Ageusia: The Complete Loss of Taste

The human ability to perceive taste serves not only as an essential evolutionary mechanism for survival and nutritional regulation but also as a primary source of hedonic pleasure and social bonding. When the neurological and physiological machinery responsible for taste processing fails entirely, an individual experiences ageusia, a rare and clinically profound sensory disorder. This comprehensive dictionary entry explores the neuroanatomy, etiology, assessment methods, and psychological ramifications of complete gustatory loss, shedding light on a condition that fundamentally disrupts the human experience of sustenance.

Ageusia

1. Concise Definition

Ageusia is the complete absence or loss of the gustatory modality, characterized by the inability of an individual to perceive any of the fundamental qualitative taste dimensions, which traditionally include sweet, sour, salty, bitter, and umami. It represents the most severe manifestation of gustatory dysfunction, distinguishing itself from partial gustatory attenuation or qualitative perceptual distortions.

In clinical neurology and otorhinolaryngology, genuine ageusia is exceedingly uncommon because the peripheral innervation of the lingual apparatus and oral cavity is redundantly distributed across multiple distinct cranial nerves. Consequently, true total ageusia typically requires extensive bilateral peripheral nerve damage, severe systemic medication toxicity, or focal central lesions within the primary gustatory cortex or medullary relay nuclei. Far more frequently, patients presenting with a subjective complaint of total taste loss are experiencing severe anosmia, wherein the cessation of retronasal olfaction impairs the complex synthesis of culinary flavor while primary tongue-based chemosensation remains neurophysiologically intact.

From an academic standpoint, ageusia must be understood as both an objective neurosensory deficit and a complex neuropsychological condition. The absolute abolition of gustatory input alters metabolic homeostasis, appetite regulation, and neuroendocrine cephalic phase responses, while also exerting substantial downstream consequences on affective wellbeing, social engagement, and quality of life.

2. Etymology & Linguistic Origin

The term ageusia is derived from classical linguistic roots, constructed through Greek morphological elements. The prefix a- (ἀ-), known as the alpha privative, denotes absence, negation, or lack. This prefix is appended to the Greek root geusis (γεῦσις), which translates directly to “taste” or “the sense of taste.” The root itself stems from the Proto-Indo-European verbal root *ǵéus-, signifying “to taste,” “to try,” or “to choose,” from which terms in various Indo-European languages emerged, including the Latin gustus and the English verb “choose.”

The suffix -ia (-ία) is an abstract noun-forming formant employed in Ancient Greek and Latinized modern medical terminology to designate pathological states, bodily conditions, or physiological abnormalities. The lexical synthesis ageusia thus literally denotes “the condition of having no taste.” The term formally entered modern scientific and medical lexicons during the late eighteenth and early nineteenth centuries as European anatomists and physiologists systematically codified disorders of the special senses, standardizing nomenclature alongside analogous sensory deficits such as anosmia (loss of smell) and ageusia’s qualitative counterpart, parageusia.

3. Pronunciation & Grammatical Form

The standard pronunciation of the term in International Phonetic Alphabet (IPA) transcription is /eɪˈɡjuːziə/ or /eɪˈdʒuːsiə/, with minor phonetic variations across British and American English dialects. In standard American English, it is most commonly articulated as ay-GEW-zee-uh or uh-GYOO-zee-uh, whereas British medical nomenclature frequently utilizes ay-JEW-zee-uh.

Grammatically, ageusia functions as an uncountable, abstract noun. It possesses several morphological derivatives across academic discourse:

• Ageusic (/eɪˈɡjuːzɪk/): Adjective denoting of, relating to, or afflicted by ageusia (e.g., “the ageusic patient exhibited no reaction to concentrated sucrose solutions”); alternatively used as a substantive noun to refer to an individual suffering from the condition.
• Ageustia (/eɪˈɡjuːstiə/): An accepted, though less common, orthographic and phonetic variant occurring primarily in archaic or specialized regional medical texts.
• Hemiageusia (/ˌhɛmi.eɪˈɡjuːziə/): A compound noun indicating the unilateral loss of taste sensation affecting precisely one lateral half of the tongue, pointing diagnostically to discrete ipsilateral neuropathology.

4. Detailed Conceptual Explanation

To fully grasp ageusia, one must rigorously disentangle the colloquial concept of “flavor” from the rigorous physiological concept of “taste.” In day-to-day parlance, individuals employ the word taste to encompass the totality of sensory impressions elicited during mastication and deglutition. Scientifically, however, flavor represents a multimodal cognitive construct assembled within secondary and tertiary association cortices, drawing upon simultaneous inputs from retronasal olfaction, trigeminal somatosensation (conveying texture, temperature, and chemesthesis such as the pungency of capsaicin or the cooling of menthol), and the gustatory system itself. Ageusia refers exclusively to the failure of the specialized gustatory sensory pathway.

The primary gustatory apparatus begins at the peripheral level within specialized neuroepithelial structures termed taste buds, which are distributed across the tongue’s fungiform, foliate, and circumvallate papillae, as well as the soft palate, pharynx, and upper esophagus. Each taste bud houses between 50 and 150 spindle-shaped taste receptor cells categorized into Types I, II, and III. Type II cells express G-protein coupled receptors responsible for transducing sweet, bitter, and umami stimuli, whereas Type III cells mediate ionotropic signaling associated with sour (acidic) and salty sensations via proton-sensitive and sodium-selective ion channels. When tastants interact with these receptor complexes, membrane depolarization triggers the release of neurotransmitters, including adenosine triphosphate (ATP) and serotonin, onto primary afferent nerve fibers.

True ageusia occurs when this signaling pathway is compromised in its entirety, either bilaterally at the receptor level or along the dedicated ascending neural conduits. Peripheral sensory transmission relies upon three distinct cranial nerves:

• Cranial Nerve VII (Facial Nerve): Specifically its chorda tympani branch and greater petrosal nerve, innervating the anterior two-thirds of the tongue and the soft palate.
• Cranial Nerve IX (Glossopharyngeal Nerve): Innervating the posterior one-third of the tongue and circumvallate papillae, playing a critical role in transducing bitter and sour compounds.
• Cranial Nerve X (Vagus Nerve): Innervating the scattered taste buds of the epiglottis, larynx, and upper digestive tract.

These primary gustatory afferents project centrally to converge upon the rostral portion of the solitary tract nucleus in the medulla oblongata, termed the gustatory nucleus. From the solitary nucleus, secondary neurons ascend ipsilaterally via the central tegmental tract to the parvocellular division of the ventroposteromedial nucleus of the thalamus (VPMpc). Tertiary thalamic projections terminate in the primary gustatory cortex, located in the anterior insula and adjacent frontal operculum. A secondary projection extends onward to the orbitofrontal cortex, where gustatory information converges with olfactory and limbic inputs to mediate hedonic valence and associative reward processing. Because of this redundant, multi-nerve bilateral organization, complete bilateral ageusia demands either widespread receptor destruction or massive, strategic disruptions along these pathways.

5. Historical Development

The scientific conceptualization of taste pathology evolved in tandem with classical neuroanatomy and physiological psychophysics throughout the nineteenth and twentieth centuries. In antiquity, Hippocratic and Galenic treatises acknowledged variations in appetite and digestive disposition, but classical scholars generally conflated lingual sensations with tactile warmth and wetness, lacking the microscopic tools necessary to distinguish specialized chemoreceptors from generic mucosal innervation.

The foundational breakthrough for modern gustatory neurology emerged during the mid-nineteenth century with the histomorphological discovery of taste buds. In 1867, German anatomist Franz von Leydig, followed closely by Christian Lovén and Gustav Schwalbe, systematically identified and documented the microscopic architecture of taste buds within mammalian papillae. These anatomical discoveries permitted physicians to conceptualize taste as an autonomous sensory modality distinct from general lingual somatosensation, laying the theoretical groundwork for identifying discrete pathological deficits such as ageusia.

In the late nineteenth and early twentieth centuries, clinical neurologists, most notably Sir William Gowers and Harvey Cushing, observed regional gustatory deficits in patients undergoing surgical interventions for acoustic neuromas, trigeminal neuralgia, and middle-ear infections. By correlating localized nerve transections with regional loss of taste, these early pioneers mapped the functional distribution of the chorda tympani and glossopharyngeal nerves. The recognition of complete ageusia as a distinct clinical entity arose through documented cases of neurotoxic drug administrations, profound head trauma involving basilar skull fractures, and cerebrovascular accidents affecting the brainstem and insula.

The late twentieth century witnessed the formalization of standardized psychophysical taste evaluation through the contributions of sensory scientists such as Linda Bartoshuk. Bartoshuk and colleagues revolutionized the quantification of taste deficits by developing specialized psychophysical scaling tools and spatial taste testing methodologies. In doing so, modern sensory science firmly differentiated true physiological ageusia from self-reported taste loss caused by olfactory pathology, solidifying the diagnostic criteria utilized today.

6. Theoretical Foundations

Understanding ageusia within modern sensory physiology requires grounding in several overarching theoretical frameworks that govern chemosensory processing, neural coding, and cognitive appraisal.

A primary theoretical architecture is the Labeled-Line versus Across-Fiber Pattern Coding Model. For decades, sensory neurobiologists debated whether individual taste qualities are mediated by discrete, dedicated neural channels (the labeled-line model) or by broad, distributed patterns of activity across an ensemble of non-specific gustatory fibers (the across-fiber pattern model). Contemporary molecular and optogenetic research supports a predominantly labeled-line configuration at the peripheral level: individual taste receptor cells, and their corresponding primary afferents, are tuned predominantly to singular basic taste modalities. Within this framework, ageusia represents the simultaneous silencing of all parallel labeled lines, distinguishing it from selective taste agnosias or partial insensitivities where individual lines remain operational.

A second crucial paradigm is the Multisensory Binding Framework. Flavor perception is an exemplar of crossmodal perceptual binding, wherein the human central nervous system integrates heterogeneous inputs from olfactory, gustatory, and trigeminal sensory channels into a unified phenomenological percept. According to predictive processing and multisensory integration theories, top-down cognitive models generate expectations of taste based on retro-olfactory odor bouquets and visual food cues. In true ageusia, the feedforward gustatory prediction error is persistently absolute; the chemical tastant fails to elicit any signal, disrupting the multisensory binding process and leaving the individual with sterile, decoupled tactile and olfactory impressions.

Finally, the Hedonic Alliesthesia Theory, originally formulated by Michel Cabanac, posits that the internal physiological state of the organism dictates the perceived pleasure or displeasure derived from a sensory stimulus. In a healthy nervous system, hunger magnifies the positive valence of caloric stimuli such as sugars and salts. In the ageusic state, alliesthesia is completely uncoupled at the primary oral interface: while a patient may cognitively understand caloric deprivation, they cannot experience gustatory pleasure, which often precipitates profound disruptions in cephalic metabolic reflexes and feeding drive.

7. Key Components, Types & Dimensions

Ageusia exhibits specific clinical profiles based on its underlying pathology, neuroanatomical locus, and temporal progression. The disorder is classified along several critical dimensions:

• Complete Ageusia: The total, bilateral incapacity to discern any of the canonical basic tastes across the entire oral cavity, including the tongue, soft palate, and pharynx.
• Partial Ageusia: A condition characterized by the selective loss of one or several specific taste qualities (such as an inability to detect sweet or bitter) while other modalities remain functional, often linked to selective receptor channelopathies or localized enzymatic failures.
• Hemiageusia: The unilateral loss of taste perception strictly confined to one lateral half of the lingual surface, typically caused by ipsilateral injury to the lingual nerve, chorda tympani, or unilateral brainstem lesions prior to decussation.
• Specific / Regional Ageusia: Loss of taste sensation localized to discrete anatomical zones of the oral mucosa (for instance, isolated anterior two-thirds loss versus posterior circumvallate loss), reflecting branch-specific cranial nerve damage.
• Peripheral Ageusia: Resulting from pathological disruptions occurring at the level of the taste receptor cells, lingual papillae, or the peripheral trajectories of cranial nerves VII, IX, or X. Etiologies include radiation therapy, severe glossitis, local surgical transection, or zinc deficiency.
• Central Ageusia: Originating from damage within the central nervous system pathways, specifically targeting the nucleus tractus solitarius, the central tegmental tract, the ventroposteromedial thalamic nucleus, or the primary gustatory cortex in the insular-opercular region.
• Transient vs. Permanent Ageusia: Variations in temporal persistence; transient forms frequently stem from reversible pharmacological toxicities, viral infections, or acute mucosal inflammation, whereas permanent ageusia reflects irreversible neuronal necrosis or complete structural avulsion of gustatory pathways.

8. Examples & Illustrative Cases

To contextualize how ageusia manifests in clinical settings, the following real-world clinical presentations provide clear illustrations of its diverse presentations:

Case 1: Iatrogenic Bilateral Nerve Injury
A 45-year-old patient underwent bilateral middle-ear tympanoplasty for extensive cholesteatomas. Postoperatively, the patient reported an absolute inability to detect sweetness, saltiness, or bitterness on the front of the mouth. Clinical gustometry demonstrated profound anterior ageusia corresponding to bilateral surgical trauma of the chorda tympani. While posterior glossopharyngeal function preserved a subtle perception of concentrated bitterness at the circumvallate papillae, the patient experienced the condition as functionally total ageusia, illustrating how anterior lingual denervation profoundly impairs routine eating experiences.

Case 2: Central Insular Infarction
A 62-year-old individual presented to a tertiary neurology clinic following an acute ischemic stroke localized to the right middle cerebral artery territory, specifically involving the anterior insula and frontal operculum. Thorough quantitative sensory mapping revealed profound left-sided hemiageusia. The patient could readily identify concentrated sucrose and sodium chloride on the right half of the tongue but perceived identical solutions as plain water on the left half, validating the anatomical mapping of the primary gustatory cortex.

Case 3: Chemotherapeutic and Radiation Toxicity
A 54-year-old patient with squamous cell carcinoma of the base of the tongue underwent high-dose external beam radiation therapy combined with cisplatin chemotherapy. Within three weeks of initiating therapy, the patient developed complete, generalized ageusia alongside severe mucositis. The rapidly dividing neuroepithelial cells of the taste buds suffered acute cytotoxic apoptosis. The patient was entirely unable to distinguish concentrated solutions of sugar, salt, citric acid, or quinine. Following treatment cessation and nutritional supplementation, partial recovery occurred over an eighteen-month period as basal progenitor cells slowly regenerated the lingual taste buds.

9. Measurement & Assessment

Accurate clinical assessment of ageusia requires distinguishing true gustatory deficits from olfactory impairments and psychological somatization. Diagnostic workups utilize both subjective psychophysical testing and objective electrophysiological measurements.

The foundational approach is Chemical Psychophysical Testing. Clinicians utilize validated kits such as “Taste Strips”—filter paper strips impregnated with graded concentrations of four or five basic tastants (sucrose, citric acid, sodium chloride, quinine hydrochloride, and monosodium glutamate). These strips are applied systematically to both sides of the tongue and the posterior pharynx. Patients identify the taste from a multiple-choice card to avoid verbal bias. A cumulative score across all concentrations establishes whether the patient falls within normal limits (normogeusia), diminished function (hypogeusia), or complete absence (ageusia). Complementary methods include whole-mouth sip-and-spit threshold tests and the three-drop method, which determine absolute detection and recognition thresholds.

A highly precise, localized method is Electrogustometry. This technique employs anodal electrical stimulation delivered via a small metallic probe to specific lingual papillae. The electrical current activates ion channels in taste bud cells, producing a distinct, metallic, galvanic taste sensation. Electrogustometry allows examiners to map regional taste thresholds rapidly and detect subtle hemiageusias without the fluid spreading associated with liquid solutions.

Advanced diagnostic evaluation frequently incorporates imaging and functional modalities. Magnetic Resonance Imaging (MRI) of the brain and skull base is essential when central or cranial nerve pathology is suspected, particularly to evaluate the cerebellopontine angle, petrous temporal bone, and insular cortices. Finally, Gustatory Evoked Potentials (GEPs) can record cortical electroencephalographic responses following automated, rapid-pulse chemical stimulation of the tongue, providing objective neurophysiological proof of gustatory pathway integrity independent of voluntary patient responses.

10. Applications & Practical Significance

The diagnosis and management of ageusia hold vital implications across diverse clinical, nutritional, and psychological disciplines. In clinical medicine, the sudden onset of ageusia serves as a crucial sentinel sign for serious underlying pathology. Unexplained taste loss can represent the presenting symptom of basilar skull fractures, neuroinvasive viral infections, demyelinating diseases such as multiple sclerosis, or occult neoplasms of the posterior cranial fossa.

In pharmacovigilance and therapeutics, ageusia is a widely recognized adverse drug reaction. Numerous pharmaceutical classes—including angiotensin-converting enzyme (ACE) inhibitors (e.g., captopril), antibiotics (e.g., metronidazole, clarithromycin), chemotherapeutic agents, and antirheumatic compounds—can induce profound gustatory inhibition. Recognizing drug-induced ageusia prevents unnecessary invasive diagnostic workups and allows clinicians to modify dosages or substitute alternative medications.

From a nutritional and metabolic perspective, the absence of taste profoundly alters dietary intake. Taste serves as an essential gatekeeper, guiding macronutrient selection and triggering cephalic phase digestive responses that prepare the gastrointestinal tract for enzymatic breakdown. Individuals with ageusia frequently experience profound anorexia, marked weight loss, and nutritional deficiencies because the sensory incentive to eat is decimated. Conversely, some patients paradoxically increase their intake of highly textured, excessively salted, or heavily spiced foods in a compensatory effort to stimulate residual trigeminal pathways, posing substantial risks for patients managing comorbid hypertension, renal disease, or diabetes mellitus.

In mental health and quality of life, the psychological impact of ageusia is profound. Eating is deeply embedded in human social interactions, celebration, and daily hedonic reward. The persistent inability to experience taste frequently precipitates anhedonia, reactive depression, and social withdrawal, underscoring the necessity of interdisciplinary supportive care involving nutritionists, psychologists, and sensory specialists.

11. Research & Empirical Evidence

Empirical research into ageusia expanded substantially following the onset of the COVID-19 pandemic, which brought post-viral chemosensory dysfunction into sharp global focus. Seminal studies by researchers such as Danielle Reed, Claire Hopkins, and the Global Consortium for Chemosensory Research (GCCR) systematically investigated patient populations experiencing acute taste and smell disturbances during SARS-CoV-2 infection. Their findings clarified that while true peripheral ageusia can occur via viral disruption of supporting cells in taste buds expressing ACE2 receptors, the vast majority of patients who initially reported total taste loss were experiencing acute anosmia, masking their preserved capacity to identify basic tastants upon controlled psychophysical testing.

Molecular research led by investigators such as Charles Zuker and Nicholas Ryba has systematically illuminated the receptor biology of taste, detailing the genetic families of T1R and T2R G-protein coupled receptors. Experimental knock-out models in rodents demonstrated that targeted ablation of genes encoding critical signaling molecules, such as phospholipase C-beta-2 (PLCβ2) or the transient receptor potential cation channel TRPM5, produces mice with phenotypic ageusia for sweet, bitter, and umami tastes while retaining sour and salty sensation, establishing the distinct intracellular signaling cascades required for different gustatory modalities.

Neuroimaging studies employing functional Magnetic Resonance Imaging (fMRI) by researchers like Dana Small have delineated the functional architecture of the human gustatory cortex. Small and colleagues demonstrated that insular cortex activation correlates directly with both perceived taste intensity and subjective pleasantness. Studies examining stroke patients have confirmed that lesions isolated specifically to the anterior dorsal insular cortex abolish taste perception bilaterally or ipsilaterally, confirming the insula as the primary human gustatory neocortex.

12. Cultural & Cross-Cultural Considerations

The cultural significance and subjective burden of ageusia vary widely based on societal relationships with food, communal dining customs, and linguistic categorizations of sensory experiences. In societies where culinary traditions form the cornerstone of daily social life, religious rituals, and family cohesion—such as Mediterranean, East Asian, and Latin American cultures—the psychological toll of ageusia can be particularly isolating. Individuals with ageusia often report feeling estranged from communal tables, unable to partake in shared culinary heritage.

Furthermore, cultural variations in the linguistic encoding of taste affect how patients articulate gustatory deficits to clinicians. While Western scientific taxonomy establishes five basic tastes, traditional culinary systems acknowledge alternative sensory frameworks. For example, traditional Chinese culinary philosophy categorizes five phases (Wu Xing) that include pungency/spiciness alongside sweet, sour, bitter, and salty. In cultures where spiciness is linguistically framed as a primary taste rather than a trigeminal somatosensory sensation, patients may report persistent “taste” perception despite suffering complete clinical ageusia, simply because their trigeminal sensitivity to chili peppers remains intact.

Cross-cultural dietary adaptations also reveal differing coping mechanisms. In cultures with rich culinary vocabularies for texture (such as the extensive Japanese lexicon for mouthfeel, or shokkan), individuals suffering from ageusia frequently adapt by shifting their culinary appreciation toward contrasting temperatures, crunchiness, and viscosities. Health professionals operating in diverse multicultural environments must account for these sensory idioms and linguistic variations during clinical interviews to avoid diagnostic misunderstandings.

13. Criticisms, Debates & Limitations

The academic study of ageusia is characterized by ongoing methodological and conceptual debates, primarily concerning diagnostics, epidemiological prevalence, and terminology.

A major point of contention is the persistent conflation of ageusia with severe anosmia in both published literature and clinical practice. Many epidemiological studies rely entirely on subjective, self-reported patient questionnaires without administering objective psychophysical tests. Chemosensory scientists criticize this methodology, pointing out that up to 90% of self-reported “taste loss” cases are actually retronasal olfactory deficits. This diagnostic imprecision leads to vastly inflated estimates of ageusia prevalence and misdirects therapeutic interventions.

A second ongoing debate concerns the definition of “basic tastes.” For decades, scientific orthodoxy recognized four canonical tastes (sweet, sour, salty, bitter), subsequently expanding to include umami (savory/glutamate). Today, researchers are actively debating whether additional modalities—such as fat (oleogustus), calcium, metallic, and water taste—should be formally recognized as autonomous gustatory qualities. The debate complicates the diagnostic threshold for complete ageusia: if an individual can detect free fatty acids through specialized lingual receptors such as CD36 and GPR120 but cannot perceive the classical five tastants, do they truly have ageusia?

Finally, there is considerable debate regarding the regenerative capacity of the peripheral gustatory apparatus and the efficacy of current therapeutic modalities. While taste receptor cells turn over rapidly (every 10 to 14 days) under normal physiological conditions, persistent post-viral, toxic, or traumatic ageusia often resists therapeutic interventions. Promoted treatments, including high-dose zinc supplementation, systemic corticosteroids, and alpha-lipoic acid, lack robust evidence from large-scale, double-blind, randomized controlled clinical trials, leaving the field without a universally accepted standard of care for permanent gustatory denervation.

14. Related Terms & Distinctions

To avoid diagnostic ambiguity, ageusia must be clearly distinguished from other chemosensory and neurological conditions:

• Hypogeusia: A quantitative reduction in taste sensitivity, where the patient retains the capacity to perceive basic tastes but requires significantly higher threshold concentrations than healthy individuals.
• Dysgeusia (Parageusia): A qualitative distortion of taste perception, where an external tastant elicits an abnormal or inappropriate sensory impression (e.g., sucrose tasting foul, metallic, or sour).
• Phantogeusia: A gustatory hallucination, defined as the persistent perception of a taste (often bitter or metallic) in the complete absence of any external chemical stimulus in the oral cavity.
• Anosmia: The total loss of the olfactory sense. While anosmia eliminates retronasal flavor identification, individuals retain full capacity to perceive the five basic tastes on the tongue.
• Ageusia vs. Gustatory Agnosia: Gustatory agnosia is a rare neuropsychological condition where the patient can physiologically detect and discriminate basic tastes at normal sensory thresholds but cannot recognize, identify, or name the meaning of the taste due to higher-order cortical lesions.

15. Summary / Key Takeaways

Ageusia represents the absolute loss of taste perception, preventing the detection of sweet, sour, salty, bitter, and umami stimuli across the oral cavity. While frequently confused with the loss of flavor stemming from olfactory dysfunction, true ageusia is an autonomous, neurophysiologically distinct deficit that is rare due to the redundant innervation provided by cranial nerves VII, IX, and X. Etiologies span peripheral damage, pharmacological toxicity, and central cerebrovascular or demyelinating lesions. Diagnosis requires objective, quantitative psychophysical testing such as taste strips or electrogustometry. The condition carries significant clinical and psychological consequences, frequently leading to anorexia, nutritional deficiencies, and reduced quality of life. An accurate understanding of ageusia enables clinicians to navigate complex sensory complaints, identify underlying neurological pathology, and provide comprehensive supportive care.

References

• Bartoshuk, L. M. (1978). History of taste research. In E. C. Carterette & M. P. Friedman (Eds.), Handbook of Perception (Vol. VIA, pp. 3–18). Academic Press. https://doi.org/10.1016/B978-0-12-161906-0.50007-4
• Doty, R. L. (2015). Handbook of Olfaction and Gustation (3rd ed.). John Wiley & Sons. https://doi.org/10.1002/9781118971758
• Hummel, T., Landis, B. N., & Hüttenbrink, K. B. (2011). Smell and taste disorders. GMS Current Topics in Otorhinolaryngology, Head and Neck Surgery, 10, Doc04. https://doi.org/10.3205/cto000077
• Parma, V., Ohla, K., Veldhuizen, M. G., Niv, M. Y., Kelly, C. E., Bakke, A. J., … & GCCR Group. (2020). More than smell—COVID-19 is associated with severe impairment of smell, taste, and chemesthesis. Chemical Senses, 45(7), 609–622. https://doi.org/10.1093/chemse/bjaa041
• Small, D. M. (2010). Taste representation in the human brain. Brain Research Reviews, 62(2), 241–259. https://doi.org/10.1016/j.brainresrev.2009.12.001