Multiple sclerosis

Last updated: September 11, 2023

Summarytoggle arrow icon

Multiple sclerosis (MS) is a chronic degenerative disease of the CNS characterized by demyelination and axonal degeneration in the brain and spinal cord, which are caused by an immune-mediated inflammatory process. The prevalence of MS is higher among women and people in temperate regions such as Europe and North America. Impaired vision (due to retrobulbar neuritis) is usually the first manifestation of MS; other neurological deficits appear as the disease progresses. The most common clinical course is characterized by exacerbations followed by periods of complete or incomplete remission. Diagnosis is made using clinical and MRI findings to identify the dissemination of CNS lesions in time and space. Characteristic MRI findings are demyelinated sclerotic plaques primarily located in white matter. Differential diagnoses of MS include other chronic demyelinating diseases and neurological infections (e.g., borreliosis, neurosyphilis). Acute exacerbations of MS are usually treated with high-dose glucocorticoids. Between exacerbations, patients may be treated with disease-modifying drugs (e.g., interferon beta, glatiramer acetate, natalizumab). There is currently no definitive treatment for MS.

Epidemiologytoggle arrow icon

  • Sex: : > (3:1) [1]
  • Age of onset: : 20–40 years of age [2]
  • Ethnicity: prevalence among the white and black population [3]
  • Prevalence: 50-300 per 100 000 people (greater among people who live further from the equator) [2]

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

The etiology of multiple sclerosis is unclear; it is believed to develop in genetically predisposed people who have been exposed to certain environmental factors.

Classificationtoggle arrow icon

Definitions [7][8]

  • Exacerbation
    • New symptoms or significant worsening of symptoms caused by CNS demyelination that last at least 24 hours and are not accompanied by fever or infection
    • Also referred to as an attack, relapse, or flare
  • Remission: a period of recovery after an exacerbation during which clinical symptoms resolve completely or almost completely
  • Pseudorelapse: recurrence or significant worsening of existing symptoms due to stressors (e.g., infection, heat)
  • Radiologically isolated syndrome (RIS) [9]
    • The presence of demyelinating lesions characteristic of MS in an asymptomatic individual
    • Not considered an MS phenotype but may progress to MS
  • Clinically isolated syndrome (CIS)
    • A single episode of neurological symptoms resulting from CNS demyelination
    • A second episode of such symptoms increases the likelihood that the symptoms are not clinically isolated and that the patient meets the diagnostic criteria for MS.
  • Diffuse cerebral sclerosis (Schilder disease) [10][11]
    • A rare inflammatory demyelinating CNS condition that affects children and young adults
    • Large areas of demyelination lead to various neurological deficits and psychological changes.

Clinical course [7][12][13]

Clinical phenotypes of multiple sclerosis [7][12][13]
Phenotype Characteristics Frequency
Relapsing-remitting MS (RR-MS)
  • Exacerbations occur.
  • Symptoms remit almost completely between exacerbations.
  • ∼ 90% (most common clinical course)
Secondary progressive MS (SP-MS)
  • A progression of RR-MS characterized by continuous worsening of neurological function that occurs independently of exacerbation events
  • ∼ 50% of patients with RR-MS develop SP-MS.
Primary progressive MS (PP-MS)
  • Symptoms continuously worsen from the onset of the disease.
  • ∼ 10%

Pathophysiologytoggle arrow icon

Clinical featurestoggle arrow icon

Fundoscopy is normal in 60% of cases of optic neuritis. Neither the patient nor the doctor are able to see anything.

Uhthoff phenomenon triggered by a viral infection may mimic an exacerbation of MS.

MS is a chronic condition that typically manifests in a relapsing-remitting form characterized by episodic CNS dysfunction (exacerbations) with at least partial recovery between episodes.

Diagnosticstoggle arrow icon

General principles [7][22]

  • Diagnosis of MS depends on a combination of clinical findings (e.g., optic neuritis, Lhermitte sign, sensory abnormalities, cerebellar signs), imaging, and laboratory results.
  • Consider early specialist (i.e., neurology) consultation for patients with history and clinical features suggestive of MS.
  • The McDonald Criteria for both DIT and DIS must both be met to confirm a diagnosis of MS: [7]
  • In some cases, electrophysiological, CSF, and laboratory studies may be necessary to support the diagnosis and exclude differential diagnoses. [23]

Clinical evidence or MRI findings consistent with the presence of CNS lesions that are disseminated in both time and space confirm the diagnosis of MS.

Imaging [7][13]

MRI is the imaging study of choice for the diagnosis and monitoring of MS.

Additional studies

Consider further testing for patients with nondiagnostic MRI and to rule out differential diagnoses.

The presence of multiple oligoclonal bands in CSF and their absence in the blood is highly suggestive of MS. [27][29]

Differential diagnosestoggle arrow icon

Autoimmune diseases associated with inflammatory demyelination

Neuromyelitis optica spectrum disorders (NMOSD; previously known as Devic disease or neuromyelitis optica) [30][31]

Diagnostic criteria of NMOSD based on AQP4-IgG status
Serological criteria Clinical criteria Additional criteria
Positive AQP4-IgG
  • Exclusion of other causes (e.g., MS)
Negative AQP4-IgG or unknown status

Acute disseminated encephalomyelitis (ADEM, acute demyelinating encephalomyelitis) [32]

Other conditions

Transverse myelitis [33]

Overview of transverse myelitis types
Types of TM Manifestations MRI findings
Longitudinally limited TM (LLTM) Acute complete TM (ACTM)
  • A single lesion spanning 1–2 vertebral segments and involves the full width of the spinal cord or the entire central part of the spinal cord
Acute partial TM (APTM)1
  • A single lesion spanning 1–2 vertebral segments that involves individual sections (i.e., spinal tracts) of the spinal cord
Longitudinally extensive TM (LETM)
  • A lesion that extends over ≥ 3 vertebral segments; usually affects > 60% of the spinal cord thickness with involvement of the central spinal cord


The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

General principles [35]

Treatment should be initiated as early as possible; the goals of treatment are to manage the primary exacerbation, prevent further exacerbations, and slow disease progression.

Management of acute exacerbations [7][38]

If an acute exacerbation of MS is suspected, a specialist should be consulted immediately for management.

Mild exacerbations that do not impact physical functioning may not require medical treatment.

Disease-modifying MS therapy

  • There are multiple disease-modifying drugs available to treat MS.
  • The decision about agent requires careful consideration of:
    • Individual patient's characteristics (e.g., clinical phenotype, comorbidities)
    • Medication side effects
    • Other factors (e.g., medication availability, route of administration)
  • All patients receiving disease-modifying therapy for MS should use birth control.

Disease-modifying therapy for MS is generally not recommended for pregnant and breastfeeding patients. [44]

Commonly used disease-modifying MS drugs by clinical phenotype
Phenotype Drugs commonly used
Clinically isolated syndrome [45]
Relapsing-remitting MS [7]
Secondary progressive MS [46]
  • All disease-modifying therapies may be used for active SP-MS.
Primary progressive MS [47]

Monoclonal antibodies (e.g., natalizumab, ocrelizumab) have the highest efficacy for reducing exacerbations, but lower efficacy medications (e.g., interferon beta, glatiramer acetate) often have fewer side effects. [7]

Overview of disease-modifying drugs in MS therapy (DMDs) [7][13][45]
Medication Mechanism of action Adverse effects

Interferon beta

Glatiramer acetate (copolymer-1)
  • Injection reactions
  • Postinjection reactions (may include chest pain, palpitations, flushing) [50]
  • Lipoatrophy

Dimethyl fumarate

  • An immunomodulator; protects nerve cells through its antiinflammatory effect [51]
  • Inhibits pyrimidine synthesis, which has an antiproliferative and antiinflammatory effect [52]
Cladribine [1][53]
Sphingosine 1-phosphate receptor modulators [54] Fingolimod


Monoclonal antibodies


Mitoxantrone [23][56]

Supportive care and symptom management [7][59][60]

Consider any of the following measures in a management plan tailored to the individual patient:

Physical therapy, occupational therapy, and psychotherapy are safe, nonpharmacological options that can improve multiple symptoms in patients with MS, including spasticity, fatigue, walking difficulties, and neuropathic pain.

Prognosistoggle arrow icon

Prognostic factors for disease progression [63][64]

  • Male sex
  • Age at MS onset > 40 years
  • Multiple symptoms with early motor and cerebellar involvement
  • Incomplete recovery after exacerbations
  • High relapse rate in the first 2 years after MS onset

Special patient groupstoggle arrow icon

Multiple sclerosis in pregnancy [7][44]



Referencestoggle arrow icon

  1. McGinley MP, Goldschmidt CH, Rae-Grant AD. Diagnosis and Treatment of Multiple Sclerosis. JAMA. 2021; 325 (8): p.765.doi: 10.1001/jama.2020.26858 . | Open in Read by QxMD
  2. Kantarci OH. Phases and Phenotypes of Multiple Sclerosis. CONTINUUM. 2019; 25 (3): p.636-654.doi: 10.1212/con.0000000000000737 . | Open in Read by QxMD
  3. Hosseiny M, Newsome SD, Yousem DM. Radiologically Isolated Syndrome: A Review for Neuroradiologists.. AJNR Am J Neuroradiol. 2020; 41 (9): p.1542-1549.doi: 10.3174/ajnr.A6649 . | Open in Read by QxMD
  4. Bacigaluppi S, Polonara G, Zavanone ML, et al. Schilder’s disease: non-invasive diagnosis?. Neurol Sci. 2009; 30 (5): p.421-430.doi: 10.1007/s10072-009-0113-z . | Open in Read by QxMD
  5. Jarius S, Haas J, Paul F, Wildemann B. Myelinoclastic diffuse sclerosis (Schilder’s disease) is immunologically distinct from multiple sclerosis: results from retrospective analysis of 92 lumbar punctures. J Neuroinflammation. 2019; 16 (1).doi: 10.1186/s12974-019-1425-4 . | Open in Read by QxMD
  6. Lublin FD, Reingold SC, Cohen JA, et al. Defining the clinical course of multiple sclerosis: The 2013 revisions. Neurology. 2014; 83 (3): p.278-286.doi: 10.1212/wnl.0000000000000560 . | Open in Read by QxMD
  7. Saguil A, Kane S, Farnell E. Multiple sclerosis: a primary care perspective.. Am Fam Physician. 2014; 90 (9): p.644-52.
  8. Dobson R, Giovannoni G. Multiple sclerosis – a review. European Journal of Neurology. 2018; 26 (1): p.27-40.doi: 10.1111/ene.13819 . | Open in Read by QxMD
  9. Thompson AJ, Baranzini SE, Geurts J, Hemmer B, Ciccarelli O. Multiple sclerosis. The Lancet. 2018; 391 (10130): p.1622-1636.doi: 10.1016/s0140-6736(18)30481-1 . | Open in Read by QxMD
  10. Langer-Gould AM, Gonzales EG, Smith JB, Li BH, Nelson LM. Racial and Ethnic Disparities in Multiple Sclerosis Prevalence.. Neurology. 2022; 98 (18): p.e1818-e1827.doi: 10.1212/WNL.0000000000200151 . | Open in Read by QxMD
  11. Schmidt H, Williamson D, Ashley-Koch A. HLA-DR15 haplotype and multiple sclerosis: A HuGE review. Am J Epidemiol. 2007; 165 (10): p.1097-1109.doi: 10.1093/aje/kwk118 . | Open in Read by QxMD
  12. Hansen T, Skytthe A, Stenager E, Petersen HC, Brønnum-Hansen H, Kyvik KO. Concordance for multiple sclerosis in Danish twins: an update of a nationwide study. Multiple Sclerosis Journal. 2005; 11 (5): p.504-510.doi: 10.1191/1352458505ms1220oa . | Open in Read by QxMD
  13. O'Gorman C, Lucas R, Taylor B. Environmental risk factors for multiple sclerosis: a review with a focus on molecular mechanisms. Int J Mol Sci. 2012; 13 (9): p.11718-52.doi: 10.3390/ijms130911718 . | Open in Read by QxMD
  14. Mitsdoerffer M, Peters A. Tertiary Lymphoid Organs in Central Nervous System Autoimmunity. Frontiers in Immunology. 2016; 7.doi: 10.3389/fimmu.2016.00451 . | Open in Read by QxMD
  15. Correale J, Gaitán MI, Ysrraelit MC, Fiol MP. Progressive multiple sclerosis: from pathogenic mechanisms to treatment.. Brain. 2017; 140 (3): p.527-546.doi: 10.1093/brain/aww258 . | Open in Read by QxMD
  16. Voss E, Raab P, Trebst C, Stangel M. Clinical approach to optic neuritis: pitfalls, red flags and differential diagnosis. Ther Adv Neurol Disord. 2011; 4 (2): p.123-134.doi: 10.1177/1756285611398702 . | Open in Read by QxMD
  17. Shaygannejad V, Golabchi K, Dehghani A, Ashtari F, Haghighi S, Mirzendehdel M, Ghasemi M. Color blindness among multiple sclerosis patients in Isfahan. J Res Med Sci. 2012; 17 (3): p.254–257.
  18. Rodriguez M, Siva A, Cross SA, O'Brien PC, Kurland LT. Optic neuritis: A population-based study in Olrnsted County, Minnesota. NEUROLOGY. 1995; 45: p.244-250.
  19. Dick JPR. The deep tendon and the abdominal reflexes. J Neurol Neurosurg Psychiatry. 2003; 74: p.150-153.
  20. Di Stefano G, Maarbjerg S, Truini A. Trigeminal neuralgia secondary to multiple sclerosis: from the clinical picture to the treatment options. The Journal of Headache and Pain. 2019; 20 (1).doi: 10.1186/s10194-019-0969-0 . | Open in Read by QxMD
  21. Hurt RW. The Pathophysiology of Trigeminal Neuralgia. Springer Berlin Heidelberg ; 2009: p. 2359-2419
  22. Thompson AJ, Banwell BL, Barkhof F, et al. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. The Lancet Neurology. 2018; 17 (2): p.162-173.doi: 10.1016/s1474-4422(17)30470-2 . | Open in Read by QxMD
  23. Calabresi PA. Diagnosis and management of multiple sclerosis.. Am Fam Physician. 2004; 70 (10): p.1935-44.
  24. Kearney H, Miller DH, Ciccarelli O. Spinal cord MRI in multiple sclerosis—diagnostic, prognostic and clinical value. Nat Rev Neurol. 2015; 11 (6): p.327-338.doi: 10.1038/nrneurol.2015.80 . | Open in Read by QxMD
  25. Filippi M, Rocca MA, Ciccarelli O, et al. MRI criteria for the diagnosis of multiple sclerosis: MAGNIMS consensus guidelines. Lancet Neurol. 2016; 15 (3): p.292-303.doi: 10.1016/s1474-4422(15)00393-2 . | Open in Read by QxMD
  26. Filippi M, Preziosa P, Banwell BL, et al. Assessment of lesions on magnetic resonance imaging in multiple sclerosis: practical guidelines. Brain. 2019; 142 (7): p.1858-1875.doi: 10.1093/brain/awz144 . | Open in Read by QxMD
  27. Deisenhammer F, Zetterberg H, Fitzner B, Zettl UK. The Cerebrospinal Fluid in Multiple Sclerosis. Frontiers in Immunology. 2019; 10.doi: 10.3389/fimmu.2019.00726 . | Open in Read by QxMD
  28. Comabella M, Montalban X. Body fluid biomarkers in multiple sclerosis.. Lancet Neurol. 2014; 13 (1): p.113-26.doi: 10.1016/S1474-4422(13)70233-3 . | Open in Read by QxMD
  29. Lamers KJ, de Reus HP, Jongen PJ. Myelin basic protein in CSF as indicator of disease activity in multiple sclerosis. Mult Scler. 1998; 4 (3): p.124-126.doi: 10.1177/135245859800400306 . | Open in Read by QxMD
  30. Barnett Y. Conventional and Advanced Imaging in Neuromyelitis Optica. American Journal of Neuroradiology. 2014.
  31. Wingerchuk D. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. American Academy of Neurology. 2015.
  32. Marchioni E, Tavazzi E, Minoli L et al. Acute disseminated encephalomyelitis. Curr Infect Dis Rep. 2008; 10 (4): p.307-314.doi: 10.1007/s10072-008-0966-6 . | Open in Read by QxMD
  33. Beh SC, Greenberg BM, Frohman T, et al.. Transverse Myelitis. Neurol Clin.. 2012.doi: 10.1016/j.ncl.2012.09.008 . | Open in Read by QxMD
  34. Jacob A, Weinshenker BG. An Approach to the Diagnosis of Acute Transverse Myelitis. Thieme Medical Publishers. 2008.
  35. Rae-Grant A., et al.. Practice guideline recommendations summary: Disease-modifying therapies for adults with multiple sclerosis: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology. 2019; 92 (2): p.112-112.doi: 10.1212/wnl.0000000000006722 . | Open in Read by QxMD
  36. Montero-Melendez T. ACTH: The forgotten therapy. Semin Immunol. 2015; 27 (3): p.216-226.doi: 10.1016/j.smim.2015.02.003 . | Open in Read by QxMD
  37. Sintzel MB, Rametta M, Reder AT. Vitamin D and Multiple Sclerosis: A Comprehensive Review. Neurol Ther. 2017; 7 (1): p.59-85.doi: 10.1007/s40120-017-0086-4 . | Open in Read by QxMD
  38. Repovic P. Management of Multiple Sclerosis Relapses. CONTINUUM. 2019; 25 (3): p.655-669.doi: 10.1212/con.0000000000000739 . | Open in Read by QxMD
  39. Burton JM, O’Connor PW, Hohol M, Beyene J. Oral versus intravenous steroids for treatment of relapses in multiple sclerosis. Cochrane Database Syst Rev. 2012.doi: 10.1002/14651858.cd006921.pub3 . | Open in Read by QxMD
  40. Olek MJ. Multiple Sclerosis. Ann Intern Med. 2021; 174 (6): p.ITC81-ITC96.doi: 10.7326/aitc202106150 . | Open in Read by QxMD
  41. Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG. Multiple Sclerosis. N Engl J Med. 2000; 343 (13): p.938-952.doi: 10.1056/nejm200009283431307 . | Open in Read by QxMD
  42. Wang C, Ruiz A, Mao-Draayer Y. Assessment and Treatment Strategies for a Multiple Sclerosis Relapse.. J Immunol Clin Res. 2018; 5 (1).
  43. Abboud H, Mente K, Seay M, et al. Triaging Patients with Multiple Sclerosis in the Emergency Department. Int J MS Care. 2017; 19 (6): p.290-296.doi: 10.7224/1537-2073.2016-069 . | Open in Read by QxMD
  44. Voskuhl R, Momtazee C. Pregnancy: Effect on Multiple Sclerosis, Treatment Considerations, and Breastfeeding. Neurotherapeutics. 2017; 14 (4): p.974-984.doi: 10.1007/s13311-017-0562-7 . | Open in Read by QxMD
  45. Metz LM. Clinically Isolated Syndrome and Early Relapsing Multiple Sclerosis. CONTINUUM. 2019; 25 (3): p.670-688.doi: 10.1212/con.0000000000000729 . | Open in Read by QxMD
  46. Cree BAC, Arnold DL, Chataway J, et al. Secondary Progressive Multiple Sclerosis. Neurology. 2021; 97 (8): p.378-388.doi: 10.1212/wnl.0000000000012323 . | Open in Read by QxMD
  47. Rae-Grant A, Day GS, Marrie RA, et al. Practice guideline recommendations summary: Disease-modifying therapies for adults with multiple sclerosis. Neurology. 2018; 90 (17): p.777-788.doi: 10.1212/wnl.0000000000005347 . | Open in Read by QxMD
  48. Dhib-Jalbut S, Marks S. Interferon-  mechanisms of action in multiple sclerosis. Neurology. 2009; 74 (Issue 1, Supplement 1): p.S17-S24.doi: 10.1212/wnl.0b013e3181c97d99 . | Open in Read by QxMD
  49. Ziemssen T. Glatiramer acetate-specific T-helper 1- and 2-type cell lines produce BDNF: implications for multiple sclerosis therapy. Brain. 2002; 125 (11): p.2381-2391.doi: 10.1093/brain/awf252 . | Open in Read by QxMD
  50. Filippi M, Bar-Or A, Piehl F, et al. Multiple sclerosis. Nat Rev Dis Primers. 2018; 4 (1).doi: 10.1038/s41572-018-0041-4 . | Open in Read by QxMD
  51. Mills EA, Ogrodnik MA, Plave A, Mao-Draayer Y. Emerging Understanding of the Mechanism of Action for Dimethyl Fumarate in the Treatment of Multiple Sclerosis. Front Neurol. 2018; 9.doi: 10.3389/fneur.2018.00005 . | Open in Read by QxMD
  52. Bar-Or A, Pachner A, Menguy-Vacheron F, Kaplan J, Wiendl H. Teriflunomide and Its Mechanism of Action in Multiple Sclerosis. Drugs. 2014; 74 (6): p.659-674.doi: 10.1007/s40265-014-0212-x . | Open in Read by QxMD
  53. Faissner S, Gold R. Oral Therapies for Multiple Sclerosis. Cold Spring Harb Perspect Med. 2018; 9 (1): p.a032011.doi: 10.1101/cshperspect.a032011 . | Open in Read by QxMD
  54. Subei AM, Cohen JA. Sphingosine 1-Phosphate Receptor Modulators in Multiple Sclerosis. CNS Drugs. 2015; 29 (7): p.565-575.doi: 10.1007/s40263-015-0261-z . | Open in Read by QxMD
  55. Berger JR, Cree BA, Greenberg B, et al. Progressive multifocal leukoencephalopathy after fingolimod treatment. Neurology. 2018; 90 (20): p.e1815-e1821.doi: 10.1212/wnl.0000000000005529 . | Open in Read by QxMD
  56. Dargahi N, Katsara M, Tselios T, et al. Multiple Sclerosis: Immunopathology and Treatment Update. Brain Sci. 2017; 7 (12): p.78.doi: 10.3390/brainsci7070078 . | Open in Read by QxMD
  57. Sellebjerg F, Blinkenberg M, Sorensen PS. Anti-CD20 Monoclonal Antibodies for Relapsing and Progressive Multiple Sclerosis. CNS Drugs. 2020; 34 (3): p.269-280.doi: 10.1007/s40263-020-00704-w . | Open in Read by QxMD
  58. Fox EJ. Mechanism of action of mitoxantrone. Neurology. 2004; 63 (Issue 12, Supplement 6): p.S15-S18.doi: 10.1212/wnl.63.12_suppl_6.s15 . | Open in Read by QxMD
  59. Tobin WO. Management of Multiple Sclerosis Symptoms and Comorbidities. CONTINUUM. 2019; 25 (3): p.753-772.doi: 10.1212/con.0000000000000732 . | Open in Read by QxMD
  60. Coyle PK. Symptom Management and Lifestyle Modifications in Multiple Sclerosis. CONTINUUM. 2016; 22 (3): p.815-836.doi: 10.1212/con.0000000000000325 . | Open in Read by QxMD
  61. Goldman MD, Cohen JA, Fox RJ, Bethoux FA. Multiple sclerosis: treating symptoms, and other general medical issues.. Cleve Clin J Med. 2006; 73 (2): p.177-186.doi: 10.3949/ccjm.73.2.177 . | Open in Read by QxMD
  62. Dunn J, Blight A. Dalfampridine: a brief review of its mechanism of action and efficacy as a treatment to improve walking in patients with multiple sclerosis. Curr Med Res Opin. 2011; 27 (7): p.1415-1423.doi: 10.1185/03007995.2011.583229 . | Open in Read by QxMD
  63. Gajofatto A, Calabrese M, Benedetti MD, Monaco S. Clinical, MRI, and CSF Markers of Disability Progression in Multiple Sclerosis. Dis Markers. 2013; 35: p.687-699.doi: 10.1155/2013/484959 . | Open in Read by QxMD
  64. Iaffaldano P, Lucisano G, Patti F, et al. Transition to secondary progression in relapsing-onset multiple sclerosis: Definitions and risk factors. Multiple Sclerosis Journal. 2020: p.135245852097436.doi: 10.1177/1352458520974366 . | Open in Read by QxMD
  65. Andersen JB, Kopp TI, Sellebjerg F, Magyari M. Pregnancy-Related and Perinatal Outcomes in Women With Multiple Sclerosis. Neurol Clin Pract. 2021; 11 (4): p.280-290.doi: 10.1212/cpj.0000000000001035 . | Open in Read by QxMD
  66. Krysko KM, Bove R, Dobson R, Jokubaitis V, Hellwig K. Treatment of Women with Multiple Sclerosis Planning Pregnancy. Curr Treat Options Neurol. 2021; 23 (4).doi: 10.1007/s11940-021-00666-4 . | Open in Read by QxMD
  67. Spiegel HE, Nowacki G, Hsiao KJ. Advances in Clinical Chemistry. Academic Press ; 2001
  68. McDonald Diagnostic Criteria for Multiple Sclerosis. . Accessed: July 28, 2017.
  69. Feinstein A . The Clinical Neuropsychiatry of Multiple Sclerosis. Cambridge University Press ; 2007
  70. Ross AP, Ben-Zacharia A, Harris C, Smrtka J. Multiple sclerosis, relapses, and the mechanism of action of adrenocorticotropic hormone. Front Neurol. 2013; 4: p.21.doi: 10.3389/fneur.2013.00021 . | Open in Read by QxMD
  71. Berkovich R, Agius MA. Mechanisms of action of ACTH in the management of relapsing forms of multiple sclerosis. Ther Adv Neurol Disord. 2014; 7 (2): p.83-96.doi: 10.1177/1756285613518599 . | Open in Read by QxMD

Icon of a lock3 free articles remaining

You have 3 free member-only articles left this month. Sign up and get unlimited access.
 Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer