Pediatric Multiple Sclerosis

Updated: Jan 03, 2022
Author: Alice K Rutatangwa, DO, MSc; Chief Editor: Stephen L Nelson, Jr, MD, PhD, FAACPDM, FAAN, FAAP, FANA 



Multiple sclerosis (MS) is primarily a disease of adults. However, MS onset in children accounts for up to 5% of all MS cases. 

Over the last 10 years, much has been learned about the epidemiology, pathophysiology, diagnosis, and treatment of MS in children. Several exciting discoveries have stressed the importance of genetic and environmental factors. Notable examples include human leukocyte antigen (HLA) subtypes and viral exposures, among others. There are phenotypic differences, including clinical, MRI, and laboratory findings, between adults and children, especially before puberty.

For example, in young children, the first presentation of MS may be indistinguishable from acute disseminated encephalomyelitis (ADEM). In addition, the initial brain MRI scan in younger patients shows more frequent involvement of the posterior fossa and higher numbers of ill-defined T2-bright foci that often partially resolve on the follow-up scan, thereby challenging early diagnosis. Finally, the spinal fluid in younger patients may fail to reveal oligoclonal bands (OCBs) or elevated immunoglobulin G (IgG) index at disease onset.

The treatment of pediatric patients with MS is based on randomized controlled data in adults. PARADIGMS, the only randomized controlled trial for safety and efficacy of fingolimod versus interferon beta-1a in pediatric patients with MS, has shown comparable efficacy and safety profile to adults. Retrospective data have shown other disease-modifying therapies to be effective. This is one of the several areas that require more study.


MS is historically defined as neurologic symptoms disseminated in time (DIT) and space (DIS). The diagnostic criteria for MS in adults have been refined over time.[1, 2, 3] The current McDonald diagnostic criteria may be applied to children if the initial presentation is not characterized by encephalopathy.

MS is a challenging diagnosis in children—especially in prepubescent children—because of the atypical clinical, biological, and MRI presentations and the broader spectrum of potential differential diagnoses specific to that age range.[4]

In 2007, the International Pediatric MS Study Group published operational definitions for acquired demyelinating diseases of the CNS in children.[5] According to these definitions, ADEM (monophasic) requires the presence of both encephalopathy and polysymptomatic presentation. ADEM may last up to 3 months, with fluctuating symptoms or MRI findings. In contrast, a clinically isolated syndrome can be either monofocal or polyfocal but usually does not include encephalopathy. The original definitions were reviewed and updated in 2013.[6]


Data concerning the pathophysiology of pediatric MS and how it may differ from adult MS are limited. Pathologic studies have offered some insights; however, brain biopsy is undertaken only in the most severe cases, so results may be biased toward a more severe phenotype. Most cases involve tumefactive demyelination. Cases with detailed pathology report a dense accumulation of lymphocytes and macrophages in a prominent perivascular distribution, with rare B cells. Axonal damage is typically limited.[7]

As in adults, identification of a self-antigen as an immunologic trigger is elusive, but T cells are believed to play a major role in CNS inflammation.[8] Several groups have studied T-cell responses to various antigenic stimuli in pediatric MS. A 2008 study of a large cohort of children with CNS inflammatory demyelination, type 1 diabetes, or CNS injury demonstrated that children with these conditions exhibited heightened peripheral T-cell responses to a wide array of self-antigens.[9] Anti–myelin oligodendrocyte glycoprotein (MOG) and anti–myelin basic protein (MBP) have been studied in both adults and children. In children, anti-myelin antibodies have been seen in patients with different demyelinating disorders, including ccute disseminated encephalomyelitis (ADEM).

CSF studies have demonstrated that children younger than 11 years exhibit a distinct cellular profile when compared with older children. Younger children with their first MS event were more likely to lack evidence of intrathecal antibody production (OCBs or an elevated IgG index) and had a higher percentage of neutrophils in their CSF, suggesting prominent activation of the innate immune response, as opposed to the typical activation of the adaptive response seen in older patients.



Several environmental factors have been shown to play a role in MS susceptibility in adults. In children, very few studies have addressed these issues. Studying the role of common viruses in the pediatric MS population provides a unique opportunity given the close temporal relationship between the infection and MS onset and the fact that exposure to those viruses is lesser in children than in adults. Several studies examining viral exposures in pediatric MS have consistently identified significantly increased frequencies of Epstein-Barr virus (EBV) seropositivity in children with MS compared to matched controls.[10, 11, 12, 13] This association is independent of age at blood draw, sex, race, ethnicity, and HLA-DRB1 status.[14]

The novel observations in this study are that in HLA-DRB1–positive individuals, a remote infection with herpes simplex virus-1 (HSV-1) decreased the MS risk by 90%. In contrast, in HLA-DRB1–negative individuals, HSV-1 seropositivity increased the MS risk fourfold.

Concern over the use of vaccinations, most recently hepatitis B vaccine, and the subsequent development of MS has been raised. Mikaeloff et al found no increased risk of developing a first episode of childhood MS up to 3 years postvaccination in the French population.[15]

Interestingly, the same group evaluated the risk of childhood-onset MS as related to exposure to passive smoking.[16] The relative risk for a first episode of MS was found to be over twice that in the control population and was even higher in those with prolonged exposure (≥10 years).

Finally, unlike in adult MS, the effect of vitamin D status on MS susceptibility is unknown, although levels of 25(OH) vitamin D have been found to be independently associated with subsequent relapse rate in patients with pediatric MS (for each 10 ng/mL increment of 25(OH) vitamin D3, risk of subsequent MS relapse was decreased by 34%).[17]

A few studies have evaluated genetic risk factors in pediatric MS. The US Pediatric MS Network has also reported that HLA-DRB1, as in adult MS, may be a risk factor for pediatric MS. In multivariate models adjusted for age, race, ethnicity, and remote viral exposures, the risk of developing MS if carrying at least one HLA-DRB1 allele was increased by 2- to 4-fold, depending on the model used.[4, 14]

Further studies on genetic and environmental risk factors are ongoing to explore the precise mechanisms that lead to disease onset. The discovery of gene-environment interactions may also shed new light on the understanding of molecular mechanisms involved in disease processes and might lead to the development of new therapeutic strategies.


While the worldwide prevalence of pediatric MS is unknown, data are available from individual countries or MS centers. Several large series[18, 19, 20, 21] report prevalence rates of MS onset in childhood or adolescence ranging from 2.2%–4.4% of all MS cases, while some MS referral centers report that up to 10% of their patients with MS experienced symptom onset prior to age 18 years.[22] In general, pediatric MS onset prior to age 10 years is rare and constitutes approximately 20% of the reported pediatric cases in large series.[8]

In 2011, a population based study in Southern California showed that, in the multiethnic cohort of Kaiser Permanente, the incidence rate of pediatric MS was 0.51 per 100,000 person-years (95% confidence interval [CI], 0.33–0.75), and the incidence of other forms of acute demyelinating syndrome, including optic neuritis, transverse myelitis, other forms of clinically isolated syndromes, and ADEM, was 1.56 per 100,000 person-years (95% CI, 1.23–1.95), for an overall incidence of acute demyelinating syndrome of 1.66 per 100,000 person-years (95% CI 1.32–2.06).[23]

It is unclear whether the incidence of pediatric MS has increased in the past decades or is merely being increasingly recognized owing to improved diagnostic criteria and medical awareness.

The sex ratio of pediatric MS varies by age. Before age 6 years, the ratio of MS in girls to boys is 0.8:1. It increases closer to the ratio observed in adults as children age.[5] The effect of ethnicity on risk of childhood-onset MS is poorly understood.


The psychosocial complications of pediatric MS encompass various problems, including feelings of self-consciousness, worries related to the future, problems with family and friends, mood disorders, and cognitive impairment.

The Schedule for Affective Disorders and Schizophrenia for School-Age Children—Present and Lifetime Version (KSADS)[24] revealed that approximately 30%-48% of children with MS or related conditions have affective disorders.[25] The most common psychiatric conditions include major depression, anxiety disorder, a combination of anxiety and depressive disorders, panic disorder, bipolar disorder, and adjustment disorder.

When the scores from the pediatric MS group were compared to age-matched healthy controls and the fifth percentile of the healthy controls was used as the cutoff for fatigue, a total of 73% of the pediatric MS group met this criterion for severe fatigue.[25]

Cognitive impairment occurs in an estimated 30%–75% of children with MS depending on which definition of impairment is applied and at what point in their course the children undergo evaluations.[25, 26, 26, 24] Similar to prior reports, the domains more frequently affected included memory, complex attention, verbal comprehension, and executive functioning. Younger age at symptom onset correlated with lower intelligence quotient (IQ) scores.[25, 27]

Children with MS appear to be more vulnerable to cognitive decline over short periods than adults with MS. In school-aged children, cognitive decline is demonstrated by poor school performance. A significant percentage of pediatric patients with MS require some type of help or altered school curriculum owing to cognitive impairments, and up to 14% are homeschooled because of their illness. Some children need classroom seating accommodations, tutoring, and in-class assistance with implementation of 504 or individualized education plans.

Disability scores are lower in pediatric patients than in adults, even when adjusted for disease duration. The median time to reach an Expanded Disability Status Scale (EDSS) score of 4 (defined as a visible, often irreversible, neurologic deficit in a patient who is still able to ambulate at least 500 meters without assistance) was approximately 20 years in pediatric MS versus 10 years in adult MS.[28] Thus, despite a slower development of irreversible disability in patients with pediatric MS, the age when these patients are confronted with disease progression and neurological deficits is 10 years younger than the population with adult-onset MS, at the time when they are expected to have a family and enter the workforce.[29]



Clinical Presentation

Initial multiple sclerosis (MS) symptoms significantly vary. A confounding factor is the difficulty associated with detecting subtle findings, such as sensory changes or mild symptoms, in young children who have limited body awareness.

Encephalopathy is a common presenting symptom of ADEM. Several studies have shown that encephalopathy may also occur with a first episode of MS or neuromyelitis optica (NMO) and is usually reported in younger patients.[30, 31, 32, 33] ADEM occurs most often in younger children. Thus, rather than being disease specific (ie, MS vs ADEM), the presence of encephalopathy may be related to immaturity of the brain or the immune system in younger patients.

Seizures as first event (as part of the encephalopathy or isolated) in the pediatric population were also reported (29%), usually in ADEM cases and less frequently in MS.[34, 32, 33, 35]

The initial clinical course in the vast majority of patients with pediatric MS is relapsing-remitting[21] to the point that a progressive course from onset in a pediatric patient with MS is a red flag. The annualized relapse rate in pediatric-onset MS has been estimated to be between 0.38 and 0.87 for the whole relapsing-remitting period in the few studies with mean disease duration of 10 years or more.[21]

A prospective study of patients with MS at a large MS center showed that patients with an onset before age 18 years had a higher relapse rate during the first few years of their disease than adults seen at the same institution.[36] While most relapsing-remitting patients have been reported to recover completely and quickly after relapses, disability can result from an incomplete recovery from relapses. In rare pediatric cases, patients later develop a more insidious progression of disability with or without superimposed exacerbations, called secondary progressive MS.



Diagnostic Considerations

In general, atypical features of pediatric multiple sclerosis (MS) include fever, encephalopathy, progressive symptoms or disease course, other organ system involvement (including the peripheral nervous system), absence of CSF OCBs, elevated IgG index, and markedly elevated CSF leukocytes.[37] The more atypical features present and the younger the child, the more consideration necessary prior to diagnosing MS.

A thorough history and physical examination, serum and CSF testing, and neuroimaging will likely provide the diagnostic specificity desired to differentiate between acquired demyelinating disorders of the CNS in children and the other disorders.


Other disorders that can mimic MS include the following:

  • Endocrine: Thyroid disorder, diabetes mellitus

  • Inflammatory: Systemic lupus erythematosus (SLE), neurosarcoidosis, Sjögren syndrome, antiphospholipid antibody syndrome (APLAS), Behçet disease, isolated angiitis

  • Mitochondrial: Myoclonic epilepsy with ragged red fibers (MERRF), mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes (MELAS), Leber hereditary optic neuropathy (LHON), Leigh syndrome, Kearns-Sayre syndrome

  • Leukodystrophy: Metachromatic leukodystrophy, adrenoleukodystrophy, Krabbe disease, Pelizaeus-Merzbacher disease, Refsum disease, vanishing white matter, leukoencephalopathy with brainstem and spinal cord involvement and elevated lactate levels, Wilson disease, Fabry disease, Alexander disease

  • Genetic/metabolic: Inborn errors of metabolism, aminoacidurias

  • Infectious: Neuroborreliosis (lyme disease), HSV encephalitis, HIV infection, neurocysticercosis, poststreptococcal infection, abscess, neurosyphilis, progressive multifocal leukoencephalopathy (PML), Whipple disease

  • Vascular: Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), Moyamoya disease, carotid dissection

  • Demyelinating: Clinically isolated syndrome, ADEM, optic neuritis, transverse myelitis, NMO, postvaccination, acute necrotizing encephalopathy

  • Nutritional: Vitamin B12, vitamin E, or folate deficiency; celiac disease

  • Neoplastic: Lymphoma, astrocytoma, medulloblastoma, metastases

  • Toxic: Radiation, chemotherapy (methotrexate, cyclosporine, cytosine-arabinoside), extrapontine myelinosis

  • Other: Langerhans cell histiocytosis, hemophagocytic lymphohistiocytosis



Laboratory Studies

The CSF profile in childhood-onset multiple sclerosis (MS) may vary by age. Typically, WBC counts range from 0-50 cells/mm3, with a lymphocytic predominance.[38] However, it has been shown that children younger than 11 years have more neutrophils in the CSF than older children.[39]

While one study reports OCB in the CSF of up to 92% of children with MS,[40] another study found OCB to be less common in younger children (43% vs 63% in adolescents).[39] By contrast, in ADEM, 0%–29% of cases are found to have OCB.[38, 30, 41, 31] Within the French KIDMUS cohort, 94% (69 of 72) of children with positive OCB results went on to develop MS.[42]

The IgG index has been found to be elevated in 68% of adolescents (>11 years) with MS but in 35% of younger children (< 11 years).[39] These features tend to depend on age rather than disease duration. This distinct CSF IgG and cellular profile in younger children tends to vanish on repeat CSF analysis (mean 19 months after initial analysis), suggesting a transient immunological phenomenon associated with disease onset.

Imaging Studies

In a small study, patients with pediatric MS were reported to have fewer brain MRI T2-bright foci and more frequent large MS lesions than reported in adults with MS.[33] However, more recent data collected at disease onset have shown that children with MS may have a higher lesion burden on their initial brain MRI scan than adults, especially in the brainstem and cerebellum.[4]

Brain lesions in younger children (< 11 years) tend to be large with poorly defined borders and frequently confluent at disease onset. New diagnostic criteria for pediatric MS (a revised version of the adult McDonald criteria) have been proposed; they are very preliminary, based on a very small retrospective cohort not including patients with ADEM or NMO.[43] The authors compared 38 children with MS with 45 children with migraine or lupus who had brain MRI abnormalities. The presence of at least 2 of the following 3 criteria distinguished MS from migraine and lupus with better sensitivity (85%) and specificity (98%): (1) 5 or more T2-bright foci, (2) 2 or more periventricular T2-bright foci, and (3) one or more T2-bright areas in the brainstem.

A companion paper included a retrospective analysis of brain MRI scans performed within 1 month of symptom onset in 48 children with an initial demyelinating event (28 with a final diagnosis of MS and 20 with ADEM).[44] They reported that the children could be categorized as having MS versus ADEM with 81% sensitivity and 95% specificity based on 2 of the following 3 brain MRI criteria: (1) absence of a diffuse bilateral T2-bright lesion pattern, (2) the presence of T1 “black holes,” and (3) the presence of 2 or more T2-bright periventricular foci.

Periventricular white matter lesions are not specific to MS, as they are also seen in other pediatric CNS demyelinating diseases, such as NMO.

Periventricular increased T2 signal, as shown in t Periventricular increased T2 signal, as shown in this FLAIR image, can be seen in neuromyelitis optica given the dense concentration of aquaporin 4 water channels in this area.
Increased T2 signal at the cervicomedullary juncti Increased T2 signal at the cervicomedullary junction, as seen in a pediatric patient with MS.
An enhancing lesion in the right superior frontopa An enhancing lesion in the right superior frontoparietal region. Image 4 shows the same lesion on FLAIR imaging.
FLAIR image of lesion in the right superior fronto FLAIR image of lesion in the right superior frontoparietal region.
This sagittal T2 image of the cervical spine shows This sagittal T2 image of the cervical spine shows small hyperintense lesions typical of MS at C2 C3.
This axial FLAIR image shows bilateral, left predo This axial FLAIR image shows bilateral, left predominant confluent signal change. There is also an area of gray matter involvement in the right frontal region. This image would not be sufficient to distinguish an episode of ADEM from pediatric MS in a pre-pubertal child.

Proposed Approach to Evaluation of White Matter Changes in a Child

Tier 1 consists of the following:

  • CSF: OCB, IgG index, cell count, protein, glucose, HSV, lyme

  • Serum: Complete blood cell (CBC) count, erythrocyte sedimentation rate (ESR), C-reactive protein, NMO antibodies (in cases of optic neuritis and/or longitudinally extensive transverse myelitis), antinuclear panel (including SSA, SSB), thyroid-stimulating hormone, vitamin B12

  • Imaging: Brain and cervical spine MRI with/without gadolinium

  • Other: Ophthalmology (if optic neuritis)

Tier 2 consists of the following:

  • CSF: EBV, cytology, bacterial, fungal, viral cultures

  • Serum: Angiotensin-converting enzyme, HIV, rapid plasma reagin/fluorescent treponemal antibody absorption

  • Imaging: Repeat brain MRI, entire spinal cord with/without gadolinium; chest radiography (sarcoid)

Tier 3 consists of the following:

  • CSF: Human T-lymphotropic virus 1, measles antibodies (subacute sclerosing panencephalitis), lactate, pyruvate

  • Serum: Serum amino acids, mitochondrial panel, WBC enzymes, very long chain fatty acids, acylcarnitine profile, lysosomal enzymes

  • Imaging: Magnetic resonance spectroscopy, magnetic resonance angiography

Low-Contrast Letter Acuity Charts

Low-contrast letter acuity charts (LCLA, Sloan charts) have been shown to provide a sensitive and reliable assessment of visual acuity in the patients with pediatric MS.[45]

Visual Evoked Potentials

Prolonged visual evoked potentials may indicate prior asymptomatic demyelination of optic nerves. Caution must be exercised in young children, as the results are highly dependent on attention.

Optical Coherence Tomography

Optical coherence tomography (OCT) uses near-infrared light to quantify the thickness of the retinal nerve fiber layer (RNFL) (which contains only nonmyelinated axons). It has been shown to provide a sensitive evaluation of the RNFL thickness in this population, a correlate of optic atrophy.[45]



Disease-Modifying Therapies

Ten disease-modifying therapies (DMT) have been approved for treatment of relapsing-remitting multiple sclerosis (MS) in the adult population, including 6 first-line therapies (glatiramer acetate [GA], intramuscular [IM] and subcutaneous [SC] interferon [IFN] beta-1a, and SC interferon-beta-1b, fingolimod [also approved in children], teriflunomide, and dimethyl fumarate) and two second-line therapies (mitoxantrone, alemtuzumab, natalizumab, and ocrelizumab). In addition, therapies such as rituximab and cyclophosphamide have been evaluated in phase II trials in adults with breakthrough disease, as have add-on therapies such as monthly steroids and intravenous immunoglobulin (IVIG).

Oral therapies

Fingolimod, teriflunomide, and dimethyl fumarate are oral disease-modifying therapies to achieve FDA approval for treatment of relapsing and remitting MS in adults. Fingolimod was also approved for children aged 10 years or older with relapsing MS in May 2018. Approval of fingolimod in children was based on the Phase 3 PARADIGMS study (n=215) that compared fingolimod to interferon beta-1a in children and adolescents. Patients were randomized to receive once-daily oral fingolimod (n=107, 0.5 mg or 0.25 mg, dependent on patients' body weight) or intramuscular interferon (IFN) beta-1a (n=108) once weekly. Compared with IFN beta-1a, fingolimod reduced the annualized rate of n/neT2 lesions by 52.6% (p< 0.001) and number of Gd+T1 lesions per scan by 66.0% (p< 0.001). Treatment with fingolimod up to Month 24 compared with IFN beta-1a significantly reduced brain atrophy (ARBA: −0.48% vs. −0.80%, p=0.014), Fingolimod significantly reduced MRI activity and slowed brain volume loss for up to 2 years compared with IFN beta-1a.[80]

Safety and efficacy of teriflunomide and dimethyl fumarate are not established in pediatric patients with MS. Off-label use of these medications should be pursued cautiously given the known adverse effects in adults. Teriflunomide labeling includes a boxed warning regarding severe liver injury and teratogenicity. Dimethyl fumarate cautions include lymphopenia, flushing, PML, angioedema, and liver injury.

Interferon-beta therapy

Interferon-beta-1a and 1b appear to be safe and well tolerated in this population, although discontinuation rates are high (30%-50%)[47] and side effects common. For example, many children on interferon (35%-65%) report flulike symptoms. Other relatively frequently observed side effects include leukopenia (8%-27%), thrombocytopenia (16%), anemia (12%), and transiently elevated transaminases (10%-62%). Injection-site reactions are very common.

Dosing of interferon-beta is not established in the pediatric population. However, most patients tolerate doses titrated following adult protocols or gradual titration to 30 µg once weekly for interferon-beta-1a IM and 22–44 µg SC 3 times/week for interferon-beta-1a. Children older than 10 years tolerate full doses of interferon-beta-1b, although decreased tolerance may exist in the younger population.[48] Limited data are available on the efficacy, effect on disability progression, and MRI effect.

Glatiramer acetate therapy

Only three published retrospective studies have evaluated the use of glatiramer acetate in pediatrics.[49, 50, 51] The medication appears well tolerated except for the typical injection-site reactions and rare and transient chest pain. The mean annualized relapse rate decreased during treatment, but the study was limited by small sample size.

Immunomodulatory and cytotoxic therapies

A small number of children continue to have MS relapses despite treatment with the first-line DMT described above, although no consensus criteria exist for the definition of breakthrough disease in pediatric MS. In general, practitioners allow at least 6 months of observation on a given treatment prior to deeming the treatment suboptimal.

Immunomodulatory and cytotoxic agents that are used in adult MS in the event of suboptimal response to interferon-beta and/or glatiramer acetate have been used in a small number of pediatric patients. There are no reports on the use of fingolimod in pediatric MS.

Natalizumab appears well tolerated by children with MS in whom first-line therapies have failed. Patients experience less clinical relapses, and MRI scans show no enhancing lesions.[52] There have been no reports to date of PML in association with natalizumab use in children.[53]

There have been no published reports of mitoxantrone use in the pediatric population except for a few cases followed at the US Pediatric MS Centers of Excellence.[54] The authors suggest caution with its use given the reported significant side effects of leukemia and cardiomyopathy.

In the pediatric MS population, only one case report of rituximab has been published.[55]

There is limited evidence to support the use of cyclophosphamide in children. Caution should be exercised given the risks of infertility and secondary neoplasm.

Symptomatic Treatments in Pediatric Multiple Sclerosis

Optimizing quality of life and function can be aided by treatment of persistent symptoms. Rehabilitative techniques, adaptive equipment, and medications can all contribute. Spasticity, fatigue, tremor, paroxysmal symptoms, cognitive impairment, and bowel and bladder dysfunction can all be improved with symptomatic treatment. Very few clinical studies have been performed in children with MS; therefore, the treatments discussed in this article are empirically derived and, in general, not FDA-approved.[56]


Spasticity can be moderated with stretching and range-of-motion exercises. Greater degrees of spasticity benefit from oral agents, including baclofen, tizanidine, or benzodiazepines; however, dosing may need to be balanced with side effects, including sedation.[53]


Fatigue is a frequent symptom in children with MS and is noted more frequently than can be easily explained by depression, exhaustion from physical disability or heat exposure, sleep disturbance, or poor bowel/bladder control. Ameliorating these potential underlying causes of fatigue is a critical first step. Medications that have been anecdotally used to address fatigue in children with MS include amantadine,[57] modafinil,[58, 59] and methylphenidate.

Bladder dysfunction

Bladder dysfunction can be treated with medications to treat or suppress infection and to decrease detrusor hyperreflexia. Intermittent bladder catheterization for urinary retention and desmopressin acetate nasal spray at bedtime for sleep-depriving nocturia unresponsive to fluid management are beneficial in some children.


Constipation occurs frequently, particularly in children with MS-related decreases in mobility. Management includes manipulating the diet, increasing fluid intake, maximizing activity levels, and adding stool softeners and additional fiber/bulk to diet.



Medication Summary

Fingolimod is the first drug approved for multiple sclerosis (MS) treatment in children.

Published studies have provided information for off-label use of beta interferons.[48, 47, 48]

Sphingosine 1-Phosphate Receptor Modulators

Class Summary

These agents may block lymphocyte capacity to egress from lymph nodes, and thereby reduce lymphocyte migration into the CNS.

Fingolimod (Gilenya, Tascenso ODT)

Fingolimod is the first drug approved for children aged ≥10 years with relapsing forms of MS. The mechanism of action for MS is unknown. It may involve a reduction of lymphocyte migration into the central nervous system. Fingolimod is available as capsules and oral disintegrating tablets.


Class Summary

Immunomodulators or receptor modulators are indicated for the treatment of adults with relapsing forms of MS. They help to slow the accumulation of physical disability and decrease the frequency of clinical exacerbations.

Interferon beta-1b (Betaseron, Extavia)

Immunomodulators or receptor modulators are indicated for the treatment of adults with relapsing forms of MS. Shown to slow the accumulation of physical disability and decrease the frequency of clinical exacerbations.

Interferon beta 1a (Avonex, Rebif)

The exact mechanism by which interferon beta-1a exerts its effects is not fully defined. Interferon beta inhibits the expression of proinflammatory cytokines, including interferon gamma, which is believed to be a major factor responsible for triggering the autoimmune reaction leading to MS.


Questions & Answers


What is pediatric multiple sclerosis (MS)?

How is pediatric multiple sclerosis (MS) defined?

What is the pathophysiology of pediatric multiple sclerosis (MS)?

What causes pediatric multiple sclerosis (MS)?

What is the prevalence of pediatric multiple sclerosis (MS)?

What is the prognosis of pediatric multiple sclerosis (MS)?


Which clinical history findings are characteristic of pediatric multiple sclerosis (MS)?


How is pediatric multiple sclerosis (MS) differentiated from acquired demyelinating disorders of the CNS?

Which conditions are included in the differential diagnoses of pediatric multiple sclerosis (MS)?


What is the role of lab tests in the workup of pediatric multiple sclerosis (MS)?

What is the role of imaging studies in the workup of pediatric multiple sclerosis (MS)?

What is the stepped approach to evaluation of white matter changes in the workup of pediatric multiple sclerosis (MS)?

How is visual acuity assessed in the workup of pediatric multiple sclerosis (MS)?

What is the role of visual evoked potentials in the workup of pediatric multiple sclerosis (MS)?

What is the role of OCT in the workup of pediatric multiple sclerosis (MS)?


What is the role of disease-modifying therapies (DMT) in the treatment of pediatric multiple sclerosis (MS)?

What is the efficacy of fingolimod in the treatment of pediatric multiple sclerosis (MS)?

What is the role of teriflunomide and dimethyl fumarate in the treatment of pediatric multiple sclerosis (MS)?

What is the role of interferon-beta therapy in the treatment of pediatric multiple sclerosis (MS)?

What is the role of glatiramer acetate therapy in the treatment of pediatric multiple sclerosis (MS)?

What is the role of immunomodulatory and cytotoxic therapies in the treatment of pediatric multiple sclerosis (MS)?

How are the symptoms of pediatric multiple sclerosis (MS) treated?

How is spasticity in pediatric multiple sclerosis (MS) treated?

How is fatigue in pediatric multiple sclerosis (MS) treated?

How is bladder dysfunction in pediatric multiple sclerosis (MS) treated?

How is constipation in pediatric multiple sclerosis (MS) treated?


Which medications are used in the treatment of pediatric multiple sclerosis (MS)?

Which medications in the drug class Immunomodulators are used in the treatment of Pediatric Multiple Sclerosis?

Which medications in the drug class Sphingosine 1-Phosphate Receptor Modulators are used in the treatment of Pediatric Multiple Sclerosis?