What is the Difference Between Transverse Myelitis and Guillain Barre Syndrome?

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Transverse myelitis (TM) and Guillain-Barré syndrome (GBS) are both immunologically mediated polyneuropathies, but they have distinct differences in their clinical manifestations and characteristics.

Transverse Myelitis:

  • Characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction.
  • Inflammatory disorder affecting the spinal cord.
  • Clinical signs are caused by an immune-mediated process.
  • Incidence of 1 to 8 new cases per million per year.

Guillain-Barré Syndrome:

  • Characterized by progressive weakness, autonomic dysfunction, and pain.
  • Acute inflammatory immune-mediated polyradiculoneuropathy.
  • Immune injury specifically takes place at the myelin sheath.
  • Incidence of 1 to 4 new cases per 100,000 per year.

Both conditions are thought to have a genetic predisposition and are considered autoimmune, although their etiologies remain enigmatic. They can be triggered by infectious agents and vaccines, and both can be diagnosed through nerve conduction tests and treated through immunotherapies.

Comparative Table: Transverse Myelitis vs Guillain Barre Syndrome

Here is a table comparing the differences between Transverse Myelitis (TM) and Guillain-Barré Syndrome (GBS):

Feature Transverse Myelitis (TM) Guillain-Barré Syndrome (GBS)
Definition TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. GBS is a form of paralysis caused by inflammation of the peripheral nerves.
Neuro-inflammation Inflammation: The clinical signs are caused by an inflammatory disorder. Inflammation: Perinodal and/or patchy demyelination, perivascular focal lymphocytic infiltration of T cells, myelin swelling, and the presence of macrophages within the nerve fibers are typical findings in GBS.
Symptoms Sensory, motor, and autonomic dysfunctions as a result of immune-mediated spinal cord injury. Symptoms include: weakness, paralysis, and sensory abnormalities, such as numbness, tingling, and pain.
Causes TM is thought to have a genetic predisposition and may be induced via molecular mimicry. GBS is thought to have a genetic predisposition and has an unknown etiology in a substantial portion of cases.
Treatment Treatment for TM is not well defined in the provided search results. Treatment for GBS may include intravenous immunoglobulin or plasmapheresis.

Both TM and GBS are immunologically mediated polyneuropathies of major clinical importance, and both are considered autoimmune, but their etiologies remain enigmatic.