By Sean Lennox, Audiologist MSc.


Vitamin B-12 deficiency
as its name implies is a syndrome that forms as a result of a lack the essential vitamin B-12 adsorption. Vitamin B-12 is involved in immunological responses, and central and peripheral nervous system maintenance and repair. The deficiency of this important metabolic agonist can lead to a cluster of neurologic, cardiovascular, and psychiatric symptoms (Oh and Brown, 2003). This disease can cause significant degeneration of the central nervous system and the peripheral and spinal nerves causing balance problems of poor gait and postural stability because of the paresthesia of the extremities as well as the joints. This nutrient is attained only through the ingestion of animal products and animal by-products (Carmel, 1997; Stabler, Lindenbaum, and Allen, 1997; Oh and Brown, 2005). B-12 binds to homocysteine or methylmelonic acid (MMA) to form important metabolites for cellular and DNA repair. B-12 is stored in the liver of mammals and it can take up to 5 years before a critical threshold of B-12 is lost as a result of disease causes listed below.

The causes of vitamin B-12 deficiency include two forms of stomach or intestinal infection or disease as well as simple poor or incomplete absorption by lack of B-12 intake or hypoacidity of stomach enzymes. Autoimmune gastritis can lead to loss of vitamin B-12 absorption and deficiency over time as important enzymes and binding proteins (IF and MMA) for the metabolism of vitamin B-12 are damaged (Carmel, 1997; Stabler et al, 1997). Type 2 gastritis also known as H pylori infection and pernicious anemia are the two most common forms of stomach conditions that can lead to deficiency. Pernicious anemia is the loss of the mucosal cells lining the stomach that are involved in the production of IF (Oh and Brown, 2005). IF is implicated in the direct absorption of Vitamin B-12 as IF binds to vitamin B-12 acting as an enzyme to break it down into useable cellular components. H pylori infection similarly reduces usable metabolic substrate homocysteine (Stabler et al, 1997). The other most common cause of this disorder is simply not ingesting enough B-12 from one’s diet or through improper absorption as a result of antacids, post gastrectomy, or even MS anti-inflammatory medications (Ariel, Korem, Almog, and Galboiz, 2005).

Disease Frequency

Incidence rates were not obtainable. However, the prevalence of vitamin B-12 deficiency appears to increase with age and is especially common in those over 65 and for those who do not eat animal products (Carmel, 1997). The prevalence has been estimated at around 15% for patients over 65 years of age and 3% of the general population (Oh and Brown, 2005).


Patients tend to report a loss of proprioception and a numbing of sensory function for the extremities leading to imbalance. This loss of balance sensation is attributed to neural degeneration at the spinal level. The patient may also report memory issues or cognitive slowing consistent with the neurologic damage of this disorder. Diagnosis of this syndrome is done through case history as well as through blood tests of serum vitamin B-12, vitamin B-12 agonists (homocysteine and MMA), as well as vitamin B-12 antagonist levels. Low serum B-12 is considered less than 200 pgs. The most sensitive diagnostic procedure is to test either serum homocysteine or MMA levels as both tests have over 95% sensitivity (Oh and Brown, 2005).

The balance assessment and audiometric profile of patients with vitamin B-12 deficiency would be normal except for tests of functional balance such as the Romberg test and posturography. The vestibular system would remain intact and as such vestibular testing would be expectedly normal (Hain, 2009).


Successful treatment is centred on increasing a patient’s B-12 intake with oral supplement or injection. Oral supplementation treatment is accomplished by having the patient take 1000 mcgs of vitamin B-12 daily for the rest of their lives (Oh and Brown, 2005). Intramuscular injections which are no more effective than oral supplementation involve an injection of 100-1000mcgs per day for life (Oh and Brown, 2005; Stabler et al, 1997).


Assuming that B-12 deficiency has been identified early in the disease progression, a physician would predict that after several months a patient’s serum B-12 should increase steadily with the amplified and continuous dosage from oral supplementation or intramuscular injection. The patient should see improved balance functioning through recovery of pressure sensory function
and proprioception, reduced pain and tingling in the extremities, and improved overall cognition and mental acuity (Oh and Brown, 2005).


Carmel. (1997) Cobalamin, the stomach and aging. American Journal of Clinical Nutrition, 66:750-759.

Hain, T. (2009) B-12 Deficiency and Unsteadiness.

Miller, Korem, Almog, and Galboiz. (2005) VitaminB12,demyelination, remyelination and repair in multiple sclerosis. Journal of Neurological Sciences. in press.

Oh DL., and Brown. (2003). Vitamin B12 deficiency, American Family Physician, 67: 979–986.

Stabler, Lindenbaum, and Allen. (1997) Vitamin B-12 deficiency in the elderly: current dilemas.American Journal of Clinical Nutrition, 66:741-749.