GUILLAIN BARRE SYNDROME (GBS)-PATHOLOGY

From NeuroRehab.wiki

SUMMARY

1. Inflammatory demyelinating polyradiculopathy: GBS is thought to result from an immune response to a preceding infection that cross-reacts with peripheral nerve components because of molecular mimicry.

2. The immune response can be directed towards the myelin or the axon of peripheral nerves, resulting in demyelinating and axonal forms of GBS.

3. Inflammation and demyelination result in varying degrees of axonal degeneration, and neurapraxia is prominent.

4. Campylobacter jejuni infection is the most commonly identified precipitant of GBS. Cytomegalovirus (CMV), Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), and Zika virus have also been associated with GBS.

5. CMV & Campylobacter jejuni have been implicated in the axonal form of GBS.


Reference(s)

Wilkinson, I., Furmedge, D. and Sinharay, R. (2017). Oxford handbook of clinical medicine. Oxford: Oxford University Press. Get it on Amazon.
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Therapeutic Guidelines. Melbourne: Therapeutic Guidelines Limited. https://www.tg.org.au [Accessed 2021].