Multiple Sclerosis: How the Immune System Attacks the Nervous System

Multiple sclerosis isn’t just a neurological condition-it’s an internal betrayal. Your own immune system, designed to protect you, turns against your brain and spinal cord, stripping away the protective coating around your nerves. This isn’t a slow decline you can ignore. It’s an active, ongoing war inside your central nervous system, and the damage builds up silently until symptoms become impossible to overlook.

What Happens When Your Immune System Goes Rogue

In multiple sclerosis (MS), the immune system mistakes parts of your nervous system for foreign invaders. Specifically, it targets the myelin sheath-the fatty insulation wrapped around nerve fibers (axons) that lets electrical signals zip through your body at lightning speed. When myelin gets damaged, those signals slow down, get scrambled, or stop entirely. That’s when you feel numbness, weakness, blurred vision, or trouble walking.

This isn’t random. It starts with immune cells-mainly T cells and B cells-breaking through the blood-brain barrier, a normally tight filter that keeps harmful substances out of the brain and spinal cord. Once inside, these cells find myelin proteins and launch an attack. Macrophages swarm in, eating away the insulation. Microglia, the brain’s own immune guards, get activated and start releasing inflammatory chemicals that make things worse. The result? Scar tissue, or plaques, form in patches across the brain and spinal cord. These are the lesions doctors see on MRIs.

Research shows this isn’t just one type of attack. There are four distinct patterns of damage seen in MS tissue. Some involve mostly T cells and macrophages. Others show heavy antibody deposits. One pattern even reveals dying myelin-producing cells without much inflammation. This complexity explains why MS affects people so differently.

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. The disease usually shows up between ages 20 and 40, though it can strike earlier or later. It’s not inherited like a gene disorder, but genetics do play a role. If you have a parent or sibling with MS, your risk goes up-though it’s still low overall.

Environmental triggers matter just as much. Epstein-Barr virus (EBV), the virus that causes mononucleosis, is the strongest known link. People who’ve had EBV are 32 times more likely to develop MS than those who haven’t. Vitamin D deficiency also increases risk-especially in people living far from the equator, where sunlight is weaker. Smoking doesn’t just harm your lungs; it doubles the chance of MS worsening over time. Even where you grew up matters. People who move from a high-risk area (like Canada or Scandinavia) to a low-risk one before age 15 lower their risk. Move after that, and your risk stays high.

The Symptoms You Can’t Ignore

Symptoms vary wildly because MS lesions can appear anywhere in the central nervous system. But some patterns show up again and again.

• Fatigue hits 80% of people with MS. It’s not just being tired. It’s a crushing, bone-deep exhaustion that doesn’t improve with rest.
• Vision problems often come first. Optic neuritis-swelling of the optic nerve-can blur vision, cause pain when moving the eye, or even lead to temporary blindness in one eye.
• Numbness or tingling in the face, arms, or legs is common. Some describe it like pins and needles, others say it feels like their limb is asleep.
• Walking difficulties affect nearly half of people with MS. Weakness, poor balance, or spasticity (muscle stiffness) make even short walks exhausting.
• Lhermitte’s sign is a telltale sign: a sharp electric shock running down your spine when you bend your neck forward. It’s caused by demyelinated nerves in the neck.

These symptoms don’t always stay. In relapsing-remitting MS (RRMS), which affects 85% of people at diagnosis, flare-ups come and go. A person might lose vision for a week, then recover fully. But each attack leaves behind some damage. Over time, recovery becomes less complete.

How MS Progresses-Relapsing vs. Progressive

There are two main types of MS progression. Most people start with RRMS. Flares last days to weeks, followed by periods of remission where symptoms fade or disappear. But even during remission, damage continues quietly. About half of untreated RRMS patients need a cane or walker within 15 to 20 years.

Then there’s primary progressive MS (PPMS), affecting 15%. No flares. No remissions. Just a steady, slow decline. Nerve damage accumulates without the inflammatory bursts seen in RRMS. This form is harder to treat because the immune system isn’t as visibly active.

The real tragedy isn’t the relapses-it’s the hidden neurodegeneration. Axons, the long wires that carry signals, start breaking down. Once they’re gone, they don’t grow back. That’s why disability gets worse over time, even if inflammation is controlled.

Current Treatments: Stopping the Attack

There’s no cure yet-but treatments have changed everything. Disease-modifying therapies (DMTs) don’t fix damaged nerves. They stop the immune system from attacking new ones.

Ocrelizumab, approved in 2017, targets B cells. It cuts relapses by 46% in RRMS and slows disability progression by 24% in PPMS. Natalizumab blocks immune cells from crossing into the brain. It’s powerful-reducing relapses by 68%-but carries a rare but deadly risk: progressive multifocal leukoencephalopathy (PML), a brain infection. That’s why doctors test for the JC virus before prescribing it.

Newer drugs like siponimod and cladribine work by trapping immune cells in lymph nodes or wiping out specific cell types. Each has trade-offs: effectiveness vs. side effects, convenience vs. monitoring needs.

The Hope: Repairing What’s Broken

The next frontier isn’t just stopping damage-it’s fixing it. Scientists are racing to find ways to rebuild myelin. One drug, clemastine fumarate, showed promise in early trials: patients improved their visual signal speed by 35%. That’s not just a lab result-it means better vision, faster reaction times, maybe even less fatigue.

Researchers are also looking at how to calm microglia and stop dendritic cells from presenting myelin as a threat. Neutrophil extracellular traps (NETs), sticky webs of DNA and toxins released by immune cells, are now known to damage the blood-brain barrier. Blocking them could be a new way to prevent attacks.

Blood tests for neurofilament light chain (sNfL) are becoming routine. Levels above 15 pg/mL mean active nerve damage is happening-even if the patient feels fine. This lets doctors adjust treatment before disability grows.

What Life With MS Looks Like Today

People with MS aren’t waiting for a miracle. They’re managing. Physical therapy keeps muscles strong. Cooling vests help with heat sensitivity. Medications for spasticity, bladder control, and depression are part of daily life. Many use mobility aids-not because they’re giving up, but because they’re staying active.

The stigma is fading. More workplaces offer flexibility. Online communities like Reddit’s r/MS are full of real stories: someone describing how they lost vision overnight, then regained it after steroids. Another talks about the terror of Lhermitte’s sign, then the relief of finding a brace that helps. These aren’t just anecdotes-they’re data points from real lives.

The message is clear: MS isn’t a death sentence. It’s a chronic condition that requires attention, but with modern tools, many people live full, active lives. The immune system may have turned traitor, but science is learning how to outsmart it.