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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- MS is an autoimmune inflammatory demyelinating disease of the CNS — lesions disseminated in time and space
- Diagnosis uses the 2017 revised McDonald criteria: clinical episodes + MRI + CSF oligoclonal bands
- Common presentations: optic neuritis, transverse myelitis, brainstem syndromes (INO, diplopia), sensory symptoms
- Relapse treatment: high-dose IV methylprednisolone 500 mg–1 g/day for 3–5 days (shortens relapse, does not alter long-term prognosis)
- Disease-modifying therapies (DMTs) for relapsing-remitting MS reduce relapse rate and disability progression
Overview
Multiple sclerosis (MS) is a chronic autoimmune inflammatory demyelinating disease of the central nervous system. It results from immune-mediated damage to myelin sheaths, oligodendrocytes, and eventually axons. The hallmark is demyelinating plaques disseminated throughout the CNS white matter. MS is classified into relapsing-remitting (RRMS, ~85% at onset), secondary progressive (SPMS), and primary progressive (PPMS, ~15%). Relapsing-remitting MS is characterised by discrete clinical attacks (relapses) with full or partial recovery, separated by periods of clinical stability.
Epidemiology
MS affects approximately 130,000 people in the UK, with an incidence of ~7 per 100,000 per year. It is most commonly diagnosed between ages 20 and 40, with a female-to-male ratio of approximately 3:1. Prevalence increases with latitude (more common in Scotland than southern England). Risk factors include vitamin D deficiency, EBV infection (particularly infectious mononucleosis), smoking, family history (15-fold increase in first-degree relatives), and HLA-DRB1*15:01 genotype. It is more common in White European populations.
Clinical Features
Symptoms
Optic neuritis: painful loss of vision in one eye, reduced colour vision (red desaturation), central scotoma
Limb weakness or numbness (pyramidal/sensory tract involvement)
Lhermitte sign: electric shock sensation radiating down the spine on neck flexion
Uhthoff phenomenon: worsening of symptoms with heat or exercise
Bladder dysfunction: urgency, frequency, retention (common and often early)
Diplopia (INO, sixth nerve palsy)
Fatigue — the most common symptom of MS and often the most disabling
Cerebellar symptoms: ataxia, intention tremor, scanning dysarthria, nystagmus
Signs
Relative afferent pupillary defect (RAPD) — Marcus Gunn pupil (optic neuritis)
Internuclear ophthalmoplegia (INO): impaired adduction on lateral gaze with nystagmus in abducting eye — classic of MS
Upper motor neurone signs: spasticity, hyperreflexia, upgoing plantars, clonus
Cerebellar signs: Charcot triad (nystagmus, intention tremor, scanning dysarthria)
Sensory level (transverse myelitis)
Pale optic disc (optic atrophy from previous optic neuritis)
Investigations
First-line
MRI brain and spinal cord (with gadolinium)Periventricular, juxtacortical, infratentorial, and spinal cord demyelinating lesions (T2 hyperintense, some enhancing with gadolinium indicating acute inflammation). Dawson fingers = periventricular lesions perpendicular to ventricles
Lumbar punctureCSF-specific oligoclonal bands (present in ~95% of MS but absent in serum). Supports diagnosis if MRI criteria for dissemination in time not met
Second-line
Visual evoked potentials (VEPs)Delayed P100 latency indicates previous optic neuritis — may demonstrate subclinical lesion
BloodsTo exclude mimics: B12, folate, HIV, syphilis serology, ANA, anti-aquaporin 4 (neuromyelitis optica), anti-MOG antibodies
Specialist
OCT (optical coherence tomography)Measures retinal nerve fibre layer thickness — thinning indicates axonal loss from optic neuritis
1
Acute relapse treatment
- IV methylprednisolone 500 mg–1 g/day for 3–5 days (or oral methylprednisolone 500 mg/day for 5 days)
- Steroids shorten relapse duration but do NOT alter long-term prognosis
- Not every relapse requires treatment — mild sensory relapses may resolve spontaneously
2
Disease-modifying therapies (DMTs)
- For relapsing-remitting MS: multiple NICE-approved DMTs including dimethyl fumarate, teriflunomide, fingolimod, natalizumab, ocrelizumab, alemtuzumab, cladribine
- Choice depends on disease activity, patient preference, risk profile — specialist decision
- Escalation approach (start moderate-efficacy, escalate if breakthrough disease) or treat-to-target (early high-efficacy)
- PPMS: ocrelizumab is the only approved DMT (NICE TA585)
3
Symptom management
- Fatigue: exercise, CBT, amantadine or modafinil may be considered (NICE NG220)
- Spasticity: baclofen, gabapentin, physiotherapy. Cannabis-based medicine (nabiximols/Sativex) for moderate-severe spasticity refractory to other treatments
- Neuropathic pain: amitriptyline, gabapentin, pregabalin (per CG173)
- Bladder dysfunction: anticholinergics, intermittent self-catheterisation, desmopressin
- Depression: screen regularly — SSRIs if indicated
4
Multidisciplinary care
- MS specialist nurse as key point of contact
- Physiotherapy, occupational therapy, psychology, continence service
- Annual comprehensive review including disability assessment, treatment review, driving advice
Complications
- Progressive disability: Approximately 50% of untreated RRMS patients develop SPMS within 15–20 years
- Cognitive impairment: Affects up to 70% — processing speed, memory, executive function
- Depression: Lifetime prevalence ~50% — screen at every review
- Osteoporosis: From reduced mobility and steroid use
- DMT-related risks: PML with natalizumab (JC virus), infections with immunosuppressive agents, cardiac effects with fingolimod
- Aspiration pneumonia and pressure injuries: In advanced MS with severe disability
UKMLA Exam Tips
- 1Young woman with optic neuritis (painful visual loss + RAPD) = think MS. Recurrent episodes in different sites = dissemination in space and time
- 2INO (internuclear ophthalmoplegia) in a young patient = MS until proven otherwise
- 3Lhermitte sign (electric shock on neck flexion) and Uhthoff phenomenon (heat worsening) are classic MS associations
- 4Oligoclonal bands: present in CSF but NOT matched in serum = intrathecal IgG synthesis = supports MS
- 5Dawson fingers on MRI: periventricular lesions perpendicular to ventricles
- 6Relapse treatment = steroids (shortens relapse but does NOT change long-term outcome). DMTs reduce relapse rate and progression
- 7NEVER diagnose MS on MRI alone (NICE NG220) — clinical correlation + McDonald criteria required
practicetest your knowledge on multiple sclerosisApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — neurology and beyond.
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Multiple Sclerosis: guidance by region
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