Help – Pain / Weight lost surgery
AnonymousJune 6, 2006 at 9:54 pm
I need some help. I got GBS in January 2005. Well that is what the Doctor told me I had. I am doing a documentary with a TV station in Canada CBC.
The lady that is working on my story told me that I don’t have GBS but some other kind of nerve problem. She was told by a doctor in the USA that BGS patient don’ t have pain.
So please let me know did you have pain with your GBS?
Also I got weight lost surgery in October of 2004, and the new people think that I got GBS or this other nerve problem because of the surgery. So if any of you GBS patient have had weight lost surgery please email me back.
This Documentary that I am doing will be my second, I also did one with the local CBC in Saskatchewan, Canada. This is the link if you would like to see the documentary
Again Thank you for your Help
AnonymousJune 6, 2006 at 10:20 pm
First Welcome to the Forums.
Second that lady has no idea what she is talking about. Just read through all the stories here and you will see how many have severe chronic pain. If she wants the truth tell her to log in here, we’ll all tell her stories that will make her head spin about GBS. I don’t know what idiot Dr told her that but if she’s a good reporter she should do her homework before making a statement like that. I get so upset by people who don’t get their facts correct and then tell other people they don’t have GBS because with GBS there is no pain. Seriously tell her to come here to get the facts from the veterans of GBS.
Yes, you could have developed GBS from the surgery. You can develope GBS from any surgery, dental work, any vaccine,food poisoning, any illness, even a simple cut on your finger can trigger your immune system to go into overdrive and cause GBS.
I wish you the best in your endeavor to get the correct story out to the people. Take care. 🙂
AnonymousJune 6, 2006 at 11:16 pm
Welcome the this growing and wonderful group.
Pain is an issue for many during GBS, in recovery and “post” GBS.
Many including myself have had expreience with neuoroligist indicating that we should be better. But we really are not better. Here is an article that gives support to the residual fatigue and pain.
Residual fatigue & pain is finally documented thx to dr. parry
here is a link to that article..
Just let me or others know if there is anything else you need.
Much success in you TV show.
AnonymousJune 7, 2006 at 5:05 am
Marie France I all for your story to be on the CBC network but make sure she gets her facts straight. We need the public to hear about GBS and CIDP but only if it’s the full truth and not the half truths. Maybe she should talk to your DR who diagnose you and if you have the foundation package and newsletter discribing post GBS symptom show her that.
AnonymousJune 7, 2006 at 8:18 am
Firstly, let me say that I am so sorry for what you are going through at the moment. I am so angered by what the stupid woman working on your story told you. I say stupid, because that is exactly what she is. I cannot believe she can possibly think she even knows what she is talking about, and mind you, I cant believe Im getting so upset about it. We have enough problems with ignorant medical workers, to throw other ignorant people in the mix doesnt help us at all. You may, or may not have GBS, but it is not for her to give you a diagnosis.
You are in my thoughts, and please do keep us updated on what is happening. 🙂
AnonymousJune 7, 2006 at 1:05 pm
Bienvenu Marie-France, 🙂
I actually encountered an Occupational Therapist while I was in hospital for my six month stay due to head to toe paralysis who kept telling me that none of her “other” GBS patients had had pain. It made my life more difficult than it needed to be. I most definately had GBS and I most definately had pain, more pain than there are words to describe. Pain is the rule with GBS to not have pain is more the exception but it is all dependant upon whether sensory nerves have been damaged in the GBS attack. I don’t think there are any words invented in the English language to describe the pain of GBS. Please tell the reporter from the CBC that for the first three months I was in hospital I could not take the weight of an ordinary cotton hospital sheet on my feet the pain was so intense, and when I needed it most I couldn’t stand my family members to touch me or hold my hand, it was out of the question as the pain was just too much. Like many other surviors here, I will have chronic pain for the rest of my life because of the permanent neurological damage GBS left me with. A quick search on “Google” using the key words “Guillain-Barre Syndrome+Pain” should bring many articles to light for the reporter to research………
GBS has been known to follow surgery, viral infections, bacterial infections, childbirth, vaccines, I just read an article that conclusively linked the development of GBS in one patient to heat stroke…….:eek: For most of us our source of GBS is idiopathic in that no one can conclusively say what brought it on at all…………in short anything that makes your immune system dysfunction could potentially bring about GBS……
my very best wishes to you, and good luck with the CBC……..:)
AnonymousJune 7, 2006 at 2:09 pm
My Fiance’s primary care physican told us that sensory nerves aren’t damaged in GBS. Whatever!! :rolleyes: It seemed those were the first affected.
The best source of info I have found is the book sent by the foundation. Even the Nurses in the hospital were borrowing it to read up on. Plus just google-ing the terms Guillian Barre with words like pain, numbness etc brings back alot of information as well.
The number one thing is to not let people generalize your condition like that. As anyone here can tell you every single person is different with GBS. The signs, symptoms, treatments and recovery will vary from person to person.
AnonymousJune 7, 2006 at 4:06 pm
Your artical said you got GBS within weeks of gastric bypass surgery. Above, you state 3 months. Which is it? It’s that you had surgery, not the type of surgery, that triggers GBS. I’m surprised, that so little is known about GBS from the medical people around you. Open one med book, or punch up an artical on the internet, and most of the basics are covered, like pain. Sounds like GBS was never determined forsure. Don’t ever go by, or take to heart what any layperson says on this subject.
CG-It’s ‘conclusive’ that a person got GBS from heat stroke? Where do you keep finding this junk?
AnonymousJune 7, 2006 at 5:49 pm
So sorry you have run into this ignorant person.
Yes, GBS often presents with pain. Big pain, awful pain, intensive pain. The first neurologist who saw me was actually puzzled by the pain and acted like he couldn’t understand what I was complaining about. I later read in a copy of his medical report that he wrote “patient doesn’t seem tolerant of pain”. No kidding, I wish he could try it for about 5 minutes and see how tolerant he was of that kind of pain!
My own bout of GBS happened about 2 weeks after I had surgery. Since I had no illness or exposure to other known triggers, the doctors tell me that it could have caused the GBS. It makes sense if you think about it, since any insult to your body can cause your immune system to react, and in the case of GBS, over-react.
Best wishes with your recovery. Don’t take any **** from anyone.
AnonymousJune 7, 2006 at 11:36 pm
hi marie-france, don’t let a reporter sell you short, you feel what you feel and no one else can tell you you don’t feel pain. pain is often related to gbs, when the nerves are trying to get the muscle to respond and the muscle doesn’t respond to the nerve that signal is interpretted as pain by the body. gbs does affect the small fibers, the ones responsible for sensory. i can not feel pain-like from a sharp object, hot/cold, or tell the difference between a hard touch and a soft touch, it all feels the same because my small fibers are damaged.
has this reporter done her homework on gbs/cidp? i would think she would want to know what she is reporting on before doing the report, otherwise it makes for bad reporting!
take care and keep a positive attitude marie-france, au revoir:).
AnonymousJune 8, 2006 at 9:39 pm
Where do I keep finding this “junk”???? This particular piece of “junk” is from the “British Journal of Medicine, and this article is also noted on the “National Library of Medicine and National Institutes of Health” website url: [url]http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?[/url]
It is also noted on the always excellent website: “All About Guillain Barre’ Syndrome” see url: [url]http://www.jsmarcussen.com/gbs/uk/incidence.htm[/url]
Scroll down to the bottom of the page and listed under “other factors” you will see Guillain-Barre’ Syndrome after Heatstroke and a link that takes you to the British Journal of Medicine article.
[U]Here is the link and full article from the British Journal of Medicine:[/U]cmd=Retrieve&db=PubMed&list_uids=10084549&dopt=Abstract
Full text below:
[B]Neurol Neurosurg Psychiatry 1999;66:408 ( March )[/B]Letters to the editor
[B]Guillain-Barré syndrome after heat stroke [/B]
Heat stroke is usually not listed among the events triggering Guillain-Barré syndrome. [B]Two cases of a Guillain-Barré syndrome-like polyneuropathy after heat stroke are on record, although without reference to electroneurography[/B].1 We report on a patient, who developed Guillain-Barré syndrome 10 days after severe heat stroke. He had electrophysiological evidence of demyelination, increased CSF protein, and high anti-GM1 antibodies. [U]Heat stroke activates the immune system by cytokine release,2 opens the blood-nerve barrier, and exposes peripheral nerve antigens and thus may induce Guillain-Barré syndrome, as suggested by results from our patient. [/U]
A 28 year old drug addict was using anticholinergic drugs against sweating during levomethadone withdrawal. He was found unresponsive in a public garden on a hot summer day (ambient temperature 32°C) after ingesting cocaine. His core temperature was 42.5°C at admission. He was in deep coma with wide unreactive pupils and without corneal and pharyngeal reflexes. Tachypnoea had induced hypocapnia. Blood pressure was 85/30 mm Hg and heart rate was 165/min. He developed disseminated intravascular coagulation, thrombopenia below 10 000 MRD/ml, and metabolic acidosis. Creatine kinase rose from 128 to 751 U/l. Leucocytes and C reactive protein remained normal. After 4 days of coma he was transferred to a closed psychiatry ward because of agitation and frightening hallucinations. After 5 more days he complained of fatigue, myalgia, and arthralgia and, 3 days later, developed fever (38.9°C), tetraplegia, and dysphagia. He required intensive care within hours. Vital capacity was 1.5 l. Proximal arm muscles had MRC grades between 2 and 3. All other limb muscles had grades 1 or 2. Facial muscle weakness increased for 2 more days. There was no ophthalmoplegia, but areflexia and stocking glove hypaesthesia for vibratory and cold stimuli. He did not respond to early intravenous immunoglobulin treatment and underwent plasma exchange from day 14 to 18. Bulbar muscles improved on day 15. Head movements improved 1 week later. Minimal hand functions recurred after 4 more weeks. He still required help with dressing and was unable to stand 14 months after disease onset.
Protein comcentration in CSF was 480 mg/l 2 days after onset of tetraparesis, and 7300 mg/l 2 weeks later. Cell count was 6 cells/mm3. He had high IgM (500 U/l; enzyme linked immunosorbent assay (ELISA); normal below 120 U/l) but only moderately increased IgA antibodies against GM1. 0nly one of 20 patients with Guillain-Barré syndrome examined in the same laboratory had higher anti-GM1 IgM antibodies. The anti-GM1 antibodies were normal 8 weeks after plasmapheresis.
Compound motor action potentials were<0.7 mV in all tested nerves from day 2 to day 95. Distal latencies were more than 150% above the upper limit of normal in the left peroneal nerve. Conduction velocities were below 70% of the lower limit of normal in the left peroneal and the left median nerve. F latency was above 150% of the upper limit of normal in the left ulnar nerve. F responses were missing in both median nerves and in the right peroneal nerve. A conduction block was present along the right ulnar nerve (wrist stimulation 0.69 mV; plexus stimulation 0.37 mV). Abnormal temporal dispersion and possible conduction block was present in the left ulnar nerve (wrist stimulation amplitude 0.36 mV; duration 8.6 ms; elbow stimulation amplitude 0.19 mV; duration 10.2 ms). Median sensory nerve conduction was normal and sural nerve conduction was moderately slowed (36 m/s) at day 2. Needle EMG disclosed abundant fibrillations and positive sharp waves in proximal and distal limb muscles at day 95.
Decreased sweating due to anticholinergic medication, cocaine induced increased heat production, and high ambient temperature precipitated heat stroke in our patient. [U]Ten days afterwards he developed an acute neuropathy that met clinical and neurophysiological criteria for Guillain-Barré syndrome. Similar time delays have been seen in two other patients with Guillain-Barré syndrome-like neuropathies after heat stroke1 and in the second of two patients reported as critical illness neuropathy after extreme hyperpyrexia.3 This patient had increased CSF protein and fasciculations which are unusual in critical illness neuropathy. He may have had Guillain-Barré syndrome as well. Weakness evolved with delay in these four patients with Guillain-Barré syndrome-like neuropathies, whereas it was present [/U][U]immediately after hyperpyrexia in five more patients, who probably did not have Guillain-Barré syndrome. One patient with heat stroke was tetraparetic when he regained consciousness.4 He had pyramidal and cerebellar signs and persistent atrophic weakness due to axonal or motor neuron loss and no neurophysiological evidence for demyelination. Four of 14 patients with cancer exposed to whole body hyperthermia and chemotherapy complained of weakness immediately after hyperthermia.5 Their nerve conduction abnormalities are reported as "compatible with scattered demyelination".[/U]
Our patient had chronic HCV infection which may be associated with vasculitic neuropathy and cryoglobulinaemia, both absent in our patient. [B]A connection between Guillain-Barré syndrome and non-A non-B hepatitis has been suggested,6 but the close temporal relation makes heat stroke a more probable cause of the disease in our patient. His high anti-GM1 antibodies suggested immune mediation. Anti-GM1 IgA is increased after Campylobacter jejuni infection, whereas IgM dominated in our patient who had no evidence of Campylobacter jejuni infection. Heat stroke disrupts the gastrointestinal mucosal wall. Endotoxins enter circulation and stimulate macrophages, which release TNF-, Il-1, Il-6, and IFN-. All these cytokines are raised after heat stroke2 and open the blood-nerve barrier. This may have exposed the GM1 epitope in our patient. IFN- induces Schwann cells to express MHC class II gene product, inviting T cell attack. TNF- is proinflammatory, myelinotoxic, and increased in Guillain-Barré syndrome. [/B]
[U]Guillain-Barré syndrome-like neuropathies have been reported from Saudia Arabia,1 where heat stroke is common, but they were not noted in connection with epidemic heat stroke in North America.7 Our patient had all features associated with fatal heat stroke: long lasting coma, shock requiring intravenous catecholamines, metabolic acidosis, and disseminated intravascular coagulation.7 [B]Guillain-Barré syndrome may occur more often after heat stroke, if more patients survive extreme hyperthermia thanks to intensive care.[/B] [/U]
Department of Neurology
Department of Internal Medicine, University Hospital Hamburg-Eppendorf, Hamburg, Germany
Correspondence to: Dr G Pfeiffer, Department of Neurology, University Hospital Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. Telephone 0049 40 4717 3771; fax 0049 40 4717 5086.
1. Bouges F, Vijayan G, Jaufferally F. Peripheral neuropathy after heatstroke. Lancet 1987;i:224.
2. Bouchama A, Parhar RS, El-Yazigi A, et al. Endotoxemia and release of tumor necrosis factor and interleukin 1 a in acute heat-stroke. J Appl Physiol 1991;70:2640-2644[Abstract/Free Full Text].
3. Wilmshurst PT, Treacher DF, Lantos PL, et al. Critical illness polyneuropathy following severe hyperpyrexia
AnonymousJune 9, 2006 at 12:24 am
GBS-like polyneuropithy. Sounds conclusive to me. Read all the med journals on heat stroke, and you start to find that many over the years, like the ones who died, really died of water overdose. I think last year, the NY marathon had two. They have concluded that most cases of heat stroke, wern’t heat stroke at all, but people gulping water so much, that the body shut down processing it. Might want to recheck the test results in Saudi Arabia to see if they had heat stroke in the first place. I hit my thumb with a hammer 3 days before onset of my GBS. Let’s put that on the list as a cause. I guess if you want something to be the cause bad enough, you can find it somewhere, in some med paper over the last 100 years. All the adjectives used in these articals sure don’t point to anything close to conclusive. That’s what people need to take stock in, and not trying so hard to be right. There are a lot of plausable causes without a doubt, but none are conclusive, and if a person has an event before onset, and can be remotely connected in some way to GBS, still doesn’t mean that had anything to do with it. I just don’t give GBS as much credit as everyone else, and build it up as something, in my opinion, that it’s not. Based only on my experiace with it.
You must be logged in to reply to this topic.