogryposis multiplex congenita
Hodgkin disease associated anterior horn disease
Macroglobulinemia associated anterior horn disease

Workup

Laboratory Studies

• Molecular genetic testing^12,13  - Routine diagnostic testing for spinal muscular atrophy (SMA) involves targeted mutation analysis to detect deletion of exons 7 and 8 of SMN1. Approximately 95-98% of individuals with a clinical diagnosis of SMA lack exon 7 in both copies of SMN1 (ie, they are homozygous for the deletion). Approximately 2-5% of individuals with a clinical diagnosis of SMA are compound heterozygotes for deletion of SMN1 exon 7 and an intragenic mutation of SMN1. Routine genetic testing detects only patients with the homozygous deletion. However, additional testing is available that includes SMN1 sequence analysis for the detection of point mutations in the SMN1 gene. Genetic testing has also been developed that uses the quantitative polymerase chain reaction to determine the SMN2 gene copy number; however, such testing is not yet widely available. The SMN2 gene copy number is variable, rangingfrom0-5.
• Other testing - Serum creatine kinase levels may be elevated, but usually not to the extent that they are elevated in persons with muscular dystrophy. Serum aldolase levels also are commonly elevated in persons with types III and IV SMA.

Imaging Studies

• Ultrasonographic imaging of the muscles has been used to assess for neurogenic atrophy in spinal muscular atrophy (SMA), but it is fairly nonspecific. Ultrasonography has lost favor as a diagnostic tool for SMA. Neuroimaging of patients with SMA reveals no brain abnormalities.

Other Tests

• Muscle biopsy reveals evidence of neurogenic atrophy and chronic reinnervation in spinal muscular atrophy (SMA). Skeletal muscle changes include atrophy with a combination of narrow fibers and large, hypertrophic fibers. These fibers are separated by abundant fat and fibrous tissues. Increase in the sarcolemmal nuclei with preservation of striations is observed. The phrenic (C3-C5) and sacral (S2-S4) sphincter motor neurons are spared. Typical findings consistent with neurogenic atrophy also are seen on biopsy and are discussed above in the Pathophysiology section.
• Electromyography (EMG) and nerve conduction studies (NCS) can be very useful for the physician in the diagnosis of SMA. Diffuse abnormalities on EMG are seen in the extremities and bulbar musculature. The findings are consistent with axonal degeneration. Fibrillation potentials, positive sharp waves, and complex, repetitive discharges are common. Large motor unit potentials are typical, but small amplitudes also have been seen. Upon recruitment, polyphasic motor unit potentials, decreased recruitment, fast firing, and synchronization of motor units are seen. A marked increase in jitter on electromyograms often is seen and helps to differentiate SMA types III and IV from ALS. Motor nerve conduction velocities are normal or slightly decreased. Motor unit action potentials (MUAPs) progressively decrease in amplitude. Sensory nerve action potentials (SNAPs) are normal.

Treatment

Rehabilitation Program

Physical Therapy

Spinal muscular atrophy (SMA) has no known cure; thus, most care for the patient with SMA is focused on symptomatic control and preventative rehabilitation.¹⁴ Maintaining the patient's joint mobility is very important, because the goal is to decrease the incidence of contractures. Plantar flexion contractures are the most common.

Ankle-foot orthotics worn at night may help to provide prolonged, passive stretching to prevent worsening of ankle plantar flexion contractures.

Stretching and strength training in patients under the care of an experienced physical therapist are very important components of the preventative rehabilitation approach. For school-age patients, a physical therapist can provide consultation regarding appropriate or adaptive physical education activities.

Aquatic therapy is an excellent way to maintain mobility, strength, and flexibility.

Because of the progressive weakness associated with SMA, patients may require the full-time use of a wheelchair. For these patients, there are multiple assistive devices available that enable them to maintain a level of independence. Patients are encouraged to use manual wheelchairs rather than electric ones, when possible, to maintain cardiovascular fitness and upper body strength.

Occupational Therapy

The occupational therapist plays an essential role in addressing the individual needs of patients with spinal muscular atrophy. Occupational therapy is useful for teaching the patient ways to increase his/her independence in activities of daily living (ADL). Fine motor skills may be affected by fatigue. Affected school-age patients may benefit from an occupational therapy consultation that addresses keyboarding and other ways to avoid fatigue from upper extremity activities in the classroom.

Patients may eventually require the use of a wheelchair on a full-time basis. In addition, multiple assistive devices are available that enable patients to maintain a higher level of independence.

Speech Therapy

Patients with spinal muscular atrophy may require consultation with a speech therapist if dysphagia is present or diet modification is needed.

Medical Issues/Complications

• Orthopedic¹⁵ - A few studies have shown that scoliosis is a major problem in half of the patients with spinal muscular atrophy (SMA) type III. However, scoliosis occurs less frequently in patients with SMA type III than it does in persons with type II, and it is not as severe. Routine radiography should be performed, and the patient may require a thoracolumbar sacral orthosis (TLSO) or may need surgery. Spinal orthoses have been shown to assist in containing the spinal deformity until instrumentation and fusion can be performed, if necessary.
  
  Hip subluxation is also common. One author reports 50% of patients with SMA type III have hip subluxation or dislocation, with rare improvement in function from surgical reduction.
• Respiratory - Pulmonary disease is the major cause of morbidity and mortality in patients with SMA types I and II and in a small portion of persons with SMA type III.^6,7,8 The presence of expiratory muscle weakness that is greater than inspiratory muscle weakness, with relative sparing of the diaphragm, leads to impaired cough, hypoventilation during sleep, chest wall underdevelopment, and the potential for recurrent infections. One author found that in SMA type III, pulmonary function was preserved until age 13 years, and that by age 17 years, pulmonary function decreased to 79%.
  
  Pulmonary function tests can be performed, with forced vital capacity (FVC) as the best predictor of respiratory reserve; these tests should be done on a regular basis. Treatments may include noninvasive ventilation, including intermittent positive pressure ventilation, bilevel positive airway pressure ventilation, and negative pressure ventilation. Infections should be treated aggressively with antibiotics, mucolytics and bronchodilators, oxygen, chest PT and postural drainage, and a cough-assist machine.
• Sleep disorders - Questions regarding sleep hygiene and fatigue should be addressed. Patients with SMA type III frequently report fatigue. One case report described a 46-year-old man with SMA type III whose increasing daytime fatigue caused by nocturnal snoring and apnea resolved with nighttime use of continuous positive airway pressure with a nasal mask.¹⁶ Another case report documented the coexistence of sleep-disordered breathing and dilated cardiomyopathy in a 53-year-old patient with SMA type III.¹⁷ Similarly, symptoms were virtually eliminated with nighttime use of continuous positive airway pressure via nasal mask. Sleep studies can be used to screen for nocturnal hypoventilation.
• Contractures - Contractures are usually mild as long as patients remain ambulatory.
• Dysphagia

Surgical Intervention

• If scoliosis develops in a patient with spinal muscular atrophy, spinal instrumentation and fusion may be necessary.¹⁸ Some upper extremity function can be lost after fusion.
• Tendon lengthenings may be needed to improve joint position.

Consultations

• Genetic counseling for spinal muscular atrophy (SMA) - Parents, patients, and extended family members may benefit from genetic counseling. Carrier detection relies on determining the number of exon 7 – containing SMN1 gene copies present in an individual. SMA carrier testing, a polymerase chain reaction – based dosage assay, is available on a limited clinical basis. For a number of reasons, test results can be difficult to interpret and should be provided in the context of formal genetic counseling.
• Vocational rehabilitation counseling - This type of counseling may be beneficial to facilitate the transition from secondary school to postsecondary education or for vocational planning.

Medication

Numerous treatment trials for spinal muscular atrophy (SMA) have been described or are currently underway.¹⁹ Medications being studied for upregulation of SMN2 protein production or for increase of exon 7 inclusion include phenylbutyrate, valproic acid, suberoylanilide hydroxamic acid, and hydroxyurea. The neuroprotective medications being investigated, including gabapentin and riluzole, are thought to provide protection from oxidative stress. Albuterol has been studied for its trophic/anabolic effects. Exercise therapy in rats has shown modest improvement in survival and modest decrease in motor neuron loss. Treatment with stem cells is also an area undergoing further study.

A single study from the Russian literature in 1980 suggested that lithium may have a role in slowing the disease progression, but this has not been corroborated. Further studies are needed to investigate this.²⁰

A study using thyrotropin-releasing hormone as a treatment for SMA types II and III in children showed promising results. More studies are warranted to further investigate this possible treatment.²¹

Merlini and colleagues performed a multicenter, randomized, controlled trial of gabapentin versus no treatment in 120 patients with SMA type II or III for 12 months.²² A significant improvement in lower extremity, maximum, voluntary isometric contraction was seen.

Follow-up

Further Outpatient Care

• Patients with spinal muscular atrophy (SMA) should have frequent follow-up care for symptomatic control of their disease. Respiratory function, nutritional state, orthopedic status, and equipment needs should be assessed at each visit. Pain control, preventative medicine, surgical intervention, and physical therapy are all essential parts of the patient's long-term care. The multidisciplinary approach, which includes family members, social workers, therapists, and physicians, is important to assist the patient in maintaining a high quality of life.

Complications

• Scoliosis
• Plantar flexion contractures
• Dysphagia

Prognosis

• Patients with spinal muscular atrophy experience a progressive loss of motor function that usually affects the legs before it does the arms, and the proximal muscles before the distal ones.
• Patients who have never climbed stairs without a rail lose walking ability by their midteens. Patients who develop normal walking skills prior to the onset of muscle weakness can maintain this ability until the third or fourth decade.
• Life expectancy for individuals with SMA type III has been shown to be similar to that of the general population.⁵
• See Mortality/Morbidity.

References

1. Bradley WG, ed. Neurology in Clinical Practice. 5^th ed. Philadelphia, Pa: Butterworth-Heinemann/Elsevier; 2008.

2. Herring JA, ed. Tachdjian's Pediatric Orthopaedics. 4^th ed. Philadelphia, Pa: Saunders/Elsevier; 2008.

3. Wang CH, Finkel RS, Bertini ES, et al. Consensus statement for standard of care in spinal muscular atrophy. J Child Neurol. Aug 2007;22(8):1027-49. [Medline].

4. Russman BS, Buncher CR, White M, et al. Function changes in spinal muscular atrophy II and III. The DCN/SMA Group. Neurology. Oct 1996;47(4):973-6. [Medline].

5. Zerres K, Rudnik-Schöneborn S, Forrest E, et al. A collaborative study on the natural history of childhood and juvenile onset proximal spinal muscular atrophy (type II and III SMA): 569 patients. J Neurol Sci. Feb 27 1997;146(1):67-72. [Medline].

6. Ioos C, Leclair-Richard D, Mrad S, et al. Respiratory capacity course in patients with infantile spinal muscular atrophy. Chest. Sep 2004;126(3):831-7. [Medline]. [Full Text].

7. Lin LC, Jong YJ. Pulmonary function assessment in patients with spinal muscular atrophy type II and type III. Acta Paediatr Taiwan. Jan-Feb 2004;45(1):15-8. [Medline].

8. Muscular Dystrophy Campaign sponsored workshop: recommendation for respiratory care of children with SMA type II and III. Neuromuscular Disord. 2003;13:184-189.

9. Moosa A, Dubowitz V. Spinal muscular atrophy in childhood. Two clues to clinical diagnosis. Arch Dis Child. May 1973;48(5):386-8. [Medline]. [Full Text].

10. Simic G. Pathogenesis of proximal autosomal recessive spinal muscular atrophy. Acta Neuropathol. Jul 16 2008;[Medline].

11. Mattis VB, Bowerman M, Kothary R, et al. A SMNDelta7 read-through product confers functionality to the SMNDelta7 protein. Neurosci Lett. Jun 26 2008;[Medline].

12. Ogino S, Wilson RB. Genetic testing and risk assessment for spinal muscular atrophy (SMA). Hum Genet. Dec 2002;111(6):477-500. [Medline].

13. Wang CC, Chang JG, Ferrance J, et al. Quantification of SMN1 and SMN2 genes by capillary electrophoresis for diagnosis of spinal muscular atrophy. Electrophoresis. Jul 2008;29(13):2904-11. [Medline].

14. Umphred DA, ed. Neurological Rehabilitation. 5^th ed. St Louis, Mo: Mosby Elsevier; 2007.

15. Rodillo E, Marini ML, Heckmatt JZ, et al. Scoliosis in spinal muscular atrophy: review of 63 cases. J Child Neurol. Apr 1989;4(2):118-23. [Medline].

16. Puruckherr M, Mehta JB, Girish MR, et al. Severe obstructive sleep apnea in a patient with spinal muscle atrophy. Chest. Nov 2004;126(5):1705-7. [Medline]. [Full Text].

17. Yasuma F, Kuru S, Konagaya M. Dilated cardiomyopathy in Kugelberg-Welander disease: coexisting sleep disordered breathing and its treatment with continuous positive airway pressure. Intern Med. Oct 2004;43(10):951-4. [Medline]. [Full Text].

18. Merlini L, Granata C, Bonfiglioli S, et al. Scoliosis in spinal muscular atrophy: natural history and management. Dev Med Child Neurol. Aug 1989;31(4):501-8. [Medline].

19. Swoboda KJ, Kissel JT, Crawford TO, et al. Perspectives on clinical trials in spinal muscular atrophy. J Child Neurol. Aug 2007;22(8):957-66. [Medline].

20. Il'ina NA, Antipova RI, Khokhlov AP. [Use of lithium carbonate to treat Kugelberg--Welander spinal amyotrophy]. Zh Nevropatol Psikhiatr Im S S Korsakova. 1980;80(11):1657-60. [Medline].

21. Tzeng AC, Cheng J, Fryczynski H, et al. A study of thyrotropin-releasing hormone for the treatment of spinal muscular atrophy: a preliminary report. Am J Phys Med Rehabil. Sep-Oct 2000;79(5):435-40. [Medline].

22. Merlini L, Solari A, Vita G, et al. Role of gabapentin in spinal muscular atrophy: results of a multicenter, randomized Italian study. J Child Neurol. Aug 2003;18(8):537-41. [Medline].

23. de Groot IJ, de Witte LP. Physical complaints in ageing persons with spinal muscular atrophy. J Rehabil Med. Jul 2005;37(4):258-62. [Medline].

24. Liveson JA. Peripheral Neurology: Case Studies in Electrodiagnosis. 2^nd ed. Philadelphia, Pa: FA Davis; 1991.

25. Menkes JH. Textbook of Child Neurology. 5^th ed. Baltimore, Md: Williams & Wilkins; 1995.

26. Swaiman KF, Ashwal S, Ferriero DM, eds. Pediatric Neurology: Principles and Practice. 4^th ed. Philadelphia, Pa: Mosby; 2006.

27. Ropper AH, Brown RH. Adams and Victor's Principles of Neurology. 8^th ed. New York, NY: McGraw-Hill Medical; 2005.

28. Younger DS, Gordon PH. Diagnosis in neuromuscular diseases. Neurol Clin. Feb 1 1996;14:135-68.

29. Zeinos M, Sampath J, Cole C, et al. Operative treatment for hip subluxations in spinal muscular atrophy. J Bone Joint Surg. 2005;87-B:1541-4.

Keywords

Kugelberg Welander spinal muscular atrophy, Kugelberg-Welander spinal muscular atrophy, Kugelberg Welander disease, Kugelberg-Welander disease, Wohlfart-Kugelberg-Welander syndrome, Wohlfart-Kugelberg-Welander disease, mild spinal muscular atrophy, spinal muscular atrophy, SMA, juvenile types III and IV spinal muscular atrophy, adult-onset spinal muscular atrophy

Contributor Information and Disclosures

Author

Joyce L Oleszek, MD, Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Colorado at Denver Health Sciences Center, The Children's Hospital of Denver
Joyce L Oleszek, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

Coauthor(s)

Stephanie E Vallee, MS, Certified Genetic Counselor, Dartmouth-Hitchcock Medical Center, Children's Hospital at Dartmouth
Disclosure: Nothing to disclose.

Michael Dichiaro, MD, Chief Resident, Department of Physical Medicine and Rehabilitation, University of Colorado at Denver Health Sciences Center
Disclosure: Nothing to disclose.

Mary Louise Caire, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Wise Regional Medical Center
Mary Louise Caire, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Stephen Kishner, MD, Residency Program Director, Professor of Clinical Medicine, Department of Medicine, Section of Physical Medicine and Rehabilitation, Louisiana State University School of Medicine
Stephen Kishner, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.

Medical Editor

Teresa L Massagli, MD, Residency Director, Professor, Department of Rehabilitation Medicine and Pediatrics, University of Washington School of Medicine
Teresa L Massagli, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Physical Medicine and Rehabilitation, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, 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: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St. Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consort
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)