Olfactory Loss
- History of olfactory loss, often manifesting as loss of the sense of taste.
- Sensory evaluation with quantitative tests indicating olfactory loss.
The sense of smell determines the flavor and palatability of food and drink. Along with the trigeminal system, it serves as a monitor of inhaled chemicals, including dangerous substances such as natural gas and smoke, and odors common to everyday life. The loss of smell or a decreased ability to smell affects approximately 1% of people under age 60 and more than half of the population beyond this age.
Abnormalities of olfaction include the following: (1) anosmia (absence of the sense of smell); (2) hyposmia (diminished olfactory sensitivity); (3) dysosmia (distorted sense of smell); (4) phantosmia (perception of an odorant when none is present); and (5) agnosia (inability to classify, contrast, or identify odor sensations verbally, even though the ability to distinguish between odorants may be normal).
Disorders of the sense of smell are caused by conditions that interfere with the access of the odorant to the olfactory neuroepithelium (transport loss), injure the receptor region (sensory loss), or damage the central olfactory pathways (neural loss). Table 10–1 summarizes the most common causes of olfactory dysfunction.
|
Transport olfactory loss can result from the following conditions: a swollen nasal mucous membrane in acute viral upper respiratory infections; bacterial rhinitis and sinusitis; allergic rhinitis; and structural changes in the nasal cavity (eg, deviations of the nasal septum, polyps, and neoplasms). It is also likely that abnormalities of mucus secretion, in which the olfactory cilia are immersed, could result in a loss of olfactory sensitivity.
Sensory olfactory loss results from damage to the olfactory neuroepithelium by any of the following causes: viral infections, neoplasms, the inhalation of toxic chemicals, drugs that affect cell turnover, and radiation therapy to the head.
Neural olfactory loss can occur in a number of ways: head trauma, with or without fracture of the base of the anterior cranial fossa or cribriform plate area; Parkinson disease; Alzheimer disease; Korsakoff psychosis; vitamin B12 deficiency; neoplasms of the anterior cranial fossa; neurosurgical procedures; administration of neurotoxic agents (eg, ethanol, amphetamines, topical cocaine, aminoglycosides, tetracycline, cigarette smoke); and in some congenital disorders such as Kallmann syndrome. Other endocrine disorders can affect smell perception, including Cushing syndrome, hypothyroidism, and diabetes mellitus.
Molecular aspects of olfaction are now becoming understood. In mammals, there are probably 300–1000 olfactory receptor genes belonging to 20 different families located on various chromosomes in clusters. The receptor genes are present at more than 25 different human chromosomal locations. Olfactory receptor proteins are G protein-coupled receptors characterized by the presence of seven alpha-helical transmembrane domains. Each olfactory neuron expresses only one or, at most, a few receptor genes, providing the molecular basis of odor distinction. The olfactory system is thus characterized by three important features: (1) the large family of receptor genes exhibits remarkable diversity allowing response to a variety of smells, (2) the receptor proteins exhibit exquisite specificity allowing for odor discrimination, and (3) odor associations are well kept in memory long after the incident that formed the association is forgotten.
Many patients experience olfactory dysfunction due to one or more of the following causes: obstructive nasal and sinus disease, post-upper respiratory infection, cranial trauma, and congenital causes. Aging, exposure to toxins, and idiopathic causes also account for the loss of smell.
Air flows through the medial and anterior to the lower part of the middle turbinate to reach the olfactory cleft. Nasal obstruction at this area or above it caused by severe mucosal swelling, tumors, nasal polyps, or bony deformities can result in hyposmia or anosmia. In addition, patients often report a loss of sense of smell during an upper respiratory infection; generally, this loss is due to airway obstruction secondary to mucosal swelling. Olfactory ability should improve or return altogether with relief of the obstruction.
Approximately 5–10% of adult patients with head trauma report olfactory loss to be in the anosmic range. The degree of olfactory loss is generally associated with two things: the severity of the trauma and the site of cranial trauma. Total anosmia is more likely to occur with occipital traumas; however, frontal blows most frequently cause olfactory loss.