Guillain–Barré syndrome post stroke: Two case reports

Guillain–Barré syndrome (GBS) is the most common and most severe acute paralytic neuropathy. There are different variants of GBS with distinct clinical and pathological features. Most GBS cases are preceded by infection or other immune stimulation that induces an aberrant autoimmune response targeting peripheral nerves and their spinal roots. Molecular mimicry between microbial and nerve antigens is clearly a major driving force behind the development of the disorder, at least in the case of Campylobacter jejuni infection. Some patients have been developing GBS either following or concomitant with head trauma, neurosurgical procedures, and rarely following stroke. The exact mechanism is not well understood probably blood–brain barrier damage may play an essential role in triggering the autoimmune activation that leads to post-stroke GBS.