Pity the poor Olfactory Nerve.

Yes, Cranial Nerve I. The "ON" in the mnemonic chanted by first-year med students to recall the cranial nerves in neuroanatomy class.

Apparently, this sensory modality is an obsolete vestige of our neurological heritage that lacks the cache of its 11 siblings.

And how do I reach this conclusion?

If you read through any typical medical chart (with or without EHR assistance), the common documentation reads "Cranial Nerves 2-12 were within normal limits."

Ergo, the ability to smell has no clinical relevance.

However, a recent study published in Neurology looked at the olfactory capability of 231 servicemen who sustained polytrauma, blast exposure, and moderate to severe TBI using a standardized quantitative olfactory assessment and compared that clinical examination with the presence of orbitofrontal abnormalities on neuroradiographic studies. While the study's intent was to reduce unnecessary use of neuroimaging, the key clinical pearl was that the presence of an abnormal quantitative olfaction score had low sensitivity, but high specificity (100% to be precise) for the presence of intracranial abnormalities on neuroimaging!

The "take home message," as I see it, is that assessment of smell in patients with suspected brain injury can provide critical information regarding structural damage intracranially. In my clinic, every new evaluation of a patient with a suspected TBI whether from sports, road traffic incident, or otherwise includes a brief olfactory assessment as follows:

1. Assessment of the patency of each nostril/nares by visual inspection with a nasal speculum followed by a functional assessment in which each nares is occluded and the air flow capacity is checked.

2. Five separate containers (I use old film canisters) containing four olfactory triggers (chocolate, coffee, peanut butter, cloves) and one trigeminal trigger (mint) to detect feigning are used.

3. With eyes closed and one nostril occluded, each smell canister is presented to the patient with the following prompt: "I will be presenting you with five different smells that are commonly found in a kitchen. Tell me if you smell anything and then, what that smell is as best you can."

4. If the patient is unable to identify any of the smells (including the trigeminal trigger), that is an alert for the possibility of malingering.

5. If the patient states they smell something, but are unable to identify the odor, they are then given the five options to select from in a multiple choice format.

6. After each nostril has been evaluated, the patient is then queried to assess for a relative asymmetry in their ability to detect smells by the following prompts: "Was there a difference between the left and right sides in terms of the intensity of smell?

7. If so, which was stronger?" They are then asked to "quantify" the intensity as follows: Peanut butter (the most pure olfactory trigger) is presented to the "stronger" side and the patient is told "If this side (stronger) is a dollar's worth of smell, how much is this side worth (when testing the "weaker" side)?" This gives a percentage estimation regarding left and right intensity that define hyposmia (reduced, but not absent, smell detection) or dysosmia (impaired sense of smell). Anosmia, unilateral or bilateral, is total loss of smell.

Finally, several clinical "pearls" to keep in mind:

Patients with unilateral abnormalities in olfactory function most typically complain of altered sense of taste or the increased use of spices, peppers, etc as 70% of what we experience as "flavor" is really the aroma of the meal. (eg., Consider how food tastes bland when one has a coryzal syndrome and airways are blocked.)

The patient's family may be the first to complain that the food cooked by the patient is too spicy!

Patients with a history of GERD may present with an increase in their symptoms or nocturnal reflux due to excessive seasoning.

Many mild TBI patients based on Glasgow Coma Score criteria (13-15) will actually be moderate in severity if one inquires regarding the duration of post-traumatic amnesia (moderate defined as >24 hours of impaired memory function).

Over the past 34 years, Dr. O'Shanick's professional career has focused on treatment, research and public policy issues affecting individuals with brain injuries while on the faculties of four medical schools (UT-Houston, Medical College of Virginia, University of Virginia, and University of Southern California), as National Medical Director Emeritus of the Brain Injury Association of America, and as president and medical director of the Center for Neurorehabilitation Services in Richmond, Va., where he continues to maintain an active clinical practice. He has consulted to numerous national and international agencies, both private and governmental, regarding diagnostic and treatment guidelines for brain injuries.