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Multiple Sclerosis (MS)

NICE guideline [NG220] Multiple sclerosis in adults: management. Last updated: Jun 2026.

NICE CKS Multiple sclerosis. Last revised: May 2024.

NICE Clinical guideline [CG148] Urinary incontinence in neurological disease: assessment and management. Last updated: Oct 2023.

Multiple Sclerosis (MS)

Multiple sclerosis (MS) is an acquired, chronic, immune-mediated, inflammatory demyelinating condition of the central nervous system that can affect the brain, brainstem, and spinal cord.

This updated UKMLA guide to MS is based on NICE NG220, which covers causes, risk factors, types, symptoms, diagnosis, and management.

Causes and Risk Factors

The exact cause of MS is unknown. It is thought to involve immune-mediated inflammation, triggered by an abnormal response to environmental factors in genetically predisposed individuals

  • T-cell-mediated inflammation damages oligodendrocytes, leading to demyelination and secondary axonal damage
  • Progressive damage within the nervous system may lead to irreversible loss of nerve function, resulting in permanent neurological symptoms and signs

Risk factors:

  • Genetics (>200 alleles have been identified)
  • Family history
  • Females (2-3x risk)
  • Vitamin D deficiency
  • Smoking
  • Diet and obesity in early life
  • EBV infection
  • Latitude

Clinical Features

Typical onset is in 20-50 y/o and is more common in females

MS may present with a wide range of symptoms affecting different body parts, most common ones (ANY of the following):

  • Optic neuritis (loss or reduction of vision in 1 eye with painful eye movements)
  • Double vision
  • Ascending sensory disturbance and/or weakness
  • Lhermitte’s sign: shock-like sensation radiating down the spine on neck flexion
  • Progressive difficulties with balance and gait

Additional supportive patterns:

  • 20-50 y/o female
  • History of previous neurological symptoms
  • Symptoms evolved >24 hours
  • Symptoms may persist over several days or weeks then improve
  • No fever or signs of infection

Key presentation patterns

Presentation Clinical features
Optic neuritis (20-30%) Optic neuritis is typically unilateral (CRAP is a useful mnemonic):

  • Central scotoma
  • RAPD (Marcus Gunn pupil) and Red desaturation
  • Acuity (visual) impairment
  • Painful eye movement (often develops a few days before visual changes)
Transverse myelitis
  • Sensory (e.g. paraesthesia) symptoms below the affected spinal level
  • Asymmetrical upper motor neuron signs below the affected spinal level
    • NB that there is an initial spinal shock phase where there are lower motor neuron signs (e.g. reduced tone, areflexia) before transitioning into upper motor neuron signs
  • Urinary symptoms (usually overactive bladder e.g. urgency, frequency, retention)
Spinal cord tract demyelination
  • Lhermitte’s sign: shock-like sensation radiating down the spine on neck flexion
  • Pyramidal tract involvement → upper motor neuron signs (e.g. ↑ tone, spasticity, hyperreflexia, +ve Babinski sign)
  • Dorsal column involvement → loss of vibration and fine-touch sensation, paraesthesia, sensory ataxia
  • Neuropathic pain
Cerebellar features
  • Ataxia
  • Charcot triad: nystagmus + intentional tremor + scanning speech
  • Vertigo
  • Dysmetria
  • Clumsiness
Brainstem syndromes
  • Internuclear ophthalmoplegia (ipsilateral eye fails to adduct and contralateral eye abducts with nystagmus)
  • Pseudobulbar palsy (e.g. dysarthria, dysphagia)
  • Cranial nerve palsies (classically bilateral CN V / VII palsy)
  • Oscillopsia
Other
  • Uhthoff phenomenon: symptoms worsening with increased body temperature (e.g. fever, warm bath, exercising)
  • Fatigue (very common, affecting up to 80% of patients)
  • Reduced mobility (85% of patients report gait disturbance as main complaint)
  • Pain (neuropathic pain and MSK pain secondary to problems with mobility and posture)
  • Bladder problems (>90% of patients)
    • Neurogenic detrusor overactivity → overactive bladder (frequency, urgency, incontinence)
  • Sexual dysfunction
  • Mental health problems
    • Depression and anxiety
    • Emotional lability (pseudobulbar affect) – patient may laugh or cry without any apparent trigger.
    • Cognitive impairment

Disability in MS can be measured and documented using the EDSS, which can be monitored for changes in disability over time

  • 0 = no signs or symptoms during assessment; 10 = death from MS
  • Increases in increments of 0.5
  • Key hallmarks
    • 5.0 = Disability severe enough to impair full daily activities
    • 6.0 = Walking aid is necessary
    • 7.0 = Restricted to wheelchair

Acute MS relapse

Characterised by:

  • Developing new symptoms OR worsening of existing symptoms, AND
  • Lasting >24 hours after a stable period of at least 1 month

It is important to rule out infection (esp. UTIs and RTIs) and to discriminate between a relapse and fluctuation in disease or progression.

Do not routinely diagnose a relapse of MS if symptoms are present for >3 months

MS Disease Patterns

There are 3 main disease patterns:

Pattern Description
Relapsing-remitting MS (RRMS) Most common disease pattern (seen in 85% of MS patients at onset)

Characterised by episodes of relapses (new or worsening symptoms), followed by remissions (partial or complete recovery) and periods of clinical stability

Secondary progressive MS (SPMS) ~2/3 of RRMS progress to SPMS

Characterised by gradual worsening symptoms and/or disability, with relapses becoming less frequent or stopping completely

Primary progressive MS (PPMS) Seen in 10-15% cases of MS

Characterised by steady progression and worsening symptoms and/or disability from the onset, without clear relapses or remissions

Differential Diagnosis

Differential diagnoses Causes and clinical clues
Other demyelinating diseases Neuromyelitis optica spectrum disorder (NMOSD)

  • Classic triad of:
    • Optic neuritis (classically bilateral, recurrent, and more severe than in MS)
    • Transverse myelitis (longitudinally extensive)
    • Area postrema syndrome (intractable nausea, vomiting, or hiccups due to brainstem involvement)
  • Associated with AQP4-IgG antibodies

Myelin oligodendrocyte glycoprotein antibody-associated Disease (MOGAD)

  • Bilateral or recurrent optic neuritis
  • Associated with myelin oligodendrocyte glycoprotein IgG antibodies

Isolated optic neuritis – optic neuritis may occur as an isolated event

Metabolic disorders
Infections
Systemic inflammatory disorders
Tumours

Investigation and Diagnosis

Note: NICE NG220 refers to the 2024 revised McDonald criteria when outlining the diagnostic approach to MS. The criteria summarised below are based on these 2024 revisions. [Ref]

If MS is suspected based on clinical features → refer to a consultant neurologist (only a consultant neurologist should make a diagnosis of MS)

1st line investigations for suspected MS

  • Clinical history and neurological examination
  • MRI brain + spinal cord (with and without gadolinium contrast) – most important investigation
  • Optic nerve imaging (MRI / OCT / VEPs) (esp. if the patient has a history of possible optic neuritis)

Further investigations:

  • Lumbar puncture for CSF analysis
  • MOG-IgG testing
    • Strongly recommended in <12 y/o presenting with a first demyelinating event to exclude MOGAD)
    • Routine testing is NOT necessary in other patients (unless clinical findings and/or MRI findings are atypical or suggestive of MOGAD rather than typical MS)

Investigation Findings

Investigation Findings in MS
MRI Key finding: T2-weighted hyperintense foci (plaques) in the CNS white matter

Some typical findings / pattern:

  • Classic MS location: periventricular lesions
  • Dawson’s fingers: ovoid periventricular lesions arranged perpendicular to the ventricles, following medullary veins
  • Spinal cord lesions are often short-segment

Dissemination in space (DIS) and dissemination in time (DIT) on MRI are fundamental components of the diagnostic criteria:

DIS: demonstrating the disease has affected distinct areas (“space”) of the CNS:

  • Typical lesions found in at least 2 out of 5 anatomical regions
  • The 5 characteristic anatomical regions: optic nerve, intracortical or juxtacortical, periventricular, infratentorial, spinal cord

DIT: demonstrating inflammatory activity is ongoing over time:

  • The presence of simultaneous gadoliniumenhancing and non-enhancing typical lesions on a single MRI scan
  • The appearance of 1 or more new T2 lesions or gadolinium-enhancing lesions on a follow-up MRI scan when compared to a previous scan

Novel MRI markers (only seen on non-conventional susceptibility-sensitive MRI sequence):

  • Central vein sign: MRI shows a distinct central vein running directly through a white matter lesion
  • Paramagnetic rim lesions: lesion with an inactive core surrounded by a characteristic rim (hypointense on T2) of activated, iron-laden microglia
Lumbar puncture and CSF analysis Classic finding: CSF-restricted oligoclonal bands

  • This refers to the presence of oligoclonal bands in the CSF, but NOT in the blood serum
  • This is indicative of an ongoing inflammatory process within the CNS, supporting MS
  • If oligoclonal bands are present in both the CSF and blood serum, this suggests a systemic immune response rather than MS (which occurs within the CNS)

Biomarker: positive kFLC Index (↑ kappa free-light chain: albumin ratio)

For diagnosis purposes, either the oligoclonal bands or biomarker can be used to fulfil the CSF criteria.

2024 McDonald Diagnostic Criteria

Key takeaway (exam-friendly and non-specialist level):

  • Classic diagnostic criteria: typical symptoms + dissemination in space (DIS) + dissemination in time (DIT)
  • In the 2024 criteria, DIT is NOT always mandatory
    • High-burden DIS alone can be diagnostic: lesions in ≥4 out of 5 typical CNS locations without DIT
    • DIS + positive CSF may also support diagnosis without separate DIT
  • The optic nerve is now recognised as a 5th CNS location to be used for DIS
  • Kappa free light chains as an alternative CSF marker to oligoclonal bands

Radiologically isolated syndrome (RIS) – i.e. asymptomatic MS criteria:

  • MRI lesions in at least 2 CNS locations, and
  • At least 1 of the following
    • +ve CSF
    • CVS on MRI

See the full diagnostic criteria here.

Management

MS management requires an MDT approach involving MS nurses, neurologists, physiotherapists, speech language therapists, psychologist, dietitians, social care etc.

Acute Relapse Management

  • 1st line: oral methylprednisolone 0.5g daily for 5 days
  • 2nd line: IV methylprednisolone 1g daily for 3-5 days
    • If oral steroids failed / not tolerated, or the patient is admitted to hospital for a severe relapse

Long-Term Management

General / Conservative Management

Manage modifiable risk factors for MS relapse / progression:

  • Regular exercise may have beneficial effects and has no harmful effects
  • Stop smoking
  • Offer routinely recommended vaccinations
    • Live vaccines should be avoided if the patient is on immunosuppressive treatment

Long-Term Management (Disease-Modifying Therapy)

Disclaimer:

NICE NG220 does not provide a single disease-modifying therapy treatment algorithm. Instead, it links to separate NICE technology appraisals for individual disease-modifying therapies and to the NHS England treatment algorithm for multiple sclerosis disease-modifying therapies.

These technology appraisals and treatment algorithms are highly specialist and extensive, with treatment choice depending on factors such as MS phenotype, disease activity, MRI findings, relapse history, safety profile, monitoring requirements, comorbidities and pregnancy plans.

For exam purposes, it should be sufficient to recognise a few classic disease-modifying therapies and, importantly, to distinguish long-term disease-modifying treatment from the acute management of MS relapses.

MS phenotype Disease-modifying therapy summary
Relapsing-remitting MS No clear 1st line option

NICE listed options include:

  • Injectables: interferon beta-1a, peginterferon beta-1b, glatiramer acetate
  • Dimethyl fumarate, diroximel fumarate
  • Ponesimod
  • Teriflunomide
  • Anti-CD20 monoclonal antibodies: ocrelizumab, ofatumumab, ublituximab
  • Cladribine

Options for highly active disease (presence of disease activity despite treatment):

  • Natalizumab (anti-integrin monoclonal antibody)
  • Anti-CD20 monoclonal antibodies: ocrelizumab, ofatumumab, ublituximab
  • Cladribine, alemtuzumab
  • Fingolimod, ponesimod
Secondary progressive MS Disease-modifying therapy is only considered when there are signs of active disease:

  • Siponimod
  • Interferon beta-1b (if there are continuing relapses)
Primary progressive MS
  • Ocrelizumab (only if there are imaging features of inflammatory activity)

Do not offer vitamin D and omega-3 / omega-6 fatty acid compounds solely for the purpose of treating MS.

Symptom / Complications Management

Complication Management
Fatigue Non-pharmacological

  • Mindfulness-based training
  • CBT
  • Fatigue management educational programmes
  • Supervised exercise programmes involving moderate progressive resistance training and aerobic exercise

Pharmacological (all off-label)

  • Amantadine
  • Modafinil
  • SSRI
Mobility problems
  • Supervised exercise programmes (involving moderate progressive resistance training and aerobic exercise) for general mobility problems
  • Vestibular rehabilitation for those with limited standing balance
Spasticity Consider referral to physiotherapy

Pharmacological:

  • 1st line: baclofen
  • 2nd line: gabapentin
Oscillopsia Consider (all off-label):

  • 1st line: gabapentin
  • 2nd line: memantine
Urinary dysfunction (usually overactive bladder) Managed similarly to those without MS, see the Urinary Incontinence in Women article for more information

Prior to treatment, the following assessment should be performed:

  • Urine dipstick
  • Fluid input / urine output charting
  • Bladder ultrasound (to measure post-void residual volume)
Pain Neuropathic pain should be managed according to standard neuropathic pain guidelines, see the Neuropathic pain article
Emotional lability Consider amitriptyline for emotional lability (involuntary laughing and crying related to a frontal lobe lesion)

MS and Pregnancy

Advise that patients should discuss with their healthcare professionals if they are planning to start or extend their family or become pregnant, especially in those who take disease-modifying therapies.

Explain that MS should not stop them from planning a family, and advise the following important points:

  • Impact on disease
    • Pregnancy does not increase the risk of MS progression
    • MS relapses may decrease during pregnancy and may increase 3 to 6 months after childbirth before returning to pre-pregnancy rates
  • Impact on pregnancy and outcome
    • Pregnancy is usually manageable with specialist input
    • Risk of the child developing MS is slightly higher than average (but overall risk is low)

References



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