Multiple Sclerosis: How the Immune System Attacks the Nervous System

Multiple sclerosis isn’t just a neurological condition-it’s a betrayal from within. Your own immune system, trained to protect you, turns against the very nerves that let you move, see, and think. This isn’t a random glitch. It’s a targeted attack on the myelin sheath, the protective coating around nerve fibers in your brain and spinal cord. When that coating gets stripped away, signals slow down, misfire, or disappear entirely. The result? Vision blurs, legs feel heavy, and fatigue hits like a wall. For 2.8 million people worldwide, this isn’t theoretical. It’s daily life.

What Happens When the Immune System Turns on the Nervous System?

The central nervous system-your brain and spinal cord-is normally shielded by the blood-brain barrier. Think of it like a security checkpoint: only approved molecules and cells get through. In multiple sclerosis, that checkpoint fails. Immune cells, especially CD4+ T cells and B cells, slip past and enter the CNS. Once inside, they mistake myelin for a foreign invader. Myelin is the fatty insulation wrapped around axons, the long wires that carry electrical signals between nerve cells. Without it, those signals can’t travel efficiently.

These immune cells don’t just attack. They recruit backup. Macrophages swarm in to clean up the debris, but they end up damaging healthy tissue too. Microglia, the brain’s own immune cells, get activated and start releasing toxic chemicals. Inflammation explodes. Lesions form-areas of scar tissue where myelin has been destroyed. These scars, called plaques, are visible on MRI scans. But the damage goes deeper than scars. Axons themselves begin to fray and die. That’s why symptoms don’t always go away, even when inflammation calms down.

The Four Patterns of Damage

MS isn’t one disease. It’s four different patterns of damage, each with its own fingerprint. Pattern I is mostly T cells and macrophages chewing through myelin. Pattern II adds antibodies-like tiny missiles-targeting myelin proteins. Pattern III shows something more disturbing: oligodendrocytes, the cells that make myelin, are dying off. And Pattern IV? That’s the worst. Oligodendrocytes are still alive, but they’re broken. They can’t repair the damage, even if the immune attack stops. This explains why some people keep getting worse, even on powerful drugs. The repair system is broken, not just the attacker.

Who Gets MS-and Why?

Women are two to three times more likely to get MS than men. The ratio jumps to 3.2:1 in places like Canada and Scandinavia, where MS is most common. Why? It’s not just hormones. Genetics play a role, but not enough to explain the spike. Environmental triggers are the real culprits. Epstein-Barr virus (EBV), the virus that causes mononucleosis, is the biggest known risk. People infected with EBV are 32 times more likely to develop MS. Vitamin D deficiency is another major factor. If your blood level drops below 50 nmol/L, your risk goes up by 60%. Smoking? It doesn’t just hurt your lungs-it speeds up disability by 80%.

MS rarely strikes before age 20 or after 50. Most people are diagnosed between 20 and 40. That’s when the immune system is most active-and most likely to go rogue. The disease doesn’t appear overnight. It builds silently for years before symptoms show up. By then, damage is already done.

What Does It Feel Like?

There’s no single MS symptom. It depends on where the attack happens. If it’s the optic nerve, vision blurs or turns gray-sometimes overnight. That’s optic neuritis. If it’s the spinal cord, you might feel electric shocks when you bend your neck. That’s Lhermitte’s sign. Fatigue hits 80% of people-not tiredness you can sleep off, but a crushing exhaustion that makes walking to the kitchen feel like climbing a mountain. Numbness, tingling, muscle spasms, bladder control issues, and trouble walking are all common. One person described it as “walking through wet sand.” Another said their legs felt like they were filled with concrete.

These aren’t random. They’re direct results of damaged wiring. A signal meant to tell your foot to lift? It never makes it. A signal meant to tell your eyes to focus? It gets scrambled. The brain tries to compensate, rerouting signals through other paths. That’s why some people have periods of remission-when the brain finds workarounds. But each flare-up leaves more damage behind.

Types of MS: Relapsing vs. Progressive

Eighty-five percent of people start with relapsing-remitting MS (RRMS). They get flare-ups-attacks of new or worsening symptoms-that last days or weeks. Then, for months or years, they’re stable. No new damage. No new symptoms. But inside, low-level inflammation is still happening. Over time, this shifts into secondary progressive MS. The relapses fade, but the decline doesn’t. Disability creeps forward, even without flares.

The other 15% have primary progressive MS (PPMS). From day one, symptoms get worse steadily. No remissions. No clear attacks. Just a slow, steady loss of function. PPMS is harder to treat. Most drugs work by calming immune flares. But in PPMS, the damage is more about degeneration than inflammation. That’s why treatments for PPMS have been slower to develop.

Treatments: Stopping the Attack, Not Just the Symptoms

There’s no cure. But there are ways to slow the damage. Disease-modifying therapies (DMTs) are the backbone of treatment. They don’t fix what’s already broken. They stop the immune system from breaking more.

Ocrelizumab targets B cells. It cuts relapses by 46% in RRMS and slows disability progression by 24% in PPMS. Natalizumab blocks immune cells from crossing the blood-brain barrier. It reduces relapses by 68%. But it comes with a risk: 1 in 1,000 people develop PML, a rare brain infection. That’s why doctors test for the JC virus before prescribing it.

These drugs work because they’re precise. They don’t wipe out the whole immune system. They hit the troublemakers. That’s a big leap from older treatments like interferons, which caused flu-like side effects and only modestly slowed progression.

The Future: Repairing the Damage

The next frontier isn’t just stopping attacks-it’s fixing what’s broken. Remyelination. Repairing the myelin sheath. For decades, scientists thought oligodendrocytes couldn’t regenerate after damage. New research shows that’s not true. The problem isn’t the cells. It’s the environment. Inflammatory chemicals in the lesion block repair. So new drugs are being tested to calm that environment and let the brain heal itself.

Clemastine fumarate, an old antihistamine, showed promise in a phase II trial. Patients improved their visual signal speed by 35%. That’s not just a lab result. It means better vision. Better function. Other drugs are targeting microglia, dendritic cells, and even neutrophil extracellular traps (NETs)-sticky webs of DNA and toxins released by immune cells that wreck the blood-brain barrier.

One of the most exciting developments is the blood test for neurofilament light chain (sNfL). When nerve fibers break, they release this protein into the cerebrospinal fluid and bloodstream. Levels above 15 pg/mL mean active damage is happening-even if you feel fine. Doctors can now see the invisible. They can adjust treatment before symptoms worsen.

What’s Next?

MS research is accelerating. The International Progressive MS Alliance has poured $65 million into projects across 14 countries. Scientists are mapping exactly which immune cells trigger damage in each person. The goal? Personalized medicine. Not one-size-fits-all drugs, but treatments tailored to your immune profile, your genetics, your disease pattern.

It’s not just about living longer. It’s about living better. Slowing progression. Reducing fatigue. Restoring function. For many, the dream isn’t a cure. It’s a future where MS doesn’t define your life.