
Am Fam Physician. 2023;108(3):240-248
Patient information: See related handout on smell and taste disorders.
Author disclosure: No relevant financial relationships.
Disorders of smell and taste are reported by approximately one-fifth of people 40 years and older, and one-third of people 80 years and older. These disorders affect quality of life and the ability to identify smoke and toxins. Smell and taste disorders can be early signs of dementia or Parkinson disease and are associated with increased mortality. Dysfunction may be apparent or may develop insidiously. Screening questionnaires are available, but many patients are unaware of their disorder. Most smell and taste disorders are due to sinonasal disease but also could be caused by smoking, medications, head trauma, neurodegenerative disease, alcohol dependence, or less common conditions. The differential diagnosis should guide the evaluation and include anterior rhinoscopy and an examination of the oral cavity, head, and cranial nerves. Further investigation is often unnecessary, but nasal endoscopy and computed tomography of the sinuses may be helpful. Magnetic resonance imaging of the head with contrast should be performed if there is an abnormal neurologic examination finding or if trauma or a tumor is suspected. Olfactory testing is indicated in refractory cases or for patients with poor quality of life and disease associated with smell or taste dysfunction. Smell and taste disorders may resolve when reversible causes are treated, but improvement is less likely when they are due to trauma, age, or neurodegenerative disease. Olfactory training is a self-administered mindful exposure therapy that may improve olfactory function. Physicians should encourage patients to ensure that smoke and other alarms are operational and to adhere to food expiration dates.
Disorders of smell and taste affect a person's quality of life, health, and safety. The COVID-19 pandemic renewed attention to these disorders, and one of the Healthy People 2030 objectives is to increase the proportion of adults with smell or taste disorders who discuss the problem with a clinician.1 Olfactory dysfunction is reported by 23% of people in the United States 40 years and older and 39% of those 80 years and older.2,3 Altered taste is reported by 19% of people 40 years and older, and 27% of those 80 years and older.2 Smell and taste disorders can affect food consumption habits, which may lead to chronic disease3 (Table 14). Depression, poor sleep, dementia, unintentional weight loss, and malnutrition are associated with disordered smell or taste.5–15 The ability to detect sources of danger, such as smoke or poison, depends on smell or taste.10,11 When directly tested, 20.3% of a nationally representative sample of adults 70 years and older without known dysfunction misidentified smoke, and 31.3% misidentified natural gas.3

Dysfunction in smell and taste occurs in 40% to 50% of patients diagnosed with COVID-19, often without rhinorrhea or nasal congestion. |
A prospective cohort study found that recovery of smell and taste after COVID-19 occurred for most patients by seven days, and more than 80% recovered by three months. |
When directly tested, 20.3% of a nationally representative sample of adults 70 years and older without known olfactory dysfunction misidentified the scent of smoke, and 31.3% misidentified the smell of natural gas. |
More than 95% of patients with Parkinson disease have smell impairment, and up to 75% have anosmia or hyposmia. |
Clinical recommendation | Evidence rating | Comments |
---|---|---|
Patients should be referred to otolaryngology for objective testing of olfactory or gustatory function in refractory cases or if they have depression, poor sleep, dementia, unintentional weight loss, or malnutrition.3,20,38–40 | B | Case series of 602 patients, multiple observational studies |
Olfactory training should be offered to patients with persistently poor quality of life due to olfactory dysfunction.63–65 | A | Consistent evidence from multiple systematic reviews and meta-analyses, including randomized controlled trials and prospective cohort studies, showing clinically significant improvement after viruses and other etiologies |
Physicians should counsel patients with olfactory dysfunction about the risks of occupational chemical exposure, adherence to food expiration dates, signs of food spoilage, and home fire and explosive gas monitoring.3,40 | C | Expert opinion and a cross-sectional study |

Disorder | Description |
---|---|
Taste | |
Ageusia | Complete loss of ability to taste |
Dysgeusia | Distorted taste perception (triggered by a taste stimulus) |
Hypogeusia | Reduced ability to taste |
Phantogeusia | Gustatory hallucination (occurs without a stimulus) |
Smell | |
Anosmia | Complete loss of ability to smell |
Hyposmia | Reduced ability to smell |
Parosmia | Distorted odor perception (triggered by a stimulus) |
Phantosmia | Olfactory hallucination (occurs without a stimulus) |
There are many clinical presentations and causes for smell and taste disorders (Table 2).16–19 Etiologies range from sinonasal disease to less common conditions such as Sjögren syndrome (Table 3).4 When only taste disorder is perceived by the patient, it is often due to olfactory dysfunction.20–26 Therefore, without an apparent taste insult, physicians should focus their evaluation on the olfactory system. Figure 1 provides an approach to evaluating smell and taste disorders in primary care.

Cause | Pathology | History |
---|---|---|
Age-related (presbyosmia) | Loss or replacement of olfactory neurons with respiratory epithelium Decreased basal cell proliferation Decrease of interneurons in olfactory bulb with reduced activity in olfactory cortex | Insidious onset; unlikely to see improvement Olfactory dysfunction predicts five-year mortality |
Neurodegenerative causes (e.g., Alzheimer disease, Parkinson disease) | Alzheimer disease: neurofibril changes in the olfactory bulb and higher olfactory network Parkinson disease: Lewy bodies deposited in the olfactory tract, olfactory bulb, and anterior olfactory nucleus17 | Insidious onset; unlikely to see improvement Onset can be early in Alzheimer and Parkinson diseases |
Other medication/toxin exposure/iatrogenic | Altered receptor function by binding G-protein coupling or affecting calcium or sodium channel activity | Sudden onset; mostly resolves with ceasing exposure; can persist in some cases requiring treatment; can have medicolegal implications18 |
Postviral olfactory dysfunction | Viral common cold pathogens, COVID-19, influenza, respiratory syncytial virus, parvovirus, HIV Long-term inflammation causes neuroepithelial remodeling to respiratory epithelium | Sudden onset with little fluctuation; often associated with parosmia; one in three recovers in the 14 months after presentation for care19 |
Posttraumatic olfactory dysfunction | Severing of olfactory nerve filament or central nervous system injury | Sudden or delayed onset; fluctuation is uncommon; phantosmia and parosmia are common 10% recover by 13 months, but up to 35% can recover depending on severity19 |
Sinonasal (e.g., chronic rhinosinusitis with polyps) | Obstruction of the olfactory cleft; temporary interference with olfactory receptor binding due to inflammation; eventual neuroepithelial remodeling/central nervous system changes | Gradual onset and fluctuation over time; typically improves with nasal/systemic corticosteroids Not commonly associated with parosmia |

Cause | Leading etiologies* |
---|---|
Most common | |
Sinonasal conditions | Upper respiratory tract infection (especially viral, including COVID-19), allergic rhinitis, chronic rhinosinusitis, nasal polyps |
More common | |
Head trauma | Damage to cribriform plate, shearing forces, and intracranial damage; facial trauma |
Neurodegenerative disorders | Parkinson disease, parkinsonism, Alzheimer disease, mild cognitive impairment, multiple sclerosis |
Less common | |
Medications | Chemotherapy, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, dihydropyridine calcium channel blockers, diuretics, intranasal zinc, antimicrobials (macrolides, terbinafine, fluoroquinolones, protease inhibitors, griseofulvin, penicillins, tetracyclines, nitroimidazoles [metronidazole (Flagyl)]), antiarrhythmics, antithyroid agents, antidepressants, anticonvulsants, lipid-lowering agents |
Intoxicants or illicit substances | Alcohol dependence, cocaine use |
Toxins | Ammonia, hairdressing chemicals, gasoline, formaldehyde, paint solvents, welding agents, benzene, sulfuric acids, cadmium, acrylates, iron, lead, chromium |
Chronic medical conditions | Renal or hepatic failure, complicated type 2 diabetes mellitus, cancer, HIV |
Structural or mechanical conditions | Ischemic stroke, subarachnoid or intracranial hemorrhage, brain or sinonasal tumor |
Nutritional deficiencies | Malnutrition, pernicious anemia or vitamin B12 deficiency, deficiencies in vitamins B6 or A, niacin, zinc, or copper |
Postsurgical state | Nasal surgery (septal or sinus) |
Postradiation | Especially to head and neck |
Congenital conditions | Kallmann syndrome, anosmia |
Psychiatric conditions | Anorexia nervosa (not bulimia), major depressive disorder, bipolar disorder, schizophrenia |
Endocrine conditions | Pregnancy, hypothyroidism, Addison disease, Cushing syndrome |
Autoimmune/inflammatory conditions | Sjögren syndrome, systemic lupus erythematosus, sarcoidosis, herpes encephalitis |

Anatomy and Physiology
Chemicals that cause smells (i.e., odorants) are absorbed through the mucosa of the nose, nasopharynx, and oropharynx. Odorants stimulate olfactory neurons in the neuroepithelium over the cribriform plate. Olfactory neurons project directly to the olfactory bulb, which communicates with the olfactory cerebral cortex. Olfactory receptors regenerate every eight to 10 days, followed by five days for the maturation of cilia.27–29 Dysfunction along these pathways can result in a smell disorder.30–32
Odorants and tastants (i.e., particles and liquids that cause the taste sensation) dissolve in saliva and directly contact gustatory receptors in dedicated cells for each of the five tastes (bitterness, saltiness, sourness, sweetness, and umami [savory]). These cells are in taste buds on the tongue, soft palate, pharynx, larynx, epiglottis, and the proximal one-third of the esophagus. Different nerves innervate the anterior two-thirds of the tongue, posterior one-third of the tongue, palate, pharynx, and larynx. The trigeminal nerve also mediates certain characteristics of smell and taste, such as irritation and temperature. Taste is mediated by several different nerves depending on anatomic location; therefore, gustatory loss is less common than olfactory loss.9,33,34
Clinical Assessment
HISTORY
Validated questionnaires help clinicians screen for subjective olfactory dysfunction (Table 4).11,35,36 A National Health and Nutrition Examination Survey used three questions that were not formally validated but are a reasonable approach to screen patients for olfactory dysfunction.2,3 There are no validated subjective tools to assess taste.16
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