Vitamin B12 deficiency: a clinical and electrophysiological profile

The present study was conducted to evaluate the clinical and electrophysiological profile of vitamin B12 deficiency syndrome and whether a correlation exists between the disease process and the various electrophysiological parameters.

40 patients with vitamin B12 deficiency neurological syndromes with low serum vitamin B12 and high homocysteine levels were subjected to a detailed motor and sensory nerve conduction studies and pattern reversal VER (P100), SSEP (P37) after stimulation of the posterior tibial nerve and median nerve (N 20) were obtained bilaterally. MR cervical spine was done in all the patients and MR brain in those who presented with neuro-psychiatric symptoms. The patients were followed up at three months, six months and one year after treatment.

On the basis of clinico-electrophysiological profile, 31 patients had myeloneuropathy, 5 isolated myelopathy, 4 isolated neuropathy. Four of the patients with myeloneuropathy, had concomitant dementia. MR imaging revealed abnormality in 12.5% of cases. Prolongation of P37 latency was observed in 39 (97.5%) patients, N 20 latency in 22 (55%), and P100 latency in 19 (47.5%) patients. Peripheral neuropathy was seen in 18 patients; optic neuropathy in 8; and combination of peripheral and optic neuropathy in 9 patients. The peripheral neuropathy was axonal in 19, and demyelinating in 6 patients. There was a significant correlation of the duration of the disease with N 20 latency (P < 0.04). Serum vitamin B12 level correlated well with the latencies of P37 (P < 0.005) and sural SNAP (P < 0.006). On treatment, normalization of P100, MRI signal, N 20 and partial recovery of P37 latencies was seen at 6 months, 9 months and one year respectively.

Differential recovery of central and peripheral syndromes was seen. This correlated with the underlying demyelinating and axonal processes, which was well reflected by the electrophysiological studies, and has an important bearing on the outcome.