Therapeutic role of Vitamin B12 in patients of chronic tinnitus: A pilot study

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918681/

Abstract

True tinnitus is a phantom auditory perception arising from a source or trigger in the cochlea, brainstem, or at higher centers and has no detectable acoustic generator. The most accepted is the famous neurophysiologic model of Jastreboff, which stresses that tinnitus, is a subcortical perception and results from the processing of weak neural activity in the periphery. The aim of this study is to determine the role of Vitamin B12 in treatment of chronic tinnitus. In this randomized, double-blind pilot study, total 40 patients were enrolled, of which 20 in Group A (cases) received intramuscular therapy of 1 ml Vitamin B12 (2500 mcg) weekly for a period of 6 weeks and Group B (20) patients received placebo isotonic saline 01 ml intramuscular. 

The patients were subjected to Vitamin B12 assay and audiometry pre- and post-therapy. Of the total patients of tinnitus, 17 were Vitamin B12 deficient that is 42.5% showed deficiency when the normal levels were considered to be 250 pg/ml. A paired t-test showed that in Group A, patients with Vitamin B12 deficiency showed significant improvement in mean tinnitus severity index score and visual analog scale (VAS) after Vitamin B12 therapy. 

This pilot study highlights the significant prevalence of Vitamin B12 deficiency in North Indian population and improvement in tinnitus severity scores and VAS in cobalamin-deficient patients receiving intramuscular Vitamin B12 weekly for 6 weeks further provides a link between cobalamin deficiency and tinnitus thereby suggestive of a therapeutic role of B12 in cobalamin-deficient patients of tinnitus.

Introduction

Tinnitus has plagued the human civilization since time immemorial and has been described in the Egyptian papyri (6000 BC). Tinnitus is experienced as ringing, roaring, or buzzing in the ears. They all originate, in one way or the other, from inside the head, and they are all known as tinnitus. In some cases, tinnitus exists because there is actually a source of acoustic energy located somewhere in the head and neck area – vascular anomalies, myoclonus, a clicking jaw, respiratory or cochlear otoacoustic emission, etc., – that can also be heard by a second person, with or without the aid of special devices. However, true tinnitus is a phantom auditory perception arising from a source or trigger in the cochlea, brainstem, or at higher centers and have no detectable acoustic generator. 

Tinnitus is classified as either primary or secondary. Primary tinnitus is used to describe tinnitus that is idiopathic and may or may not be associated with sensorineural deafness. Secondary tinnitus is tinnitus that is associated with a specific underlying cause (other than sensorineural deafness) or an identifiable organic condition. It is a symptom of a range of auditory and nonauditory system disorders that include simple cerumen impaction of the external auditory canal; middle ear diseases such as otosclerosis or Eustachian tube dysfunction; cochlear abnormalities such as Meniere's disease; and auditory nerve pathology such as vestibular schwannoma.

Although the exact mechanism of tinnitus still eludes us, the most accepted is the famous neurophysiological model of Jastreboff, which stresses that tinnitus, is a subcortical perception and results from the processing of weak neural activity in the periphery. The tinnitus-related neural activity occurring usually near the periphery of the system undergoes processing in subcortical auditory pathways and finally perceived at a conscious level as sound. The loudness and pitch of tinnitus depend on the strengths and pattern of electrical activity arriving at the cortex of the temporal lobe after subcortical signal detection, and pattern matching has occurred, the process being the same as for any neural activity generated by the external sounds by the cochlea.

There has been no promising treatment for tinnitus until date mainly because the etiology of tinnitus is still not clear. The generation of tinnitus has been attributed to the auditory system and neighboring anatomical regions, but at present, no test can identify these regions accurately.[1] Current consensus is that tinnitus results from aberrant neural activity in the auditory system, generally of excitatory nature.[2] New drugs have been emerging frequently which claim to play a role in managing tinnitus. Shemesh et al. in the year 1993 found Vitamin B12 deficiency in tinnitus patients, and its supplementation was found to help these patients.[3] The aim of this study is to determine the role of Vitamin B12 in the treatment of tinnitus. 

One of the mechanisms believed to be at play in Vitamin B12 deficiency neuropathy is hypomethylation in the central nervous system. Cochlear function is dependent on adequate vascular supply and the normal functioning of nerve tissue. B12 deficiency is associated with axonal degeneration, demyelination, and subsequent apoptotic neuronal death. Vitamin B12 deficiency may cause the demyelination of neurons in the cochlear nerve, resulting in hearing loss.[4,5,6] In addition, low levels of Vitamin B12 and folate are associated with the destruction of the microvasculature of the stria vascularis, which might result in decreased endocochlear potential and in hearing loss and tinnitus.[7] The objective of the study was to assess the prevalence of Vitamin B12 deficiency in chronic subjective tinnitus patients in Indian population and therapeutic effect of Vitamin B12 injection on tinnitus.

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The results suggest role of evaluating serum Vitamin B12 levels in patients of chronic tinnitus in view of the significant prevalence of cobalamin deficiency in North Indian population. This pilot study sheds light onz and its supplementation playing a therapeutic role in tinnitus ...