Regarding the nasal diseases responsible for bilateral hyposmia or anosmia, the most frequent are those in which hypertrophy and hyperemia of the nasal mucosa prevent olfactory stimuli from reaching the receptor cells. Heavy smoking is the most frequent cause of this type of hyposmia in practice. Chronic atrophic rhinitis; sinusitis of allergic, vasomotor, or infective types; nasal polyposis; and overuse of topical vasoconstrictors are other common causes. Biopsies of the olfactory mucosa in cases of allergic rhinitis have shown that the sensory epithelial cells are still present, but their cilia are deformed and shortened and are buried under other mucosal cells. Influenza, herpes simplex, and hepatitis virus infections may be followed by hyposmia or anosmia caused by destruction of receptor cells; if the basal cells are also destroyed, this may be permanent. These cells may also be affected as a result of atrophic rhinitis and local radiation therapy or by a rare type of tumor (esthesioneuroblastoma) that originates in the olfactory epithelium. There is also a group of uncommon diseases in which the primary receptor neurons are congenitally absent or hypoplastic and lack cilia. One of these is the Kallmann syndrome of congenital anosmia and hypogonadotropic hypogonadism. A similar disorder occurs in Turner syndrome and in albinism because of an ill-defined congenital structural defect.
Anosmia that follows head injury is most often a result of tearing of the delicate filaments of the receptor cells as they pass through the cribriform plate, especially if the injury is severe enough to cause fracture. The damage may be unilateral or bilateral. With closed head injury, complete anosmia is relatively infrequent (6 percent of Sumner’s series of 584 cases), but lesser degrees are common in our experience. Some recovery of olfaction occurs in about one-third of cases over a period of several days to months. Beyond 6 to 12 months, recovery is negligible. Cranial surgery, subarachnoid hemorrhage, and chronic meningeal inflammation may have similar effects.
In some of the cases of traumatic anosmia, there is also a loss of taste (ageusia). Ferrier, who first described traumatic ageusia in 1876, noted that there was always anosmia as well—an observation subsequently corroborated by Sumner. Often, the ageusia also clears within a few weeks. A bilateral traumatic lesion near the frontal operculum and paralimbic region, where olfactory and gustatory receptive zones are in close proximity, would best explain this concurrence, but this has not been proven. As stated earlier, the interruption of olfactory filaments alone would explain a reduction in the ability to perceive the subtleties of specific flavors, but does not explain ageusia.
Olfactory acuity varies throughout the menstrual cycle, possibly through a imputed vomeronasal system in humans, and may be disordered during pregnancy as well. Nutritional and metabolic disorders such as thiamine deficiency (Wernicke disease), vitamin A deficiency, adrenal and perhaps thyroid insufficiency, cirrhosis, and chronic renal failure may give rise to anosmia, all as a result of sensorineural dysfunction. A large number of toxic agents—the more common ones being organic solvents (benzene), metals including platinum-containing chemotherapies, dusts, cocaine, corticosteroids, methotrexate, aminoglycoside antibiotics, tetracyclines, opiates, and l-dopa—can damage the olfactory epithelium (Doty et al). Alcoholics with Korsakoff psychosis also have a defect in odor discrimination (Mair et al). In this disorder, anosmia is presumably caused by degeneration of neurons in the higher-order olfactory systems involving the medial thalamic nuclei.