Clinical Olfactory Disorders
Olfactory disorders can be classified as either the loss of ability to detect odorants or the distortion of odors and are classified as “-osmias.” Anosmia refers to complete loss of the ability to detect odorants, whereas hyposmia is a decreased ability to smell. Dysosmia refers to distortion of the quality of odors, and includes parosmia, the perception of an altered sense of smell. Patients may complain that a particular odorant now has a new, often unpleasant odor, such as food smelling foul or putrid, and can be associated with loss of smell sensitivity. Phantosmia, another form of dysosmia, is the perception of an odor when no odorant is present. Dysosmias are far less common than either hyposmia or anosmia. However, parosmia and phantosmia can be significantly disruptive for patients, as the odors they perceive tend to be quite unpleasant and may smell like leaking gas, burning, or rotten fumes and may not be masked by foods, thus affecting their ability to eat or enjoy daily activities.12,13
Surveys of randomly selected adults have found a 1.4% prevalence of self-reported olfactory disorders in the general population.6 The actual prevalence of olfactory disorders, as identified by odor identification objective testing, occurs at a much higher range of up to 20%, with nearly 5% with anosmia and 15% with hyposmia.7,8 This discrepancy may be due partly to older adults not recognizing their loss of olfactory ability. Although only 1% of the population younger than 65 years has major olfactory dysfunction, the sense of smell decreases significantly with age, with a 50% incidence of olfactory loss in persons between 65 and 80 years and over 60% incidence after age 80.3,5
Similar to the classification of hearing loss, disorders of olfaction can also be divided into conductive or sensorineural loss, including both peripheral and central causes ( Table 4.1 ). Epidemiologic studies of olfactory disorders find the most common causes to include post-upper respiratory infection (URI; 26–36%); nasal and sinus disease (both obstructive polypoid disease and inflammatory disease of the neural olfactory epithelium; 15–21%); head trauma (17–18%); and toxins/drugs, congenital, and idiopathic (18–22%). However, reviews of olfactory disorders have listed over 200 etiologies.1
Conductive Olfactory Disorders
The presence of sinonasal polyps can decrease nasal airflow and block the access of odorants to the olfactory epithelium; however, patients may still have some retro-nasal airflow, allowing the ability to detect the flavor of food. Other causes of decreased nasal airflow include nasal septal deformities, tracheostomy, previous laryngectomy, or nasal cavity tumors. Although rhinosinusitis may cause a conductive loss, and a change in the sense of smell is one of the most predictive symptoms of true rhinosinusitis, evidence also points to a sensorineural olfactory loss especially with long-standing inflammatory disease.14,15 Sinonasal tumors, including esthesioneuroblastomas, inverted papillomas, or sinonasal malignancies, may cause a conductive olfactory loss and may be associated with epistaxis, headache, or airflow obstruction.
Sensorineural Olfactory Disorders
Post-Upper Respiratory Infections
Loss of olfaction after a URI is one of the most common causes of smell disorders, and occurs more commonly in women and the elderly.1,16 Olfactory dysfunction during a URI can initially be conductive, but persistence of loss of smell after resolution of other symptoms indicates sensorineural injury to the olfactory epithelium. In patients with post-viral olfactory dysfunction, the presence of rhinovirus, coronavirus, parainfluenza virus, and Epstein-Barr virus have been detected in the nasal discharge.17 Patients may present with hyposmia, anosmia, or dysosmia, with a higher incidence of hyposmia than is seen with other sensorineural causes of olfactory disorders and more parosmias than other causes.1,16 The exact mechanism of injury is unknown, but biopsies of olfactory epithelium reveal patchy degeneration, suggesting direct injury to the olfactory epithelium, either from viral injury or the inflammatory reaction. The epithelium exhibits marked disorganization with few receptors in patients with anosmia and reduced numbers of receptors in patches in patients with hyposmia, and the olfactory bulb has decreased volume.18,19 Patients with post-URI loss can experience some degree of recovery, but the likelihood of recovery decreases with increasing age, severity of loss, and duration of loss. Improvement varies in different studies, with 32 to 67% of patients showing significant improvement after URI olfactory loss, but less than 10% improve into the absolute normal range and less than 15% into the age-adjusted normal range.20–22
Conductive | |
Rhinosinusitis | |
Nasal polyposis | |
Nasal cavity tumor | |
Sensorineural | |
Post-URI/viral | |
Trauma and head injury | |
Congenital | |
Toxins | |
Medications | |
Aging | |
Neurodegenerative disorders | |
Alzheimer disease | |
Parkinson disease | |
Abbreviations: URI, upper respiratory infection. | |
The viral-associated loss of olfactory neurons may actually be protective; the death of virally infected olfactory neurons may prevent the passage of viruses to the central nervous system (CNS). Certain viruses can enter the brain through an olfactory route, as the olfactory neurons provide a direct connection from the environment at the epithelial level to their first synapse within the olfactory bulb.23,24 During the polio outbreak of the early 20th century, poliovirus was initially thought to penetrate the CNS through the olfactory epithelium, and in North America, attempts to prevent polio infection in children included treatment of the nose with zinc sulfate and Pontocaine. This did not prevent spread of the infection (later found to spread by fecal-oral transmission) and left ~10 to 15% of the patients anosmic.25 Some strains of influenza A have been found in the brains of mice infected through an olfactory transmission, whereas other strains of the virus cause apoptosis of olfactory neurons. The viral particles are enclosed in apoptotic bodies of dying cells and cleared by the surrounding olfactory epithelium and are not transmitted to the olfactory bulb. Herpes simplex virus (HSV) causing encephalitis localizes to the fronto-temporal regions of the brain, and HSV antigen has been found in the olfactory tract and cortex. These findings support the theory that virally infected olfactory epithelium undergoes apoptosis to prevent viral CNS infection, resulting in a loss of olfactory neurons and olfactory dys-function after URI.23,24 Although the mechanism of injury may differ from direct viral invasion of the olfactory epithelium, patients infected with HIV exhibit increased olfactory thresholds early in the disease.26
Trauma and Head Injury
Posttraumatic loss of smell is characterized by a sudden onset of olfactory dysfunction. Unlike post-URI loss, traumatic injury more commonly results in complete anosmia or dysosmia.1–3 The mechanism includes injury anywhere along the olfactory tract, including stretching or shearing of olfactory fibers through the cribriform plate, injury to the olfactory bulb or frontal cortex, or central brain trauma to the olfactory regions. A mouse model of traumatic injury includes surgical removal of the olfactory bulb or olfactory nerve axotomy in mice, causing retrograde degeneration of the olfactory receptor neurons. Regenerating ORNs attempts to regrow them through the cribriform plate to resynapse with the olfactory bulb, but if they are unable to reconnect, the ORNs do not survive.27 Biopsies in patients with posttraumatic olfactory dysfunction reveal disorganization of the epithelium with fewer mature neurons and an increased number of immature neurons lacking projecting cilia with receptors.18 A disordered reconnection of olfactory neuron axons to the olfactory bulb or a loss of some of the receptors responsible for complex odor identification is hypothesized to be responsible for dysosmias following traumatic injury with perception of changes in odor, similar to synkinesis after a facial nerve injury.27
The severity of head injury is associated with the severity of olfactory loss. Loss of consciousness, facial or skull fractures, or occipital and lateral blows are more likely to be associated with anosmia than less severe head injuries or frontal blows.28–30 Although some studies have found a lower rate of recovery of olfactory ability after head trauma compared with URI olfactory loss, more recent research has found a similar likelihood of recovery.20–22 The authors concluded that the amount of olfactory loss, not the origin or causative factor, is the determinant of prognosis, and more severe loss is less likely to improve significantly.20 Due to comorbidities associated with significant head injury, olfactory deficits may not be noted at the time of the trauma and patients may not present until after recovery from other injuries. Sinonasal fractures causing conductive loss are extremely rare. Finally, iatrogenic injury to the olfactory nerves or bulb may occur with an anterior craniotomy or neurosurgical procedures, resulting in anosmia.
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