The Role of Vitamin B12 in the Management and Optimization of Treatment in Patients With Degenerative Cervical Myelopathy

Abstract

Study design: Narrative review.

Objectives: To discuss the relationship between degenerative cervical myelopathy (DCM) and vitamin B₁₂ deficiency. Specifically, it is the aim to outline the rational for future research into assessment and therapeutic optimization of vitamin B₁₂ in the treatment of DCM.

Methods: Literature review.

Results: DCM is the commonest cause of spinal cord impairment, with an average age of presentation in the sixth decade. Patients at this age have also been reported to have a high prevalence of vitamin B₁₂ deficiency, with estimates of up to 20% in the elderly. Vitamin B₁₂ deficiency can result in subacute combined degeneration of the spinal cord (SACD), and several case reports have pointed to patients with both DCM and SACD. Both SACD and reversible compressive injury due to DCM necessitate remyelination in the spinal cord, a process that requires adequate vitamin B₁₂ levels. Basic science research on nerve crush injuries have shown that vitamin B₁₂ levels are altered after nerve injury and that vitamin B₁₂ along with dexamethasone or nonsteroidal anti-inflammatory drugs can reduce Wallerian degeneration. Furthermore, it has been suggested that a combination of B-vitamins can reduce glutamate-induced neurotoxicity.

Conclusions: Given the high prevalence of clinical and subclinical vitamin B₁₂ deficiency in the elderly, the role of vitamin B₁₂ in myelination, and vitamin B₁₂ deficiency as a differential diagnosis of DCM, it is important to investigate what role vitamin B₁₂ levels play in patients with DCM in terms of baseline neurological function and whether optimization of vitamin B₁₂ levels can improve surgical outcome. Furthermore, the routine assessment of vitamin B₁₂ levels in patients considered for DCM surgery should be considered.

Keywords: anemia; cobalamin; nitrous oxide; nutrition; spinal cord; subacute combined degeneration.

Figure 1.

Vitamin B₁₂ coenzyme function. B₁₂ acts as a coenzyme in the conversion of homocysteine to methionine in the cytosol, and the conversion of methylmalonyl-CoA to succinyl-CoA in the mitochondrion. The cytoplasmic reaction requires folate, as the methyl group that is added to homocysteine is removed from 5-methyl tetrahydrofolate. Tetrahydrofolate is a precursor in the synthetic pathway for purines and pyrimidines, while succinyl-CoA enters the Krebs cycle and is important for lipid and carbohydrate synthesis. Reprinted with permission from Springer: Nature Reviews Gastroenterology and Hepatology (Nielsen et al).

Figure 2.

Axial T2-wieghted MRI of a patients with degenerative cervical myelopathy and concomitant B₁₂ deficiency. On the left, a characteristic reverse V-shaped hyperintensity is visible in the posterior column (arrow). On the right significant spinal cord compression is demonstrated. Reprinted with permission from Elsevier: The Spine Journal (Miyazaki et al).