FLAIR image": note the abnormal lesions (circled) in the periventricular area suggesting white matter pathology.MRI image of the cervical spinal cord in<unk>  showing subacute combined degeneration. (A) The midsagittal T2 weighted image shows linear hyperintensity in the posterior portion of the cervical tract of the spinal cord (black arrows). (B) Axial T2 weighted images reveal the selective involvement of the posterior columns. Physiology The total amount of vitamin<unk>  stored in the body is between two and five milligrams in adults. Approximately 50% is stored in the liver, but approximately 0.1% is lost each day, due to secretions into the gut—not all of the vitamin in the gut is reabsorbed. While bile is the main vehicle for<unk>  excretion, most of this is recycled via enterohepatic circulation. Due to the extreme efficiency of this mechanism, the liver can store three to five years worth of vitamin<unk>  under normal conditions and functioning. However, the rate at which<unk>  levels may change when dietary intake is low depends on the balance between several variables. Pathophysiology<unk>  causes particular changes to the metabolism of two clinically relevant substances in humans: # Homocysteine (homocysteine to methionine, catalysed by methionine synthase) leading to hyperhomocysteinemia # Methylmalonic acid (methylmalonyl-CoA to succinyl-CoA, of which methylmalonyl-CoA is made from methylmalonic acid in a preceding reaction) Methionine is activated to S-adenosyl methionine, which aids in purine and thymidine synthesis, myelin production, protein/neurotransmitters/fatty acid/phospholipid production and DNA methylation. 5-Methyl tetrahydrofolate provides a methyl group, which is released to the reaction with homocysteine, resulting in methionine. This reaction requires cobalamin as a cofactor. The creation of 5-methyl tetrahydrofolate is an irreversible reaction. If<unk>  is absent, the forward reaction of homocysteine to methionine does not occur, homocysteine concentrations increase, and the replenishment of tetrahydrofolate stops. Because<unk>  and folate are involved in the metabolism of homocysteine, hyperhomocysteinuria is a non-specific marker of deficiency. Methylmalonic acid is used as a more specific test of<unk>  deficiency. Nervous system Early changes include a spongiform state of neural tissue, along with edema of fibers and deficiency of tissue. The myelin decays, along with axial fiber. In later phases, fibric sclerosis of nervous tissues occurs. Those changes occur in dorsal parts of the spinal cord and to pyramidal tracts in lateral cords and are called subacute combined degeneration of spinal cord. Pathological changes can be noticed as well in the posterior roots of the cord and, to lesser extent, in peripheral nerves. In the brain itself, changes are less severe: They occur as small sources of nervous fibers decay and accumulation of astrocytes, usually subcortically located, and also round hemorrhages with a torus of glial cells. MRI of the brain may show periventricular white matter abnormalities. MRI of the spinal cord may show linear hyperintensity in the posterior portion of the cervical tract of the spinal cord, with selective involvement of the posterior columns.
Vitamin B12 deficiency
Vitamin A deficiency
Copper deficiency
Biotin deficiency
Megavitamin-B6 syndrome
Vitamin E deficiency
Fluorine deficiency
Zinc deficiency