By Marcello Cherchi, MD PhD

For patients

Zinc is an element found in the diet. Some patients with gastrointestinal problems may not be able to get zinc out of the food they eat. A very small amount of research has reported eye movement problems in patients with zinc deficiency.

For clinicians

Overview

Zinc influences the activity of several neurotransmitter receptor systems, including ones relevant to vestibular function such as GABA, glutamate, potassium and NMDA. There is almost no literature on the vestibular effects of zinc deficiency, but one study reported abnormalities in horizontal and vertical saccades, and horizontal smooth pursuit.

Introduction

Zinc influences the activity of several neurotransmitter receptor systems, including some that are relevant to vestibular function.

Pathophysiological mechanism of disease

Zinc modulates activity at numerous neurotransmitter receptors, including GABA, glutamate, potassium and NMDA (Smart, Xie, Krishek 1994). Since all of these neurotransmitter systems are found in the vestibular system (Soto, Vega, Sesena 2013), it is reasonable to suspect that abnormalities in zinc metabolism may have vestibular effects. Candidate neuroanatomical locations of these effects include vestibular hair cells, vestibular nuclei and the cerebellum (Ferreira et al. 2009).

Testing: vestibular

Abnormalities in zinc metabolism have been little studied from the otoneurological perspective. Ferreira and Cury (Ferreira et al. 2009) studied videonystagmography in 9 patients with zinc deficiency and reported that they exhibited abnormalities in horizontal saccades (specifically leftward saccadic latencies and bilateral saccadic accuracies), vertical saccades (upward saccadic latencies), and reduced smooth pursuit gain. However it should be noted that this single study involved patients who (1) had malabsorption syndrome due to small intestinal resection for treatment of mesenteric thrombosis; (2) had received perioperative aminoglycoside antibiotics; and (3) had magnesium deficiency. In other words, the observed abnormalities may not be attributable only to zinc deficiency.

Treatment

Zinc deficiency may be treated with supplementation. Supplementation may be administered orally, but should be given parenterally (by injection) in patients with malabsorption syndromes.

References

Ferreira GD, Cury MC, Oliveira JA, Manfredi AK, Vannucchi H (2009) Vestibular evaluation using videonystagmography of chronic zinc deficient patients due to short bowel syndrome. Braz J Otorhinolaryngol 75: 290-4. doi: 10.1016/s1808-8694(15)30792-8

Smart TG, Xie X, Krishek BJ (1994) Modulation of inhibitory and excitatory amino acid receptor ion channels by zinc. Prog Neurobiol 42: 393-441. doi: 10.1016/0301-0082(94)90082-5

Soto E, Vega R, Sesena E (2013) Neuropharmacological basis of vestibular system disorder treatment. J Vestib Res 23: 119-37. doi: 10.3233/VES-130494

Page first published on August 19, 2023. Page last updated on September 19, 2023

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