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B12 Deficiency - Loss of Vibratory Sense

Updated: Jan 13, 2020

What is vitamin B12?

Vitamin B12 is a water soluble vitamin and is part of a group of cobalamins which have a cobalt in the center of its molecule. B12 is a coenzyme often bonded to a protein and is found in meats, fish, eggs, and milk, though microorganisms can make B12 (McLaren, Meguid, 1988; Schrier, S., Mentzer, W., & Tirnauer, J. n.d.).

Vitamin B12 deficiency causes, signs, symptoms

When an individual first presents with a B12 deficiency, they are often asymptomatic (Schrier, S., Mentzer, W., & Tirnauer, J., n.d.). Serum B12 can show deficiency long before signs and symptoms clinically manifest. Then, slowly signs and symptoms develop including neurological changes (tingly fingers and toes, tremors). Lastly, hematological changes (such a pernicious anemia, fatigue) will present. Those with advanced B12 deficiency and pernicious anemia will have an increased risk for gastrointestinal malignancy (Schrier, S., Mentzer, W., & Tirnauer, J., n.d.).

Vitamin B12 deficiency may singularly manifest in veganism/vegetarianism, but in other states of undernutrition vitamin B12 deficiency is often paired with other deficiencies, particularly folic acid. Vitamin B12 deficiency also presents in malabsorptive states such as with liver disease, celiac disease, or kidney disease. And those with hyperthyroidism need more B12 (McLaren, Meguid, 1988) than otherwise healthy individuals.

Nervous System Changes

Degeneration of the nerves of the spinal cord and peripheral nervous system can occur as a subacute sign of B12 deficiency. Neurological symptoms include tingling fingers and toes, numbness, tremors, dizziness, anxiety, and weakness. This is seen in combination with megaloblastosis, histamine-fast achlorhydria, dorsal funiculi syndrome, and pyramidal syndrome (McLaren, Meguid, 1988). Subnormal serum B12 concentration of <120 pg/mL may present with glossitis (inflammation of the tongue) and paresthesia (tingling, burning, or numb sensation of the fingers or toes). It is important to note that nutritional deficiencies are always bilateral affecting both hands or both feet, for example.

What is apallasthesia, and what causes it?

Apallesthesia is the inability to perceive vibrations usually by the hand or foot and is also known as the loss of vibratory sense. Nutrient imbalances associated with this loss of vibratory sense are deficiencies of B12, thiamine, copper, and B6 (pyridoxine). Vitamin B12 is one of the most common nutritional causes of apallasthesia.

Hematological Changes

Faster Red Blood Cell Destruction

In pernicious anemia which is caused by severe vitamin B12 deficiency, red blood cells are enlarged and pale in color. In Vitamin B12 anemia, there is an increased rate of red blood cell and megaloblast (enlarged red blood cell) destruction. Weakness, fatigue, and pallor are symptoms of anemia. A high level of indirect bilirubin as related to this increased rate of destruction can manifest as jaundice of the skin and conjunctiva of the eye as seen by the yellowing of the "whites of the eye". Some people call this scleral icterus but it is more accurately referred to as conjunctival icterus, because the conjunctiva overlays the sclera and the conjunctiva is what is yellowed by bilirubin.

The hematological changes (changes of the blood) of pernicious anemia also occur in folate anemia but take longer to manifest (McLaren, Meguid, 1988).

Nutrition-Focused Physical Exam and Considerations for APALLESTHESIA (loss of vibratory sense)

Legend: A- acute, C – chronic, MI – mild, M – moderate, S – Severe, R – rare, L – likely

Diagnostic Tool for Apallesthesia

Recommendations for medical and clinical nutrition practice should include examination procedures (nutrition-focused physical exam) involving the tuning fork method for apallesthesia detection, examination of the tongue and skin as detailed in the table above.

Youtube videos for pallesthesia examination technique:

Neuropathy (360WoundCare, 2015)

Apallesthesia (Weng, Q., 2013)


Schilling test will be negative with pernicious anemia. Vitamin B12 deficiency can cause intestinal damage. Therefore, oral supplementation of vitamin B12 to treat deficiency may have malabsorption of the nutrient at first but will resolves slowly with treatment (McLaren, Meguid, 1988). In the pernicious anemic, individuals will have increasing amounts of urine MMA (methylmalonic acid). Urine MMA is considered a sensitive test for B12 deficiency and responds positively to B12 treatment. Though, urine MMA will remain until anemia is completely resolved and serum B12 is normalized. It is possible that someone with normal B12 status can have serum B12 <150 pg/mL. Treating B12 requires weeks for stores to be replenished. B12 can be administered via shot (intramuscularly or IV), orally, sublingually, and topical patch. Two oral supplements are cyanocobalamin and hydroxocobalamin. For maintenance, cyanocobalamin can be given monthly and hydroxocobalamin once every 2-3 months (Schrier, S., Mentzer, W., & Tirnauer, J., n.d.). Parenteral B12 prescription of 1000 mcg per week until deficiency is corrected OR every other month with hydroxocobalamin. OR oral supplementation of 1000 mcg once per day (Schrier, S., Mentzer, W., & Tirnauer, J., n.d.).

Monitoring treatment

With B12 deficiency treatment, the following responses are typical: Lactate dehydrogenase and indirect bilirubin decline in 1-2 days; increase in reticulocyte count in 3-4 days (indicates new red blood cell production); anemia improves (measured by hemoglobin and hematocrit) 4-8 weeks; potassium may drop slightly due to red blood cell potassium uptake; hypersegmented neutrophils disappear in 10-14 days; leukopenia/thrombocytopenia improves in 2-4 weeks; serum folate & B12 will normalize. Symptoms to consider: increased energy and feeling of wellbeing associated with normalizing hemoglobin and hematocrit. Neuropsychiatric symptoms take a longer period of time to improve of 3 months to 1 year (Schrier, S., Mentzer, W., & Tirnauer, J., n.d.).


Addressing quality of evidence is significant for clinical decisions to be based upon and hopefully the reader will find citations herein helpful. This article is meant to provoke thought and clinical reasoning on the topic of vitamin B12 deficiency but not to be a substitute for professional advice. Please comment below any resources you have found particularly helpful on this topic.


Azhary, H., et al. (2010). Peripheral neuropathy: differential diagnosis and management.

American Family Physician, 81(7), 887-892.

Becker, D., et al. (2012). The neurological complications of nutritional deficiency following

bariatric surgery. Journal of Obesity, 2012.

Heaney, R. P. (2014). Guidelines for optimizing design and analysis of clinical studies of

nutrient effects. Nutrition Reviews, 72(1), 48–54. doi:10.1111/nure.12090

LeBlond, RF, Brown, DD, Suneja, M & Szot, J. (Ed.). (2015). DeGowin’s Diagnostic

Examination (10th ed.). New York: McGraw Hill.

McLaren, D., & Meguid, M. (1988). Nutrition and its disorders (4th ed.). NY: Churchill


Schrier, S., Mentzer, W., & Tirnauer, J. (n.d.). Treatment of vitamin B12 and folate

deficiencies. Retrieved from

Weng, Q. (2013, December 01). 7 apallesthesia 3. Retrieved from


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