Anosmia has been found in some patients with temporal lobe epilepsy and particularly in such patients who had been subjected to anterior temporal lobectomy. In these conditions, Andy and coworkers have found impairment in discriminating the quality of odors and in matching odors with test objects seen or felt.
As with other sensory modalities, olfaction (and taste) is diminished with aging (presbyosmia). The receptor cell population is depleted, and if the loss is regional, neuroepithelium is slowly replaced with respiratory epithelium (which is normally present in the nasal cavity and serves to filter, humidify, and warm incoming air). Neurons of the olfactory bulb may also be reduced as part of the aging process.
Bilateral anosmia has been a manifestation of malingering, now that it has been recognized as a compensable disability. The fact that true anosmics will complain inordinately of a loss of taste (but show normal taste sensation) may help to separate them from malingerers. If it were to be perfected, testing of olfactory evoked potentials would be of use here.
The nasal epithelium or the olfactory nerves themselves may be affected in Wegener granulomatosis and by craniopharyngioma, respectively. A meningioma of the olfactory groove may implicate the olfactory bulb and tract and may extend posteriorly to involve the optic nerve, sometimes with optic atrophy; if combined with papilledema on the opposite side, these abnormalities are known as the Foster Kennedy syndrome (see Chap. 12). A large aneurysm of the anterior cerebral or anterior communicating artery may produce a similar constellation. With tumors confined to one side, the anosmia may be strictly unilateral, in which case it will not be reported by the patient but will be found on examination. The limitations of testing each side of the nose separately have been mentioned earlier. These defects in the sense of smell are attributable to lesions of either the receptor cells and their axons or the olfactory bulbs, and current test methods do not distinguish between lesions in these two localities. In some cases of increased intracranial pressure, olfactory sense has been impaired without evidence of lesions in the olfactory bulbs.
The term specific anosmia has been applied to an unusual olfactory phenomenon in which a person with normal olfactory acuity for most substances encounters a particular compound or class of compounds that is odorless to him, although obvious to others. In a sense, this is a condition of “smell blindness,” analogous to color blindness. The basis of this disorder is unclear although there is evidence that specific anosmia for musky and uriniferous odors is inherited as an autosomal recessive trait (see Amoore).
Whether a true hyperosmia exists is a matter of conjecture, but it is so frequently reported by migraineurs that the problem seems worthy of attention. Anxious, highly introspective individuals may complain of being unduly sensitive to odors, but for the most part there is no proof of an actual change in their threshold of perception of odors. Interestingly, Menashe and colleagues have linked enhanced sensitivity to the odorant isovaleric acid to single nucleotide polymorphism (SNP) variants of the olfactory receptor gene OR11H7P, and more associations of this kind may be elucidated.