A cross-reaction between peripheral nerve antigens and microbial/viral components through molecular mimicry is thought to drive the inflammatory process of this illness. MFS and GBS are thought to result from an aberrant acute autoimmune response to a preceding infection (e.g., Campylobacter jejuni, Cytomegalovirus, Epstein-Barr virus, or human immunodeficiency virus (HIV). Miller Fisher later characterized it in 1956, classifying it as a unique entity within the GBS spectrum. James Collier first discovered the variant in 1932 and described it as a triad of symptoms including ophthalmoplegia, ataxia, and areflexia.
The focus of our review will be the Miller Fisher syndrome (MFS), a rare variant of GBS. Acute, immune-mediated demyelinating polyneuropathies (AIDP) are classified within the spectrum of Guillain-Barre syndrome (GBS), named after the French physicians who discovered it. Demyelinating neuropathies include toxic, hereditary, and immune-mediated etiologies the latter can be further be classified as acute and chronic depending on the onset. Schwann cells are glial cells that play an important role in the peripheral nervous system including saltatory conduction of nerve impulses along axons, nerve development and regeneration, modulation of neuromuscular synaptic activity, and presentation of antigens to T lymphocytes. Demyelinating neuropathies produce abnormalities because Schwann cells do not interact appropriately with axons. Axonal neuropathies cause symptoms related to axon damage and loss and are caused by a broad number of systemic illnesses.
Polyneuropathies are dysfunction in multiple nerves and divided into 2 broad categories: axonal or demyelinating.
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