International Journal of Scientific & Technology Research

Home About Us Scope Editorial Board Blog/Latest News Contact Us
10th percentile
Powered by  Scopus
Scopus coverage:
Nov 2018 to May 2020


IJSTR >> Volume 4 - Issue 11, November 2015 Edition

International Journal of Scientific & Technology Research  
International Journal of Scientific & Technology Research

Website: http://www.ijstr.org

ISSN 2277-8616

A Case Study Of Dietary Deficiency On Peripheral Nerve Functions In Chronic Alcoholic Patient

[Full Text]



Arbind Kumar Choudhary, Tanwir Alam, Sadawarte Sahebrao Kishanrao.



Keyword: Alcoholic, Neuropathy, Vitamin-B12, Nutrient.



Abstract: Alcoholic neuropathy is most likely result of dietary deficiency rather than direct neurotoxic effect of alcohol. A male alcoholic patient, aged 34- years old with clear clinical sign of peripheral neuropathy was examined after his habit of six years chronic alcoholic drinking. Conduction velocities, latencies and nerve action potential amplitudes was measured from median, radial, common peroneal and sural nerves on respective upper and lower limb and the results showed that there was decrease in conduction velocity of common peroneal, and posterior tibial in lower limbs. However, sensory nerve conduction (SNCV) of sural nerve (right and left) was normal in lower limb. Based on the results observed in our study, we conclude that the combination of vitamin B12, uridine, and cytidine can be safe and effective in the treatment of patients presenting alcoholic polyneuropathy. So the prognosis of alcoholic peripheral neuropathy is good and independent of age provided that intake of alcohol is withdrawn completely.



[1] Koike, H; Iijima, M; Sugiura, M; Mori, K; Hattori, N; Ito, H. Hirayama, M; Sobue, G. 2003. Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy. Ann Neurol, 54: 19–29.

[2] Koike, H; Sobue, G. 2006. Alcoholic neuropathy, Curr Opin Neurol, 19: 481–486.

[3] Wang, Z.B., Gan, Q., Rupert, R.L., Zeng, Y.M., and Song, X.J. 2005. Thiamine, pyridoxine, cyancobalamin and their combination inhibit thermal, but not mechanical hyperalgesia in rats with primary sensory neuron injury. Pain, 114: 266-277.

[4] Saperstein, D.S; Barohn, R.J. 2002. Peripheral neuropathy due to cobalamin deficiency. Curr Treat Options Neurol, 4: 197–201.

[5] Wilson, J.A. Vitamin deficiency and excess. In: Harrison’s Principles of Internal Medicine. 14th Ed. 1998, Fauci, A.S; Braunwald, E; Isselbacher, K. (eds). McGraw-Hill, New York, p. 481.

[6] Oh, R., Brown, D.L. 2003. Vitamin B12 deficiency. American Family Physician, 67:979-986.

[7] Weir, D.G; Scott, J.M. 1995. The biochemical basis of the neuropathy in cobalamin deficiency. Baillieres Clin Haematol, 8: 479–497.

[8] Carmel, R. 2000. Current concepts in cobalamin deficiency. Annual Review of Medicine, 51:357-375.

[9] Gomes, A.V.C., Coutinho, C., Geller, M.2006. Therapeutic properties of the Bcomplex vitamins (B1, B6, B12) and their pharmacologic associations. Revista Brasileira de Medicina, 63(3): 111-117.
[10] Wattig, B., Schalow, G., Heydenreich, F., Warzok R., and Cervos-Navarro J. 1992. Enhancement of nerve fibre regeneration by nucleotides after peripheral nerve crush damage Electrophysiologic and morphometric investigations. Arzneimittel- Forschung/Drug Research, 42(9): 1075- 1078.