Vitiams, Medication & Alchol – Miller Fisher
AnonymousOctober 9, 2006 at 10:44 am
I was dx’d with Miller Fisher in 3/06 – my protien count was 93, had 5 IVGs –
My Drs. do not know much about Vitiams and my immune system is still out of whack – the health food store told me about a vitiam/herb supplement called Plaanetary Formula for the Myelin Sheath to start growing back – has anyone heard of this?
Meds – I am taking Lexapro, Lyrica & xanax – I wonder if this is keeping my Myeline Sheathing from growing back?
Alcohol – has anyone been told not to drink wine.
It has been 7 months and still am very tired and my mouth, tongue and face still feel awful. Felt I quit improving after 4 months – thats when I went back to work – stressful job.
Thanks for any feed back I can get.
AnonymousOctober 9, 2006 at 11:29 am
General heath can be helped by Vitamins. I am not familiar with the supplement you mentioned. It is a long recovery for the Demyelinating cased by the syndrom. I am almost 6 years out from GBS and still recovery is occurring however very slowly.
As far as alcohol (wine) there others on this forum have indicated that it does not contribute to GBS problems. My moto is that any thing taken in excess can hurt you.
The fact you were able to return to work after four months is a good sign. It is harder than it sounds much grief can be prevented by paying attention to the signals your body gives you. Here is some information regarding Residual Effects.
residual fatigue & pain is finally documented thx to dr. parry
GBS Newsletter – The Communicator Spring 2003
Residual Effects Following Guillain-Barre
Gareth J. Parry, MD Professor of Neurology, University Of Minnesota
Guillain-Barr~ syndrome is a disorder whose excellent prognosis is invariably emphasized. Widely accepted figures suggest that 75%-85% of patient make a complete recovery. However, many of my patients have complained to me of minor but annoying persistent symptoms continuing for years after the initial paralytic event. Although I have made no systematic study of the proportion of patients with these residual complaints it is certainly more than the 15%-25% that the figures in the literature would suggest. The great majority of studies of the ultimate outcome in GBS are based on telephone interviews or retrospective chart reviews and seemingly minor complaints may have been missed or disregarded. Thus, patients are often asked if they have returned to their previous work or other previous activities but they may not have been asked whether they have more difficulty performing their former activities. A note of caution was sounded in one small study from Dr. J. McLeod and his colleagues in Australia (J. Neurol Sci 1976; 27:438-443) who objectively evaluated a small group of 18 recovered GBS patients and found that half of them had objective residual neurological abnormalities. Even then the residual abnormalities were considered to be significant in only four patients. A recent important paper from Dr. I.S.J. Merkies and colleagues in Holland (Neurology 1999; 53:16481654) has established that residual effects from both GBS and CIDP are much more common than has been generally reported and that seemingly minor neurologic abnormalities may still result in annoying disabilities. The study used a validated index of fatigue severity to assess residual disability. It included 83 patients who had suffered from GBS an average of five years previously. About 80% of these patients experienced fatigue that was considered severe enough to interfere with their life despite the fact that the majority had normal strength or only minor weakness. They noted also that the fatigue did not seem to improve over time; the fatigue index score was the same in patients in whom many years had elapsed as it was in patients whose acute illness had occurred only 6-12 months previously. This paper provides sound scientific support for the validity of the observations of my patients who regularly complain of fatigue even when they have returned to all or most of their former activities and who are working full time at their former jobs. Although their strength may be normal when they are examined in the doctor’s office they are clearly unable to sustain the same level of physical activity that they had performed prior to their GBS.
A second under-appreciated symptom that may persist for many years is pain. Certainly, severe disabling pain is very rare. However, a number of my patients complain of persistent discomfort in their feet. The discomfort may take the form of annoying paresthesias (tingling) or there may be a vague aching discomfort. Occasionally there is more severe burning or stabbing pain. The symptoms have the same characteristics as typical neuropathic pain in that they tend to be worse in the evening or at night and are particularly annoying following days during which the patients have been up on their feet a lot. The discomfort is not particularly responsive to analgesics but usually does respond to antiepileptic drugs such as gabapentin, or antidepressant drugs such as amitriptyline, drugs typically used in the treatment of neuropathic pain. However, these medications have to be taken on a daily basis to be effective and one problem with deciding whether to treat this residual symptom is that the discomfort is usually rather mild. Thus, patients may be daily irritated by their symptom but be reluctant to take a drug every day for a symptom that significantly bothers them only once or twice a month. I have seen no mention in the medical literature of this phenomenon. It is possible that I see a highly selected group of patients in my practice who had initially been more severely affected and that the prevalence of this annoying residual symptom is much higher in my patients than in the usual population of recovered GBS patients. I would be most interested to learn whether the group of patients reported by Merkies and colleagues also suffered from minor persistent discomfort.
The basis for both of these seemingly minor residual symptoms (fatigue and pain) is probably axonal degeneration. During the acute illness the predominant underlying pathology in most patients is segmental demyelination, a completely reversible phenomenon. However, some degree of axonal degeneration is almost invariable and in some patients it is severe. As recovery occurs function is restored by a number of mechanisms. Axonal regeneration of motor axons probably plays very little role in restoration of function except in the more severe cases. Rather, surviving axons send out small branches called collateral sprouts that restore the nerve supply to those muscle fibers whose nerves have been damaged. This process of collateral sprouting is very effective at restoring strength to a muscle but the efficiency of the muscle suffers the muscle must work harder to achieve its goals. Thus, fatigue may result even when there appears to be full restoration of strength. On the sensory side, even a small number of damaged sensory axons may be sufficient to generate spontaneous discharges that are registered as pain or discomfort.
It is entirely appropriate that the good outcome of GBS should be emphasized during the acute illness. During this time, the patient is losing control of many motor functions, sometimes including life-preserving functions, and constant reassurance from the attending physicians plays a vital role in the recovery process. However, it is equally important to be aware that residual problems are experienced by “recovered” GBS patients. Acknowledgment that such residual problems exist will go a long way towards helping patients deal with the frustration of their incomplete recovery.
More research is needed to discover an effective treatment for the residual fatigue. In addition, since these persistent symptoms are probably related to the degree of axonal damage that occurs at the time of the initial attack, we also need to continue to strive for earlier and more effective treatment of the acute stage of the disease so that these residual problems are minimized.
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