Talk:Guillain–Barré syndrome

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"a result of an acute polyneuropathy"

--  I have found several sources that call this a "polyradiculopathy"  

L - Landry-Guillain-Barré Syndrome (GB) or Acute Inflammatory Demyelinating Polyradiculopathy to Local Anesthetic Pharmacology pp. 387-397 By May C. M. Pian-Smith and Lisa Leffert. — Preceding unsigned comment added by Tmbirkhead (talkcontribs) 04:33, 8 January 2015 (UTC)


"These two treatments are equally effective"

 No problem with this

"and a combination of the two is not significantly better than either alone."

 Big problem with this

I had Guillain-Barre (and 100% recovery, thank goodness) and received both treatments. It is very important to realize that the two treatments are completely incompatible. That is, they absolutely cannot be administered simultaneously, but if administered consecutively, the end result can be superior to just using one of them (or not). With intravenous immunoglobulins (aka IVIG) you are getting other people's white blood cells, in the hope that it makes your own white blood cells behave themselves, as opposed to what they are doing (destroying your peripheral nervous system's myelin sheath). With plasmapheresis, on the other hand, (almost) all of your white blood cells are being removed from your blood, in the hope that the new white blood cells generated by your system (bone marrow) will behave themselves. Stay with me here, either you are getting a whole bunch of extra white blood cells, or you are losing a whole bunch of the white blood cells you already have. You cannot do both at the same time, don't you agree? The idea is to (a) use IVIG to shock the system into some kind of stability, although it is not a cure then (b) once stability but not cure is achieved, to use plasmapheresis to effect a cure. At least, that is what my doctors told me they were doing. And it worked. So my experience is that IVIG, followed by plasmapheresis, *is* significantly better than either alone. Not too sure what to do about providing a reference. IVIG is extremely expensive, so may not be an option in every health-care context. Plasmapheresis is, essentially, just a form of dialysis, so it is not that expensive and should be generally available. — Preceding unsigned comment added by Gsa703 (talkcontribs) 19:09, 7 October 2013 (UTC)

Very nice that the combination worked for you. We prefer to base wikipedia on scientific research. The immunoglobulins are way smaller particles than white blood cells, so plasmapheresis of just the white blood cells (and not the plasma fluid with the ivig in it) can be done simultaneosly to ivig administration. But if you're convinced otherwise, please provide scientific sources that contradict the currently used reference. PizzaMan (♨♨) 15:22, 11 December 2014 (UTC)


This section does not appear to have rigorous references.

"Recovery usually starts after the fourth week.."

I had Guillain-Barre. My experience with my doctors was that my recovery time was a direct reflection of my time-to-diagnosis. That is, the sooner I was diagnosed, the less my recovery time. In my case, I was diagnosed in about 50 hours and had a recovery time of about 50 weeks. So one week for every hour until diagnosis (and treatment).

That said, let's talk about when recovery starts. Presumably that means when things start stabilizing. Again, I suggest that it totally depends upon how fast the patient gets to a knowledgeable physician. In my case, I think my recovery started after the second week, but that is not a reflection of Guillain-Barre, nor of the physician, but solely of how fast I noticed that I had a problem, and did something about it.

"About 80% of patients have a complete recovery.."

Where does this come from? My doctors said that 98% of patients have a recovery in which there are no long-term disabilities, such as having to use a cane, or a walker, or take medication, etc. Aside from the fact that I should probably not donate blood, I have zero effects upon my well-being from having had Guillain-Barre. — Preceding unsigned comment added by Gsa703 (talkcontribs) 19:39, 7 October 2013 (UTC)

I've added a reference and a little bit of text based on the reference. Note that the reference doesn't support the statement of recovery starting after four weeks. As for the 98%, that's a bit optimistic. For example: "Among severely affected patients, 20% remain unable to walk 6 months after the onset of symptoms." (NEJM 2012). Unfortunately, the appendix doesn't contain the prognostic models it's supposed to when i try to download. And you're right that the onset of therapy is a prognostic factor: "Days between onset of weakness and admission, Medical Research Council sum score, and presence of facial and/or bulbar weakness were the main predictors of mechanical ventilation" (Walgaard, Ann Neurol. 2010).PizzaMan (♨♨) 15:41, 11 December 2014 (UTC)

Distinguishing between Gilbert and Guillain–Barré Syndromes[edit]

I feel that it would be a good idea to add a "not to be confused with" label at the top of the page to distinguish between Gilbert's and Guillain–Barré syndromes. The latter is often pronounced like "gillie-bear" while Gilbert's is sometimes pronounced "jill-bear" (apologies for the bad formatting), opening up the possibility of people looking at the incorrect article, so I'm going to add a tag to both articles. I leave this section open to discussion of the topic as both can be confusing to spell given their non-English etymologies. Zedtwitz (talk) 02:32, 18 February 2014 (UTC)

I really doubt that anyone will make the confusion, because Gilbert is one name, and "Guillain-Barré" is always used together. Wikipedia:Hatnote describes the guidance. JFW | T@lk 14:25, 20 February 2014 (UTC)

Why are the H1N1 vaccine cases not included in the cause section?[edit]

I recently added info and links from a 2009 study of H1N1 influenza vaccines and had it removed citing a link supposedly 'fisking' the ones I provided. Why are recent studies not included in this article? It's currently dated to be archaic (1977?, really?). Editing is still new to me, so please help modify the cause section to include recent info.

I removed the sources because they did not meet the criteria outlined in WP:MEDRS; we prefer secondary sources in high-quality publications. I am particularly worried by the reference to MCT lawyers - this is a no-win no-fee outfit, and their content is not peer reviewed. JFW | T@lk 19:26, 30 June 2014 (UTC)

Guillain-Barre Syndrome Notable Cases[edit]

This help request has been answered. If you need more help, you can ask another question on your talk page, contact the responding user(s) directly on their user talk page, or consider visiting the Teahouse.

Discussion closed for archiving. JFW | T@lk 15:54, 29 October 2014 (UTC)


The classification of GBS has been revised. doi:10.1038/nrneurol.2014.138 discusses it. JFW | T@lk 12:32, 29 October 2014 (UTC)

Epidemiology papers: doi:10.1159/000184748 (2009) and doi:10.1159/000324710 (2011); different approaches and probably both worth citing.
Association with vaccines: doi:10.2165/00002018-200932040-00005 (2009) and doi:10.7774/cevr.2014.3.1.50 (2014). JFW | T@lk 09:10, 30 October 2014 (UTC)
Brighton criteria were brought about by vaccine worries: doi:10.1016/j.vaccine.2010.06.003 JFW | T@lk 23:54, 30 November 2014 (UTC)


This article has needed tidying up for some time.

  1.  Done Signs and symptoms - needs to be more detailed on the clinical distinction between subtypes
  2.  Done Causes - currently not written; this needs to list the common infectious triggers (chlamydia, campylobacter, herpesviruses, mycoplasma)
  3.  Done Mechanism - needs updating in general, especially with some discussion about the serological signals
  4.  Done Diagnosis - better sourcing for the importance of each test
  5.  Done Treatment - good sources are available, need more about the rehabilitation aspects
  6.  Done Prognosis - recently some information added, although some more QOL information would be valuable
  7.  Done Epidemiology - vaccine triggers should be discussed here discussed under "causes" instead
  8.  Done History - good secondary sources exist for this
  9.  Done Notable cases - should be migrated to its own subarticle
  10.  Done Research directions - we may need to talk about eculizumab
  11.  Done References
  12.  Done Further reading - should be integrated in the content; the book listed there currently is a good candidate for this section
  13.  Done External links - should be minimalist


Will try to do some stuff here. Help appreciated as always. JFW | T@lk 00:00, 2 November 2014 (UTC)

I've got that book "Guillain-Barré:From diagnosis to recovery". I'll get more info up and cite it. Let me know if/when I do that incorrectly? Regards,  Aloha27 talk  13:24, 3 November 2014 (UTC)
Review in children (in addition to Ryan2013). I have no access: doi:10.1542/pir.33-4-164 JFW | T@lk 08:43, 1 January 2015 (UTC)


Epidemiology[edit] In Western countries, the incidence (number of episodes per year) per 100,000 people has been estimated to be between 0.89 and 1.89 cases. The risk increases by 20% for every decade.[29]

My concern is that the sentence "The risk increases by 20% for every decade" could be misinterpreted to mean that the risk of GBS is increasing with every decade for the population as a whole, rather than as the age-related increase observed. The cited study says that "GBS incidence increased by 20% for every 10-year increase in age." [1]

I've not done any editing on Wikipedia, which is why I'm commenting rather than editing myself. Wikimol03 (talk) 06:02, 5 December 2014 (UTC)

Thanks Wikimol03. I will rephrase. Always feel free to change something yourself; great articles come about because folk like yourself are BOLDly updating pages. JFW | T@lk 21:11, 6 December 2014 (UTC)

Acute autonomic neuropathy[edit]

I removed the following:

  • Acute panautonomic neuropathy is the rarest variant of GBS, sometimes accompanied by encephalopathy. It is associated with a high mortality rate, owing to cardiovascular involvement, and associated dysrhythmias. Frequently occurring symptoms include impaired sweating, lack of tear formation, photophobia, dryness of nasal and oral mucosa, itching and peeling of skin, nausea, dysphagia, and constipation unrelieved by laxatives or alternating with diarrhea. Initial nonspecific symptoms of lethargy, fatigue, headache, and decreased initiative are followed by autonomic symptoms including orthostatic lightheadedness, blurring of vision, abdominal pain, diarrhea, dryness of eyes, and disturbed micturition. The most common symptoms at onset are related to orthostatic intolerance, as well as gastrointestinal and sudomotor dysfunction.[2] Parasympathetic impairment (abdominal pain, vomiting, constipation, ileus, urinary retention, dilated unreactive pupils; loss of accommodation) may also be observed.

The reason for this removal is the fact that none of the reviews (NEJM2012, NatRevNeurol2014 and others) mention it as a GBS subtype, and doi:10.1136/jnnp-2012-302833 states that inclusion is "disputed". A very recent classification system (still need to cite) by Wakerley et al does not include it (doi:10.1038/nrneurol.2014.138). I am happy to be corrected, but for now I will stick to the classifications introduced by the key sources. JFW | T@lk 22:06, 7 December 2014 (UTC)

Babinski in Bickerstaff[edit]

Thanks to user:TylerDurden8823 for the contribution. But why remove babinski reflexes from the Bickerstaff symptoms? That's not just a decreased reflex. PizzaMan (♨♨) 08:17, 12 December 2014 (UTC)

The source I saw describing BBE did not mention Babinski at all. If you have a source for Bickerstaff that mentions Babinski sign (not a symptom but a medical sign), feel free to add it back in. I didn't think that was something a major review would gloss over and if it were really a prominent feature of BBE, I figured the Nature Review would probably have at least mentioned it once. I'm not opposed to adding it back in though if you or someone else can demonstrate it is part of BBE with a reputable source. TylerDurden8823 (talk) 13:48, 12 December 2014 (UTC)
Recent reviews point out that hyperreflexia may occur in the early stages of all cases. I don't think Bickerstaff's is unique. JFW | T@lk 15:32, 12 December 2014 (UTC)
So, we don't need to mention it specifically then for BBE? TylerDurden8823 (talk) 22:48, 12 December 2014 (UTC)
Very interesting for a disease of the peripheral nervous system. And so would a babinski be, because that's typically caused by a damaged piramidal tract. But yes, in that case it should be mentioned in general then in stead of specifically with Bickerstaff. JFW, can you point us to one of those reviews? Again, TylerDurden8823, thank you for contributing to this article. PizzaMan (♨♨) 13:29, 13 December 2014 (UTC)
PizzaMan The finding of hyperreflexia is already mentioned in "Signs and symptoms". The NEJM2012 and NatRevNeurol2014 sources do not actually mention abnormal plantar reflexes, so perhaps that finding is unique to BBE. JFW | T@lk 20:22, 13 December 2014 (UTC)
If we do find a good review that does specifically mention this, I have no objection to saying that Babinski is part of BBE. I just want to see verification. TylerDurden8823 (talk) 22:39, 13 December 2014 (UTC)

Guillain-Barré mechanism[edit]

The cited NEJM article and 15 July 2014 Nature Neurology review on Guillain-Barré by van den Berg et al. states that BOTH AMAN and AIDP are caused by antibody formation, albeit directed towards different peripheral nerve targets. AIDP is less well characterized, but involves antibodies formed against unidentified antigens of the Schwann cell itself. AMAN is caused by antibodies against GM1 and GD1a gangliosides located in the node of Ranvier. These antibodies are formed via molecular mimicry from Campylobacter lipo-oligosaccharide outer membrane. Please see Figure 2 in the cited NEJM article or Figure 2 in the Nature review.

Nature Reviews Neurology 10, 469–482 (2014) doi:10.1038/nrneurol.2014.121 Published online 15 July 2014 — Preceding unsigned comment added by (talk) 15:57, 2 May 2015 (UTC)

The NEJM review uses guarded language ("autoantibodies may bind to myelin antigens") and in the text itself does not mention the antibodies nor their possible epitopes. The van den Berg review similarly is vague on this (apart from discussing anti-GM2 in CMV infections). I will have a look at the wording. Presumably someone has tried to demonstrate the actual presence of IgG on the myelin sheath, but the reviews don't cite this evidence. Thanks for bringing this up. JFW | T@lk 21:40, 23 June 2015 (UTC)

Another push[edit]

So, having some time available, I might just be able to finish the work on this and get it nominated for GA:

  •  Done Address the point of the anonymous editor in the previous section
  •  Done Finish the "neurophysiology" section with sources listed above (Uncini in particular) - a neurology colleague has explained the key points of NCS/EMG
  •  Done "Citation needed" in "clinical subtypes" with regards to Bickerstaff
  •  Done Complete the "rehabilitation" section, replacing the content that is based on primary sources.
  •  Done In "prognosis", incorporate the HRQL discussion from doi:10.1111/jns5.12051
  •  Done In "prognosis", address the "citation needed" tags

Help appreciated as always. JFW | T@lk 20:54, 22 June 2015 (UTC)

possible references[edit]

Brain human normal inferior view

I would also recommend this image in symptoms section as half of those affected experience cranial nerve involvement perhaps these can help--Ozzie10aaaa (talk) 22:18, 25 June 2015 (UTC)

@Ozzie10aaaa: I wasn't planning on adding more sources, and you will find that I've referenced the relevant Cochrane reviews. JFW | T@lk 18:26, 26 June 2015 (UTC)


  1. ^
  2. ^ Suarez, G. A.; Fealey, R. D.; Camilleri, M.; Low, P. A. (1 September 1994). "Idiopathic autonomic neuropathy: Clinical, neurophysiologie, and follow-up studies on 27 patients". Neurology 44 (9): 1675–1675. doi:10.1212/WNL.44.9.1675. PMID 7936295.