Trigeminal neuralgia is a disorder of the fifth cranial (trigeminal) nerve that causes episodes of intense, stabbing, electric shock-like pain. The first line of treatment of trigeminal neuralgia is usually in the form of anticonvulsant drug, especially carbamezepine.

When medication does not satisfactorily manage pain, various surgical options are available, including microvascular decompression, radiofrequency ablation and stereotactic radiosurgery, with a gamma knife. The sustained pulsatile during nerve compression, demyelinates sensory axons in the nerve and nerve root. Microvascular decompression is the only procedure that has successfully provided long term pain relief  due to remyelination after the decompression.

Cyanocobalamin has been shown to reduce spinal nerve ligation induced alloydnia and tactile allodynia in rats and therefore may have a role in humans. Vitamin B12 functions as a methyl donor and works with folic acid in the synthesis of DNA and RBCs & is vitally important in maintaining the health of the myelin sheath that surrounds nerve cells. Methylcobalamin as a form of Vitamin B12 protects against neurological diseases and aging. The liver converts cyanocobalamin into methylcobalamin within the body but larger amounts of methylcobalamin are necessary to correct neurological defects. The high doses of methylcobalamin are needed to regenerate neurons as well as the myelin sheath that protects nerve axons and the peripheral nerves. The treatment of trigeminal neuralgia can be challenging and in the search for alternatives, vitamin B12 has been found to be a clinically useful pharmacological useful tool for patients with neuropathic pain. In previous time large dose of vitamin B12 were used with good effect in therapy of trigeminal neuralgia.

Causes of Low Vitamin B12:

a. Low HCl in the stomach: Cobalamin malabsorption due to gastric dysfunction and may be exacerbated by the use of acid- lowering agents such as H2 blockers, antacids and proton pump inhibitors. Approx.80% of plasma B12 is bound to  plasma proteins transcobalamin I (TCI).  Transcobalamin II (TCII ) is the principal B12 binding protein for the delivery of B12 to cells.

b) Immune System – Intrinsic factor in the stomach: Caused by an immune system problem where antibodies attack the stomach lining and damage the cells that produce intrinsic factor.

c) Bacterial overgrowth and infestation with tapeworms or other intestinal parasites that can compete for dietary vitamin B12 in the small bowel.

d) Antibiotics: The use of antibiotics may alter the intestinal microflora and may decrease the possible contribution of vitamin B12 by certain inhabitants of the microflora.

e) Lack of calcium

f) Megadoses of vitamin C and/or copper.

Once absorbed, vitamin B12 binds to transcobalamin II & is transported throughout the body. Congenital transport-protein deficiencies, including transcobalamin II deficiency, are another rare cause of vitamin B12 deficiency. It has also been suggested that in the presence of heavy metals the cobalt atom is oxidized from CO2+ to CO3+ at the same time as the heavy metal is reduced. The properties of the cobalamin are hypothetically changed and vitamin B12 has lost its biological properties.


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