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This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.
The Bottom Line
- MS is CNS demyelination disseminated in time and space
- MRI brain/spine with gadolinium is the key diagnostic test
- CSF oligoclonal bands support diagnosis
- Acute relapse is treated with high-dose corticosteroids
- Disease-modifying therapy reduces relapses and disability accumulation
Overview
Multiple sclerosis is an immune-mediated demyelinating disease affecting brain, optic nerves, and spinal cord. Diagnosis requires dissemination in space and time with exclusion of better explanations. Typical attacks include optic neuritis, internuclear ophthalmoplegia, sensory symptoms, weakness, and myelitis.
Epidemiology
MS usually begins between ages 20 and 40 and is more common in women. Risk factors include family history, northern latitude, low vitamin D, smoking, obesity in adolescence, and prior Epstein-Barr virus infection. It affects CNS only, not peripheral nerves.
Clinical Features
Symptoms
Painful monocular vision loss and reduced color vision
Sensory symptoms, Lhermitte sign, weakness, ataxia
Diplopia from internuclear ophthalmoplegia
Bladder urgency, constipation, sexual dysfunction, fatigue
Heat-related transient worsening suggests Uhthoff phenomenon
Signs
UMN signs: hyperreflexia, spasticity, Babinski
INO: impaired adduction with abducting nystagmus
Afferent pupillary defect after optic neuritis
Cerebellar dysmetria or scanning speech
Peripheral areflexia suggests another diagnosis
Investigations
First-line
MRI brain/spinal cord with gadoliniumPeriventricular, juxtacortical, infratentorial, and spinal cord lesions
CSF analysisOligoclonal bands and elevated IgG index support MS
Second-line
Visual evoked potentialsShow prior optic nerve demyelination
Rule-out labsB12, HIV, syphilis, Lyme, AQP4/MOG when phenotype suggests
OCTDocuments optic nerve injury
Specialist
JCV antibodyRisk stratification before natalizumab
DMT safety labsCBC, LFTs, hepatitis/TB/VZV depending therapy
1
Acute relapse
- High-dose IV or oral corticosteroids
- Plasma exchange for severe steroid-refractory relapse
- Treat pseudo-relapse triggers such as fever/infection
- Rehabilitation for residual deficits
2
Disease-modifying therapy
- Start DMT for relapsing MS unless contraindicated
- Options include interferon, glatiramer, fumarates, S1P modulators, natalizumab, anti-CD20 therapy
- Ocrelizumab is approved for primary progressive MS
- Choose based on activity, pregnancy plans, comorbidities, monitoring burden
3
Symptoms
- Baclofen/tizanidine for spasticity
- Gabapentin/duloxetine/amitriptyline for neuropathic pain
- Treat bladder dysfunction and fatigue
- Exercise and PT
4
Prevention
- Smoking cessation
- Vitamin D repletion if low
- Vaccination planning before immunosuppression
- Pregnancy counseling for DMT washout
Complications
- Progressive disability: Motor, visual, bladder, sensory, and cognitive impairment
- Pseudo-relapse: Worsening with heat or infection
- PML: Natalizumab and immunosuppression risk
- Falls and depression: Common chronic issues
USMLE Step 2 CK Exam Tips
- 1Young woman with deficits separated in time and space = MS
- 2Painful monocular vision loss = optic neuritis
- 3INO in young adult = MS until proven otherwise
- 4MRI Dawson fingers + CSF oligoclonal bands is classic
- 5Uhthoff phenomenon = heat worsens symptoms
- 6Acute relapse = high-dose corticosteroids
- 7Peripheral areflexia is not typical MS
practicetest your knowledge on multiple sclerosisApply what you've learnt with USMLE Step 2 CK-style questions from the iatroX Q-Bank — neurology and beyond.
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