Demüelination

Demüelination, more commonly spelled demyelination, is the loss or disruption of the myelin sheath that surrounds nerve fibers in the central nervous system (CNS) and/or peripheral nervous system (PNS). Myelin acts as an insulating layer that accelerates and stabilizes the transmission of electrical impulses along axons. When myelin is damaged, conduction becomes slower, unreliable, or blocked, and, with ongoing injury, axons may degenerate.

Causes and mechanisms vary. Demyelination can occur in autoimmune disorders such as multiple sclerosis (CNS) and chronic inflammatory demyelinating polyneuropathy (PNS). It can follow inflammatory infections, vascular injury, or ischemia, and may be seen in metabolic disorders, genetic leukodystrophies, or exposure to toxins. In many diseases, immune-mediated processes target myelin or oligodendrocytes (CNS) and Schwann cells (PNS), leading to focal or disseminated lesions.

Clinical features depend on the location and extent of demyelination. CNS involvement can produce visual disturbances, weakness, sensory changes, ataxia, or cognitive problems. PNS involvement often presents as symmetric or asymmetric numbness, tingling, weakness, or gait disturbances. Symptoms may occur in relapsing–remitting or progressive patterns, and some patients experience partial recovery with remyelination.

Diagnosis relies on a combination of clinical assessment and investigations. Magnetic resonance imaging (MRI) is central for CNS demyelination. Nerve conduction studies help distinguish demyelinating from axonal injury in the PNS. Cerebrospinal fluid analysis and evoked potentials can support diagnosis and monitor disease activity.

Treatment targets the underlying disorder and its inflammatory component, using immunomodulatory or immunosuppressive therapies, plasma exchange, or IV immunoglobulins in selective conditions. Rehabilitation and symptom management are important for functional recovery. Prognosis varies with disease type and extent of demyelination.