B12 as a Treatment for Peripheral Neuropathic Pain: A Systematic Review

Abstract

Neuropathic pain describes a range of unpleasant sensations caused by a lesion or disease of the somatosensory nervous system. The sensations caused by neuropathic pain are debilitating and improved treatment regimens are sought in order to improve the quality of life of patients. One proposed treatment for neuropathic pain is vitamin B12, which is thought to alleviate pain by a number of mechanisms including promoting myelination, increasing nerve regeneration and decreasing ectopic nerve firing. In this paper, the evidence for B12 as a drug treatment for neuropathic pain is reviewed. Twenty four published articles were eligible for inclusion in this systematic review in which a range of treatment regimens were evaluated including both B12 monotherapy and B12 in combination with other vitamins or conventional treatments, such as gabapentinoids. Overall, this systematic review demonstrates that there is currently some evidence for the therapeutic effect of B12 in the treatment of post-herpetic neuralgia (level II evidence) and the treatment of painful peripheral neuropathy (level III evidence).

Vitamin B12 Supplementation in Diabetic Neuropathy: A 1-Year, Randomized, Double-Blind, Placebo-Controlled Trial

“…Though our patients did not present with extremely painful neuropathy (mean pain score about 19 out of 38) [ 53 ], the pain level in the present study significantly decreased by 7%. Similar effects could be shown in our previous study [ 51 ] and other studies [ 3 , 33 , 63 , 75 ]. These findings once again confirm the analgesic action of B12 [ 63 , 73 ], possibly mediated by an increase of the availability and effectiveness of noradrenaline and 5-hydroxytryptamine [ 76 ] in the descending inhibitory pain modulation system (endogenous opioid system).…”

“…There is thus an urgent need for an effective drug therapy that would act either causally or by modifying the pathophysiology of DN. Among other drugs and supplements (e.g., alpha lipoic acid, carnitine, folate, and superoxide dismutase), vitamin B12 has perhaps been the most often used [ 3 , 33 , 34 , 35 , 36 , 38 , 61 , 62 , 63 , 64 ]. This is because vitamin B12 deficiency is commonly found in patients with DM2 and vitamin B12 deficiency may cause a variety of neurological disorders resembling or accelerating DN.…”

“…In other studies, combinations of B12 with other supplements or agents, not solely B12, were given [ 3 , 33 , 34 , 36 , 38 , 51 , 61 , 62 , 64 , 65 ]. In addition, there was a great variation in these studies in terms of the baseline blood levels (150–450 pmol/L), dose (25–2000 μg), duration (from 12 to 24 weeks), molecular form (cyano-, methyl-, or hydroxocobalamin) [ 31 , 35 , 62 , 63 , 66 ], and mode of administration (orally or parenterally) of B12 [ 31 ], as well as the inclusion criteria of the study participants (without or with established DN, DPN, or painful DN) [ 3 , 33 , 34 , 36 , 38 , 51 , 61 , 62 , 64 , 65 ].…”

“…Most trials had a follow-up period of 12–24 weeks [ 33 , 34 , 35 , 36 , 38 , 65 ], and no one exceeded 24 weeks, as was the case in the present trial, which lasted one year. In these trials, B12 had been administered in a dose varying from 250 to 2000 μg when given orally and from 1000 to 2000 μg when given intramuscularly [ 35 , 63 , 67 , 68 ]. For instance, doses of 250 mcg cyanocobalamin for one year [ 51 ] and 1500 mg methylcobalamin for four months [ 33 ] led to improvements in neurophysiological parameters and a substantial increase of B12 levels.…”

B Vitamins and One-Carbon Metabolism: Implications in Human Health and Disease

“…While the above research suggests that supplementation with FA and B12 could potentially be harmful, B12 supplementation, even in patients with normal serum B12 levels, has been explored to counteract certain neurological defects, given that B12 deficiency can cause neurological symptoms. B12 treatment does have potential as a therapy for peripheral neuropathic pain [156] and acute herpetic neuralgia [157,158]. This may be due to the restoration of MUT enzymatic activity, which is inversely associated with neuronal damage.…”