AUTHOR AND EDITOR INFORMATION

Section 1 of 8  

• Authors and Editors
• Introduction And Background
• Anatomy And Physiology
• Etiology Of Smell And Taste Disorders
• Diagnosis Of Smell And Taste Disorders
• Treatment Of Olfactory And Gustatory Dysfunction
• Summary
• References

INTRODUCTION AND BACKGROUND

Section 2 of 8  

• Authors and Editors
• Introduction And Background
• Anatomy And Physiology
• Etiology Of Smell And Taste Disorders
• Diagnosis Of Smell And Taste Disorders
• Treatment Of Olfactory And Gustatory Dysfunction
• Summary
• References

Introduction

Disorders of taste and smell generally have been difficult to diagnose and treat, often because of a lack of knowledge and understanding of these senses and their disease states. An alteration in taste or smell may be a secondary process in various disease states, or it may be the primary complaint.

A 1994 survey revealed that 2.7 million American adults have an olfactory problem, and 1.1 million report a gustatory problem. An earlier study found that 66% of people are aware of a period in their life in which they had decreased smell acuity. Although often discounted and overlooked in the basic examination, deficiencies in taste and smell can cause anxiety, depression, and even nutritional deficiencies due to decreased enjoyment of food.

Loss of smell and/or taste may be life threatening, impairing detection of smoke in a fire or ability to identify spoiled food. Because approximately 80% of taste disorders are truly smell disorders, much of this article focuses on smell function and its lack, with additional discussion of taste and its disorders.

Terminology

The disorders of smell are classified as "-osmias" and those of taste as "-geusias."

• Anosmia - Inability to detect odors
• Hyposmia - Decreased ability to detect odors
• Dysosmia - Distorted identification of smell
  • Parosmia - Altered perception of smell in the presence of an odor, usually unpleasant
  • Phantosmia – Perception of smell without an odor present
  • Agnosia - Inability to classify or contrast odors, although able to detect odors
• Ageusia - Inability to taste
• Hypogeusia - Decreased ability to taste
• Dysgeusia – Distorted ability to taste

Smell and taste disorders can be total (all odors or tastes), partial (affecting several odors or tastes), or specific (only one or a select few odors or tastes).

ANATOMY AND PHYSIOLOGY

Section 3 of 8  

• Authors and Editors
• Introduction And Background
• Anatomy And Physiology
• Etiology Of Smell And Taste Disorders
• Diagnosis Of Smell And Taste Disorders
• Treatment Of Olfactory And Gustatory Dysfunction
• Summary
• References

Olfactory system

The olfactory neuroepithelium is located at the upper area of each nasal chamber adjacent to the cribriform plate, superior nasal septum, and superior-lateral nasal wall. It is a specialized pseudostratified neuroepithelium containing the primary olfactory receptors. In neonates, this area is a dense neural sheet, but, in children and adults, the respiratory and olfactory tissues interdigitate. As humans age, the number of olfactory neurons steadily decreases. In addition to the olfactory neurons, the epithelium is composed of supporting cells, Bowman glands and ducts unique to the olfactory epithelium, and basal cells that allow for the regeneration of the epithelium.

The sense of smell is mediated through stimulation of the olfactory receptor cells by volatile chemicals. To stimulate the olfactory receptors, airborne molecules must pass through the nasal cavity with relatively turbulent air currents and contact the receptors. Important determinants of an odor's stimulating effectiveness include duration, volume, and velocity of a sniff.

Each olfactory receptor cell is a primary sensory bipolar neuron. The average nasal cavity contains more than 100 million such neurons. The olfactory neurons are unique because they are generated throughout life by the underlying basal cells. New receptor cells are generated approximately every 30-60 days.

Each regenerating receptor cell extends its axon (cranial nerve I) into the CNS as a first-order olfactory neuron and forms synapses with target mitral and tufted cells in the olfactory bulb. The olfactory bulb cells, like all other CNS cells, do not regenerate, but they are able to accept new synapses from the receptor cells.

The bipolar olfactory neurons have a short peripheral process and a long central process. The peripheral process extends to the mucosal surface to end in an olfactory knob, which has several immobile cilia forming a dense mat at the mucosal surface. The cilia express the olfactory receptors that interact with odorants. The odorant receptors comprise part of a G-protein receptor superfamily associated with adenylate cyclase. Humans have many hundreds of different olfactory receptors, but each neuron expresses only one receptor type. This forms the basis of an olfactory map. Receptor-like neurons throughout the epithelium send axons that converge together within the bundled axons of the fila olfactoria deep to the epithelium.

These axons project through the cribriform plate to the ipsilateral olfactory bulb. The olfactory bulb cells contacted by the olfactory receptor cells include the mitral and tufted cells, arranged in specialized areas termed glomeruli. The axon terminals of receptor-like neurons synapse within the same glomeruli, forming an early topographical odorant map. Therefore, an odor is thought to activate a set of odorant receptors based on its chemical composition. The corresponding glomeruli of the olfactory bulbs are in turn activated, creating a unique pattern of excitation in the olfactory bulb for each odorant.

The glomerular cells are the primary output neurons of the olfactory bulb. Axons from these cells travel to the olfactory cortex, which is divided into 5 parts, including (1) the anterior olfactory nucleus, connecting the 2 olfactory bulbs through the anterior commissure, (2) the olfactory tubercle, (3) the pyriform cortex, which is the main olfactory discrimination region, (4) the cortical nucleus of the amygdala, and (5) the entorhinal area, which projects to the hippocampus.

The olfactory pathway does not involve a thalamic relay prior to its cortical projections. Relays from the olfactory tubercle and the pyriform cortex project to other olfactory cortical regions and to the medial dorsal nucleus of the thalamus and probably involve the conscious perception of odors.

Conversely, the cortical nucleus of the amygdala and the entorhinal area are limbic system components and may be involved in the affective, or hedonic, components of odors. Regional cerebral blood flow (measured with positron emission tomography) is significantly increased in the amygdala with introduction of a highly aversive odorant, and it is associated with subjective ratings of perceived aversiveness.

The vomeronasal organ (VNO), or Jacobson organ, is a bilateral membranous structure located within pits of the anterior nasal septum, deep to the nasal respiratory mucosa and next to the septal perichondria. Its opening in the nasal vestibule is visible in 91-97% of adult humans, and it is 2 cm from the nostril at the junction of the septal cartilage with the bony septum.

The VNO is believed by some to detect external chemical signals termed pheromones or vomeropherins through neuroendocrine-type cells found within the organ. These signals are not detected as perceptible smells by the olfactory system and may mediate human autonomic, psychologic, and endocrine responses.

Free trigeminal nerve endings, which are stimulated by aversive stimuli (eg, ammonia), exist in the nasal mucosa. These are processed via separate pathways from those in the olfactory system, described above.

Gustatory system

Individual taste buds with multiple receptor cells in each bud mediate taste perception. The taste buds are modified epithelial cells, not direct neurons as in olfactory function. These cells have a life span of approximately 10 days and arise continuously from the underlying basal cell layer in a process of constant turnover, similar to olfactory receptor cells.

Afferent nerve branches making synaptic contact with receptor cells penetrate the base of the taste bud. Taste buds occupy papillae, projections embedded in the tongue epithelium. A single nerve fiber innervates multiple taste papillae, and the nerve contact exerts trophic influences on the epithelium.

The specificity of the gustatory receptor cells is determined by the epithelium in which it resides, not by the particular nerve innervating the bud. A single fiber in the chorda tympani may respond to multiple types of tastes, some tastes more than others. This ability of single nerve fibers to respond to multiple types of stimuli is referred to as broad tuning, and it is shared by the olfactory system.

Lingual papillae have 4 forms, each occupying different areas of the tongue. In general, each form involves different aspects of taste.

• Fungiform papillae are located in the anterior two thirds of the tongue. People have an average of 33 fungiform papillae with approximately 114 buds per papilla. Innervation is through cranial nerve (CN) VII via the chorda tympani.
• Circumvallate papillae are located in the posterior two thirds of the tongue, consisting of 8-12 papillae, approximately 250 buds each, for an average of 3000 total buds. Cranial nerve IX innervates these, along with the entire posterior one third of the tongue.
• Foliate papillae reside in folds and clefts at the lateral borders of the tongue, with approximately 1280 buds. Cranial nerve IX innervates these buds.
• Filiform papillae have no taste buds.

Other locations of taste buds include the following:

• Soft palate - Innervated by CN VII via the greater superficial petrosal nerve
• Epiglottis and larynx - Supplied by the superior laryngeal branch of CN X
• Pharynx - Supplied by branches from CN IX and CN X

Free trigeminal nerve endings exist on the tongue; these detect strong, often displeasing or irritating sensations in the nasal cavity.

Five different taste qualities–salty, sweet, sour, bitter, and umami (monosodium glutamate/ 5' nucleotide)–have been identified. They can be detected in all regions of the tongue, but certain areas of the tongue have lower thresholds for each quality. Sweetness is most readily detected at the tip of the tongue, whereas salty taste receptors focus on the anterolateral borders. Sour tastes are best perceived along the lateral border, and bitter sensations are tasted most in the posterior one third. Another proposed taste quality is chalky (calcium salts).

ETIOLOGY OF SMELL AND TASTE DISORDERS

Section 4 of 8  

• Authors and Editors
• Introduction And Background
• Anatomy And Physiology
• Etiology Of Smell And Taste Disorders
• Diagnosis Of Smell And Taste Disorders
• Treatment Of Olfactory And Gustatory Dysfunction
• Summary
• References

Olfactory dysfunction

Disturbances in olfaction can result from pathologic processes at any level along the olfactory pathway. They can be thought of similarly to otologic dysfunctions as conductive or sensorineural defects.

In conductive (ie, transport) defects, transmission of an odorant stimulus to the olfactory neuroepithelium is disrupted. Sensorineural defects involve the more central neural structures. Overall, the most common causes of primary olfactory deficits are nasal and/or sinus disease, prior viral upper respiratory infections (URIs), and head trauma.

• Conductive defects
  • Inflammatory processes cause a large portion of olfactory defects. These may include rhinitis of various types, including allergic, acute, or toxic (eg, cocaine use). Chronic sinus disease causes progressive mucosal disease and often leads to decreased olfactory function despite aggressive allergic, medical, and surgical intervention.
  • Masses may block the nasal cavity, preventing the flow of odorants to the olfactory epithelium. These include nasal polyps (most common), inverting papilloma, and any malignancy.
  • Developmental abnormalities (eg, encephaloceles, dermoid cysts) also may cause obstruction.
  • Patients with laryngectomies or tracheotomies experience hyposmia because of a reduced or absent nasal airflow. Children with tracheotomies who are cannulated very young and for a long period may have a continued problem with olfaction even after decannulation because of a lack of early stimulation of the olfactory system.
• Central/sensorineural defects
  • Infectious and Inflammatory processes contribute to central defects in olfaction and in transmission. These include viral infections (which may damage the neuroepithelium), sarcoidosis (affecting neural structures), Wegener granulomatosis, and multiple sclerosis.
  • Congenital causes may be associated with neural losses. Kallman syndrome includes anosmia due to failed olfactory structure ontogenesis and hypogonadotropic hypogonadism. One study found the VNO to be absent in patients with Kallman syndrome.
  • Endocrine disturbances (eg, hypothyroidism, hypoadrenalism, diabetes mellitus) affect olfactory function.
  • Head trauma, brain surgery, or subarachnoid hemorrhage may stretch, damage, or transect the delicate fila olfactoria and result in anosmia.
  • Toxicity of systemic or inhaled drugs (eg, aminoglycosides, formaldehyde) can contribute to olfactory dysfunction. Many other medications and compounds may alter smell sensitivity, including alcohol, nicotine, organic solvents, and direct application of zinc salts.
  • Nutritional deficiencies (eg, vitamin A, thiamine, zinc) have been found to affect olfaction.
  • The number of fibers in the olfactory bulb decreases at an approximate rate of 1% per year throughout one's lifetime. These olfactory bulb losses may be secondary to sensory cell loss in the olfactory mucosa and a general decline in the CNS cognitive processing functions.
  • Degenerative processes of the central nervous system (eg, Parkinson disease, Alzheimer disease, normal aging) have been found to cause hyposmia. In the case of Alzheimer disease, olfactory loss can be the first symptom of the disease process. The sense of smell, more than taste, is impaired with aging, with a noticeable average decline in function during the seventh decade of life.

Once thought to be mostly a conductive defect through mucosal edema and polyp formation, chronic rhinosinusitis also appears to disrupt the neuroepithelium with irreversible loss of olfactory receptors through upregulated apoptosis.

Gustatory dysfunction

Much of what is perceived as a taste defect is truly a primary defect in olfaction, which alters flavor. The components that comprise the sensation of flavor include the food's smell, taste, texture, and temperature. Each of these sensory modalities is stimulated independently to produce a distinct flavor when food enters the mouth.

Taste may be enhanced by tongue movements, which increase the distribution of the substance over a greater number of taste buds. Adaptation in taste perception exerts a greater influence than in other sensory modalities.

Other than smell dysfunction, the most frequent causes of taste dysfunction are prior URI, head injury, and idiopathic causes, but many other causes can be responsible.

• Lesions at any site from the mucosa, taste buds, unmyelinated nerves, or cranial nerves to the brain stem may impair gustation.
• Oral cavity and mucosal disorders including oral infections, inflammation, and radiation-induced mucositis can impair taste sensation. The site of injury with radiotherapy is probably the microvilli of the taste buds, not the taste buds themselves, since taste buds are thought to be radioresistant.
• Poor oral hygiene is a leading cause of hypogeusia and cacogeusia. Viral, bacterial, fungal, and parasitic infections may lead to taste disturbances because of secondary taste bud involvement.
• Normal aging produces taste loss due to changes in taste cell membranes involving altered function of ion channels and receptors rather than taste bud loss.
• Malignancies of the head and neck, as well as of other sites, are associated with decreased appetite and inability to appreciate flavors.
• Use of dentures or other palatal prostheses may impair sour and bitter perception, and tongue brushing has been shown to decrease taste acuity.
• Surgical manipulation may alter taste permanently or temporarily.
  • Laryngectomy alters airflow, decreasing taste perception.
  • Resection of the tongue and/or portions of the oral cavity decreases the number of taste buds.
  • In otologic surgery, unilateral stretching of the chorda tympani nerve may result in temporary dysgeusia. Bilateral injury still may not result in permanent taste dysfunction because of the alternate innervation through the otic ganglion to the geniculate ganglion via the greater superficial petrosal nerve.
• Nutritional deficiencies are involved in taste aberrations. Decreased zinc, copper, and nickel levels can correlate with taste alterations. Nutritional deficiencies may be caused by anorexia, malabsorption, and/or increased urinary losses.
• Endocrine disorders also are involved in taste and olfactory disorders. Diabetes mellitus, hypogonadism, and pseudohypoparathyroidism may decrease taste sensation, while hypothyroidism and adrenal cortical insufficiency may increase taste sensitivity. Hormonal fluctuations in menstruation and pregnancy also influence taste.
• Heredity is involved in some aspects of gustation. The ability to taste phenylthiourea (bitter) and other compounds with an –N-C= group is an autosomal dominant trait. Studies have shown that phenylthiourea tasters detect saccharin, potassium chloride (KCl), and caffeine as more bitter. Type I familial dysautonomia (ie, Riley-Day syndrome) causes severe hypogeusia or ageusia because of the absence of taste bud development.
• Direct nerve or CNS damage, as in multiple sclerosis, facial paralysis, and thalamic or uncal lesions, can decrease taste perception.
• Many other diseases can affect gustation (eg, lichen planus, aglycogeusia, Sjögren syndrome, renal failure with uremia and dialysis, erythema multiforme, geographic tongue, cirrhosis).

DIAGNOSIS OF SMELL AND TASTE DISORDERS

Section 5 of 8  

• Authors and Editors
• Introduction And Background
• Anatomy And Physiology
• Etiology Of Smell And Taste Disorders
• Diagnosis Of Smell And Taste Disorders
• Treatment Of Olfactory And Gustatory Dysfunction
• Summary
• References

The first step in diagnosing any deficit of taste and smell is obtaining a thorough history and physical examination. Give attention to any antecedent URI, nasal or sinus pathology, history of trauma, other medical problems, and medications taken.

Order sinus CT scans if indicated by the history and examination. Generally, olfactory loss in the absence of CNS symptoms or an abnormal neurologic examination is highly unlikely to be associated with an intracranial mass such as a meningioma. However, an MRI of the brain is often recommended when the history is not straightforward or a secondary neurologic symptom or sign is obtained. Although a standard laboratory panel is not recommended, tests to evaluate for allergy, diabetes mellitus, thyroid functions, renal and liver function, endocrine function, and nutritional deficiencies may be obtained based on history and the physical examination. Olfactory epithelium biopsy is used primarily as a research technique.

Clinical measurement of olfaction

Quantitative measurement of smell and taste dysfunctions is most important when chemosensory dysfunction is the primary complaint. The major goal of sensory testing is to assess the degree of chemosensory dysfunction.

Clinical assessment can be time-consuming and difficult to perform precisely, but some approaches developed at the Connecticut Chemosensory Clinical Research Center and the University of Pennsylvania Clinical Smell and Taste Research Center attempt to standardize these efforts.

Three tests of olfactory function that evaluate threshold of odor detection and odor identification have been developed and are considered standard measurements of olfactory function. When given together and correlated, they can provide a reliable measure of olfactory ability. The Connecticut tests employ butanol threshold and odor identification. The University of Pennsylvania Smell Identification Test (UPSIT) is an odor identification test. Another test, the olfactory evoked response, has been used in research centers along with odor identification tests to evaluate aberrant olfaction with relation to neurologic disease.

• Butanol threshold test
  • The butanol threshold test used at the Connecticut Chemosensory Clinical Research Center involves a forced-choice test using an aqueous concentration of butyl alcohol in one sniff bottle and water in the other. The patient is asked to identify the bottle containing the odorant, with each nostril tested separately.
  • After each incorrect response, the concentration of butanol is increased by a factor of 3 until the patient either achieves 5 correct responses or fails to correctly identify the bottle with 4% butanol.
  • The detection threshold is recorded as the concentration at which the patient correctly identifies the butanol on 5 consecutive trials. The scoring relates the patient's threshold to a normal subject population.
• Connecticut odor identification test
  • The odor identification test used at the Connecticut Chemosensory Clinical Research Center involves 10 items separately presented to each nostril in opaque jars. The items include 7 odorants, including baby powder, chocolate, cinnamon, coffee, mothballs, peanut butter, and soap. The test also includes 3 trigeminal stimulants.
  • The patient is given a list of 20 items with the 10 stimuli and 10 other names as distractors and is asked to choose the name of the stimulus from this list. If the patient's choice is incorrect, a second chance is given to correctly identify the item.
  • The function score is derived from the number of odorants correctly identified, and it relates the patient's performance to a normal control group's performance.

The performances on the butanol threshold and the odor identification tests are averaged to determine a composite function score.

• University of Pennsylvania Smell Identification Test
  • The UPSIT involves 40 microencapsulated odors in a scratch-and-sniff format, with 4 response alternatives accompanying each odor. The patient takes the test alone, with instructions to guess if not able to identify the item.
  • Anosmic patients tend to score at or near chance (10/40 correct). The scores are compared against sex- and age-related norms, and the results are analyzed. This test has excellent test-retest reliability.
  • A chart is available relating scores to varying patient populations, including patients with multiple sclerosis, with Korsakoff syndrome, and those feigning anosmia. Those in the latter group tend to score much lower on the test than expected by chance.

The 3 above tests, given together and correlated, can provide a reliable measure of olfactory ability. Two more tests can be used; however, they are less reliable.

• Cross-Cultural Smell Identification Test
  • A variant of the UPSIT, which can be given in 5 minutes, was proposed for a quick measure of olfactory function. The 12-item Cross-Cultural Smell Identification Test (CC-SIT) was developed using input on the familiarity of odors in several countries, including China, Colombia, France, Germany, Italy, Japan, Russia, and Sweden.
  • The odorants chosen include banana, chocolate, cinnamon, gasoline, lemon, onion, paint thinner, pineapple, rose, soap, smoke, and turpentine. Representatives from each country identified these odorants most consistently.
  • This test is an excellent alternative for measuring olfactory function in the clinical setting, especially when time is limited, since it is rapid and reliable.
  • The disadvantage of this test is that its brevity limits its sensitivity in detecting subtle changes in olfactory function.
• Olfactory evoked response
  • To standardize the patient reaction to eye movements, electroencephalogram (EEG) electrodes and an electrooculogram measure olfactory evoked potentials. A visual tracking task is performed to ensure constant alertness to the task, and headphones playing white noise are worn to mask auditory clues.
  • Either carbon dioxide (no odor but a trigeminal stimulant) or hydrogen sulfide is delivered via an olfactometer to the nose in a constantly flowing air stream. N1 is the first negative peak measured, and P2 is the second positive trough. Latencies are measured to these 2 values.
  • In patients with neurologic disease, the UPSIT revealed abnormality more frequently than olfactory evoked responses.

For clinical olfactory function testing, the authors' experience is that the self-administered UPSIT test allows for practical use during a busy clinical practice. However, in the absence of the olfactory tests described above, a simple screening test using a common alcohol pad can be used. The envelope is opened at one end and presented to the patient. With the patient's eyes closed, the pad is then positioned at the level of the umbilicus and slowly brought closer to the nose. The patient is instructed to notify the tester when the alcohol is again detected. The distance of the pad from the nose correlates with the patient's olfactory ability, with a distance of less than 20 cm indicating a less-than-average smell function.

Clinical measurement of taste

Evaluation of taste disorders is not as well developed as that of olfaction. It involves measurement of detection or recognition thresholds. No comparable approach to odor identification tests is available because only 4 basic taste sensations exist.

Salivary adaptation and size of the tongue area stimulated influence the threshold assessment. Thus, these tests are extremely variable. Changes in threshold detection do not necessarily indicate correlation to changes in suprathreshold taste intensity. Testing of the taste thresholds alone does not provide a full picture of the level of gustatory function or dysfunction. For example, a patient after radiation therapy may recover recognition thresholds for all 4 taste qualities, but the magnitude of the perceived tastes still may be quite depressed.

• Magnitude matching
  • Suprathreshold testing involves assessment of the patient's perceptions of taste intensities at levels above threshold. One method of measuring this quality is with a psychophysical procedure known as magnitude matching.
  • Other tests of suprathreshold tastes have involved assigning numbers to their sensations, but no direct comparison across individuals can be made. Specific numbers, such as 10 or 100, do not have any intrinsic psychologic value.
  • Conversely, magnitude matching makes use of one sensory modality that is presumed to be normal (in this case, hearing) in comparison to a deficiency in another sensory modality (taste) by using the following procedure:
    • Several concentrations of sodium chloride, sucrose, citric acid, and quinine hydrochloric acid, along with several loudness levels of a 1000-Hz tone, are provided for the magnitude matching task.
    • The patient sips each solution and expectorates, and the tones are presented via headphones. The patient provides estimates of perceived magnitude for each stimulus.
    • The results are scaled in relation to loudness functions to reveal abnormalities of taste as depressed psychophysical functions. In other words, patients with hypogeusia associate stronger taste concentrations with weaker tones than normal patients.
    • The major limitations of this testing modality are its dependence on normal hearing and its complicated design, which takes a significant amount of time to administer and analyze.
• Spatial test
  • Taste function in the various areas of the tongue and oral cavity can be measured using a spatial test. Because the gustatory system is multiply innervated, damage to one of the 3 major nerves (ie, chorda tympani, glossopharyngeal, greater superficial petrosal) or their ganglia may cause a disturbance of taste that can be evaluated only by testing the anatomic areas supplied by those nerves.
  • To test these areas, 4 standardized sizes of filter paper are soaked with strong concentrations of the 4 basic tastes. The papers are randomly placed on the 4 quadrants of the tongue and on both sides of the soft palate. Patients then identify the quality of the taste and rate its intensity using the same scale as in whole mouth assessment.

TREATMENT OF OLFACTORY AND GUSTATORY DYSFUNCTION

Section 6 of 8  

• Authors and Editors
• Introduction And Background
• Anatomy And Physiology
• Etiology Of Smell And Taste Disorders
• Diagnosis Of Smell And Taste Disorders
• Treatment Of Olfactory And Gustatory Dysfunction
• Summary
• References

Treatment of olfactory dysfunction

Any treatment of olfactory disorders must first treat the specific causative abnormality if it has been identified from diagnostic tests, history, and physical examination.

• Local nasal and/or sinus conditions should be optimally managed with nasal sprays, decongestants, antihistamines, antibiotics, and/or nasal and systemic steroids, if applicable. Polyps and sinus disease that are resistant to medical management should be surgically addressed to remove the conductive defect.
• Aggressive treatment of these disorders, if present, provides a good chance of improvement. In general, conductive olfactory losses are the most amenable to treatment.
• A few of the sensorineural olfactory defects also have specific treatments, but these are fewer and have less chance of success. Generally, viral processes that damage the olfactory neuroepithelium, sarcoidosis, and multiple sclerosis do not have specific remedies; however, steroids may be administered in an attempt to limit the inflammation.
• Endocrine disturbances may be addressed by administration of the deficient hormone, as with hypothyroidism. Control of diabetes mellitus may slow neural degeneration of the olfactory system.
• Nutritional deficits may be reversed with zinc, vitamin A, thiamine, or any other specific nutrient that may be lacking.
• Idiopathic cases of olfactory loss are not amenable to specific treatment, although some unproven remedies have been attempted. The best known of these is zinc sulfate. It has not been proven beneficial and is generally regarded as ineffective. In addition, over-the-counter zinc nasal sprays have been implicated in the cause of smell loss, although this has not been proven.
• Other unproven remedies include pharmacologic doses of vitamins, steroid tapers, and tricyclic antidepressants (for their effect on CSF catecholamines). Steroid tapers, once thought to benefit only those with polyp disease, have recently shown to improve olfactory function in patients with sensorineural defects as well as conductive disorders.
• A viral URI can cause extensive scarring and replacement of the olfactory neuroepithelium with respiratory epithelium, but studies suggest that stem cells remain, allowing for potential regeneration of the olfactory epithelium. Recovery of smell in these cases can take weeks to months and, in some instances, may never occur. Unfortunately, besides the possibility of oral steroids as mentioned above, no proven therapy exists to improve function in these patients.
• Eliminating toxins (eg, cigarette smoke, airborne pollutants) may help.
• Overall, the patient with olfactory disorders needs reassurance that these generally are not life-threatening problems and that many other individuals experience them. In some patients, psychiatric evaluation and treatment may be warranted. Most importantly, the physician is responsible for warning the patient with olfactory disorders of the hazards associated with the inability to smell odors such as smoke, natural gas leaks, and spoiled food. Smoke detectors, as well as natural gas and propane gas detectors, are commercially available to help eliminate such risks.

Treatment of gustatory dysfunction

As with olfactory problems, direct initial treatment of gustatory dysfunction toward the causative abnormality, if possible.

• Address any nasal pathology causing decreased olfaction and thus affecting taste.
• Treat mucosal disorders (eg, infections, inflammations).
• Treat oral candidiasis and other local factors, and replete any vitamin deficiency that may cause glossitis.
• Aid patients in eliminating local irritants (eg, mouthwashes, ill-fitting dentures)
• In mucositis or dry mouth as a result of radiation therapy, artificial saliva or salivary stimulants and local anti-inflammatory medications may improve some taste dysfunction.
• Correcting endocrine disorders with the appropriate hormone replacement may improve the taste disorder.
• Consider eliminating a medication suspected of causing dysgeusia unless the medication is crucial in treating another medical problem and cannot be substituted.
• In the case of familial dysautonomia, in which patients have a complete lack of lingual taste buds, subcutaneous administration of methacholine has been reported to normalize previously elevated taste thresholds for all taste qualities. The cholinergic mechanism is probably related to taste transduction via free nerve endings because these patients have no taste receptors.
• Some gustatory deficits are untreatable (eg, some cases of nerve or CNS damage, end-stage diabetic neuropathy, multiple sclerosis). Certain mechanical aids exist to enable the patient to make use of whatever taste function is left.
• Advise patients that chewing food well increases the release of the tastant and increases saliva production to further distribute the chemicals. Switching foods during the meal decreases the phenomenon of adaptation and can improve detection of the tastes.
• Finally, for patients who are anosmic or hyposmic (including many elderly people), simulated odors are available to use while cooking to augment the sensation of flavor. A drawback of these simulated odors is that, to normosmic people, the smell is quite pungent. Thus, these odors cannot be used in mixed groups of anosmic and normosmic individuals.

SUMMARY

Section 7 of 8  

• Authors and Editors
• Introduction And Background
• Anatomy And Physiology
• Etiology Of Smell And Taste Disorders
• Diagnosis Of Smell And Taste Disorders
• Treatment Of Olfactory And Gustatory Dysfunction
• Summary
• References

Smell and taste disorders traditionally have been overlooked in most aspects of medical practice because these specialized senses often are not considered critical to life. However, they affect everyday enjoyment of food, and they impair detection of the potentially dangerous smells of smoke or spoiled food.

Anxiety and depression, as well as anorexia and nutritional deficiencies, may result from taste and smell disorders. Many causes of smell and taste disorders exist, and the modalities of treatment begin with treating the specific deficit, if possible.

Unfortunately, much about the diagnosis and treatment of taste and smell dysfunction remains to be discovered. Most taste defects are truly alterations in perception of flavor due to smell defects, and they should be treated accordingly.

Some standardized tests, such as the butanol threshold, odor identification, UPSIT, and olfactory evoked potentials, can help diagnose and measure olfactory dysfunction; however, diagnosis remains an imprecise science. Measurement of gustatory disturbances is even less precise and more difficult.

Reassurance is one of the most important aspects of treatment in these disorders because cures are often difficult to obtain and may take weeks, months, or years.

REFERENCES

Section 8 of 8

• Authors and Editors
• Introduction And Background
• Anatomy And Physiology
• Etiology Of Smell And Taste Disorders
• Diagnosis Of Smell And Taste Disorders
• Treatment Of Olfactory And Gustatory Dysfunction
• Summary
• References

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• Dodd J, Castellucci VF. Smell and taste: the chemical senses. In: Kandel ER, Schwartz JH, eds. Principles of Neural Science. NY:. Elsevier Science;1991:512-529.
• Doty RL, Marcus A, Lee WW. Development of the 12-item Cross-Cultural Smell Identification Test (CC- SIT). Laryngoscope. Mar 1996;106(3 Pt 1):353-6. [Medline].
• Downey LL, Jacobs JB, Lebowitz RA. Anosmia and chronic sinus disease. Otolaryngol Head Neck Surg. Jul 1996;115(1):24-8. [Medline].
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Article Last Updated: Jun 8, 2006