The olfactory nerve is a sensory nerve with but one function, smell. Only volatile substances soluble in lipids or water are perceived as odors. In true anosmia there is loss of ability to perceive or recognize not only scents but also flavors, for much of what is interpreted as taste involves smell. Flavor is a synthesis of sensations derived from the olfactory nerves, taste buds, and other sensory end-organs. A patient with olfactory impairment may complain of loss of taste rather than of smell. Patients with unilateral anosmia may be unaware of any impairment. Olfaction is a phylogenetically ancient sensation. In lower mammals where olfaction is extremely important, the olfactory cortex constitutes a large part of the cerebral hemispheres. In higher primates and man, the area of the uncus and anterior hippocampal gyrus is likely the primary olfactory cortex. The connections between the olfactory system, hypothalamus, certain brainstem nuclei, and autonomic centers is pertinent to the understanding of many visceral functions. Olfaction is the only sensation not directly processed in the thalamus.

Important historical points to address in a patient with a smell or taste disturbance include past head injury; smoking; recent upper-respiratory infection; systemic illness; nutrition; and exposure to toxins, medications, or illicit drugs. Changes in the flavor of coffee may be particularly informative. Unilateral loss of smell is more significant than bilateral, which may be caused by many conditions, primarily conductive (Table 8.1). Impairments due to anosmia are not trivial. The problem is not merely that patients with disturbances of smell sensation miss out on some of life’s pleasures; they may also miss olfactory danger signals, such as spoiled food, smoke, and leaking gas. As with hearing, olfactory deficits are sometimes divided into (a) conductive deficits, due to processes interfering with the ability of odorants to contact the olfactory epithelium, such as nasal
polyps; and (b) sensorineural or neurogenic deficits, due to dysfunction of the receptors or their central connections.