CIDPUSA.ORG Autoimmune

Nutritional Neuropathy

God Our Guide

Main Links Cidpusa.org

Home page
Autoimmune Diseases Guide
F.A.Q. Autoimmune
F.A.Q.
Help page
services contact page
Treatment Page

Vitamin Deficient Diet

Search Cidpusa web

Strachans Syndrome

Strachan's syndrome is  polynutritional in origin; therefore, a battery of vitamin deficiencies should be sought, including thiamin, niacin, pyridoxine, and cobalamin. The pathophysiology of post-gastroplasty neuropathy is probably multifactorial, due perhaps to a polynutritional and an endogenous toxin produced as the result of the abnormal anatomy created by the surgical procedure. This toxic hypothesis is supported by the fact that some have reported a resolution of the symptoms following reversal of the surgical procedure whereas nutritional replacement alone
does not. Alternatively, there may be a nutritional factor that cannot be replaced adequately until the procedure has been reversed.

Pyridoxine deficiency will cause elevations in serum homocysteine and cystathionine, and assays are commercially available. Urinary assays for xanthurenic acid and other pyridoxine metabolites may be performed following tryptophan loading.


Vitamin E deficiency can be reliably investigated using the serum alpha- tocopherol level. Adult patients without malabsorption and a clinical picture consistent with Friedrich's ataxia and neuropathy should be investigated for an autosomal recessive defect in the tocopherol transporter protein gene of chromosome 8. Tocopherol transporter protein incorporates tocopherol into chylomicrons. The serum tocopherol levels in these patients may be in the normal range;
however, they respond to high dose supplementation.

Treatment of suspected thiamine deficiency in the setting of post-gastroplasty neuropathy, Strachan's syndrome, or Wernicke-Korsakoff syndrome begins with the immediate administration of 100 mg thiamine intravenously followed by 100 mg intramuscularly daily for 3 to 5 days and parenteral multivitamins. Patients are then maintained on 50 mg thiamin orally along with multivitamins daily.


For cobalamin deficiency, the total body store of cobalamin is 2000 to 5000 μg, half of which is stored in the liver. The recommended daily allowance is 6 μg/day, and the average diet provides 20 μg/day. Treatment may begin with intramuscular injections of 1000 μg of cobalamin for 5 days, then 500 to 1000 μg intramuscularly every month. Oral replacement is an alternative for those patients who cannot tolerate intramuscular injections, or for whom they are impractical.
Because 1% of all ingested cobalamin may be absorbed by passive diffusion, cobalamin requirements can be satisfied with oral therapy, even in patients with pernicious anemia (Kuzminski, 1998). A daily dose of 1000 μg/day orally will yield 10 μg of absorbed cobalamin, which exceeds the recommended daily allowance.

Sublingual cobalamin 2000 ug/ day is also effective and may be superior to IM injections for some patients (Delpre, 1999).

It may be practical to replenish cobalamin stores first using injections of cyanocobalamin for 1 week, and then to maintain patients using a 1000 μg daily oral supplement. The effectiveness of treatment, regardless of route, can be confirmed by demonstrating normal serum or urine methylmalonic acid levels three to four weeks after beginning B12 replacement.
The management of post gastroplasty neuropathy begins with a recognition and replacement of vitamin deficiency, particularly thiamine and B12. However, vitamin supplementation alone is rarely successful. A toxic hypothesis is supported by the fact that some have reported a resolution if the symptoms following reversal of the surgical procedure whereas nutritional replacement alone does not.
The management of gluten sensitivity neuropathy is preliminary given its uncertainty. Further] study of the efficacy of a gluten free diet in patients with anti gliadin antibodies and a peripheral neuropathy is warranted. .

Go to gluten free diet page