Pernicious Neurological degeneration

A frequent cause of vitamin B12 deficiency is atrophic gastritis leading to a lack of intrinsic factor. Besides megaloblastic anemia, damage to mucosal linings and degeneration of myelin sheaths with neurological sequelae will occur (pernicious anemia). 

Walton et al. (1954) report their findings in 130 cases of pernicious anemia. Abnormal electroencephalograms were common, not only in those showing subacute combined degeneration of the cord but also in those without clinical evidence of neurological involvement. There was no correlation with hemoglobin levels or with age. The records tended to improve in the first 7 to 10 days after B12 therapy, and in some cases further improvement occurred over a period of months or years. 

Treatment of subacute combined degeneration with masmve doses of citrovorum factor did not prevent neurological deterioration (Ungley, unpublished), and it appears very unlikely that this compound will protect the nervous system in pernicious anemia. Treatment with folic acid or citrovorum factor has no effect on the serum Bw levels of patients with pernicious anemia (Mollin and Ross, 1953b). 

Vitamin 8,2 deficiency results in pernicious anaemia. In this condition there is a delayed maturation of erythrocytes due to the impairment of DNA synthesis. This results in the appearance of megaloblasts in the blood. Deficiency of vitamin 8,2 also results in a neurological condition (subacute combined degeneration of the spinal cord). 

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