Multiple Sclerosis (MS) is a chronic condition of the central nervous system (CNS) that targets the brain and spinal cord. The fundamental process driving this disease is a misdirected inflammatory response. Inflammation in MS is the core biological activity that causes damage to nervous tissue and underlies the symptoms experienced by patients. This destructive inflammation is initiated by the body’s own immune system, which mistakenly identifies components of the CNS as foreign invaders. The disease course and severity are directly linked to the intensity and location of this inflammatory activity within the CNS.
The Immune System Attack on the Central Nervous System
Multiple Sclerosis is classified as an autoimmune disorder, meaning the immune system launches an attack against the body’s own tissues. This attack begins when specialized white blood cells, primarily T-lymphocytes and B-lymphocytes, become activated in the peripheral immune system. These activated immune cells are programmed to attack the myelin sheath, the fatty protective layer that insulates nerve fibers, or axons, in the brain and spinal cord.
To initiate the inflammatory cascade, these lymphocytes must first breach the blood-brain barrier, a highly selective membrane that normally protects the brain. Once inside the CNS, T-cells and B-cells release pro-inflammatory signaling molecules called cytokines, activating resident immune cells.
T-cells directly attack the myelin sheath, while B-cells contribute to the damage by producing antibodies and amplifying the inflammatory signals. This localized inflammation results in the formation of focal lesions, or plaques, which are areas of active immune infiltration and tissue destruction. This process makes MS an active disease state.
Acute Attacks Versus Chronic Inflammation
The inflammation in Multiple Sclerosis manifests in two distinct patterns. Acute inflammation is the characteristic feature of relapses, often seen in the relapsing-remitting form of MS. This pattern involves sudden, intense immune cell infiltration and the formation of new, localized inflammatory lesions within the white matter. These acute attacks cause the sudden onset of new or worsening neurological symptoms.
In contrast, chronic inflammation is a low-grade, persistent process that occurs even without an acute relapse. This smoldering inflammation is often found in the deeper gray matter and the rims of older lesions, known as chronic active lesions. These lesions are characterized by a persistent presence of activated immune cells, particularly microglia, the brain’s resident immune cells, at their edges.
The progressive forms of MS, where disability steadily accumulates, are linked to this persistent inflammation. While acute inflammation drives the relapses, the ongoing chronic inflammation contributes to the long-term, irreversible degeneration of nervous tissue.
Consequences of Inflammation
The inflammatory response in the CNS leads directly to physical damage that disrupts nervous system signaling. The immediate consequence of the immune attack is demyelination, the stripping away of the myelin sheath from the nerve fiber. Without this insulation, electrical impulses traveling along the axon are slowed, distorted, or blocked, leading to neurological dysfunction.
The persistent inflammatory environment also results in damage to the nerve fiber itself, a process known as axonal loss. Unlike myelin, axons have a limited capacity for regeneration. Axonal loss is considered the primary driver of long-term disability accumulation in MS, even without acute relapses.
The body attempts to repair the damage by creating scar tissue, a process called gliosis, which further impedes signal transmission. This physical damage—demyelination, axonal loss, and gliosis—translates into common neurological symptoms of MS. These symptoms include muscle weakness, difficulty with balance and coordination, and visual impairment.
Targeting the Inflammatory Response
Current therapeutic strategies for Multiple Sclerosis focus on reducing the inflammatory response. Disease-Modifying Therapies (DMTs) aim to modulate or suppress the overactive immune system to halt the destructive process. These treatments seek to reduce the frequency and severity of inflammatory attacks and slow the accumulation of disability.
The mechanisms of action for DMTs fall into general categories, all focused on disrupting the inflammatory cascade. Some therapies prevent T-cells and B-cells from leaving the lymph nodes or block their ability to cross the blood-brain barrier and enter the CNS. Other treatments reduce the overall number of circulating immune cells or suppress their inflammatory activity.
By interfering with the movement or function of the immune cells, these therapies reduce inflammation in the CNS. This limits the resulting demyelination and axonal damage, dampening the destructive autoimmune response.