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

被引:26
作者
Nouri, Aria [1 ,2 ]
Patel, Kishan [1 ]
Montejo, Julio [1 ]
Nasser, Rani [2 ]
Gimbel, David A. [2 ]
Sciubba, Daniel M. [3 ]
Cheng, Joseph S. [1 ,2 ]
机构
[1] Yale Univ, Dept Neurosurg, New Haven, CT USA
[2] Univ Cincinnati, Dept Neurosurg, Cincinnati, OH USA
[3] Johns Hopkins Univ, Dept Neurosurg, Baltimore, MD USA
关键词
nutrition; anemia; subacute combined degeneration; spinal cord; nitrous oxide; cobalamin; SUBACUTE COMBINED DEGENERATION; NITROUS-OXIDE ANESTHESIA; SERUM METHYLMALONIC ACID; COBALAMIN DEFICIENCY; SPONDYLOTIC MYELOPATHY; SPINAL-CORD; REVERSIBLE MYELOPATHY; NERVE REGENERATION; SCIATIC-NERVE; HOLOTRANSCOBALAMIN;
D O I
10.1177/2192568218758633
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Study Design: Narrative review. Objectives: To discuss the relationship between degenerative cervical myelopathy (DCM) and vitamin B-12 deficiency. Specifically, it is the aim to outline the rational for future research into assessment and therapeutic optimization of vitamin B-12 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 B-12 deficiency, with estimates of up to 20% in the elderly. Vitamin B-12 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 B-12 levels. Basic science research on nerve crush injuries have shown that vitamin B-12 levels are altered after nerve injury and that vitamin B-12 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 B-12 deficiency in the elderly, the role of vitamin B-12 in myelination, and vitamin B-12 deficiency as a differential diagnosis of DCM, it is important to investigate what role vitamin B-12 levels play in patients with DCM in terms of baseline neurological function and whether optimization of vitamin B-12 levels can improve surgical outcome. Furthermore, the routine assessment of vitamin B-12 levels in patients considered for DCM surgery should be considered.
引用
收藏
页码:331 / 337
页数:7
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