Guest guest Posted August 18, 2004 Report Share Posted August 18, 2004 my doc says 2 CCs at least 3 x per week joseph Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 19, 2004 Report Share Posted August 19, 2004 Hi Tom, Do you know how often one should have a B12 injection? Audrey --- Bayuk <tbayuk@...> wrote: > Folate, vitamin B12, and neuropsychiatric disorders. > Bottiglieri T > H. Courtwright and ph W. Summers > Institute of Metabolic Disease, Baylor University > Medical Center, Dallas, Texas, USA. > > Folate and vitamin B12 are required both in the > methylation of homocysteine to methionine and in the > synthesis of S-adenosylmethionine. > S-adenosylmethionine is involved in numerous > methylation reactions involving proteins, > phospholipids, DNA, and neurotransmitter metabolism. > Both folate and vitamin B12 deficiency may cause > similar neurologic and psychiatric disturbances > including depression, dementia, and a demyelinating > myelopathy. A current theory proposes that a defect > in methylation processes is central to the > biochemical basis of the neuropsychiatry of these > vitamin deficiencies. Folate deficiency may > specifically affect central monoamine metabolism and > aggravate depressive disorders. In addition, the > neurotoxic effects of homocysteine may also play a > role in the neurologic and psychiatric disturbances > that are associated with folate and vitamin B12 > deficiency. > > Gen Hosp Psychiatry 1994 May;16(3):224-228 > > Dietary vitamin B12 deficiency in a patient with > multiple sclerosis. > Gruener DM, Kunkel EJ, Snyderman DA, Infante MR, > Rodgers C, Field HL > Department of Psychiatry and Human Behavior, > Jefferson Medical College, Philadelphia, PA. > > The authors present a case of dietary vitamin B12 > deficiency in a patient with multiple sclerosis. A > simple schemata for evaluating patients for vitamin > B12 deficiency is included as a clinical aid for > physicians. > > Ger J Ophthalmol 1993 Aug;2(4-5):234-240 > > Uncommon chiasmal lesions: demyelinating disease, > vasculitis, and cobalamin deficiency. > Wilhelm H, Grodd W, Schiefer U, Zrenner E > Universitats-Augenklinik Tubingen, Abteilung fur > Pathophysiologie des Sehens and Neuroophthalmologie, > Germany. > > We report on eight patients who presented for > evaluation of unexplained visual loss. They all > showed a typical chiasmal visual field defect > (bitemporal hemianopia, junction scotoma). In all > patients, high-resolution computer-assisted > tomographic (CT) scans of the sellar region were > normal, and neither the medical history nor > additional ophthalmological findings pointed to any > explanation for the underlying disease. Six patients > seemed to have suffered from chiasmal optic > neuritis. Magnetic resonance imaging (MRI) scans > could elucidate the diagnosis in five cases: > white-matter lesions typical of multiple sclerosis > (MS) were found and, additionally, in four cases an > enlargement of the chiasm or barrier defect was > revealed in post-gadolinium MRI. In one patient, MRI > was normal. He recovered completely after megadose > steroid therapy. One patient developed motoric > symptoms of MS during the following year, another > patient had mild sensory symptoms and recurrence of > severe optic neuritis. An MR-proven chiasmal lesion > due to a leukocytoclastic immunovasculitis combined > with small subcortical white-matter lesions was > diagnosed in another patient. The field defects > disappeared spontaneously. In a 28-year-old woman a > low vitamin B12 level was found in routine blood > samples. Parenteral vitamin B12 substitution led to > an almost complete recovery of the visual field > defects. Chiasmal optic neuritis may occur isolated > or during the course of MS. Megadose steroids may be > of value if contraindications have been ruled out. A > chiasmal visual field defect caused by vitamin B12 > deficiency is very uncommon. A similar case was > reported in 1961. > > Int J Neurosci 1993 Jul;71(1-4):93-99 > > Vitamin B12 and its relationship to age of onset of > multiple sclerosis. > Sandyk R, Awerbuch GI > NeuroCommunication Research Laboratories, Danbury, > CT 06811. > > Attention has been focused recently on the > association between vitamin B12 metabolism and the > pathogenesis of multiple sclerosis (MS). Several > recent reports have documented vitamin B12 > deficiency in patients with MS. The etiology of this > deficiency in MS is unknown. The majority of these > patients do not have pernicious anemia and serum > levels of the vitamin are unrelated to the course or > chronicity of the disease. Moreover, vitamin B12 > does not reverse the associated macrocytic anemia > nor are the neurological deficits of MS improved > following supplementation with vitamin B12. It has > been suggested that vitamin B12 deficiency may > render the patient more vulnerable to the putative > viral and/or immunologic mechanisms widely suspected > in MS. In the present communication, we report that > serum vitamin B12 levels in MS patients are related > to the age of onset of the disease. Specifically, we > found in 45 MS patients that vitamin B12 levels were > significantly lower in those who experienced the > onset of first neurological symptoms prior to age 18 > years (N = 10) compared to patients in whom the > disease first manifested after age 18 (N = 35). In > contrast, serum folate levels were unrelated to age > of onset of the disease. As vitamin B12 levels were > statistically unrelated to chronicity of illness, > these findings suggest a specific association > between the timing of onset of first neurological > symptoms of MS and vitamin B12 metabolism. In > addition, since vitamin B12 is required for the > formation of myelin and for immune mechanisms, we > propose that its deficiency in MS is of critical > pathogenetic significance. > > J Neurol 1993 May;240(5):305-308 > > Decreased vitamin B12 and folate levels in > cerebrospinal fluid and serum of multiple sclerosis > patients after high-dose intravenous > methylprednisolone. > Frequin ST, Wevers RA, Braam M, Barkhof F, Hommes OR > Department of Neurology, University Hospital > Nijmegen, The Netherlands. > > Twenty-one patients (15 women, 6 men) with definite > multiple sclerosis (MS) were treated with 1000 mg > intravenous methylprednisolone-succinate (MP) daily > for 10 days. Before MP treatment there was a > negative correlation (r = 0.59, P = 0.0084) between > serum vitamin B12 and progression rate, defined as > the ratio of the score on Kurtzke's Expanded > Disability Status Scale and disease duration. A > significant decrease was demonstrated in the > cerebrospinal fluid (CSF) and serum levels of folate > and in the CSF level of vitamin B12 after MP > treatment. The decrease in serum B12 was not > statistically significant. After MP treatment all > median levels of vitamin B12 and folate were below > the reference medians. We hypothesize that low or > reduced vitamin B12/folate levels found in MS > patients may be related to previous corticosteroid > treatments. Otherwise a more causal relationship > between low vitamin B12/folate and MS cannot be > excluded. Further studies may be required to clarify > the vitamin B12 and folate metabolism in patients > with MS. > > J Neuroimmunol 1992 Oct;40(2-3):225-230 > > Multiple sclerosis and vitamin B12 metabolism. > Reynolds EH > Maudsley Hospital, London, UK. > > Multiple sclerosis (MS) is occasionally associated > with vitamin B12 deficiency. Recent studies have > shown an increased risk of macrocytosis, low serum > and/or CSF vitamin B12 levels, raised plasma > homocysteine and raised unsaturated R-binder > capacity in MS. The aetiology of the vitamin B12 > deficiency in MS is often uncertain and a disorder > of vitamin B12 binding or transport is suspected. > The nature of the association of vitamin B12 > deficiency and MS is unclear but is likely to be > more than coincidental. There is a remarkable > similarity in the epidemiology of MS and pernicious > anaemia. Vitamin B12 deficiency should always be > looked for in MS. The deficiency may aggravate MS or > impair recovery. There is evidence that vitamin B12 > is important for myelin synthesis and integrity but > further basic studies are required. > > Arch Neurol 1992 Jul;49(7):683-684 > > Biologically significant serum vitamin B12 > deficiency in multiple sclerosis inadequately > documented. > [LETTER] > > > Goodkin DE, sen DW, Green R > Vitamin B12 metabolism in multiple sclerosis. > Reynolds EH, Bottiglieri T, Laundy M, Crellin RF, > Kirker SG > Department of Neurology, King's College Hospital, > London, England. > > We have previously described 10 patients with > multiple sclerosis (MS) and unusual vitamin B12 > deficiency. === message truncated === ___________________________________________________________ALL-NEW Messenger - all new features - even more fun! http://uk.messenger. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 18, 2008 Report Share Posted February 18, 2008 Hi Auggie, During my college years I had B6 and 12 injections periodically, as I was eating way too much junk, drinking and very vitamin deficient. Got me to feeling better and straightened me out, temporarily, lol Gretchen Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 18, 2008 Report Share Posted February 18, 2008 Caution is needed in taking *Megadoses* of the B Vitamins in persons who have CMT. (Some of the weight loss OTC supplements have a large additive of B6 and B12) A megadose would be anything greater than the RDA allowance. Any of the B vitamins I had were always for theraputic reasons given by an MD familiar with CMT and peripheral neuropathy. There is some information from CMT doctor Garreth Parry on B6 in our files. Gretchen Quote Link to comment Share on other sites More sharing options...
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