https://pubmed.ncbi.nlm.nih.gov/22336700/ Notably, 47% of participants reported long term fatigue on the questionnaires. Unfortunately, this wasn't a true prospective study, nor did they use objective measures of functioning or fatigue. Anecdotally, some post-GBS patients do suffer from PEM and clinically there is strong overlap with ME diagnoses.
A shorter-term study (median 6 year followup) https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1468-1331.2008.02311.x
https://emedicine.medscape.com/article/315632-overview I've said before, I see a lot of similarities between ME/CFS and GBS. I have not understood why ME/CFS is viewed so sceptically when GBS is acknowledged to exist. My symptoms occurred after a not particularly remarkable gastrointestinal illness. Numbness/pins and needles of my hands was a very marked symptom of the early months and it comes back when there is a flare. In the first year, I had occasional foot falls. When I was seen by an infectious diseases associate professor (a very experienced well-regarded doctor), quite some months into the illness, she was unable to find my knee reflexes. She tried really hard, had me doing distracting things, had me lying on my side... I think if they were there, she would have found them. She referred me to a neurologist, it took months to get an appointment. He of course found the reflexes and was very dismissive of everything, including the infectious diseases doctor and most certainly me. I have long thought the absence of reflexes might have been a clue. So, taken together with the fact that some people with GBS seem to stay fatigued, and Snow Leopard tells us that there are anecdotal reports of PEM, why can't ME/CFS be a variant of GBS?
GBS is characterised by severe paresis/paralysis that starts in the extremities, typically the legs, though sometimes the arms. Occasionally there is a facial variant. Foot drop associated with GBS is never 'occasional', but continuous and takes months to recover from (if there is full neurological recovery). What is notable however is the ongoing symptoms that are similar to ME/CFS, that are not explained by abnormalities in typical nerve conduction tests, similar to ME/CFS. (https://link.springer.com/article/10.1007/s00415-006-0962-9 etc) There have been a few authors who discuss the possibility of "sub-clinical" GBS and I sometimes wonder if that is what some people with ME/CFS diagnoses really had? I also wonder about whether the symptoms are perpetuated by ongoing neuropathy, such as single-fibre neuropathy. I know that Jonathan Edwards recently remarked about the association of SFN with Fibromyalgia not explaining the symptoms (he suggested the neuropathy would lead to lower sensitivity), but different types of single fibre neuropathies are possible, depending on the tissue type. There is also the possibility that it is not a reduction in nerve fibres that is the problem, but that some nerve fibres that recovered could have become sensitised (or even to other stimuli) in the process. On the topic of tachycardia or orthostatic intolerance, authors have proposed a different mechanism to that typical of POTS: "Correlation analysis suggested that tachycardia in the context of GBS might be caused by a reduction of sympathetically mediated peripheral vascular tone rather than by vagal failure." https://onlinelibrary.wiley.com/doi/abs/10.1002/ana.410420207
