Pathophysiology and Variant Forms

The pathophysiology of GBS is thought to be an autoimmune response against peripheral nerve components namely the myelin sheath (causing AIDP) OR the axonal membranes (causing AMAN/ AMSAN)

The most common variant bilaterally affects motor and sensory nerves.

The key findings in GBS are profoundly-delayed conduction in nerve fibres, secondary to axonal demyelination. This occurs primarily in peripheral nerves and spinal roots, but may affect cranial nerves as well.

There is growing evidence that, at least in some cases, GBS is caused by an aberrant immune response to an infective trigger.


Subtypes include:

  • Acute inflammatory demyelinating polyneuropathy (AIDP). A subtype of GBS that has both sensory and motor symptoms. This is the most common form in the USA and western Europe
  • Acute motor axonal neuropathy (AMAN). This is a purely motor presentation, and more prevalent in children
  • Acute Sensorimotor Axonal Polyneuropathy (AMSAN).
  • Miller Fisher syndrome.¬†This is a clinical variant of AIDP that is most commonly seen in the far east.
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