Multiple sclerosis: an animated, cited guide

This page needs JavaScript for its animations. The outline and key answers are below, and every claim in the full version carries a numbered citation.

Not medical advice. MS Companion is an educational synthesis of published literature. It does not replace a clinician.

What is in it

What MS is Who gets it, the numbers, and where in the nervous system it strikes.
Myelin and demyelination How signals jump along a myelinated nerve fibre, and what a lesion does to them.
The immune attack T cells, B cells and the blood-brain barrier, step by step.
Genes and risk factors HLA-DRB1*15:01, Epstein-Barr virus, vitamin D, smoking and teenage obesity.
Relapse and remission over time Relapsing, secondary progressive and primary progressive MS on one timeline.
A relapse, week by week Onset, steroids and recovery, and how a pseudo-relapse differs.
Measuring disability: EDSS The 0 to 10 scale and what confirmed worsening means.
McDonald criteria calculator Dissemination in space and time, CSF, and the 2017 and 2024 rules.
The differential NMOSD, MOGAD and other conditions that look like MS.
How the drugs work Where each disease-modifying therapy acts.
The DMT ladder Escalation, early high-efficacy treatment and stopping in later life.
Safety and monitoring PML and the JCV index, infections, vaccines and rebound.
Toward a cure Remyelination, BTK inhibitors, stem-cell transplantation and EBV.
Symptoms and rehabilitation Fatigue, spasticity, bladder, walking, mood and cognition.
Living with MS Pregnancy, work, heat, exercise and planning.
Nursing care Assessment, giving the medicines, monitoring and teaching.
History and people From Carswell and Charcot to the 2024 criteria.
Flashcards, quiz and glossary Revision for students.
Sources Every reference behind the app.

Part 4 · Treatment

How the drugs work

Each MS disease-modifying therapy blocks a different step of the immune attack: holding cells in lymph nodes, stopping them entering the brain, or removing them. Pick a drug class to watch where it acts, then compare continuous and pulsed treatment over two years.

Published label and trial information only. Doses below are quoted from the US labels or trial reports so the mechanisms make sense. They are not instructions. Which medicine suits a particular person is a decision for that person and their MS team.

Timeline

Schematic, not to scale. The number of moving cells and the three meters are illustrative, not measured effect sizes. Orange cells marked T are T cells; violet cells marked B are B cells; teal shapes are the drug.

The untreated pathway, step by step, is in 1.3 The immune attack. Choosing between these medicines is covered in 4.2 The DMT ladder, and their monitoring in 4.3 Safety & monitoring.

Continuous or pulsed: lymphocyte counts over 24 months

Continuous therapies work only while they are being given. Pulsed immune reconstitution therapies are given as two short yearly courses: they knock lymphocyte counts down, and the immune system then rebuilds itself. Drag through two years and watch the four patterns side by side. Numbered dots mark the published timing anchors the curves pass through.

What if

Month

Schematic curves. Heights are relative to each person's starting count and are not to scale, except the alemtuzumab B-cell overshoot. Timings pass through the published anchors listed below. The S1P lane has no published count anchors in our sources, so it is drawn entirely schematically.

All the disease-modifying therapies at a glance

Filter by route or efficacy tier, and sort by any underlined column. Relapse-rate effects are the published headline results of each pivotal trial, against the comparator named. Trials with different comparators cannot be compared directly.

Route

Tier

Efficacy tiers are this guide's grouping, built from the AAN 2018 statement on higher-efficacy drugs and the Cochrane 2024 network meta-analysis; they are not an official ranking. Drugs that neither source rates are placed by class and by their head-to-head trials. ^171,394 ARR = annualised relapse rate. SC = under the skin; IM = into muscle; IV = into a vein.

What is still debated

Debated

Why does anti-CD20 work?

One view: through B cells presenting antigen and making cytokines, not antibody, because the benefit arrives before immunoglobulin falls and oligoclonal bands persist. The other gives antibody and complement a role in at least some lesions. Both may operate. ^{48,87,282,288,400}

Regulators differ

Tolebrutinib

The EU authorised it in June 2026 for SPMS without relapses in the last 2 years; the FDA issued a complete response letter in December 2025. Both looked at the same HERCULES data, which carry a liver-enzyme signal. ^125,156,419

Off-label

Rituximab

RIFUND-MS found it superior to dimethyl fumarate, yet it remains unapproved for MS in the US and EU, and AAN 2018 mentions it only in PML counselling. ^394,455

Mixed

Relapses fall, but disability?

CARE-MS I and ULTIMATE showed no significant disability benefit over their comparators; CARE-MS II, OPERA and ASCLEPIOS did. Cochrane rates the cladribine disability evidence as low certainty and possibly null, despite the CLARITY hazard ratio of 0.67. ^{74,83,85,165,186,187,452}

In plain wordsDisease-modifying therapies act on the immune attack, not on damage that is already done. They differ in where they act: some keep immune cells inside the lymph nodes, one stops them climbing into the brain, and some remove whole groups of immune cells for a while.

Exam hookMatch drug to step. S1P modulators: node exit (sequestration, reverses on stopping). Natalizumab: VLA-4 docking on VCAM-1 at the barrier. Anti-CD20: B-cell lysis that spares CD20-negative plasma cells. Cladribine and alemtuzumab (CD52): pulsed immune reconstitution. Teriflunomide: DHODH. BTK inhibitors: B cells and microglia behind the barrier. ^{14,163,175,257,279,473}