Multiple Sclerosis is a chronic, immune-mediated disease where the body’s defense system incorrectly attacks the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. This inflammatory process damages structures within the CNS, producing the varied symptoms associated with the condition. The disease is thought to develop in individuals with a genetic predisposition following a trigger from one or more environmental factors.
The Autoimmune Attack
In MS, the immune system fails to recognize its own components, a concept known as autoimmunity. This loss of self-tolerance leads to a targeted inflammatory response against healthy parts of the central nervous system. While the precise trigger for this process has not been identified, the resulting cascade of immune activity is well-documented.
The attack is orchestrated by specific types of white blood cells called lymphocytes, primarily T-cells and B-cells. Normally, T-cells identify and destroy infected cells, while B-cells produce antibodies that neutralize pathogens. In MS, certain T-cells become activated in the lymphatic system and are programmed to recognize components of the central nervous system as threats.
Once activated, these T-cells interact with and stimulate B-cells, prompting them to mature and produce antibodies that also target the CNS. Furthermore, B-cells can present antigens to T-cells, effectively amplifying and sustaining the immune response.
This coordinated effort results in a multifaceted attack. The activated T-cells release chemicals that promote inflammation, while the antibodies produced by B-cells can bind to their targets, marking them for destruction. The attack persists because regulatory T-cells, which are supposed to suppress inflammation, do not function correctly.
Breaching the Central Nervous System
The brain and spinal cord are protected by a highly selective border known as the blood-brain barrier (BBB). This barrier is formed by endothelial cells lining the blood vessels and is designed to prevent harmful substances and most immune cells from entering the central nervous system. The BBB’s integrity is one of the first structures to be compromised in MS.
The breakdown of this protective wall is initiated by the same activated T-cells that lead the autoimmune attack. As these T-cells circulate, they release inflammatory chemicals called cytokines. These cytokines signal the endothelial cells of the BBB, causing them to become “leaky” by disorganizing the tight junctions that hold them together.
This increased permeability is a key event in the disease’s progression. The breach allows activated T-cells, B-cells, and the antibodies they produce to migrate from the bloodstream into the brain and spinal cord tissue, initiating the localized damage that characterizes MS lesions.
Demyelination and Axonal Damage
Once inside the central nervous system, immune cells attack their primary target: a fatty substance called myelin. Myelin forms a protective, insulating sheath around nerve fibers, known as axons. This covering can be compared to the insulation on an electrical wire; it protects the axon and increases the speed and efficiency of electrical signal transmission.
The process where immune cells destroy this protective layer is called demyelination. Infiltrating T-cells release chemicals that cause inflammation, while antibodies produced by B-cells bind to the myelin sheath, marking it for destruction by other immune cells. This inflammatory assault strips the myelin away, leaving the underlying axon exposed. The sites where this occurs form hardened scars, or scleroses, which give the disease its name.
The body has a capacity to repair damaged myelin through a process called remyelination, but this repair is often incomplete. The new myelin sheath is thinner and less effective, and repeated attacks can overwhelm the cells responsible for the repair, known as oligodendrocytes. Eventually, these repair cells can be destroyed, halting the remyelination process.
The damage is not always confined to the myelin sheath, as prolonged inflammation can also directly harm the axon itself. Axons can be cut within the inflammatory lesions, and unlike myelin, they have a very limited ability to regenerate. This axonal damage is a contributor to permanent neurological disability.
Disruption of Nerve Signals
The loss of the myelin sheath has immediate consequences for nerve function. In a healthy nerve, electrical impulses leap rapidly from one gap in the myelin to the next, ensuring swift communication. When demyelination occurs, this efficient pathway is destroyed. The nerve signal slows down, becomes distorted, or may be blocked completely.
These areas of damage and the resulting scar tissue, or lesions, further impede the flow of electrical signals along nerve pathways. The central nervous system can sometimes reroute nerve signals around damaged areas, an ability known as plasticity. However, this compensation is often not enough to fully restore function, and messages may still be delayed.
The specific symptoms experienced by an individual with MS are entirely dependent on where these lesions occur within the central nervous system. If the optic nerve is affected, a person might experience vision problems. Damage in the spinal cord can lead to muscle weakness or numbness, while lesions in the brain can affect balance, coordination, and cognitive functions.