February 2018

Biochemical Mechanisms Cause Smell Loss in Patients with Traumatic Brain Injury (TBI)

TBI is a common cause of smell loss. However, the mechanisms which cause smell loss have been described as anatomical — related to “shearing” or “tearing” of the small olfactory nerve fibers from their location on the olfactory plate, the cribriform plate, the bony structure in the skull through which these small fibers pass to make their way to form the olfactory bulb in the brain. It has been considered that a head injury tears these fibers from the cribriform plate so that smell function is lost.

While logical, this concept is wrong. There is no clinical or scientific basis for this type of event although it has been considered to be the major cause for smell loss after TBI. Indeed, physicians have usually told patients who experienced TBI that because of this shearing they would never be able to recover their smell function.

We and others have demonstrated that the olfactory system is usually anatomically intact after TBI. We have demonstrated by use of magnetic resonance imaging (MRI) and computerized tomography (CT) scans taken of the brain after TBI that the olfactory nerves are present, albeit sometimes decreased in diameter. We have also shown the anatomical areas of the brain dedicated to olfaction are usually intact after TBI and without any significant pathology. We have also shown by use of functional MRI of brain that patients following TBI may have a significant loss of smell function but they retain the anatomical brain structures necessary to support olfaction (1).

Thus, if not anatomical, what is the cause of smell loss after TBI? We have determined that the cause of smell loss after TBI is related to biochemical changes — biochemical abnormalities in olfactory function which occur after TBI (2). Others before us have also considered this but have not formalized this concept as the primary cause of smell loss after TBI.

We and others have discovered multiple biochemical changes in olfactory function after TBI. We have defined several of these changes in an attempt to understand the nature of these biochemical abnormalities so that these biochemical abnormalities can be corrected and patients can regain their smell function after TBI. By use of this knowledge we have helped many of these patients to restore their smell function after TBI (2).

Reference

1. Levy LM, Henkin RI, Lin CS, Hutter A, Schellinger D. Increased brain activation in response to odors in patients with hyposmia after theophylline treatment demonstrated by fMRI. J Comput Assist Tomogr. 1998;22:760-770.

2. Henkin RI, Levy LM, Fordyce A. Taste and smell function in chronic disease: A review of clinical and biochemical evaluation of taste and smell dysfunction in over 5000 patients at The Taste and Smell Clinic in Washington, DC. Am J Otolaryngol. 2013;34:477-489.