Neurology: Multiple Sclerosis and inflammatory disease

• Multiple sclerosis: What is MS? | Symptoms and Signs of MS | Diagnosing MS | Treating Relapses | Disease-modifying Treatments | DMT Safety and Monitoring | Managing MS Symptoms | MS in Women and Pregnancy | Progressive MS and Advanced Care
• Other inflammatory conditions: Optic Neuritis | Transverse Myelitis | Neuromyelitis Optica Spectrum Disorder | MOG Antibody-associated Disease | Acute Disseminated Encephalomyelitis | Autoimmune Encephalitis | Neurosarcoidosis and CNS Vasculitis
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🧩 Multiple sclerosis and related inflammatory conditions are the commonest cause of neurological disability in young adults in the UK. MS treatment has been transformed: high-efficacy drugs started early can prevent much of the long-term disability. It is also important to recognise MS "mimics" such as NMOSD and MOGAD, because some MS drugs make them worse.
Your four questions for every patient: Is this demyelination, and is it typical of MS? Is there infection or heat triggering a "pseudo-relapse"? Is the patient on the right disease-modifying treatment, with the right safety monitoring? Are symptoms such as bladder, spasticity, fatigue, pain and mood being treated?

What is MS?

What it is: A chronic immune-mediated disease. The immune system damages myelin and nerve fibres in the brain, optic nerves and spinal cord, producing patches ("plaques") of inflammation that are "disseminated in time and space".

Who gets it:

• About 150,000 people in the UK.
• Women 3 times more than men.
• Usually diagnosed at 20–40.
• Commoner further from the equator (Scotland has one of the highest rates in the world).

Risk factors:

• Low vitamin D and low sunlight.
• Epstein–Barr virus infection (almost all people with MS have had EBV).
• Smoking.
• Obesity in adolescence.
• Genetics (HLA-DRB1*15:01; about 2–3% risk for a sibling).

Disease courses:

• Clinically isolated syndrome (CIS) - a first episode of demyelination.
• Relapsing–remitting MS (about 85% at onset) - relapses with full or partial recovery.
• Secondary progressive MS - gradual worsening after a relapsing phase (often 10–20 years later), with or without relapses.
• Primary progressive MS (about 10–15%) - steady progression from the start, often a spinal cord syndrome; older onset; equal sex ratio.
• Each course is described as "active" (relapses or new MRI lesions) or "not active".

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Symptoms and Signs of MS

Symptoms usually develop over hours to days, last more than 24 hours, and improve over weeks.

• Optic neuritis - pain on eye movement and blurred vision in one eye.
• Sensory symptoms - numbness or tingling spreading up the legs or trunk; "band-like" feelings.
• Lhermitte's sign - an electric shock down the spine on bending the neck (cervical cord lesion).
• Motor - weakness, spasticity, foot drop.
• Brainstem - double vision (INO or sixth nerve palsy), vertigo, facial numbness, trigeminal neuralgia in a young person.
• Cerebellar - ataxia, intention tremor, dysarthria.
• Bladder and bowel - urgency, frequency, incomplete emptying, constipation; sexual dysfunction.
• Fatigue - very common and disabling.
• Cognitive problems - processing speed, memory; depression and anxiety.
• Pain - neuropathic pain, spasms.
• Uhthoff's phenomenon - symptoms worsen temporarily with heat (hot bath, exercise, fever).

💡 Clinical Pearl: Before diagnosing an MS relapse, check for a "pseudo-relapse" - old symptoms returning with infection (especially UTI), fever, heat or stress. Dip the urine and treat the trigger; steroids are not needed.

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Diagnosing MS

Principle: Show dissemination in space (lesions in different parts of the CNS) and dissemination in time (lesions at different times), and exclude other causes (McDonald criteria, 2017, with 2024 revisions).

• MRI brain and spinal cord (with contrast):
  • Typical sites: periventricular (perpendicular to the ventricles - "Dawson's fingers"), juxtacortical/cortical, infratentorial (brainstem, cerebellum), spinal cord; the optic nerve is included in the 2024 revision.
  • Dissemination in time - enhancing and non-enhancing lesions together, or new lesions on a later scan.
  • The "central vein sign" helps distinguish MS from small vessel disease.
• Lumbar puncture:
  • CSF-specific oligoclonal bands (present in over 90%) can stand in for dissemination in time.
  • Kappa free light chains are an alternative.
• Evoked potentials - show previous optic neuritis (delayed visual evoked potentials).
• Blood tests to exclude mimics:
  • B12.
  • ANA, ANCA, antiphospholipid antibodies.
  • Syphilis, HIV.
  • AQP4 and MOG antibodies when features are atypical.
  • ACE (sarcoid).
  • TFTs.
• Red flags suggesting another diagnosis:
  • Age over 50 at onset.
  • Severe bilateral optic neuritis.
  • Long spinal cord lesions (3 or more segments - NMOSD).
  • Intractable hiccups or vomiting (area postrema - NMOSD).
  • Encephalopathy; headache; fever.
  • Peripheral nerve involvement.
  • Normal MRI.
• White matter spots on MRI are common in migraine, small vessel disease and older age - don't diagnose MS from a scan alone.
• Radiologically isolated syndrome - typical MS lesions found by chance in someone without symptoms. Many later develop MS; specialist follow-up.

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Treating Relapses

• A relapse: New or worsening symptoms lasting more than 24 hours, at least 30 days after a previous relapse, without infection or fever.
• Check first: Urine dip and culture, temperature, inflammatory markers (exclude pseudo-relapse).
• Steroids for relapses that affect function (NICE NG220):
  • Oral methylprednisolone 500 mg daily for 5 days.
  • IV methylprednisolone 1 g daily for 3–5 days if oral treatment has failed or isn't tolerated, or for severe relapses needing admission.
  • Start within 14 days of onset.
• Steroids speed recovery but don't improve the final outcome or prevent future relapses.
• Steroid risks: High glucose, mood change, insomnia, GI upset, infection, avascular necrosis with repeated courses. Give a PPI and check glucose (especially in diabetes).
• Severe relapses that don't respond: plasma exchange.
• Every relapse should trigger a review of disease-modifying treatment - it may need escalating.
• Rehabilitation (physiotherapy, occupational therapy).

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Disease-modifying Treatments

Disease-modifying treatments (DMTs) reduce relapses and new MRI lesions and slow disability. They do not repair damage, so the trend is to start effective treatment early. Prescribing follows the NHS England MS treatment algorithm.

Moderate-efficacy treatments:

• Interferon beta (injections) - flu-like symptoms, depression, abnormal LFTs.
• Glatiramer acetate (injections) - injection-site reactions; safe in pregnancy.
• Teriflunomide (tablet) - hair thinning, abnormal LFTs. Teratogenic and stays in the body for up to 2 years - needs a washout with colestyramine before pregnancy.
• Dimethyl fumarate and diroximel fumarate (tablets) - flushing, GI upset, low lymphocytes (rare PML).

High-efficacy treatments:

• Anti-CD20 antibodies (B-cell depletion):
  • Ocrelizumab (IV every 6 months, or subcutaneous).
  • Ofatumumab (monthly self-injection).
  • Ublituximab.
  • Ocrelizumab is also licensed for early active primary progressive MS.
• Natalizumab (IV or SC every 4–6 weeks) - very effective, but carries a risk of PML (see below).
• S1P receptor modulators (tablets) - fingolimod, ozanimod, ponesimod, and siponimod (active secondary progressive MS).
• Cladribine (tablets) - two short courses a year apart ("immune reconstitution").
• Alemtuzumab (IV, two courses) - very effective but high risk of secondary autoimmune disease; now restricted.
• Autologous haematopoietic stem cell transplant - for highly active MS despite treatment, in specialist centres.

Everyone with MS:

• Stop smoking.
• Vitamin D if deficient.
• Regular exercise.
• Healthy weight.
• Manage vascular risk factors.

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DMT Safety and Monitoring

• Before starting (as for other immunosuppression):
  • Hepatitis B and C, HIV, varicella immunity, TB screening (for some drugs).
  • FBC and LFTs; pregnancy test.
  • Vaccinations, including live vaccines before starting.
• Progressive multifocal leukoencephalopathy (PML):
  • Brain infection by JC virus - progressive weakness, visual, speech and cognitive problems. Often fatal or disabling.
  • Natalizumab carries the highest risk - highest in people who are JCV antibody-positive (high index), on treatment for over 2 years, and with previous immunosuppression.
  • Check JCV antibody status regularly; MRI surveillance; extended-interval dosing lowers the risk.
• Anti-CD20 drugs:
  • Infusion reactions.
  • Infections; low immunoglobulins with long use.
  • Hepatitis B reactivation.
  • Reduced vaccine responses (including COVID-19 and influenza).
• S1P modulators (fingolimod):
  • First-dose bradycardia and heart block - ECG and monitoring.
  • Macular oedema - eye check at 3–4 months.
  • Low lymphocytes; herpes infections; skin cancer.
  • Severe rebound relapse if stopped suddenly.
• Alemtuzumab:
  • Autoimmune thyroid disease (about 40%), ITP, anti-GBM kidney disease.
  • Monthly blood and urine tests for 4 years after the last dose.
  • Stroke and arterial dissection around infusions.
• Cladribine: Low lymphocytes; shingles; teratogenic - contraception for 6 months after each course.

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Managing MS Symptoms

• Spasticity and spasms:
  • Physiotherapy and stretching; treat triggers (infection, constipation, pressure sores, pain).
  • Baclofen or gabapentin first; tizanidine.
  • Botulinum toxin for focal spasticity.
  • Nabiximols (cannabis-based oral spray) for moderate to severe spasticity (NICE NG144).
  • Intrathecal baclofen for severe cases.
• Fatigue:
  • Look for causes - depression, poor sleep, anaemia, thyroid, drugs, infection.
  • Energy management; aerobic exercise; CBT.
  • Amantadine is sometimes tried.
• Bladder:
  • Check post-void residual volume (bladder scan).
  • Urgency - antimuscarinics (beware cognitive side effects; trospium is less likely to cause them) or mirabegron.
  • Incomplete emptying (residual over 100 mL) - intermittent self-catheterisation.
  • Nocturia - desmopressin (watch sodium).
  • Botulinum toxin to the bladder; urology input.
• Bowel: Constipation and urgency - laxatives, bowel routines, transanal irrigation.
• Pain:
  • Neuropathic pain - amitriptyline, duloxetine, gabapentin, pregabalin.
  • Trigeminal neuralgia - carbamazepine.
  • Musculoskeletal pain - physiotherapy.
• Mobility: Physiotherapy; walking aids; foot drop splints or functional electrical stimulation. Fampridine improves walking speed in some (not routinely funded by NICE).
• Tremor: Hard to treat - physiotherapy, occupational therapy, propranolol, DBS rarely.
• Oscillopsia (shaky vision from nystagmus): Gabapentin or memantine.
• Mood and cognition: Screen for depression (common) and treat; cognitive rehabilitation.
• Sexual dysfunction: PDE5 inhibitors; specialist support.
• Bone health (steroids, immobility), vaccinations, and driving (tell the DVLA).

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MS in Women and Pregnancy

• MS doesn't affect fertility, and having children doesn't worsen long-term disability.
• Relapse rate falls during pregnancy (especially the third trimester) and rises in the 3 months after delivery.
• Plan pregnancy with the MS team - ideally when the disease has been stable for a year.
• DMTs in pregnancy:
  • Interferon and glatiramer can be continued.
  • Anti-CD20 drugs - often given before conception (long effect); breastfeeding is possible.
  • Natalizumab - sometimes continued in highly active disease (stopping can cause severe rebound); the baby needs a blood count check.
  • Avoid teriflunomide (washout needed), fingolimod and other S1P modulators (stop 2 months before, with rebound risk), cladribine, alemtuzumab (wait 4 months) and mitoxantrone.
• Delivery: Normal vaginal birth and epidural are fine.
• Breastfeeding: Possible on several DMTs; discuss individually.
• Vitamin D and folic acid supplementation.
• Restart DMTs promptly after delivery if needed.

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Progressive MS and Advanced Care

• Treatment options are limited for progressive MS without activity.
  • Ocrelizumab - early, active primary progressive MS.
  • Siponimod - active secondary progressive MS.
  • Newer drugs (e.g. BTK inhibitors) are in development.
• Stopping DMTs may be considered in older people with long-standing stable, non-relapsing disease.
• Rehabilitation and MDT care:
  • Physiotherapy, occupational therapy, speech and language therapy.
  • Continence services.
  • Wheelchair and seating; pressure care.
  • Dietitian.
  • Psychology.
  • Social care and carer support.
• Complications of advanced MS:
  • Aspiration pneumonia.
  • Urinary sepsis.
  • Pressure sores.
  • Contractures; osteoporosis and fractures.
  • VTE.
• Advance care planning and palliative care for symptoms (pain, spasms, swallowing, breathing).
• Life expectancy is reduced by about 7 years on average, largely from complications.

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Optic Neuritis

What it is: Inflammation of the optic nerve. It is often the first sign of MS, but can also be due to NMOSD, MOGAD, sarcoid, infection or autoimmune disease.

Typical (MS-associated) features:

• Young adult, often female.
• Pain on eye movement.
• Reduced vision over hours to days, in one eye.
• Reduced colour vision (red desaturation); central scotoma.
• RAPD.
• The disc is often normal ("retrobulbar"), or mildly swollen.
• Starts to recover within 2–3 weeks, without treatment.

Atypical features - think NMOSD, MOGAD, or other causes:

• Both eyes.
• Very severe loss (no light perception).
• No pain.
• Marked disc swelling or haemorrhages.
• No recovery after 3 weeks.
• Steroid-dependence.
• Age over 50 - consider ischaemic optic neuropathy and GCA.

Investigation:

• MRI brain and orbits - white matter lesions predict MS (risk about 60–70% at 15 years with lesions, about 25% without).
• AQP4 and MOG antibodies if atypical.
• ESR and CRP if over 50.

Treatment:

• Typical optic neuritis often needs no treatment. High-dose steroids speed recovery but don't change the final vision.
• Atypical or severe - urgent IV methylprednisolone, with plasma exchange for NMOSD.
• Oral prednisolone at standard doses alone is not recommended (higher recurrence in the ONTT trial).

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Transverse Myelitis

What it is: Inflammation across the spinal cord.

• Features:
  • Weakness and sensory loss below a level, developing over hours to days.
  • Bladder and bowel dysfunction.
  • Band-like pain at the level.
• Urgent MRI of the whole spine - exclude compression first (see the Neurological Emergencies chapter).
• Lesion length guides the cause:
  • Short, partial lesions (under 2 segments, off-centre) - MS.
  • Longitudinally extensive (3 or more segments, central) - NMOSD, MOGAD, sarcoid, infection, SLE, Sjögren's syndrome.
• Other causes:
  • Infection - HSV, VZV, HIV, syphilis, Lyme, TB, schistosomiasis.
  • Post-infectious.
  • B12 and copper deficiency (posterior columns - mimics).
  • Spinal cord infarction (sudden onset).
  • Dural arteriovenous fistula (progressive, worse with exercise).
  • Radiation.
  • Paraneoplastic.
• Tests: MRI brain; LP (cells, oligoclonal bands, infection PCR); AQP4 and MOG antibodies; ANA, ENA; B12 and copper; HIV and syphilis serology.
• Treatment:
  • IV methylprednisolone 1 g daily for 3–5 days.
  • Plasma exchange if severe or no response.
  • Treat any infection.
  • Bladder care, VTE prophylaxis, pressure care, rehabilitation.

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Neuromyelitis Optica Spectrum Disorder

What it is: An autoimmune disease caused by antibodies against aquaporin-4 (AQP4), a water channel on astrocytes. It is different from MS and is treated differently.

Who gets it:

• Mostly women (about 9:1).
• Older average onset than MS (about 40).
• Commoner in people of African, Caribbean and Asian descent.
• Associated with other autoimmune disease (SLE, Sjögren's syndrome, myasthenia).

Core features:

• Severe optic neuritis - often bilateral, with poor recovery.
• Longitudinally extensive transverse myelitis (3 or more vertebral segments).
• Area postrema syndrome - intractable hiccups, nausea and vomiting.
• Brainstem, diencephalic (narcolepsy, low sodium) and cerebral syndromes.

Diagnosis:

• Serum AQP4 antibody (cell-based assay).
• MRI.
• CSF (oligoclonal bands usually absent; may have neutrophils).

Treatment:

• Attacks - urgent IV methylprednisolone and early plasma exchange. Attacks cause stepwise disability, so prevent them.
• Prevention (lifelong):
  • Rituximab.
  • Newer targeted drugs: inebilizumab (anti-CD19), satralizumab (anti-IL-6 receptor), eculizumab and ravulizumab (complement inhibitors - need meningococcal vaccination).
  • Azathioprine or mycophenolate with steroids.
• Avoid MS drugs - interferon beta, natalizumab and fingolimod can make NMOSD worse.
• Managed by the national NMO service in England.

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MOG Antibody-associated Disease

• What it is: Inflammatory demyelination with antibodies to myelin oligodendrocyte glycoprotein (MOG). It is separate from MS and NMOSD.
• Who gets it: Children and adults, men and women equally.
• Features:
  • Optic neuritis - often bilateral, with marked disc swelling and severe pain.
  • Myelitis - often long, and involving the conus (bladder, bowel and erectile problems).
  • ADEM (especially in children).
  • Cortical encephalitis with seizures; brainstem attacks.
• Course: Often a single episode; about half relapse. Recovery is usually better than in NMOSD.
• Diagnosis: Serum MOG antibody (cell-based assay) with a compatible clinical picture - low-titre results can be false positives.
• Treatment:
  • Attacks: IV methylprednisolone, then a slow oral steroid taper (relapses often occur when steroids are reduced quickly); plasma exchange or IVIg if severe.
  • Relapsing disease: maintenance IVIg, azathioprine, mycophenolate or rituximab. Newer targeted drugs are in development.

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Acute Disseminated Encephalomyelitis

• What it is: A single episode of widespread brain and spinal cord inflammation.
• Who: Usually children, often days to weeks after an infection or (rarely) vaccination.
• Features:
  • Encephalopathy (confusion, drowsiness, behaviour change) - required for diagnosis.
  • Multifocal signs - weakness, ataxia, optic neuritis, seizures.
  • Fever and headache.
• MRI: Large, fluffy, poorly defined white and grey matter lesions, often in the basal ganglia and thalamus, all of the same age.
• CSF: Lymphocytes and raised protein; oligoclonal bands usually absent. Exclude infective encephalitis.
• Test for MOG antibodies - positive in about half of children with ADEM.
• Treatment: IV methylprednisolone, then an oral taper; IVIg or plasma exchange if no response.
• Outlook: Most recover well. Relapses suggest MOGAD or MS.

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Autoimmune Encephalitis

Acute assessment of encephalitis is covered in the Neurological Emergencies chapter. Autoimmune encephalitis is now as common as infectious encephalitis.

• Anti-NMDA receptor encephalitis:
  • Young women and children.
  • A viral-like illness, then psychiatric symptoms (psychosis, agitation), memory loss, seizures, abnormal movements (orofacial dyskinesia), reduced consciousness, autonomic instability and breathing problems.
  • Ovarian teratoma in about a third of adult women - look for it (pelvic ultrasound or MRI) and remove it.
  • Can follow HSV encephalitis.
• LGI1 encephalitis:
  • Older men.
  • Faciobrachial dystonic seizures (brief jerks of the face and arm on one side, many times a day).
  • Low sodium.
  • Memory loss (limbic encephalitis).
• CASPR2: Neuromyotonia, pain, insomnia (Morvan syndrome), encephalitis.
• Paraneoplastic encephalitis (anti-Hu, anti-Ma2) - poorer response; treat the cancer.
• Diagnosis:
  • MRI (medial temporal changes, often normal in NMDA).
  • EEG.
  • CSF (lymphocytes, oligoclonal bands).
  • Serum and CSF antibodies (NMDA antibodies are more reliable in CSF).
  • Screen for cancer.
• Treatment (start early, often before antibody results):
  • First line: IV methylprednisolone, IVIg and/or plasma exchange.
  • Second line: Rituximab or cyclophosphamide.
  • Remove any tumour.
  • Recovery can take many months; rehabilitation.
• Checkpoint inhibitor-related neurological toxicity (encephalitis, myasthenia, myositis, neuropathy) is increasingly seen.

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Neurosarcoidosis and CNS Vasculitis

Neurosarcoidosis (about 5–10% of people with sarcoidosis):

• Features:
  • Cranial neuropathies - especially facial nerve palsy (can be bilateral); optic neuropathy.
  • Chronic meningitis.
  • Hypothalamic and pituitary involvement - diabetes insipidus, hormone deficiencies.
  • Myelitis.
  • Peripheral neuropathy; myopathy.
• Tests:
  • MRI with contrast (meningeal enhancement).
  • CSF.
  • CT chest and PET to find a site for biopsy (lymph nodes).
  • Serum ACE (non-specific).
  • Calcium.
• Treatment: Steroids, then steroid-sparing drugs (methotrexate, mycophenolate); infliximab for severe or refractory disease.

CNS vasculitis:

• Primary angiitis of the CNS - rare.
  • Headache, cognitive decline, multiple strokes of different ages, seizures.
  • CSF is usually abnormal (raised protein and cells).
  • Angiography or brain biopsy.
  • Mimic: Reversible cerebral vasoconstriction syndrome (thunderclap headache, normal CSF).
• Secondary vasculitis:
  • SLE; ANCA vasculitis; Behçet's disease (brainstem lesions, venous sinus thrombosis, with mouth and genital ulcers).
  • GCA (posterior circulation strokes).
  • Infections - VZV vasculopathy, TB, syphilis, HIV.
  • Drugs (cocaine, amphetamines).
• Treatment: High-dose steroids with cyclophosphamide or rituximab; treat any infection.
• Susac syndrome - rare: encephalopathy, branch retinal artery occlusions and hearing loss, with corpus callosum lesions. Immunosuppression.

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Drug Reference Table

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Spot the Diagnosis

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Exam-style Scenarios

1. A 29-year-old woman has 5 days of numbness spreading up from her feet to her waist. MRI shows a short cervical cord lesion and several periventricular lesions, some enhancing.
Answer: Relapsing MS (dissemination in space and time on one scan).

• Exclude mimics (B12, AQP4 and MOG antibodies if atypical).
• Oral methylprednisolone 500 mg daily for 5 days if the symptoms affect function.
• Discuss early DMT (consider high-efficacy treatment); stop smoking; vitamin D.

2. A man with MS has worsening leg weakness for 2 days with a temperature of 38.2 °C and a positive urine dip.
Answer: Pseudo-relapse due to UTI.

• Treat the infection (urine culture, antibiotics); paracetamol for fever.
• No steroids; review after the infection settles.
• Check post-void residual volume.

3. A 40-year-old Afro-Caribbean woman has severe bilateral visual loss and, a month later, a myelitis spanning 5 segments.
Answer: NMOSD - test AQP4 antibodies.

• IV methylprednisolone and early plasma exchange.
• Long-term prevention (rituximab, inebilizumab, satralizumab or eculizumab).
• Avoid MS DMTs (interferon, natalizumab, fingolimod).

4. A woman with MS on natalizumab for 3 years has a high JCV antibody index.
Answer: High PML risk.

• Discuss switching (e.g. to an anti-CD20 drug) or extended-interval dosing with MRI surveillance.
• Plan the switch carefully to avoid rebound relapses.

5. A man with MS has urgency and frequency. His post-void residual is 180 mL.
Answer: Incomplete bladder emptying.

• Exclude UTI.
• Teach intermittent self-catheterisation.
• Then treat urgency (antimuscarinic or mirabegron); continence or urology referral.

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Key Points

• MS: young women; symptoms over days lasting more than 24 hours; optic neuritis, sensory, brainstem (INO), cord and cerebellar features.
• Diagnosis needs dissemination in space and time (MRI, oligoclonal bands) and exclusion of mimics. Don't diagnose MS from a scan alone.
• Exclude pseudo-relapse (infection, heat) before giving steroids.
• Relapse: oral methylprednisolone 500 mg for 5 days (IV 1 g for 3–5 days if needed). It speeds recovery only.
• Start DMTs early; high-efficacy options include anti-CD20 drugs, natalizumab, S1P modulators, cladribine and alemtuzumab.
• Natalizumab: PML risk - JCV antibody index. Fingolimod: bradycardia, macular oedema, rebound. Alemtuzumab: thyroid disease and ITP.
• Treat spasticity, bladder (check residual - self-catheterisation if over 100 mL), fatigue, pain and mood.
• MS relapses fall in pregnancy and rise after delivery; avoid teriflunomide, S1P modulators and cladribine.
• Atypical optic neuritis (bilateral, painless, severe, swollen disc, no recovery) - test AQP4 and MOG.
• Longitudinally extensive myelitis or intractable hiccups and vomiting: NMOSD. Some MS drugs make NMOSD worse.
• MOGAD: bilateral optic neuritis with disc swelling, conus myelitis, ADEM; usually recovers better.
• Anti-NMDA encephalitis: psychiatric symptoms, seizures, dyskinesia - look for ovarian teratoma.
• Always image the whole spine urgently in a new myelopathy to exclude compression.

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Guidelines and Further Reading

• NICE NG220: Multiple sclerosis in adults - management (2022)
• NHS England: Treatment algorithm for multiple sclerosis disease-modifying therapies
• McDonald criteria for MS (2017) and 2024 revisions
• NICE NG144: Cannabis-based medicinal products
• Association of British Neurologists: guidelines for prescribing DMTs in MS
• International consensus diagnostic criteria for NMOSD (2015) and MOGAD (2023)
• Association of British Neurologists: autoimmune encephalitis guidance
• MS Society; MS Trust
• BNF - for current doses

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