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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D., Julinka Auta Fernandes

Overview

Medical therapy for multiple sclerosis includes disease-modifying therapy (DMT) for eligible relapsing or progressive phenotypes, high-dose glucocorticoid treatment and selected medical rescue treatment for functionally significant acute relapses, and medication-based treatment of established symptoms. Treatment choice should be individualized according to disease activity, prognostic factors, comorbidities, reproductive plans, treatment risks, patient preferences, and local regulatory approval.[1][2][3]

Medical Therapy

Disease-modifying therapies are used to reduce MS disease activity and do not eliminate the need for medication-based treatment of established symptoms.[4]

The American Academy of Neurology (AAN) guideline on disease-modifying therapies was published in 2018 and reaffirmed on October 19, 2024. It remains an important American evidence-based guideline for starting, switching, and stopping disease-modifying treatment.[1][4]

The joint European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS)/European Academy of Neurology (EAN) guideline remains an important European reference for pharmacological disease-modifying treatment of MS. It addresses treatment selection, response, switching, safety, and special situations including pregnancy.[2] An updated joint guideline is in development; until it is published, the 2018 guideline should be interpreted alongside newer European consensus work, including the Association of British Neurologists (ABN) 2024 guidance and topic-specific ECTRIMS consensus statements.[5][3]

Principles of disease-modifying treatment

  • DMT should be offered as early as practical to eligible patients with active relapsing disease after the diagnosis has been confirmed. Activity may be demonstrated by clinical relapse or new/enlarging or contrast-enhancing lesions on magnetic resonance imaging.[1][3]
  • Treatment should be selected through shared decision-making. Important considerations include expected efficacy, serious and common adverse effects, route and frequency of administration, monitoring burden, comorbidities, pregnancy plans, adherence, access, and patient preference.[1][2]
  • An escalation strategy and an early high-efficacy strategy are both used in contemporary practice. The ABN guidance recommends considering a high-efficacy DMT as a first treatment option when the anticipated benefit-risk balance is favorable.[3]
  • DMT reduces future inflammatory disease activity but does not reverse established neurological injury; symptom-directed medical treatment should be provided when indicated.

Current disease-modifying therapies

The following table summarizes major contemporary DMT classes. Availability, approved phenotype, age range, formulation, and required monitoring differ between jurisdictions; current national labeling and specialist guidance should be checked before treatment.[3][6]

Class and usual route Agents General considerations
Injectable platform therapies Interferon beta-1a, interferon beta-1b, peginterferon beta-1a, and glatiramer acetate Generally considered moderate-efficacy therapies with extensive long-term safety experience. Injection reactions, influenza-like symptoms, laboratory monitoring, and adherence should be considered.
Oral fumarates and pyrimidine-synthesis inhibition Dimethyl fumarate, diroximel fumarate, monomethyl fumarate where authorized, and teriflunomide Generally moderate-efficacy therapies. Treatment-specific risks include lymphopenia and infection with fumarates and hepatotoxicity, teratogenicity, and prolonged elimination with teriflunomide.
Oral sphingosine-1-phosphate receptor modulators Fingolimod, siponimod, ozanimod, and ponesimod Indications and selectivity differ. Pretreatment cardiac, ophthalmic, hepatic, infection, and vaccination assessments may be required. Abrupt cessation can be followed by severe disease reactivation.
Oral immune-reconstitution therapy Cladribine tablets A higher-efficacy option for eligible relapsing disease. Lymphocyte counts, infection screening, malignancy risk, contraception, and cumulative treatment limits require attention.
Anti-integrin monoclonal antibody Natalizumab A high-efficacy therapy. Risk stratification for progressive multifocal leukoencephalopathy includes John Cunningham virus antibody status, treatment duration, and prior immunosuppressant exposure. Long gaps after stopping should be avoided because of disease reactivation.
Anti-CD20 monoclonal antibodies Ocrelizumab, ofatumumab, and ublituximab High-efficacy B-cell-depleting therapies. Hepatitis B screening, immunoglobulin assessment, infection risk, vaccination timing, and product-specific administration reactions should be addressed. Ocrelizumab also has an indication for primary progressive MS.
Anti-CD52 monoclonal antibody Alemtuzumab A high-efficacy immune-reconstitution therapy whose use is restricted by serious autoimmune, infectious, vascular, malignant, and infusion-related risks and prolonged post-treatment monitoring.
Oral Bruton's tyrosine kinase inhibitor Tolebrutinib Authorized in the European Union for adults with secondary progressive MS without relapses during the preceding 2 years. Hepatotoxicity is an important risk, requiring pretreatment and regular liver-function monitoring. This authorization is region-specific.[7]

Daclizumab must not be listed as a current MS therapy. Its marketing authorization was withdrawn in 2018 following reports of serious and potentially fatal inflammatory brain disorders.[8]

Mitoxantrone is not a routine contemporary DMT. Because of cardiotoxicity, therapy-related leukemia, and other serious toxicities, the AAN recommends that it not be prescribed unless the potential therapeutic benefit clearly outweighs the risks.[1]

Selected mechanisms and safety considerations

  • Interferon beta has pleiotropic immunomodulatory effects, while glatiramer acetate alters antigen-specific immune responses. Both remain options when their efficacy, safety, route, and reproductive profile match the patient's priorities.[9][10]
  • Teriflunomide inhibits dihydro-orotate dehydrogenase and de novo pyrimidine synthesis, thereby limiting proliferation of activated lymphocytes.[11]
  • Sphingosine-1-phosphate receptor modulators reduce egress of lymphocytes from lymphoid tissue. Their cardiac, ophthalmic, hepatic, infectious, pregnancy, and rebound risks differ by agent.[12]
  • Natalizumab blocks alpha-4 integrin-mediated leukocyte trafficking across the blood-brain barrier. Its benefit must be balanced against PML and rebound risks.[13]
  • Ocrelizumab, ofatumumab, and ublituximab target CD20-expressing B cells. Ocrelizumab reduces clinical and MRI activity in relapsing MS and slows disability accumulation in eligible patients with primary progressive MS.[14][15]
  • Alemtuzumab targets CD52 and produces prolonged lymphocyte depletion and repopulation. Serious autoimmune disease, infection, infusion reactions, stroke, and malignancy necessitate restricted use and long-term monitoring.[16]

Monitoring, switching, and stopping DMT

  • A treatment-specific clinical and laboratory baseline should be obtained before starting DMT. Immunization status should be reviewed before immune-depleting or immune-sequestering therapy. Live-attenuated vaccines are generally avoided during immunosuppressive therapy, and the timing needed to obtain an immune response varies by DMT.[17]
  • A new MRI baseline is commonly obtained approximately 3–6 months after treatment initiation, followed by brain MRI at approximately annual intervals when clinically appropriate. The protocol and frequency should be individualized according to disease activity, DMT, pregnancy, age, and safety considerations.[18][3]
  • Clinical relapse, meaningful new MRI activity, progressive disability, adverse effects, laboratory abnormalities, nonadherence, or changing patient circumstances should prompt reassessment. Apparent treatment failure should be interpreted in light of adherence and the time required for the DMT to become effective.[1][3]
  • When switching from natalizumab or a sphingosine-1-phosphate receptor modulator, unnecessary washout should be avoided because of rebound risk. The next therapy and timing should be planned before the current treatment is stopped.[3]
  • De-escalation or discontinuation should be individualized. Age, disease duration and activity, disability, comorbidity, infection and malignancy risk, DMT mechanism, and the possibility of rebound must be considered, with continued clinical and MRI surveillance after a change.[19][20]

Pregnancy, lactation, and pediatric treatment

Pregnancy planning should be discussed before DMT initiation and revisited during treatment. Decisions about continuing, timing, or stopping a DMT require drug-specific assessment of fetal exposure, durability of treatment effect, rebound risk, maternal disease activity, postpartum relapse risk, breastfeeding, and vaccination of the mother and infant. Abrupt withdrawal of natalizumab or a sphingosine-1-phosphate receptor modulator without a transition plan can expose the patient to significant disease reactivation. Recent UK consensus recognizes that transfer of many monoclonal antibodies into breast milk is low, so treatment during lactation may be considered after individualized assessment.[21]

Pediatric-onset MS requires specialist treatment oversight. In the United States, intravenous ocrelizumab is approved for relapsing-remitting MS in patients aged 10 years and older who weigh at least 25 kg.[22]

Treatment of progressive multiple sclerosis

Progressive MS should be characterized as active or not active and as progressing or stable. Progressive disease is not an indication for nonspecific immunosuppression solely on the basis of accumulated disability.[3]

  • Primary progressive MS (PPMS): Ocrelizumab is an approved treatment for PPMS. The benefit-risk balance is generally most favorable earlier in the progressive course and when there is evidence of inflammatory activity.[15][3]
  • Active secondary progressive MS (SPMS): Siponimod is an approved option in relevant jurisdictions; interferon beta-1b and DMTs authorized for relapsing forms of MS may also be options according to the patient's activity and local labeling.[23][3]
  • Non-relapsing secondary progressive MS in the European Union: Tolebrutinib is authorized for adults with SPMS without relapses during the preceding 2 years. Liver injury is an important risk, and pretreatment and regular liver-function monitoring are required. This indication is region-specific and should not be generalized to countries in which the medicine is not authorized.[7]

Autologous haematopoietic stem cell transplantation

Autologous haematopoietic stem cell transplantation (AHSCT) is a specialized immune-reconstitution medical therapy rather than conventional surgery. Haematopoietic stem cells are mobilized and collected from the patient, an immunosuppressive conditioning regimen is administered to remove or profoundly suppress autoreactive immune cells, and the stored autologous cells are reinfused to restore haematopoiesis. AHSCT aims to control inflammatory MS activity; it does not directly regenerate myelin or reverse established neurological injury.[24]

ECTRIMS/European Society for Blood and Marrow Transplantation (EBMT) recommendations support considering AHSCT for carefully selected patients with highly active inflammatory MS, generally after failure of at least one high-efficacy DMT and before irreversible disability has developed. The best-supported candidates are usually younger, have shorter disease duration, remain ambulatory, and have recent clinical or MRI inflammatory activity. It is not recommended for late-stage non-inflammatory progressive MS. Because conditioning and immune suppression can cause severe infection, infertility, organ toxicity, secondary autoimmune disease or malignancy, and treatment-related death, AHSCT should be performed only in experienced accredited centers after multidisciplinary assessment.[24]

Treatment of acute exacerbation of multiple sclerosis

Before diagnosing a relapse, infection—particularly urinary or respiratory infection—and other causes of transient symptom worsening should be excluded. Not every relapse requires corticosteroids; treatment is generally offered when symptoms impair usual activities or when faster recovery is clinically important.[25]

  • National Institute for Health and Care Excellence (NICE) recommends oral methylprednisolone 0.5 g daily for 5 days for an acute relapse. Intravenous methylprednisolone 1 g daily for 3–5 days may be considered when oral treatment has failed or is not tolerated, or when the relapse is severe or requires hospital monitoring.[25]
  • High-dose corticosteroids accelerate recovery but do not provide long-term disease modification. Potential adverse effects include insomnia, mood disturbance or psychosis, hyperglycemia, gastrointestinal symptoms, and infection; patient-specific risks should be assessed.[26]
  • Therapeutic plasma exchange is an accepted second-line medical rescue treatment for severe acute demyelinating relapses that respond inadequately to high-dose corticosteroids. It is not a treatment for chronic progressive MS.[27]

Medical treatment of established symptoms

Symptom-directed medication should be individualized. Reversible medical contributors—including infection, pain, sleep disorder, depression, medication adverse effects, anemia, vitamin B12 deficiency, thyroid disease, and constipation—should be treated before medication is escalated.[25]

Bladder dysfunction

Treatment should be matched to storage or emptying dysfunction. Antimuscarinic drugs such as oxybutynin, tolterodine, and solifenacin or a beta-3 agonist may be considered for storage symptoms. Refractory neurogenic detrusor overactivity may be treated with intradetrusor botulinum toxin medication in specialist care.[28][29]

Sexual dysfunction

Contributory pain, spasticity, bladder symptoms, fatigue, depression, endocrine disease, and medication adverse effects should be treated. Phosphodiesterase-5 inhibitors are effective for many men with erectile dysfunction, subject to contraindications and cardiovascular risk assessment.[30][29]

Cognitive symptoms

No medication has sufficient evidence for routine treatment of MS-related cognitive impairment. A multicenter Class I trial found that donepezil was not superior to placebo, and a systematic review concluded that the overall evidence for pharmacological cognitive treatment was insufficient. Donepezil and other cognitive enhancers should therefore not be presented as established treatment solely for MS-related cognitive impairment.[31][32]

Fatigue

Medical causes of fatigue—including sleep disorders, depression, anemia, vitamin B12 deficiency, thyroid disease, infection, pain, and medication effects—should be treated. NICE discusses amantadine, modafinil, and selected serotonin reuptake inhibitors through shared decision-making; these uses may be off-label and benefits are often modest. Response and adverse effects should be reviewed, and ineffective medication should be stopped.[25]

Walking impairment

Fampridine (called dalfampridine extended release in the United States) can improve walking speed or walking ability in a subset of adults with MS-related walking disability. In the European Union, fampridine is authorized for adults with an Expanded Disability Status Scale score of 4–7; response should be assessed after 2–4 weeks and treatment stopped when walking has not improved, has worsened, or the patient reports no benefit.[33] NICE does not recommend offering fampridine through the National Health Service because it is not cost effective at its current list price; this does not apply to patients who have already started treatment and continue it with their clinician.[25] The U.S. label recommends 10 mg approximately every 12 hours, requires renal-function assessment before and at least annually during treatment, and contraindicates dalfampridine in patients with a seizure history or creatinine clearance of 50 mL/min or less.[34]

Optic neuritis

High-dose corticosteroids may accelerate recovery from functionally significant acute optic neuritis but do not improve the final long-term visual outcome. Treatment should follow the acute-relapse principles above.[26]

Trigeminal neuralgia

Carbamazepine or oxcarbazepine is recommended as first-line long-term pharmacological treatment. Lamotrigine, gabapentin, pregabalin, baclofen, or phenytoin may be used alone or as add-on medication in selected patients.[35]

Neuropathic pain, dysesthesias, and Lhermitte sign

Neuropathic pain and painful dysesthesias may be treated with gabapentin, pregabalin, duloxetine, or amitriptyline according to comorbidity and adverse-effect profile. Lhermitte sign is often brief and may not require medication.[36]

Spasticity

NICE recommends oral baclofen as first-line pharmacological treatment and gabapentin as an alternative when baclofen is ineffective, contraindicated, or not tolerated. Diazepam and dantrolene should not be presented as routine first-line treatment.[25]

The 2026 Deutsche Gesellschaft für Neurologie (DGN; German Neurological Society) living guideline recommends beginning oral antispastic treatment with baclofen and/or tizanidine. When functionally impairing spasticity remains inadequately controlled, the guideline recommends adding standardized oromucosal nabiximols (delta-9-tetrahydrocannabinol [THC] and cannabidiol [CBD]) where it is authorized and clinically appropriate.[37]

For adults with moderate-to-severe MS spasticity that has not responded adequately to other pharmacological treatment, NICE recommends a specialist-supervised 4-week trial of THC:CBD oromucosal spray when applicable prescribing criteria are met. Treatment is continued only after at least a 20% reduction in spasticity-related symptoms on a 0–10 patient-reported scale.[38]

Prescription THC:CBD spray is a regulated symptomatic pharmacotherapy. No cannabis, cannabis-derived, or cannabis-related drug is approved by the U.S. Food and Drug Administration specifically for treatment of MS; European availability and recommendations should therefore not be generalized to the United States.[39]

For focal spasticity that remains functionally significant despite initial treatment, botulinum toxin A may be considered in specialist care. For severe generalized or multisegmental spasticity that responds inadequately to, or causes unacceptable adverse effects with, oral or oromucosal medication, intrathecal baclofen may be considered. The implantation and device-management aspects of intrathecal baclofen therapy are addressed in Multiple sclerosis surgery.[37]

Oscillopsia

Gabapentin may be considered as first-line pharmacological treatment for MS-related oscillopsia, with memantine as a second-line option. These uses may be off-label. Specialist advice is appropriate when neither treatment is effective or adverse effects prevent continued treatment.[25]

Emotional lability

Amitriptyline may be considered for emotional lability characterized by involuntary laughing or crying related to a frontal-lobe lesion. This use may be off-label, and contraindications, anticholinergic effects, sedation, and withdrawal considerations should be reviewed.[25]

Tremor and ataxia

No medication has consistently demonstrated substantial benefit for MS-related tremor or ataxia. The 2026 DGN living guideline states that a carefully monitored trial of propranolol, primidone, topiramate, or levetiracetam may be considered for functionally impairing tremor, either individually or in selected combinations. Botulinum toxin may be considered when disabling tremor remains treatment-resistant. The evidence for these treatments remains limited, and adverse effects should be considered.[37]

Cannabinoids are not effective for MS-related tremor. Medication is generally ineffective for MS-related ataxia; topiramate may occasionally be tried in a carefully selected patient, but evidence is limited and no medication should be presented as routinely effective.[37]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Rae-Grant A, Day GS, Marrie RA, et al. (April 2018). "Practice guideline recommendations summary: Disease-modifying therapies for adults with multiple sclerosis". Neurology. 90 (17): 777–788. doi:10.1212/WNL.0000000000005347. PMID 29686116.
  2. ↑ 2.0 2.1 2.2 Montalban X, Gold R, Thompson AJ, Otero-Romero S, Amato MP, Chandraratna D, Clanet M, Comi G, Derfuss T, Fazekas F, Hartung HP, Havrdova E, Hemmer B, Kappos L, Liblau R, Lubetzki C, Marcus E, Miller DH, Olsson T, Pilling S, Selmaj K, Siva A, Sorensen PS, Sormani MP, Thalheim C, Wiendl H, Zipp F (February 2018). "ECTRIMS/EAN guideline on the pharmacological treatment of people with multiple sclerosis". Mult Scler. 24 (2): 96–120. doi:10.1177/1352458517751049. PMID 29353550.
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 Rashid W, Ciccarelli O, Leary SM, et al. (February 2025). "Using disease-modifying treatments in multiple sclerosis: Association of British Neurologists (ABN) 2024 guidance". Pract Neurol. 25 (1): 18–24. doi:10.1136/pn-2024-004228. PMID 39532459 Check |pmid= value (help).
  4. ↑ 4.0 4.1 "Practice Guideline: Disease-modifying Therapies for Adults with Multiple Sclerosis". American Academy of Neurology. April 2018. Retrieved 2026-08-29.
  5. ↑ "Ongoing Guidelines: ECTRIMS/EAN guideline on the pharmacological treatment of people with multiple sclerosis (update)". European Academy of Neurology. Retrieved 2026-08-29.
  6. ↑ "Briumvi (ublituximab): European public assessment report". European Medicines Agency. Retrieved 2026-08-29.
  7. ↑ 7.0 7.1 "Cenrifki (tolebrutinib): European public assessment report". European Medicines Agency. 2026. Retrieved 2026-08-29.
  8. ↑ "Zinbryta (daclizumab beta): European public assessment report". European Medicines Agency. 2018. Retrieved 2026-08-29.
  9. ↑ Kasper LH, Reder AT (August 2014). "Immunomodulatory activity of interferon-beta". Ann Clin Transl Neurol. 1 (8): 622–631. doi:10.1002/acn3.84. PMC 4184564. PMID 25356432.
  10. ↑ Arnon R, Aharoni R (October 2004). "Mechanism of action of glatiramer acetate in multiple sclerosis and its potential for the development of new applications". Proc Natl Acad Sci U S A. 101 (Suppl 2): 14593–14598. doi:10.1073/pnas.0404887101. PMC 521994. PMID 15371592.
  11. ↑ Zeyda M, Poglitsch M, Geyeregger R, et al. (September 2005). "Disruption of the interaction of T cells with antigen-presenting cells by the active leflunomide metabolite teriflunomide". Arthritis Rheum. 52 (9): 2730–2739. doi:10.1002/art.21255. PMID 16142756.
  12. ↑ Cohen JA, Chun J (May 2011). "Mechanisms of fingolimod's efficacy and adverse effects in multiple sclerosis". Ann Neurol. 69 (5): 759–777. doi:10.1002/ana.22426. PMID 21520239.
  13. ↑ Rice GP, Hartung HP, Calabresi PA (April 2005). "Anti-alpha4 integrin therapy for multiple sclerosis: mechanisms and rationale". Neurology. 64 (8): 1336–1342. doi:10.1212/01.WNL.0000158329.30470.D0. PMID 15851719.
  14. ↑ Hauser SL, Bar-Or A, Comi G, et al. (January 2017). "Ocrelizumab versus interferon beta-1a in relapsing multiple sclerosis". N Engl J Med. 376 (3): 221–234. doi:10.1056/NEJMoa1601277. PMID 28002679.
  15. ↑ 15.0 15.1 Montalban X, Hauser SL, Kappos L, et al. (January 2017). "Ocrelizumab versus placebo in primary progressive multiple sclerosis". N Engl J Med. 376 (3): 209–220. doi:10.1056/NEJMoa1606468. PMID 28002688.
  16. ↑ Ruck T, Bittner S, Wiendl H, Meuth SG (July 2015). "Alemtuzumab in multiple sclerosis: mechanism of action and beyond". Int J Mol Sci. 16 (7): 16414–16439. doi:10.3390/ijms160716414. PMC 4519957. PMID 26204829.
  17. ↑ Otero-Romero S, Lebrun-Frénay C, Reyes S, et al. (July 2023). "ECTRIMS/EAN consensus on vaccination in people with multiple sclerosis: Improving immunization strategies in the era of highly active immunotherapeutic drugs". Mult Scler. 29 (8): 904–925. doi:10.1177/13524585231168043. PMC 10338708 Check |pmc= value (help). PMID 37293841 Check |pmid= value (help).
  18. ↑ Wattjes MP, Ciccarelli O, Reich DS, et al. (August 2021). "2021 MAGNIMS-CMSC-NAIMS consensus recommendations on the use of MRI in patients with multiple sclerosis". Lancet Neurol. 20 (8): 653–670. doi:10.1016/S1474-4422(21)00095-8. PMID 34139157 Check |pmid= value (help).
  19. ↑ Androdias G, Lünemann JD, Maillart E, et al. (May 2025). "De-escalating and discontinuing disease-modifying therapies in multiple sclerosis". Brain. 148 (5): 1459–1478. doi:10.1093/brain/awae409. PMID 39707906 Check |pmid= value (help).
  20. ↑ van der Walt A; Strijbis EMM; Bridge F; et al. (August 2025). "Advancing multiple sclerosis management in older adults". Nat Rev Neurol. 21 (8): 432–448. doi:10.1038/s41582-025-01115-5. PMID 40702382 Check |pmid= value (help).
  21. ↑ Mullan G, Ford HL, Blackall P, et al. (August 2026). "UK consensus on pregnancy in multiple sclerosis: An update to Association of British Neurologists guidance". Mult Scler. 32 (9): 885–896. doi:10.1177/13524585261454551. PMID 42397849 Check |pmid= value (help).
  22. ↑ "Ocrevus (ocrelizumab), BLA 761053/S-038: Supplement approval" (PDF). U.S. Food and Drug Administration. May 8, 2026. Retrieved 2026-08-29.
  23. ↑ Kappos L; Bar-Or A; Cree BAC; et al. (March 2018). "Siponimod versus placebo in secondary progressive multiple sclerosis (EXPAND): a double-blind, randomised, phase 3 study". Lancet. 391 (10127): 1263–1273. doi:10.1016/S0140-6736(18)30475-6. PMID 29576505.
  24. ↑ 24.0 24.1 Muraro PA, Mariottini A, Greco R, et al. (March 2025). "Autologous haematopoietic stem cell transplantation for treatment of multiple sclerosis and neuromyelitis optica spectrum disorder—recommendations from ECTRIMS and the EBMT". Nat Rev Neurol. 21 (3): 140–158. doi:10.1038/s41582-024-01050-x. PMID 39814869 Check |pmid= value (help).
  25. ↑ 25.0 25.1 25.2 25.3 25.4 25.5 25.6 25.7 "Multiple sclerosis in adults: management (NG220)". National Institute for Health and Care Excellence. August 26, 2026. Retrieved 2026-08-29.
  26. ↑ 26.0 26.1 Brusaferri F, Candelise L (June 2000). "Steroids for multiple sclerosis and optic neuritis: a meta-analysis of randomized controlled clinical trials". J Neurol. 247 (6): 435–442. PMID 10929272.
  27. ↑ Connelly-Smith L, Alquist CR, Aqui NA, et al. (April 2023). "Guidelines on the use of therapeutic apheresis in clinical practice—evidence-based approach from the Writing Committee of the American Society for Apheresis: The ninth special issue". J Clin Apher. 38 (2): 77–278. doi:10.1002/jca.22043. PMID 37017433 Check |pmid= value (help).
  28. ↑ Ginsberg DA, Boone TB, Cameron AP, et al. (November 2021). "The AUA/SUFU guideline on adult neurogenic lower urinary tract dysfunction: Treatment and follow-up". J Urol. 206 (5): 1106–1113. doi:10.1097/JU.0000000000002239. PMID 34495688 Check |pmid= value (help).
  29. ↑ 29.0 29.1 "EAU Guidelines on Neuro-urology". European Association of Urology. 2026. Retrieved 2026-08-29.
  30. ↑ Fowler CJ, Miller JR, Sharief MK, Hussain IF, Stecher VJ, Sweeney M (May 2005). "A double blind, randomised study of sildenafil citrate for erectile dysfunction in men with multiple sclerosis". J Neurol Neurosurg Psychiatry. 76 (5): 700–705. doi:10.1136/jnnp.2004.038695. PMC 1739638. PMID 15834030.
  31. ↑ Krupp LB, Christodoulou C, Melville P, et al. (April 2011). "Multicenter randomized clinical trial of donepezil for memory impairment in multiple sclerosis". Neurology. 76 (17): 1500–1507. doi:10.1212/WNL.0b013e318218107a. PMC 3087469. PMID 21519001.
  32. ↑ Chen MH, Goverover Y, Genova HM, DeLuca J (June 2020). "Cognitive efficacy of pharmacologic treatments in multiple sclerosis: A systematic review". CNS Drugs. 34 (6): 599–628. doi:10.1007/s40263-020-00734-4. PMC 7275014 Check |pmc= value (help). PMID 32361940 Check |pmid= value (help).
  33. ↑ "Fampyra (fampridine): European public assessment report". European Medicines Agency. Retrieved 2026-08-29.
  34. ↑ "Dalfampridine extended-release tablets: Prescribing information". U.S. National Library of Medicine, DailyMed. July 28, 2025. Retrieved 2026-08-29.
  35. ↑ Bendtsen L, Zakrzewska JM, Abbott J, et al. (June 2019). "European Academy of Neurology guideline on trigeminal neuralgia". Eur J Neurol. 26 (6): 831–849. doi:10.1111/ene.13950. PMID 30860637.
  36. ↑ "Neuropathic pain in adults: pharmacological management in non-specialist settings (CG173)". National Institute for Health and Care Excellence. September 2020. Retrieved 2026-08-29.
  37. ↑ 37.0 37.1 37.2 37.3 Deutsche Gesellschaft für Neurologie (27 April 2026). "Diagnose und Therapie der Multiplen Sklerose, Neuromyelitis-optica-Spektrum-Erkrankungen und MOG-IgG-assoziierten Erkrankungen: S2k-Living Guideline, Version 9.0". AWMF Registry Number 030-050 (in German). Deutsche Gesellschaft für Neurologie. Retrieved 2026-08-30.
  38. ↑ "Cannabis-based medicinal products (NG144): Recommendations". National Institute for Health and Care Excellence. November 11, 2019. Retrieved 2026-08-29.
  39. ↑ U.S. Food and Drug Administration. "FDA Regulation of Cannabis and Cannabis-Derived Products, Including Cannabidiol (CBD)". U.S. Food and Drug Administration. Retrieved 2026-08-30.

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