STUDY - Technical - New Dacian's Medicine
Taste
disorders
Translation Draft
Many patients who have lost their sense of smell also blame the loss of taste. In psychophysical tests, most of these patients have normal detection thresholds for taste sensations. Taste disorders are much rarer than olfactory ones.
Taste receptors are located in taste buds, spherical groups of cells, arranged similar to the segments of a citrus fruit. On the surface, the taste buds present a pore through which the microemine of the receiving cells. Taste buds look the same, no matter where they're located.
Unlike the olfactory analyzer, the taste receptor cell is not the proton. Instead, the related taste nerve fibers come into contact with individual taste receptors. The transmission of the message depends on the activity of the second messengers coupled with the G protein, but differs in detail for each taste sensation. The sense of taste is mediated by the facial, glossopharynx and vague nerves.
The taste analyzer consists of at least five populations of receiving cells. Taste buds are located in the leafy papillae on the lateral edges of the tongue, in the fungiform papillae on the dorsal face of the tongue, in the circumvalated papillae located at the junction between the dorsal face and the base of the tongue and in the palate, epiglottis, larynx and esophagus.
The cord of the eardrum, branch of the facial nerve, serves the taste sensations coming from the previous two thirds of the tongue. The posterior third of the tongue is innervated by the lingual branch of the glossopharynx nerve. The palatine adhesions reach through the large superficial rocky nerve to the genicular ganglion and then, through the facial nerve, to the brain stem. The internal branch of the upper laryngeal nerve (branch of the vagus nerve) contains taste adhesions from the larynx, including the epiglottis and the esophagus.
The central connections of the nerves end in the brain stem, in the nucleus of the solitary tract. The fibers of the timpapanic cord and the large superficial rocky nerves reach the cephalic portion of the nucleus. Glosopharyngeal taste fibers end in the middle portion of the nucleus and the fibers of the upper laryngeal nerve reach the caudal portion of the nucleus.
From the nucleus of the solitary tract, the central path is projected into the ipsilateral parabrahial pontine nuclei. Two divergent paths leave the parabrahial walnuts. One of them has an upward trajectory to the taste relay in the dorsal thalamus, where it makes synapses, then continues to the island's cortex. There is also a direct pathway linking the parabrahial contractions to the cortex.
The sense of smell and taste seem to be unique among the analyzers, in that at least some fibers shun the thalamus. The other way from the parabrahial nuclei reaches the ventral part of the brain, including the lateral hypothalamus, the unnamed substance, the central nucleus of the tonsil and the terminal is stria.
Taste stimuli reach the receiving cells through the taste pores. Four types of tastes are known: sweet, salty, sour and bitter. Individual taste related fibers almost always respond to a number of different chemicals. Models of the responses of aferate taste axons can be grouped into several categories based on the chemical stimulus that produces the strongest response.
For example, for neurons that respond best to sucrose, the second stimulus in terms of sensitivity is almost always sodium chloride. The fact that individual taste fibers respond to a large number of different chemicals generated the theory of "cross-response" for the coding of taste stimuli, while the analysis of the strongest stimulus generated the concept of "labeled" afferences.
It appears that labelled fibres play an important role in the coarse determination of quality, but for qualitative discrimination of chemicals, cross-response fibres with maximum sensitivity to a certain category of stimuli are required.
For example, sweet taste can be transported by neurons with maximum sensitivity to sucrose, but differentiation between sucrose and fructose may require a comparison of the relative activities of neurons with maximum sensitivity to sucrose, salt or quinine. As with the olfactory analyzer and other analyzers, the intensity appears to be encoded by the amplitude of neural activity.
Taste disorders are caused by disorders that interfere with access to taste stimuli to the receiving cells in the taste buds (loss of transport), damage the receiving cells (sensory loss) or affect the taste nerves and central taste pathways (neural loss).
Taste losses of transport are caused by xerostomia due to several causes, including Sjogren's syndrome, heavy metal poisoning and bacterial colonization of the taste pore. The salivary environment in which receptors are found may be important for the various causes of taste loss.
Sensory taste losses are caused by inflammatory and degenerative diseases of the oral cavity, a large number of drugs, especially those that interfere with the cellular turn-over, such as antithyroids and antineoplastic agents, radiotherapy of the oral cavity and pharynx, viral infections, endocrine disorders, neoplasia, the aging process.
Neural taste losses occur in neoplasias, traumas and surgeries in which taste damage is related. Taste buds degenerate when their taste adhesions are severed but remain unchanged if their somatosensitive aferences are severed.
Let's move on to clinical manifestations. From a psychological and physical point of view, taste disorders can be classified either on the basis of patients' accusations, either on the basis of objective sensory determinations in total ageusia (inability to qualitatively detect tastes of sweet, salty, bitter or sour), partial ageusia (inability to qualitatively detect the taste of certain substances), total hypogheusia (low sensitivity to all taste stimuli), partial hypogheusia (low sensitivity to some taste stimuli) and dysgeusia (distortion of the perception of a taste stimulus , that is, the misperception of the quality of an existing taste stimulus or the perception of a taste stimulus in the absence of ingestion of taste substances).
Confusions between sour and bitter taste are common and can sometimes result in errors of a semantic nature. However, often these confusions have physiological or physiopathological bases. There is the possibility of differentiating the lack of recognition of flavors in patients with olfactory losses that also blame loss of taste and smell, asking them if they can feel the sweet taste of carbonated drinks, the salty taste of fries, etc.
Patients who report taste loss should be evaluated psychologically and physically for assessment of taste and olfactory function. The first step is to determine the perception for the entire oral cavity of the qualitatively superior taste threshold and the feeling of pleasure using sucrose, citric acid, caffeine and sodium chloride. For the quantification of the sense of taste, sensitivity thresholds are obtained by progressive application of dilutions on the dials of the tongue or throughout the oral cavity. Finally, estimating the amplitude of the over-threshold can be used to better understand the patient's accusations.
Electrical taste testing (electrogustometry) is used in the clinic to identify taste deficits of different dials of the tongue. Biopsy of the foliated or fungiform papillae for the histopathological study of taste buds is in the experimental stage, but is promising in terms of the classification of taste disorders.
It's the turn of differential diagnosis. As with olfaction, no psychic and physical methods are available for differentiating taste transport losses from sensory or neural ones. Once a taste disorder is objectively highlighted, it is important to establish, as with other neurological deficits, an anatomical diagnosis before the etiological one. The history of the condition often provides important clues for etiological diagnosis.
For example, the absence of taste sensitivity in the anterior two thirds of the tongue, associated with facial paralysis, indicates that the lesion is located proximal to the point of the junction of the eardrum cord branch with the facial nerve in the mastoid.
Taste loss therapy remains limited. Some patients with salivary disorders benefit from treatment with artificial saliva. Treatment of bacterial and fungal infections of the oral cavity is indicated and may be helpful. Discontinuation of medication affecting cellular turnover is usually useful if the patient's general condition allows it. Some doctors are in favour of zinc and vitamin therapy of taste loss, but its effectiveness has not been demonstrated. There are no therapeutic strategies for neurosensory taste disorders.
Many patients who have lost their sense of smell also blame the loss of taste. In psychophysical tests, most of these patients have normal detection thresholds for taste sensations. Taste disorders are much rarer than olfactory ones.
Taste receptors are located in taste buds, spherical groups of cells, arranged similar to the segments of a citrus fruit. On the surface, the taste buds present a pore through which the microemine of the receiving cells. Taste buds look the same, no matter where they're located.
Unlike the olfactory analyzer, the taste receptor cell is not the proton. Instead, the related taste nerve fibers come into contact with individual taste receptors. The transmission of the message depends on the activity of the second messengers coupled with the G protein, but differs in detail for each taste sensation. The sense of taste is mediated by the facial, glossopharynx and vague nerves.
The taste analyzer consists of at least five populations of receiving cells. Taste buds are located in the leafy papillae on the lateral edges of the tongue, in the fungiform papillae on the dorsal face of the tongue, in the circumvalated papillae located at the junction between the dorsal face and the base of the tongue and in the palate, epiglottis, larynx and esophagus.
The cord of the eardrum, branch of the facial nerve, serves the taste sensations coming from the previous two thirds of the tongue. The posterior third of the tongue is innervated by the lingual branch of the glossopharynx nerve. The palatine adhesions reach through the large superficial rocky nerve to the genicular ganglion and then, through the facial nerve, to the brain stem. The internal branch of the upper laryngeal nerve (branch of the vagus nerve) contains taste adhesions from the larynx, including the epiglottis and the esophagus.
The central connections of the nerves end in the brain stem, in the nucleus of the solitary tract. The fibers of the timpapanic cord and the large superficial rocky nerves reach the cephalic portion of the nucleus. Glosopharyngeal taste fibers end in the middle portion of the nucleus and the fibers of the upper laryngeal nerve reach the caudal portion of the nucleus.
From the nucleus of the solitary tract, the central path is projected into the ipsilateral parabrahial pontine nuclei. Two divergent paths leave the parabrahial walnuts. One of them has an upward trajectory to the taste relay in the dorsal thalamus, where it makes synapses, then continues to the island's cortex. There is also a direct pathway linking the parabrahial contractions to the cortex.
The sense of smell and taste seem to be unique among the analyzers, in that at least some fibers shun the thalamus. The other way from the parabrahial nuclei reaches the ventral part of the brain, including the lateral hypothalamus, the unnamed substance, the central nucleus of the tonsil and the terminal is stria.
Taste stimuli reach the receiving cells through the taste pores. Four types of tastes are known: sweet, salty, sour and bitter. Individual taste related fibers almost always respond to a number of different chemicals. Models of the responses of aferate taste axons can be grouped into several categories based on the chemical stimulus that produces the strongest response.
For example, for neurons that respond best to sucrose, the second stimulus in terms of sensitivity is almost always sodium chloride. The fact that individual taste fibers respond to a large number of different chemicals generated the theory of "cross-response" for the coding of taste stimuli, while the analysis of the strongest stimulus generated the concept of "labeled" afferences.
It appears that labelled fibres play an important role in the coarse determination of quality, but for qualitative discrimination of chemicals, cross-response fibres with maximum sensitivity to a certain category of stimuli are required.
For example, sweet taste can be transported by neurons with maximum sensitivity to sucrose, but differentiation between sucrose and fructose may require a comparison of the relative activities of neurons with maximum sensitivity to sucrose, salt or quinine. As with the olfactory analyzer and other analyzers, the intensity appears to be encoded by the amplitude of neural activity.
Taste disorders are caused by disorders that interfere with access to taste stimuli to the receiving cells in the taste buds (loss of transport), damage the receiving cells (sensory loss) or affect the taste nerves and central taste pathways (neural loss).
Taste losses of transport are caused by xerostomia due to several causes, including Sjogren's syndrome, heavy metal poisoning and bacterial colonization of the taste pore. The salivary environment in which receptors are found may be important for the various causes of taste loss.
Sensory taste losses are caused by inflammatory and degenerative diseases of the oral cavity, a large number of drugs, especially those that interfere with the cellular turn-over, such as antithyroids and antineoplastic agents, radiotherapy of the oral cavity and pharynx, viral infections, endocrine disorders, neoplasia, the aging process.
Neural taste losses occur in neoplasias, traumas and surgeries in which taste damage is related. Taste buds degenerate when their taste adhesions are severed but remain unchanged if their somatosensitive aferences are severed.
Let's move on to clinical manifestations. From a psychological and physical point of view, taste disorders can be classified either on the basis of patients' accusations, either on the basis of objective sensory determinations in total ageusia (inability to qualitatively detect tastes of sweet, salty, bitter or sour), partial ageusia (inability to qualitatively detect the taste of certain substances), total hypogheusia (low sensitivity to all taste stimuli), partial hypogheusia (low sensitivity to some taste stimuli) and dysgeusia (distortion of the perception of a taste stimulus , that is, the misperception of the quality of an existing taste stimulus or the perception of a taste stimulus in the absence of ingestion of taste substances).
Confusions between sour and bitter taste are common and can sometimes result in errors of a semantic nature. However, often these confusions have physiological or physiopathological bases. There is the possibility of differentiating the lack of recognition of flavors in patients with olfactory losses that also blame loss of taste and smell, asking them if they can feel the sweet taste of carbonated drinks, the salty taste of fries, etc.
Patients who report taste loss should be evaluated psychologically and physically for assessment of taste and olfactory function. The first step is to determine the perception for the entire oral cavity of the qualitatively superior taste threshold and the feeling of pleasure using sucrose, citric acid, caffeine and sodium chloride. For the quantification of the sense of taste, sensitivity thresholds are obtained by progressive application of dilutions on the dials of the tongue or throughout the oral cavity. Finally, estimating the amplitude of the over-threshold can be used to better understand the patient's accusations.
Electrical taste testing (electrogustometry) is used in the clinic to identify taste deficits of different dials of the tongue. Biopsy of the foliated or fungiform papillae for the histopathological study of taste buds is in the experimental stage, but is promising in terms of the classification of taste disorders.
It's the turn of differential diagnosis. As with olfaction, no psychic and physical methods are available for differentiating taste transport losses from sensory or neural ones. Once a taste disorder is objectively highlighted, it is important to establish, as with other neurological deficits, an anatomical diagnosis before the etiological one. The history of the condition often provides important clues for etiological diagnosis.
For example, the absence of taste sensitivity in the anterior two thirds of the tongue, associated with facial paralysis, indicates that the lesion is located proximal to the point of the junction of the eardrum cord branch with the facial nerve in the mastoid.
Taste loss therapy remains limited. Some patients with salivary disorders benefit from treatment with artificial saliva. Treatment of bacterial and fungal infections of the oral cavity is indicated and may be helpful. Discontinuation of medication affecting cellular turnover is usually useful if the patient's general condition allows it. Some doctors are in favour of zinc and vitamin therapy of taste loss, but its effectiveness has not been demonstrated. There are no therapeutic strategies for neurosensory taste disorders.
Have a good day!
Dorin, Merticaru