Multiple Sclerosis (MS) is a chronic condition that affects the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. The disorder is classified as an autoimmune disease, meaning the body’s own immune system mistakenly launches an attack against healthy tissue. This immune attack is characterized by a severe inflammatory response that is the core destructive mechanism of the disease. Consequently, inflammation is the central driving force in MS, initiating damage that leads to the neurological symptoms experienced by patients.
Multiple Sclerosis: An Autoimmune Attack on the CNS
The abnormal immune response in MS is directed specifically at components within the CNS. The primary target of this attack is the myelin sheath, a fatty, protective coating that insulates nerve fibers (axons) for rapid signal transmission. When the immune system attacks myelin, it causes demyelination, stripping away this protective layer. This immune-mediated destruction results in the formation of scar-like tissue, known as lesions or plaques, throughout the CNS. Damage to the myelin sheath and underlying axons slows or blocks nerve signal transmission, leading to the physical, mental, and sensory symptoms of MS.
The Cellular Mechanism Driving CNS Inflammation
The inflammation in MS begins when specific immune cells, primarily T-cells and B-cells, become activated in the peripheral circulation. These activated cells gain access to the CNS by breaching the blood-brain barrier (BBB), a highly selective membrane that normally protects the brain and spinal cord.
Once inside, these lymphocytes are reactivated and begin an inflammatory cascade, with T-cells recognizing myelin components as foreign and initiating the destructive process. They, along with B-cells and macrophages, release signaling molecules called cytokines. These highly pro-inflammatory cytokines, such as Interleukin-17 (IL-17), recruit more immune cells from the bloodstream, amplifying the attack. This perpetuates the cycle of inflammation, which directly damages the myelin and leads to the degeneration of the axons.
Acute Relapses Versus Chronic Inflammation
Inflammatory activity in MS manifests in two distinct patterns: acute relapses and chronic, low-level inflammation. An acute relapse, characteristic of relapsing-remitting MS (RRMS), is a sudden, intense burst of inflammation defined by new or worsening neurological symptoms lasting at least 24 hours. These attacks are associated with blood-brain barrier breakdown, visible on MRI as new or enhancing lesions. After the acute attack subsides, a period of remission follows where symptoms may partially or completely resolve.
However, a continuous, low-grade inflammatory process persists even during clinical remission. This chronic inflammation, often called “smoldering,” is driven by immune cells already residing within the CNS, such as activated microglia. This ongoing process contributes significantly to the progressive worsening of disability and causes neurodegeneration.
Therapeutic Strategies Targeting the Inflammatory Response
Because inflammation is the root cause of damage in MS, therapeutic strategies focus on modulating or suppressing the abnormal immune response. The primary goal of disease-modifying therapies (DMTs) is to reduce the frequency and severity of inflammatory attacks and slow the rate of chronic progression. These treatments work by targeting different aspects of the immune system.
DMTs function in several ways. Some act as immunomodulators, shifting the immune system toward an anti-inflammatory state. Others are immunosuppressants, broadly reducing the activity of immune cells like T-cells and B-cells, or block the migration of immune cells across the blood-brain barrier.
For acute relapses, high-dose corticosteroids (steroids) are commonly administered for a short course. These medications rapidly suppress the intense inflammation associated with the attack, helping to shorten its duration and severity.