STUDY - Technical - New Dacian's Medicine
Odor
disorders
Translation Draft
I'll start with a few general things about olfaction: The olfactory sense determines the flavor and palatability of food and drink. Together with the trigeminal system it serves to monitor inhaled chemicals, including hazardous ones, such as natural gas, smoke and pollutants in the air, etc.
Although the quality of olfactory sensations is determined by the olfactory neuroepithelial, many substances are able to produce somatic sensations of cold, warm and irritation through trigeminal, glossopharynx and vagal effects of the nose, oral cavity, tongue, pharynx and larynx. The sense of smell should be included in chemosensory systems, as most chemicals initiate olfactory, trigeminal and taste perceptions.
The olfactory neuroepithelium is located in the upper part of the nasal cavity and contains an orderly arrangement of receiving bipolar olfactory cells, microvil cells, supportive cells and basal cells. The dendritic process of bipolar cells presents at its end a bulb-shaped button that penetrates the mucous layer and possesses 6 to 9 cilia. The receiving sites for odor molecules are located on the cilia.
Microvil cells are located adjacent to the receiving cells on the surface of the neuroepithelium. Supportive cells, unlike homologous cells in the respiratory epithelium, do not secrete mucus. Their function is unknown. Basal cells generate other types of cells in the olfactory neuroepithelium, including bipolar receptor cells.
There is a regular turnover of the receiving bipolar cells, which act as primary sensory neurons. In addition, damage to the cellular body or axon leads to the replacement of the receiving cell with a differentiated basal cell, which restores the central neural connection. Therefore, these primary sensory neurons are unique among sensory systems in that they are regularly replaced and regenerate after damage.
The nonmyelinized axons of the receiving cells form the threads of the olfactory nerve, pass through the riddled blade of the ethmoid bone and end with the spherical formations of the neuropils, called glomeruli, in the olfactory bulb. Glomeruli are the seat of a high degree of convergence of information, the inferences being much more numerous than the events.
The second main neuron is represented by the mitral cell. The primary dendrite of each mitral cell connects with a single glomer. Mitral cell axons are projected together with the axons of adjacent ciliated cells into the limbic system, including the anterior olfactory nucleus, the prepiriform cortex, the periamigdalian cortex, the olfactory tuber, the nucleus of the lateral olfactory tract and the corticomedial nucleus of the amygdala. Awareness of olfactory sensations requires stimulation of the prepiriform cortex or tonsil nuclei.
Odorous substances are absorbed by the mucus that covers the olfactory neuroepithelium, diffuses to the cilia and binds reversibly to the membrane's receiving sites. This process leads to changes in the conformation of receiving proteins, which induce a chain of biochemical events that result in the generation of potential action in primary neurons. The transduction depends on the activation of the second messengers coupled with the protein G. Intensity appears to be encoded by the amount of pulses incoming from the related neurons.
Indeed, in humans, there is a clear correlation between the psychophysical parameters of intensity and the amplitude of the potentials evoked at the level of the olfactory neuroepithelial. The discovery of a vast family of genes for receptors suggests the existence of specific receptors for each odorant substance. A single receptor neuron expresses only one receptor subtype of a multigene family. All receptor neurons expressing a specific receptor subtype project their axons to one or two glomerules in the olfactory bulb.
Olfactive sense disorders are caused by conditions that interfere with the access of the odortous substance to the olfactory neuroepithelium (transport damage), damage the receiving region (sensory damage) or damage the central olfactory pathways (neural damage).
Loss of olfactory transport may be the result of inflammation of the nasal mucous membrane from acute viral infections of the upper respiratory tract, rhinitis and bacterial sinusitis, allergic rhinitis and structural changes in the nasal cavity, such as septum deviations, polyps and neoplasms. It is also possible that abnormalities in mucus secretion, in which the olfactory cilia are immersed, may lead to loss of olfactory sensitivity.
Olfactive sensory losses are caused by the destruction of olfactory neuroepithelial by viral infections, neoplasms, inhalation of toxic chemicals, drugs that affect cell turnover and cranial radiotherapy. Olfactive neural losses occur in head trauma, with or without fracture of the base of the anterior cranial fossa or riddled ethmoid blade (BP, BA, Korsakoff psychosis and vitamin B12 deficiency, anterior cranial fossa neoplasms, neurosurgical interventions, administration of neurotoxic agents such as ethanol, amphetamines, topical cocaine, aminoglycosides, tetracycline, cigarette smoke, and in some congenital diseases such as Kallmann syndrome). Other endocrine conditions, including Cushing syndrome, hypothyroidism and diabetes mellitus can affect the perception of smell.
From a psychophysical point of view, olfactory sense disorders can be classified either by the patient's accusations or by objective sensory determinations, in: total anosmia (general anosmia) - the inability to qualitatively detect any olfactory sensation; partial anosmia - the ability to qualitatively detect some, but not all, olfactory sensations; specific anosmia - loss of ability to detect one or a very limited number of odorants; total hyposmia (general hyposmia) - reduced sensitivity to all odorous substances; partial hyposmia - reduced sensitivity to certain odorous substances; dysosmia (cacosmia or paraosmia) - distortion of the perception of a smell, such as the perception of an unpleasant odor in the presence of a pleasant one or the perception of odors that do not exist in that environment; total hyperosmia (general hyperosmia) - increased sensitivity to all odorants; partial hyperosmia - increased sensitivity to certain odorous substances; agnosia - inability to classify, differentiate or verbally identify olfactory sensations, although the ability to distinguish or recognize odorous substances may be normal.
Let's move on to the clinical evaluation! The history of the onset and progression of the olfactory disease may be of paramount importance in establishing the etiological diagnosis. Unilateral anosmia is rarely a charge. can only be detected by separate testing of the olfactory perception of each nasal cavity. On the other hand, bilateral anosmia causes patients to report to the doctor. Usually, patients with anosmia accuse loss of taste sensations, although their taste thresholds may be within normal limits. In fact, they blame the loss of flavour detection, which is mainly an olfactory function. The appreciation of flavors depends on the olfactory detection of volatile substances in solid and liquid foods as well as the sense of taste.
The physical examination will include a complete examination of the ears, upper respiratory tract, head and neck. Neurological examination with an emphasis on cranial nerves is essential. Computerized cranial tomography (CT) with amplification is necessary to exclude anterior cranial fossa neoplasms, unsuspected fractures of the anterior cranial fossa, paranasal sinusitis and nasal cavity neoplasms and paranasal sinuses.
Sensory evaluation of olfactory function is necessary to corroborate the patient's accusations, assess the effectiveness of treatment and determine the degree of permanent impairment. The first step in sensory evaluation is to determine the degree to which qualitative sensations are present. For this evaluation, a smell identification set comprising 40 microcapsulated odorants, forcibly chosen (scratch and sniffing paradigm) is used.
For example, in one of the samples, the patient is asked the following problem: "This odorous substance most likely smells: a. chocolate, b. banana, c. onion, d. fruit", and the patient is instructed to respond with one of the variants. The test is very accurate and sensitive to differences due to age and sex. It represents a precise quantitative determination of the relative degree of the olfactory deficit. People with total loss of olfactory function have a score between 7-19 out of 40. The average score for total anosmia is slightly higher than expected, as substances that act by trigeminal stimulation are included.
The second step is to establish the olfactory threshold for odorant phenylethylene alcohol, using a gradual stimulation. The sensitivity of each nasal passage is determined by detecting the threshold for phenyl-ethyl-ethyl carinol. Nasal resistance is measured by anterior rhinomanometry for each nasal fossa. Although techniques for biopsy of olfactory neuroepithelial have been developed, given the wide spread of olfactory neuroepithelial degeneration and respiratory epithelium intercalation in olfactory areas in adults without manifest olfactory dysfunction, the biopsy material should be interpreted with great caution.
For differential diagnosis, there are currently no psychophysical methods for differentiating the sensory causes of olfactory and neural losses. Fortunately, anamnesis provides important clues for elucidating etiology. The main causes of olfactory disorders are head trauma and viral infections.
Head trauma is a more common cause of anosmia in children and young adults, and viral infections are more important causes of anosmia in older adults. Head trauma is followed in 5-10% of cases by uni or bilateral damage to the eye. The frontal lesions and fractures fragment the riddled blade of the ethmoid bone and damage the olfactory axons that pass through it. Sometimes a rhinorrhea is associated with cerebrospinal fluid (CRL), resulting in the rupture of the hard mater covering the riddled blade of the ethmoid bone and the paranasal sinuses.
Anosmia may also be a result of strikes in the occipital region. Once it occurs, traumatic anosmia is usually definitive, with only 10% of patients showing improvement or healing. Perverting the olfactory sense may occur as a phase of the healing process. Viral infections destroy the olfactory neuroepithelium, which is replaced by respiratory epithelium.
Congenital anosmias are rare, but important. Kallmann syndrome is a neuronal migration defect for which the X-linked gene (KAL) has been cloned. It is characterized by congenital anosmia and hypogonadotropic hypogonadism. Hypothalamic and olfactory disorders are due to the lack of migration from the olfactory placode of the olfactory receptor neurons and gonadotropin-releasing hormone synthesizer neurons. Anosmia can also occur in albinism. The receiving cells exist, but they are hypoplastic, have no cilia and no proemin above the surrounding supporting cells.
The meninioma of the lower frontal region is the most common neoplastic cause of anosmia (rarely, anosmia can occur within the glioma of the frontal lobe). Occasionally, pituitary adenomas, craniopharyngioamenes, suprasal meningiomas and aneurysms of the lower part of the Willis polygon, previously expand and affect olfactory structures. These tumors and hematomas can also induce epilepsy with olfactory hallucinations, indicating damage to the temporal lobe.
Dysosmia, the subjective distortion of olfactory perception, can occur in intranasal diseases that partially affect the olfactory sense or may represent a phase of the recovery of a neurological anosmia. Most disosmious disorders consist of the perception of unpleasant or non-existent olfactory sensations and may be associated with changes in the sense of taste. Dysosmia is associated with depressive syndrome.
Treatment of patients with olfactory transport losses due to allergic rhinitis, bacterial rhinitis and sinusitis, polyps, neoplasms and structural abnormalities of the nasal passages, can be addressed rationally, with a high chance of improvement. Treatment of allergic phenomena, antibiotic therapy, topical and systemic glucocorticoid therapy, surgery for nasal polyps, nasal septum deviations and chronic hyperplastic sinusitis are frequently effective in the rehabilitation or restoration of olfactory perception.
There is no effective treatment for sensory and neuronal loss of the olfaction. Fortunately, spontaneous healings often occur. Some doctors rule in favor of treatment with zinc and vitamins. Severe zinc deficiency can certainly lead to loss and distortion of the sense of smell, but does not pose clinical problems, except in very small geographical areas, Vitaminotherapy consists mainly in the administration of vitamin A. Epithelial degeneration associated with vitamin A deficiency may cause anosmia, but is not a common clinical problem.
See you tomorrow, with the taste disturbances!
I'll start with a few general things about olfaction: The olfactory sense determines the flavor and palatability of food and drink. Together with the trigeminal system it serves to monitor inhaled chemicals, including hazardous ones, such as natural gas, smoke and pollutants in the air, etc.
Although the quality of olfactory sensations is determined by the olfactory neuroepithelial, many substances are able to produce somatic sensations of cold, warm and irritation through trigeminal, glossopharynx and vagal effects of the nose, oral cavity, tongue, pharynx and larynx. The sense of smell should be included in chemosensory systems, as most chemicals initiate olfactory, trigeminal and taste perceptions.
The olfactory neuroepithelium is located in the upper part of the nasal cavity and contains an orderly arrangement of receiving bipolar olfactory cells, microvil cells, supportive cells and basal cells. The dendritic process of bipolar cells presents at its end a bulb-shaped button that penetrates the mucous layer and possesses 6 to 9 cilia. The receiving sites for odor molecules are located on the cilia.
Microvil cells are located adjacent to the receiving cells on the surface of the neuroepithelium. Supportive cells, unlike homologous cells in the respiratory epithelium, do not secrete mucus. Their function is unknown. Basal cells generate other types of cells in the olfactory neuroepithelium, including bipolar receptor cells.
There is a regular turnover of the receiving bipolar cells, which act as primary sensory neurons. In addition, damage to the cellular body or axon leads to the replacement of the receiving cell with a differentiated basal cell, which restores the central neural connection. Therefore, these primary sensory neurons are unique among sensory systems in that they are regularly replaced and regenerate after damage.
The nonmyelinized axons of the receiving cells form the threads of the olfactory nerve, pass through the riddled blade of the ethmoid bone and end with the spherical formations of the neuropils, called glomeruli, in the olfactory bulb. Glomeruli are the seat of a high degree of convergence of information, the inferences being much more numerous than the events.
The second main neuron is represented by the mitral cell. The primary dendrite of each mitral cell connects with a single glomer. Mitral cell axons are projected together with the axons of adjacent ciliated cells into the limbic system, including the anterior olfactory nucleus, the prepiriform cortex, the periamigdalian cortex, the olfactory tuber, the nucleus of the lateral olfactory tract and the corticomedial nucleus of the amygdala. Awareness of olfactory sensations requires stimulation of the prepiriform cortex or tonsil nuclei.
Odorous substances are absorbed by the mucus that covers the olfactory neuroepithelium, diffuses to the cilia and binds reversibly to the membrane's receiving sites. This process leads to changes in the conformation of receiving proteins, which induce a chain of biochemical events that result in the generation of potential action in primary neurons. The transduction depends on the activation of the second messengers coupled with the protein G. Intensity appears to be encoded by the amount of pulses incoming from the related neurons.
Indeed, in humans, there is a clear correlation between the psychophysical parameters of intensity and the amplitude of the potentials evoked at the level of the olfactory neuroepithelial. The discovery of a vast family of genes for receptors suggests the existence of specific receptors for each odorant substance. A single receptor neuron expresses only one receptor subtype of a multigene family. All receptor neurons expressing a specific receptor subtype project their axons to one or two glomerules in the olfactory bulb.
Olfactive sense disorders are caused by conditions that interfere with the access of the odortous substance to the olfactory neuroepithelium (transport damage), damage the receiving region (sensory damage) or damage the central olfactory pathways (neural damage).
Loss of olfactory transport may be the result of inflammation of the nasal mucous membrane from acute viral infections of the upper respiratory tract, rhinitis and bacterial sinusitis, allergic rhinitis and structural changes in the nasal cavity, such as septum deviations, polyps and neoplasms. It is also possible that abnormalities in mucus secretion, in which the olfactory cilia are immersed, may lead to loss of olfactory sensitivity.
Olfactive sensory losses are caused by the destruction of olfactory neuroepithelial by viral infections, neoplasms, inhalation of toxic chemicals, drugs that affect cell turnover and cranial radiotherapy. Olfactive neural losses occur in head trauma, with or without fracture of the base of the anterior cranial fossa or riddled ethmoid blade (BP, BA, Korsakoff psychosis and vitamin B12 deficiency, anterior cranial fossa neoplasms, neurosurgical interventions, administration of neurotoxic agents such as ethanol, amphetamines, topical cocaine, aminoglycosides, tetracycline, cigarette smoke, and in some congenital diseases such as Kallmann syndrome). Other endocrine conditions, including Cushing syndrome, hypothyroidism and diabetes mellitus can affect the perception of smell.
From a psychophysical point of view, olfactory sense disorders can be classified either by the patient's accusations or by objective sensory determinations, in: total anosmia (general anosmia) - the inability to qualitatively detect any olfactory sensation; partial anosmia - the ability to qualitatively detect some, but not all, olfactory sensations; specific anosmia - loss of ability to detect one or a very limited number of odorants; total hyposmia (general hyposmia) - reduced sensitivity to all odorous substances; partial hyposmia - reduced sensitivity to certain odorous substances; dysosmia (cacosmia or paraosmia) - distortion of the perception of a smell, such as the perception of an unpleasant odor in the presence of a pleasant one or the perception of odors that do not exist in that environment; total hyperosmia (general hyperosmia) - increased sensitivity to all odorants; partial hyperosmia - increased sensitivity to certain odorous substances; agnosia - inability to classify, differentiate or verbally identify olfactory sensations, although the ability to distinguish or recognize odorous substances may be normal.
Let's move on to the clinical evaluation! The history of the onset and progression of the olfactory disease may be of paramount importance in establishing the etiological diagnosis. Unilateral anosmia is rarely a charge. can only be detected by separate testing of the olfactory perception of each nasal cavity. On the other hand, bilateral anosmia causes patients to report to the doctor. Usually, patients with anosmia accuse loss of taste sensations, although their taste thresholds may be within normal limits. In fact, they blame the loss of flavour detection, which is mainly an olfactory function. The appreciation of flavors depends on the olfactory detection of volatile substances in solid and liquid foods as well as the sense of taste.
The physical examination will include a complete examination of the ears, upper respiratory tract, head and neck. Neurological examination with an emphasis on cranial nerves is essential. Computerized cranial tomography (CT) with amplification is necessary to exclude anterior cranial fossa neoplasms, unsuspected fractures of the anterior cranial fossa, paranasal sinusitis and nasal cavity neoplasms and paranasal sinuses.
Sensory evaluation of olfactory function is necessary to corroborate the patient's accusations, assess the effectiveness of treatment and determine the degree of permanent impairment. The first step in sensory evaluation is to determine the degree to which qualitative sensations are present. For this evaluation, a smell identification set comprising 40 microcapsulated odorants, forcibly chosen (scratch and sniffing paradigm) is used.
For example, in one of the samples, the patient is asked the following problem: "This odorous substance most likely smells: a. chocolate, b. banana, c. onion, d. fruit", and the patient is instructed to respond with one of the variants. The test is very accurate and sensitive to differences due to age and sex. It represents a precise quantitative determination of the relative degree of the olfactory deficit. People with total loss of olfactory function have a score between 7-19 out of 40. The average score for total anosmia is slightly higher than expected, as substances that act by trigeminal stimulation are included.
The second step is to establish the olfactory threshold for odorant phenylethylene alcohol, using a gradual stimulation. The sensitivity of each nasal passage is determined by detecting the threshold for phenyl-ethyl-ethyl carinol. Nasal resistance is measured by anterior rhinomanometry for each nasal fossa. Although techniques for biopsy of olfactory neuroepithelial have been developed, given the wide spread of olfactory neuroepithelial degeneration and respiratory epithelium intercalation in olfactory areas in adults without manifest olfactory dysfunction, the biopsy material should be interpreted with great caution.
For differential diagnosis, there are currently no psychophysical methods for differentiating the sensory causes of olfactory and neural losses. Fortunately, anamnesis provides important clues for elucidating etiology. The main causes of olfactory disorders are head trauma and viral infections.
Head trauma is a more common cause of anosmia in children and young adults, and viral infections are more important causes of anosmia in older adults. Head trauma is followed in 5-10% of cases by uni or bilateral damage to the eye. The frontal lesions and fractures fragment the riddled blade of the ethmoid bone and damage the olfactory axons that pass through it. Sometimes a rhinorrhea is associated with cerebrospinal fluid (CRL), resulting in the rupture of the hard mater covering the riddled blade of the ethmoid bone and the paranasal sinuses.
Anosmia may also be a result of strikes in the occipital region. Once it occurs, traumatic anosmia is usually definitive, with only 10% of patients showing improvement or healing. Perverting the olfactory sense may occur as a phase of the healing process. Viral infections destroy the olfactory neuroepithelium, which is replaced by respiratory epithelium.
Congenital anosmias are rare, but important. Kallmann syndrome is a neuronal migration defect for which the X-linked gene (KAL) has been cloned. It is characterized by congenital anosmia and hypogonadotropic hypogonadism. Hypothalamic and olfactory disorders are due to the lack of migration from the olfactory placode of the olfactory receptor neurons and gonadotropin-releasing hormone synthesizer neurons. Anosmia can also occur in albinism. The receiving cells exist, but they are hypoplastic, have no cilia and no proemin above the surrounding supporting cells.
The meninioma of the lower frontal region is the most common neoplastic cause of anosmia (rarely, anosmia can occur within the glioma of the frontal lobe). Occasionally, pituitary adenomas, craniopharyngioamenes, suprasal meningiomas and aneurysms of the lower part of the Willis polygon, previously expand and affect olfactory structures. These tumors and hematomas can also induce epilepsy with olfactory hallucinations, indicating damage to the temporal lobe.
Dysosmia, the subjective distortion of olfactory perception, can occur in intranasal diseases that partially affect the olfactory sense or may represent a phase of the recovery of a neurological anosmia. Most disosmious disorders consist of the perception of unpleasant or non-existent olfactory sensations and may be associated with changes in the sense of taste. Dysosmia is associated with depressive syndrome.
Treatment of patients with olfactory transport losses due to allergic rhinitis, bacterial rhinitis and sinusitis, polyps, neoplasms and structural abnormalities of the nasal passages, can be addressed rationally, with a high chance of improvement. Treatment of allergic phenomena, antibiotic therapy, topical and systemic glucocorticoid therapy, surgery for nasal polyps, nasal septum deviations and chronic hyperplastic sinusitis are frequently effective in the rehabilitation or restoration of olfactory perception.
There is no effective treatment for sensory and neuronal loss of the olfaction. Fortunately, spontaneous healings often occur. Some doctors rule in favor of treatment with zinc and vitamins. Severe zinc deficiency can certainly lead to loss and distortion of the sense of smell, but does not pose clinical problems, except in very small geographical areas, Vitaminotherapy consists mainly in the administration of vitamin A. Epithelial degeneration associated with vitamin A deficiency may cause anosmia, but is not a common clinical problem.
See you tomorrow, with the taste disturbances!
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