Cranial nerve I (CN I) constitutes the primary receptor cells for the sense of smell. This nerve monitors the intake of airborne agents into the human respiratory system and largely determines, along with the sense of taste, the flavor and palatability of foods and beverages. In addition to purveying esthetic pleasures, CN I warns of spoiled foods, leaking natural gas, polluted air, and smoke, and mediates elements of basic communication (e.g., mother-infant interactions). Of particular interest to the neurologist is the fact that alterations in the ability to smell are among the first, if not the first, signs of Alzheimer's disease and idiopathic Parkinson's disease.

Olfactory dysfunction can affect a patient's safety, nutritional status, and quality of life. Among 750 consecutive patients presenting to the University of Pennsylvania Smell and Taste Center with mainly olfactory problems, 68 percent experienced an altered quality of life, 46 percent reported changes in appetite or body weight, and 56 percent noted adverse influences on daily living or psychological well-being. [1 Many anosmics report increased use of sugar and seasonings to compensate for their olfactory disorder, a situation detrimental to persons with diabetes and salt-sensitive hypertension. In experimental settings, older persons with diminished smell function ingest foods that younger persons find distasteful, implying that such individuals are at considerable risk for food poisoning. It is well documented that a disproportionate number of elderly persons die from accidental gas poisoning, which is due, in large part, to their decreased ability to smell.

Most patients presenting with decreased "taste" function actually have decreased smell function. The perception of decreased ability to "taste" during deglutition is usually due to a loss of flavor sensations derived from retronasal stimulation of the olfactory receptors rather than to a loss of taste bud-mediated sensations per se. Thus, such flavors as coffee, chocolate, vanilla, strawberry, pizza, licorice, steak sauce, root beer, and cola disappear when CN I is markedly damaged, leaving intact only sweet, sour, salty, bitter, and umami (monosodium glutamate-like) sensations. Whole-mouth taste function is much more resilient to pathological or trauma-related alterations than is olfactory function, in large part because the taste buds have redundant innervation from several cranial nerves (i.e., CN VII, IX, and X).

The nomenclature for olfactory dysfunction is straightforward. Anosmia refers to a loss of ability to smell, whereas hyposmia or microsmia refers to diminished ability to smell. Dysosmia is distorted or perverted smell perception, such as when a rose smells more like garbage than a rose ( parosmia, cacosmia) or when a medicine-like smell is present in the absence of odor stimulation following head trauma ( phantosmia). General or total anosmia implies inability to smell all odorants on both sides of the nose. Partial anosmia implies an inability to smell certain odorants. In some cases, partial anosmia is indicative of a decreased sensitivity to a broad spectrum of odorants (general hyposmia), with the decrement exceeding the absolute threshold for only some odorants. Specific anosmia, the inability to smell one or a few odorants in the presence of an otherwise normal sense of smell, is rarely a reason for medical consultation. Hyperosmia is a rare condition of abnormally acute smell function. This occurs, for example, in some epileptic patients prior to the onset of ictal activity.

Olfactory dysfunction can be either bilateral or unilateral

(sometimes termed binasal or uninasal). Thus, if a person has anosmia on the left side of the nose but not the right, the condition is described as unilateral left anosmia. Anosmia that is present on both sides of the nose is termed bilateral anosmia, or, as noted previously, total anosmia.

Occasionally, complaints of dysosmia reflect foul odors that are produced either within the nasal cavity (e.g., as a result of infections within the nose) or within the body proper (e.g., as a result of altered metabolism). In the latter case, bad odors may come from saliva, exhaled breath, skin secretions, or urine. Although the basis of a number of such problems has nothing to do with alterations in any element of the olfactory pathway, the term dysosmia is still appropriate for describing the complaint but not the clinical syndrome. Examples are trimethylaminuria (fish odor syndrome), in which a metabolic defect results in excretion of fishlike smelling amines, and cat's odor syndrome, a childhood neurological disorder associated with a defect in the enzyme beta-methyl-crotonyl-CoA carboxylase.


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