In patients with multiple sclerosis, the immune responses trigger activation of immune cells such as T and B cells, CD4+ helper T-cells that cross the blood-brain barrier.
These cells activate autoantigens that produce an auto-immune cytotoxic effect within the central nervous system (CNS).
👉👉 Phagocytic activity of macrophages May contributes to the demyelination of neurons.
An acute inflammatory event occurs.
Edema and infiltrates (e.g., monocytes, macrophages, and microglia) surround the acute lesion and cause abnormally increased pressure that further interfere with the conductivity of nerve fibers.
During, the early stage of multiple sclerosis oligodendrocytes survive and produce remyelination.
As the disease becomes chronic the oligodendrocytes become involved and myelin repair cannot occur.
Demyelinated areas are filled with fibrous astrocytes and undergo a process called gliosis.
Gliosis is a proliferation of neuroglial tissue within the central nervous system and results in glial scars (Plaque).
This is the main cause of permanent neurological disability.
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