Multiple Sclerosis: How the Immune System Attacks the Nervous System

Multiple sclerosis isn’t just a neurological condition-it’s an immune system attack on the body’s own nervous system. Imagine your nerves as electrical wires, wrapped in a protective plastic coating called myelin. That coating helps signals travel fast and clear from your brain to your muscles, eyes, and organs. In multiple sclerosis (MS), your immune system, which is supposed to protect you from viruses and bacteria, turns against those myelin sheaths. It doesn’t just damage them-it strips them away, leaving nerves exposed and signals scrambling. The result? Vision blur, numbness, fatigue, walking trouble, and sometimes permanent disability.

What Happens Inside the Nervous System?

The attack starts when immune cells-mainly T cells and B cells-break through the blood-brain barrier, a natural shield that normally keeps harmful substances out of the brain and spinal cord. Once inside, these cells mistake myelin for a foreign invader. They release inflammatory chemicals, recruit more immune fighters, and begin tearing down the fatty insulation around nerve fibers. This process is called demyelination.

What’s worse is that the damage doesn’t stop at the coating. Over time, the bare nerve fibers themselves-called axons-start to degenerate. Unlike skin or liver cells, nerve cells in the central nervous system don’t regenerate easily. Once an axon dies, the connection is gone for good. That’s why early treatment matters so much: it’s not just about stopping flare-ups, it’s about saving the wiring.

Scientists have identified four distinct patterns of this damage in MS patients. Some show mostly T cells and macrophages chewing through myelin. Others show antibodies sticking to the damaged areas. One pattern even reveals that the myelin-producing cells, called oligodendrocytes, are dying off without being replaced. In all cases, the environment becomes toxic-like a war zone where repair crews can’t get in because the fighting never stops.

Who Gets MS and Why?

About 2.8 million people worldwide live with MS. Women are two to three times more likely to be diagnosed than men, especially between the ages of 20 and 40. But it’s not just about gender. Geography plays a big role too. People living farther from the equator-like in Canada, Scandinavia, or northern U.S. states-have much higher rates. Why? Sunlight. Less sun means less vitamin D, and low vitamin D levels are linked to a 60% higher risk of developing MS.

Another major trigger is the Epstein-Barr virus (EBV), the same virus that causes mononucleosis. A 2022 Harvard study found that people infected with EBV are 32 times more likely to develop MS than those who weren’t. It’s not that EBV causes MS directly-it’s that in genetically vulnerable people, the virus seems to confuse the immune system, making it start attacking myelin.

Smoking also increases your risk by 80% and speeds up disability. Genetics matter too. If a parent or sibling has MS, your risk goes up-but even then, most people with a family history never develop it. It’s a mix: genes load the gun, environment pulls the trigger.

What Do the Symptoms Feel Like?

Symptoms vary wildly because MS can strike anywhere in the brain or spinal cord. One person might lose vision in one eye. Another might feel like their legs are made of concrete. Fatigue hits 80% of patients-not the kind you can fix with coffee. It’s a deep, bone-tired exhaustion that comes on suddenly, even after a good night’s sleep.

Numbness or tingling in the arms, legs, or face is common. Some describe it like a limb falling asleep-but it doesn’t wake up. Walking becomes harder as muscles lose their signal. About 42% of people with MS report trouble with balance or coordination.

Then there’s Lhermitte’s sign: a sudden electric shock that runs down your spine when you bend your neck. It’s caused by damaged nerves in the cervical spinal cord. Or optic neuritis-when the optic nerve gets inflamed, vision blurs or turns gray over 24 to 48 hours. For many, it’s the first warning sign.

These symptoms don’t happen all the time. Most people start with relapsing-remitting MS (RRMS), where flare-ups come and go. During a relapse, immune cells flood the CNS, creating new lesions. Then, for weeks or months, things calm down. But each attack leaves behind some damage. Over time, the gaps between relapses shrink, and recovery gets harder.

How Is It Treated Today?

There’s no cure yet-but there are tools to slow the damage. Disease-modifying therapies (DMTs) are the backbone of treatment. They don’t fix existing damage, but they stop the immune system from making new attacks.

Ocrelizumab is one of the most powerful. It targets B cells, which make up a big part of the problem. In clinical trials, it cut relapses by 46% in RRMS and slowed disability progression by 24% in primary progressive MS. Natalizumab blocks immune cells from crossing the blood-brain barrier. It’s incredibly effective-reducing relapses by 68%-but carries a rare but serious risk: progressive multifocal leukoencephalopathy (PML), a brain infection that can be fatal. Doctors test patients for the JC virus before starting it.

Newer drugs are being developed to go beyond suppression. One promising approach is remyelination-helping the body regrow myelin. Clemastine fumarate, originally an antihistamine, showed in a phase II trial that it improved nerve signal speed by 35% in MS patients. That’s not a cure, but it’s the first real sign that repair might be possible.

Blood tests are also becoming more precise. Serum neurofilament light chain (sNfL) levels above 15 pg/mL indicate active nerve damage with 89% accuracy. This lets doctors see if a treatment is working before symptoms get worse.

What’s on the Horizon?

Researchers are now looking at the role of dendritic cells-immune sentinels that hang out near blood vessels in the brain. In MS patients, these cells are found holding up pieces of myelin like wanted posters, showing T cells exactly what to attack. Blocking these cells could stop the attack before it starts.

Neutrophils, usually seen as short-term fighters, are also turning out to be troublemakers. They release sticky webs called NETs that tear apart the blood-brain barrier. In 78% of acute MS relapses, these NETs are present. New drugs targeting NETs are in early trials.

The International Progressive MS Alliance has invested $65 million into research since 2014. Projects span 14 countries, focused on understanding why MS becomes progressive-when damage keeps growing even without flare-ups. That’s the hardest form to treat, and the one that leads to long-term disability.

What Can You Do?

If you’ve been diagnosed, the most important thing is to start treatment early. Delaying increases the chance of permanent damage. Avoid smoking. Get regular sun exposure or take vitamin D supplements-especially if you live in a northern climate. Stay active. Exercise doesn’t cure MS, but it helps maintain strength, balance, and mental health.

If you’re worried you might have MS-because of sudden vision loss, unexplained numbness, or extreme fatigue-see a neurologist. Early diagnosis means early intervention. MRIs can show lesions before symptoms even start in some cases.

MS isn’t a death sentence. With modern treatments, many people live full, active lives. The immune system may have turned against the nervous system, but science is learning how to turn it back.