Electrophysiological profile of serum vitamin B12 levels, correlation with serum methylmalonic acid levels, and determination of subclinical peripheral nerve involvement

Abstract

Background/Aim: Vitamin B12 is essential for normal neural conduction in peripheral nerves. This study aimed to investigate the electrophysiological profile for varying degrees of serum B12 levels and to determine whether a correlation existed between electrophysiological profiles and serum methylmalonic acid (MMA) levels. Also, determination of subclinical peripheral nerve involvement with cold administration was planned in serum B12 levels. Methods: A total of 101 (63 females, 38 males) subjects with known serum vitamin B12 levels were selected randomly from the neurology outpatient clinic for this study. The subjects were divided into three groups based on the serum total Vitamin B12 levels: (1) B12 deficiency (<126 pg/mL), (2) low B12 (126-250 pg/mL), and (3) normal B12 (250–500 pg/mL). Serum MMA and nerve conduction studies (NCS) were assessed and compared between the three groups. After the cooling procedure was applied to the ulnar and sural nerves, NCS was repeated. Results: There were 13 subjects in the B12 deficiency group, 44 subjects in the low B12 group, and 44 subjects in the normal group. We found that ulnar sensory nerve action potential amplitudes were significantly decreased (P = 0.009), ulnar F latency (P = 0.003; P < 0.001)) was prolonged, and peroneal combined muscle action potential amplitudes decreased (P = 0.026) in the B12 deficiency when compared with the low and normal B12 groups. Sural nerve amplitude and conduction velocities were found to be significantly abnormal after the cold application in all groups (P < 0.001). The increase in sural nerve sensory nerve amplitude potentials (SNAP) amplitudes was higher in the B12 deficiency group than in the other groups. Mean serum MMA levels were high in all groups. A correlation of nerve conduction study (NCS) changes with serum vitamin B12 and MMA was not observed in the groups after cold application. Conclusion: Vitamin B12 deficiency may cause subclinical sensorial and motor axonal nerve conduction changes. Nerve conduction changes may not always reach pathological values based on electrophysiological studies but may be detected after cooling administration even in the normal serum B12 levels. A correlation between serum MMA and vitamin B12 levels was found. Therefore, serum levels of vitamin B12, which is important for nerve conduction, should be carefully evaluated in clinical practice.