It is commonly believed that smell loss following a head injury is associated with the severing of the olfactory nerves along the cribriform plate. This severing is believed to cause a loss of connectivity between the odor and the brain and that this loss is irrevocable.

While this may initially appear logical, careful examination of olfactory bulbs, in situ, reveal that these neural structures may not be damaged following a head injury. Indeed, the olfactory nerves and the olfactory bulbs are not rigid structures but rather pliable organs that lie bathed in a gel-like fluid that surrounds and protects them. Rather than being rigid, these structures are more like pieces of fruit placed into “jello”. Thus, when a blow to the head applies force to these structures they bend or move in response to the blow much like movement in a dish of “jello”—much like the abdomen of the Pillsbury doughboy after a finger is poked into it — the abdomen moves inward but when the finger is removed, it pops back out.

We have demonstrated in several published papers that smell loss can be restored in patients who have experienced head injuries even if the injury was severe, such as the blow were contra coup, against the back of the head (1, 2). We have also demonstrated the intact nature of this system by use of functional magnetic imaging (fMRI) of the brain in which brain activation to olfactory stimuli occurs in a totally objective manner (1). These studies demonstrate that patients with head injury and smell loss must be anatomically intact or else the brain would not activate or “light up” in response to olfactory stimuli delivered into the nose.

However, these results were not definitive in demonstrating that the system was anatomically intact. In order to demonstrate that following a severe head injury with accompanying smell loss that the system was anatomically intact, we initiated another series of studies using what is called “tracer” techniques. In these studies it is possible to follow neural activity along an axon and its dendrite in the brain to determine the origin of the action potential and its destination into specific anatomical regions in the brain.

In patients with severe smell loss following head injury we demonstrated by use of fMRI that after introduction of an odor into the nose the sensory stimulus activates the olfactory nerve and the subsequent neural activity and its pathway into various portions of the brain can be “traced” visually and in color. Thus, we have demonstrated that neural pathways in patients with head injury and smell loss are intact and are not severed, as has been the common, but mistaken, concept. These neural connections, in fact, are intact and functioning despite severe head injury as previously stated (1, 2).

With these present tracer studies we have demonstrated that the anatomy between nerve and brain is intact following a severe head injury that results in severe smell loss. The neural pathways from the olfactory nerve, through the olfactory bulb into appropriate association centers in the brain, are intact and functioning in response to odors. These odors can be quite pleasant such as amyl acetate which smells like banana oil, or menthone which smells like mint.

The pathology related to loss of smell following a head injury is not in the severing of neural connections to the brain but rather in pathological biochemical changes which occur in the sensory receptors of the olfactory epithelium as we had previously described (3). These receptor changes, once identified biochemically, can be treated effectively with restoration of smell function even after severe head injury (1, 2).

Thus, the dire prediction of total and irrevocable loss of smell following head injury is simply an old shibboleth.

References

1. Levy, L.M., Henkin, R.I., Hutter, A., Lin, C.S., Schellinger, D. Increased brain activation in response to odors in patients with hyposmia after theophylline treatment demonstrated by fMRI. J. Comp. Asst. Tomog. 1998;22:760-770.

2. Thatcher, B.J., Doherty, A.E., Orvisky, E., Martin, B.M., Henkin, R.I. Gustin from human parotid saliva is carbonic anhydrase VI. Biochem. Biophys. Res. Comm. 1998;250:635-641.

3. Henkin, R.I., Velicu, I., Papathanasiu, A. cAMP and cGMP in human parotid saliva: relationships to taste and smell dysfunction, gender and age. Amer. J. Med. Sci. 2007;334:431-440.