The olfactory area is located high in the nasal vault above the superior turbinate. The neurons of the first cranial nerve penetrate the cribriform plate and travel to the cortex at the base of the frontal lobe on top of the cribriform plate.

The most common mechanism of acute anosmia or hyposmia is nasal obstruction, which prevents air from reaching olfactory areas high in the nose. Food is tasteless while the problem persists. In most instances, such as those related to the common cold or allergic rhinitis, the process is fully reversible, but sometimes more lasting damage is done. Influenza is known for its ability to cause permanent destruction of the nasal receptors especially in the elderly; the onset is often acute. Viral syndromes are also common causes of hyposmia or anosmia. Another mechanism of acute anosmia is head trauma, in which the nerve filaments coming through the cribriform plate are damaged due to shear injury; the prognosis for recovery after head trauma is poor. Topically applied intranasal medications may compromise smell. Increasingly implicated is zinc spray for the treatment of the common cold, as evidence accumulates of an association with acute hyposmia and anosmia.

More gradual onset of reduced smell is typical of an expanding mass lesion at the base of the frontal lobe. Meningiomas, neuroblastomas, and aneurysms of the anterior cerebral circulation are the most important sources of this problem. Upward extension of a mass lesion into the frontal lobe is manifested by a lack of initiative, personality change, and forgetfulness; posterior extension may involve the optic chiasm.

Parosmia can result from local nasal pathology, such as empyema of the nasal sinuses or ozena, a chronic rhinitis of unknown etiology that causes thick, greenish discharge and crusting (see Chapter 219). In some cases, ozena is reflective of atrophic rhinitis, most commonly resulting from nasal surgeries. These patients often complain about nasal crusting and parosmia or cacosmia (a constant foul smell within the nose). Klebsiella and Pseudomonas and other polymicrobial flora are often cultured from the discharge. Olfactory hallucinations are central in origin and may present as the aura of a seizure. The responsible lesion is typically found in the area of the uncus. Olfactory delusions are reported by schizophrenic patients, whereas their sense of smell remains intact.

The mechanisms of reduced smell associated with hypothyroidism, hypogonadism, and hepatitis are not understood. Speculation has centered on the deficiencies of various trace metals, particularly copper and zinc, but replacement therapy has been disappointing.

The tongue, the seventh and ninth cranial nerves, and the hippocampal region of the cerebral cortex make up the taste apparatus. The front of the tongue detects sweet and salty tastes, the sides of the tongue sense sour tastes, and the large circumvallate papillae in the back detect bitter tastes. The pharynx also has the ability to sense taste. The taste buds are concentrated in the anterior two thirds of the tongue, which is innervated by the chorda tympani branch of the seventh cranial nerve. The posterior third of the tongue and palate are supplied by the special sensory fibers of the glossopharyngeal nerve.

The most frequent source of diminished fine taste is impairment of smell because the appreciation of taste is at least one third to one half olfactory in origin. Isolated taste impairment is 40 times less common than is olfactory impairment. In addition, the taste buds may be directly injured by alcohol use and smoking. The common observation that food tastes better after these habits are terminated is due to improvement in both the olfactory receptors and the taste buds. Aging results in small but measurable changes in acuity for salty and bitter tastes but not for sweet or sour ones. Elderly men differ from elderly women in that men selectively lose sensitivity to low concentrations of salt, whereas women have a more progressive loss of salt sensitivity.

Diseases and drugs that dry the mouth—for example, Sjögren syndrome and tricyclic antidepressants—reduce the threshold for taste. Chorda tympani and seventh nerve lesions are rarely bilateral and therefore do not produce a complete loss of taste. Cerebral mass lesions usually do not involve the hippocampal gyrus. Depression, endocrinopathies, and a host of drugs are associated with complaints of altered taste. The mechanisms are unknown, but in many instances, the primary disturbance seems to be, in part, an alteration of smell. Other factors, such as poor dentition, that negatively influence oral cavity hygiene can also negatively affect the sense of taste.