Serum B12, Homocysteine Levels, and their Effect on Peripheral Neuropathy in Parkinson's Disease: Indian Cohort

Background: Cobalamin deficiency, either due to dietary inadequacy or increased consumption attributable to levodopa-mediated metabolic disturbance, and resultant hyperhomocysteinemia may contribute to peripheral neuropathy (PN) in Parkinson's disease (PD). Aim: The aim of the study is to assess the prevalence of Vitamin B12 deficiency, hyperhomocysteinemia in Indian PD patients, and their association with PN. Materials and Methods: Clinical details were collected in 93 patients over a period of 2 years. Seventy controls were included in the study. Serum B12, homocysteine, folate, electroneurography, and autonomic function tests were done. The prevalence of B12 deficiency and hyperhomocysteinemia in PD patients and controls was assessed. The association of B12 and homocysteine levels with patients' age, disease duration, levodopa equivalent daily dose, cumulative levodopa dose, Unified Parkinson's Disease Rating Scale-III off score, modified Hoehn and Yahr score, and presence or absence of PN was studied. Results: Serum B12, homocysteine levels, prevalence of B12 deficiency, and hyperhomocysteinemia were no different between cases and controls. Seven of 93 (9.68%) PD patients had PN. The median values of serum B12, folate, and homocysteine levels across patients with or without PN could not be compared as only seven of our patients had PN. Conclusion: The prevalence of B12 deficiency, hyperhomocysteinemia, and incidence of PN among our patients is very less when compared to the Western population. The conjecture that PN in PD patients may be secondary to B12 deficiency/hyperhomocysteinemia stands as a speculation.