Medical Articles
Most patients with GBS exhibit absent or profoundly-delayed conduction in action nerve fibres. This aberrant conduction results from demyelination of nerve cell axons. Peripheral nerves and spinal roots are the major sites of demyelination, but cranial nerves also may be involved.
GBS is believed to result from an autoimmune response, both humoral and cell mediated, to a recent infection or any of a long list of medical problems. Recovery is typically associated with remyelination. In a subset of patients, GBS is associated primarily with myelin-sparing axonal damage resulting from a direct cellular immune attack on the axon itself.
The acute inflammatory demyelinating polyneuropathy (ATDP) subtype of GBS is by far the most commonly identified form. It is generally preceded by an antecedent bacterial or viral infection. Nearly 40% of patients are seropositive for Campylobacter jejuni. Lymphocytic infiltration and macrophage-mediated demyelination of the peripheral nerves are present. Symptoms generally resolve with remyelination.
The acute motor axonal neuropathy (AMAN) subtype is a purely motor subtype, which is more prevalent amongst paediatric age groups. Nearly 70-75% of patients are seropositive for Campylobacter. One third of these cases may actually be hyperreflexic. AMAN is generally characterised by a rapidly progressive weakness, ensuing respiratory failure, and good recovery.
Acute motor-sensory axonal neuropathy (AMSAN) is an acute severe illness similar to AMAN except that AMSAN also affects sensory nerves and roots. Patients are typically adults with both motor and sensory dysfunction, marked muscle wasting, and poor recovery.
Acute panautonomic neuropathy involves both the sympathetic and parasympathetic nervous systems. Cardiovascular involvement is common, and dysrhythmias are a significant source of mortality in this form of the disease. The patient may also experience sensory symptoms. Recovery is gradual and often incomplete.
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