8 Evaluation and Treatment of Olfactory Disorders Often overlooked in comparison to our other senses, the sense of smell is still an important way by which we experience the world around us. As in other animals, smell at its basic level tells us whether a substance or environment is good or bad, safe or dangerous. It can act as a warning system detecting smoke from a fire or the stench of spoiled food. Smell also imparts flavor to food, and by doing so, changes a necessity of daily survival into a matter of enjoyment. It greatly affects our quality of life and can trigger some of our deepest memories; it triggers emotion with the smell of a holiday dinner or of a spouse’s cologne or perfume. The quality and intensity of this perception depend on the anatomic state of the nasal epithelium and the status of the peripheral and central nervous systems. Dysfunction at any one of the many steps along the olfactory pathway can disable a patient’s sense of smell and greatly affect his or her quality of life. The relevant anatomy and physiology of olfaction explain how an odor is carried into the nose and eventually is perceived by the brain as a distinct smell. Before an odorant can activate a receptor it must first reach the olfactory cleft. The pathway of odorant exposure to the nasal cavity is usually thought to occur through an anterior pathway via the nares and anterior nasal cavity. It has become clear, however, that a retronasal stimulation of the olfactory epithelium is also important and probably plays a role in flavor appreciation during eating.1 This secondary pathway is important in cases of anterior nasal obstruction from polyp disease, in which odor identification appears to be more effective through a retronasal route.2 As the odorant molecule traverses the narrow passageway of the nasal cavity, it must first cross from the air phase to the mucus phase to gain access to the olfactory receptors. The odorant molecules must be not only soluble in the mucus but also free enough within the mucus to interact with receptors on the olfactory epithilium.3 Changes in the character of the mucus can influence the diffusion time required for odorant molecules to reach the receptor sites.4 The olfactory epithelium corresponds to an area in the superior recess of the right and left nasal cavities, between the septum and middle/superior turbinates, and below the cribriform plate, termed the olfactory cleft. The epithelium is a continuous sheet at birth but develops irregular borders and is progressively replaced with respiratory epithelium in patches thereafter.5 This respiratory metaplasia is thought to increase in size even in normal-functioning adults. The area of olfactory epithelium in adults generally includes the surface of the superior turbinates and occasionally the anterior extent of the middle turbinates, covering an area of roughly 1 to 2 cm2.6,7 The olfactory mucosa is a pseudostratified columnar neuroepithelium. In the deepest layer are the basal cells, which are the putative stem cells that give rise to all components of the epithelium. In all primates and mammals the olfactory neurons are continually being replaced by the dividing basal cells. The combined presence of immature olfactory neurons with mature neurons and mitotic cells in the basal layer of the olfactory epithelium in human autopsy specimens strongly supports the presence of regenerating olfactory neurons in humans.7 It is this unique ability of the olfactory mucosa to renew itself that enables the possibility of full recovery after injury to the epithelium. In fact, intensive research studying the multipotency of these basal cells is ongoing. The cells have been shown to harbor the ability to become neuronal, as well as nonneuronal, cells outside of the olfactory system.8 Microvillar-capped sustentacular cells occupy the most apical layer of the epithelium. Beneath the basement membrane, serous Bowman glands send ducts through the epithelium to the surface. The olfactory neurons occupy the region superficial to the basal cells, with more mature cell bodies residing apically. They are bipolar in shape with dendrites terminating in knobs with immotile cilia at the surface of the mucosa. These cilia contain the olfactory receptors providing increased surface area for sampling the odorants introduced into the nasal cavity. The olfactory axons exit through the basal lamina and converge with other axons into nerve bundles, termed fila olfactoria (cranial nerve I), that travel through the lamina propria and eventually traverse the cribriform plate to contact the olfactory bulb. The axons are surrounded by special olfactory ensheathing cells that are unique because they share characteristics that are common with both Schwann cells and central glial cells. Because of the unique regenerative properties of this neuroepithelium, there has been interest in the role of the ensheathing cells in this process and its possible therapeutic potential for repair of peripheral nerve injury. These same axons make first-order synapses in the glomeruli of the olfactory bulb. Further signal transduction proceeds along the olfactory tract to higher processing centers of the olfactory cortex at the base of the frontal lobes and medial aspect of the temporal lobes. From the olfactory cortex, information is sent to the insular cortex in the thalamus where olfactory and taste information is integrated.9 The gene family responsible for olfactory receptors is the largest within the human genome, coding for close to 700 different transmembrane G-protein receptor types, although a large proportion of these are nonfunctional pseudogenes.10 Each olfactory neuron expresses one single receptor type. In rodents, olfactory neurons with the same receptor type converge on an average of two glomeruli per bulb, creating the beginning of a specialized odorant map. It is clear that one odorant does not activate one receptor type but many receptor types are activated to various degrees. Therefore, by stimulating a combination of different receptor types, a pattern of glomerular activation occurs. In this way, the system can encode an almost limitless number of different odorants. The most important element in the evaluation of a patient with an olfactory disorder is obtaining the history. A detailed history will provide a diagnosis in the vast majority of cases. The physician should first assess what type of olfactory disorder the patient is describing. Quantitative disorders are deficiencies of detection. Hyposmia is the decreased ability to detect odors, and anosmia is an inability to detect odors. Patients with qualitative disorders may have difficulty identifying an odor (parosmia) or they may perceive odors when none are present (phantosmia). Although there are many proposed etiologies of olfactory disorders, the most common are because of upper respiratory infections (URIs), head trauma, and rhinosinusitis; therefore, significant time should be directed toward identifying these causes in the history.11–15 Given the large contributions of smell to flavor, it is not unusual for patients to describe a loss of taste as the presenting complaint. By confirming that the patient can detect salty, sweet, sour, or bitter tastes, one may then focus specifically on olfaction. This also gives the clinician an opportunity to educate patients on the differences between smell, taste, and flavor. Patients should be asked about the severity of the smell loss and how it affects their everyday life. Descriptions of hazardous events including the inability to detect cooking fires, natural gas leaks, or spoiled food are often relayed by the patient and it presents an opportunity to counsel the patient on the risks of smell loss. Timing of the onset of the disorder can be very helpful. Sudden onset of smell loss is usually related to an URI or trauma, whereas gradual smell loss is usually associated with causes such as aging, neurodegenerative disease, and long-term chronic rhinosinusitis (CRS). Fluctuation in the ability to smell is associated frequently with CRS and polyps. Having no memory of the ability to smell implies a congenital smell loss. In this case, further questions relating to a delay in sexual maturity and family history of the same should be asked to check for Kallmann syndrome and an endocrine referral should be considered if the patient is prepubescent.16 Physicians should inquire about the presence of URI symptoms, head trauma (regardless of severity), acute or chronic exposure to chemicals, changes in medications, and use of over-the-counter medications. Inquiry should be made into the use of topical nasal zinc preparations. These medications, designed to prevent or shorten URIs, have been implicated in causing sudden smell loss.17,18
Anatomy and Physiology
Evaluation
History
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