The value of the olfactory analyzer is not limited only to the function of smell perception.

Different odors have different effects on the functional interaction of the analyzer with the brainstem and the autonomic nervous system, and many reflex brainstem mechanisms are activated, which can have an exciting effect on the cerebral cortex. A close connection between the olfactory analyzer and the vascular system has been revealed: depending on the type of odorous substance, a change (increase or decrease) in vascular tone may occur, manifested by narrowing or dilation of blood vessels.

The prevalence of smell disorders, according to various authors, is high and does not tend to decrease. The US National Institute of Health in 1969 identified olfactory disorders in 2 million people in this country, and in 1981 - already in 16 million people. This pronounced dynamics is largely due to environmental factors. There is little data on the prevalence of specific forms of olfactory disorders: according to a number of researchers, parosmia prevails among olfactory disorders in the general population. Olfactory dysfunction is a violation of a person’s ability to sense and differentiate odors that affect his olfactory analyzer. Disorders of the olfactory function are manifested by a number of characteristic signs, united by the term “dysosmia”.

Classification. Currently, several options for subdividing olfactory disorders have been proposed, but there is no unified classification. Quantitative changes in the sense of smell are characterized by the following concepts:
normosmia - normal sense of smell;
hyposmia - increased odor perception thresholds;
hyperosmia - heightened sense of smell: increased sensitivity to odors, sometimes even to the weakest;
anosmia - complete loss of smell;
Specific anosmia is the inability to smell a specific smell.

Both anosmia and hyposmia can be complete or total, manifested by either the impossibility or limitation of the perception of all odors, and partial or partial, relating only to individual odors. Below are qualitative changes in the sense of smell.
Aliosmia is a distorted perception of odors, when odorous substances are perceived as one of the odors of the environment:
cacosmia - either constant or periodic perception of unpleasant (putrefactive, fecal) odors;
torcosmia - constant or periodic perception of odors that are absent in the inhaled air (chemical, bitter smell, burning smell, metal);
parosmia is a specific transformation of the recognition of odors, their incorrect recognition (the patient feels odors, but perceives them inadequately, odors change qualitatively).
Phantosmia is manifested by olfactory hallucinations.
Heterosmia - incorrect discrimination of odors.
Allosteresia is the sensation of odors on the side opposite to irritation.
Pseudosmia is a hallucinatory description of olfactory stimuli.
Agnosmia is a violation of odor identification: lack of recognition of a smell when it is felt.

According to etiology, all olfactory disorders are divided into two large subgroups: congenital and acquired. In children, congenital defects and developmental anomalies are extremely diverse; These include such as lateral trunk (unilateral and bilateral), median cleft nose (complete and partial), lateral cleft nose, fistulas of the nasal dorsum, dermoid cysts, choanal atresia, etc. Acquired olfactory disorders, taking into account the location of the lesion and clinical features , are divided into two subgroups: rhinogenic (conductive), neurosensory (perceptual).

Neurosensory olfactory disorders are divided into the following groups:
peripheral disturbances of smell (damage at the level of neuroepithelial cells of the nasal cavity, olfactory nerves);
central disturbances of the sense of smell: in the anterior cranial fossa (at the level of the olfactory bulb, tract, triangle); damage to the central cortical sections of the olfactory analyzer in the temporo-basal regions of the brain (hippocampal gyrus).

A number of authors classify smell disorders as a separate group due to damage to the nerves that play an auxiliary role in the act of smell (trigeminal, glossopharyngeal, facial nerves). Division of dysosmia both in form and severity. There are three forms of dysosmia: perceptual, conductive and mixed. It should be noted that a violation of the acuity of smell is possible in all three forms of dysosmia, either by the type of anosmia (lack of perception and recognition of odors) or by the type of hyposmia (decreased ability to perceive and adequately recognize odorous substances). There are three degrees of hyposmia: I degree - lack of recognition while maintaining the perception of odors, II degree - decreased ability to perceive and recognize odors, III degree - decreased ability to judge the intensity of a stimulus. Impaired differentiation of odors is possible with perceptual and mixed dysosmia and manifests itself as aliosmia (including cacosmia, torcosmia, parosmia), phantosmia. If the patient has both conductive and perceptual components of dysosmia, its mixed (perceptual-conductive) form is distinguished.

Clinical picture. The most typical symptom of dysosmia is a decrease in the acuity of smell without impaired differentiation of odorous substances (rare). Often, a change in the sense of smell is combined with a loss of the range of taste sensations while the perception of sweet, salty, and bitter tastes is preserved, which is due to a violation of the olfactory reception of the “smell of food” in dysosmia. It must be remembered that when patients turn to an otolaryngologist, the disorder of smell bothers them less than other symptoms: high fever, headache, lack of nasal breathing, copious nasal discharge, dry mucous membranes, lacrimation, etc. The patient complains of a disorder of smell then when the main painful symptoms subside.

Olfactory disturbances of a conductive nature can be unilateral or bilateral (depending on the localization and prevalence of the pathology of the nasal cavity) and can manifest themselves in the form of hyposmia or anosmia (depending on the degree of disruption of the passage of air flow into the olfactory cleft). Patients usually complain of impaired perception of weaker odors, difficulty in nasal breathing, and dry nose. Due to the fact that hyposmia is subjectively less painful for the patient than other nasal dysfunctions, the patient may not have active complaints about changes in the sense of smell. Nasal breathing is usually difficult. Rhinoscopy reveals changes leading to narrowing of the nasal passages and degenerative changes in the mucous membrane. After improving the patency of the nasal passages due to anemization, a clear decrease in the thresholds of smell is determined. Moisturizing the mucous membrane (if it is dry) leads to improved perception of odors. However, there are no significant changes in the neurological status of these patients.

Rhinogenic disorders of smell can also be in the form of cacosmia. There are subjective cacosmia, in which the patient perceives an odor, despite its absence in the external environment, and objective, in which both the patient and often those around them perceive an odor, the source of which is in the patient’s respiratory tract or in the neighborhood, with the function of the olfactory analyzer unchanged. So, with chronic sphenoiditis, the smell from the nose is felt by the patient himself, but not by those around him; this is a very painful sensation for patients, since the excretory opening opens in the olfactory area. The flow of discharge along the anterior wall of the main sinus, along the arch of the nasopharynx and the posterior wall of the pharynx leads to the occurrence of this symptom. Nasal congestion and discharge are usually absent. Other causes of objective cacosmia may be pathology of the digestive system, carious teeth, periodontal disease, chronic tonsillitis, purulent sinusitis, adenoiditis, tumors of the respiratory tract and esophagus.

Neurogenic olfactory disorders can manifest themselves as a variety of neurodynamic phenomena, symptoms of irritation (hyperosmia, parosmia, olfactory hallucinations, phase phenomena in the olfactory analyzer) and symptoms of loss (reduction, absence of smell, impaired recognition of odors).

With hyperosmia, there is often increased sensitivity to many or all odors, less often to just one. An isolated increase in only olfactory sensitivity is associated with damage to the olfactory analyzer. Hyperosmia, which occurs against the background of a general increase in sensitivity to any irritations (tactile, auditory, visual) and is accompanied by clear motor-effective reactions, is usually caused by damage to the subcortical structures (visual thalamus) and is an unfavorable diagnostic symptom, indicating the deep location of the process.

Increased sensitivity to odors can result not only from a sharp increase in the sensitivity of the olfactory analyzer itself, but also from other systems. As a result of olfactory irritation, persistent insomnia, focal epileptic seizure, and migraine attack can develop. Increased pathological irradiation of excitation, similar to a pathological reflex, can also spread to the autonomic nervous system that innervates internal organs: a certain smell can cause an attack of bronchial asthma.

Olfactory hallucinations - a feeling of a non-existent smell, often unpleasant. More often these are some vague smells that the patient has never smelled, less often it is a specific smell that the patients encountered earlier in life. Olfactory hallucinations are often unpleasant in nature and can be combined with parosmia or autonomic-visceral, vestibular, taste and other disorders. In some cases, this symptom occurs first and then often repeats. Olfactory hallucinations can be the leading manifestation of primary damage to the cortical part of the olfactory analyzer in the mediobasal parts of the temporal lobe of the brain (irritation syndrome of the hippocampus and surrounding areas). They occur independently or as an aura before the onset of a generalized epileptic seizure. Olfactory hallucinations must be differentiated from objective cacosmia, caused by an objectively existing odor, often in connection with a focus of chronic infection.

Phase phenomena in the olfactory analyzer are manifested in the inadequacy of the increase in olfactory sensations with increasing intensity of the stimulus. When the source of the smell approaches the nose, patients do not feel the smell, however, when the odorous substance is moved away from the patient and the smell becomes weaker, they feel and distinguish it well. In this case, a paradoxical phase occurs in the olfactory analyzer - a strong olfactory stimulus at a close distance produces a weaker effect than a weak stimulus at a further distance. Pathological increased adaptation with central damage is manifested in the fact that, after inhaling 1-2 times, patients then cease to smell, and after 2-3 minutes of rest, the olfactory perception of this odorous substance is quickly restored. When the excitation processes in the olfactory analyzer are inert, approaching olfactory hallucinations, patients can continue to smell for a long time, even after the olfactory stimulation has long ceased to act. With complete anosmia and olfactory hallucinations, inhalation of trigeminal odors (cologne, ammonia) can intensify olfactory hallucinations. Hyperosmia is also classified as a phase phenomenon in the olfactory analyzer.

Hyperosmia, olfactory hallucinations, phase phenomena in the olfactory analyzer - all these are symptoms of a neurodynamic nature; they are usually unstable, labile, appear at a certain stage of the disease, and then disappear or are replaced as the process progresses by a decrease, loss of smell, or impaired recognition of odors. With hyposmia (decreased sense of smell), patients perceive all odors, but on the affected side the olfactory perception is weakened, weak odors may not be felt. Reduction and loss of smell can be unilateral or bilateral. Hyposmia may be a manifestation of damage to the trigeminal nerve on the trigeminal side. Loss of smell - anosmia - is expressed in the absence of the sensation of smell acting on the olfactory nerve. However, even with a complete anatomical break of the olfactory nerve, patients still feel odorous substances acting primarily on the trigeminal nerve (ammonia and wine alcohol, acetic acid) and the glossopharyngeal nerve (chloroform). Impaired odor recognition manifests itself in the absence of discrimination between even the most opposite odors in quality. At the same time, patients feel all odors.

Local significance is a decrease and loss of the sense of smell, impaired recognition of odors, olfactory hallucinations, and hyperosmia. Phase phenomena in the olfactory analyzer can occur if there is a disturbance in any part of the analyzer from the periphery to the olfactory cortex. Allosteresia is caused by tissue proliferation (tumor, anterior cerebral artery aneurysm) within the bulb and olfactory tract, as a result of which olfactory impulses pass through commissural fibers to the opposite hemisphere.

Olfactory receptors are exposed to all environmental influences that are associated with breathing. The result of the influence of damaging factors on the structures of the olfactory epithelium is partial or complete destruction and degeneration of olfactory receptor cells and, as a result, a decrease in olfactory function. In many diseases of the nasal cavity, damage occurs to the olfactory cells and olfactory filaments - the initial part of the olfactory nerve. In these cases, anosmia and hyposmia are usually observed on both sides. Lesions of the peripheral, conductive and central parts of the olfactory analyzer always lead to a violation of the sense of smell on the side of the lesion, even if the lesion is located in the olfactory cortex. Peripheral olfactory disorders mainly manifest themselves in the form of neuritis of the olfactory nerve. They are characterized by an isolated decrease or loss of smell, often on both sides, in which there are no other symptoms of damage from the peripheral and central nervous system. Adaptation in peripheral neuritis decreases slightly, readaptation increases slightly relative to the norm. Thresholds for olfactory substances acting on the trigeminal and facial nerves increase.

Olfactory neuritis is a large group of diseases of the first neuron of the olfactory tract: from neuroepithelial cells to the central endings of their axons in the glomeruli of the olfactory bulbs. A distinction is made between primary olfactory neuritis, which is an independent disease, and secondary olfactory neuritis, which occurs against the background of diseases of the upper respiratory tract, either due to the spread of the pathological process to the olfactory nerve, or as a result of its prolonged inactivity. Primary olfactory neuritis most often occurs after common infectious diseases, especially influenza. Much less often they develop due to intoxication with antibiotics, food poisons, and other substances: due to injuries (including electrical injuries). Secondary olfactory neuritis is observed in patients with scleroma (with olfactory disorders), allergic rhinosinusopathy, acute and chronic purulent sinusitis, in patients with tumors of the nose and paranasal sinuses. Neuritis of the olfactory nerve is manifested by a decrease or loss of smell and is not accompanied by other symptoms from the central nervous system.

During olfactory neuritis there are three stages:
Stage I is the stage of inflammatory changes (neuritis itself). Smell impairments are more of a qualitative nature; parosmia and cacosmia are observed. Odor thresholds are normal or slightly elevated; there is a progressive increase in odor recognition thresholds. Treatment of olfactory neuritis at this stage usually gives a good effect.
Stage II is the stage of progressive decline in the function of the olfactory nerve: the thresholds of perception and, to an even greater extent, the thresholds of odor recognition are steadily increasing. Initially, patients lose the ability to perceive purely olfactory (floral, aromatic) odors, and then mixed (“pungent”, “kitchen”) odors. Parosmia is observed, and cacosmia disappears. Treatment leads to incomplete restoration of the sense of smell, often leaving partial anosmia.
Stage III is the stage of loss of function of the olfactory nerve. Odors are either not perceived at all, or their trigeminal or glossopharyngeal components are perceived. The smells are characterized as “sweet”, “salty”, “pungent”, “spicy”. Treatment is unsuccessful.

Central olfactory disorders. These include, first of all, disturbances of the sense of smell associated with diseases of the central nervous system. In this case, the nature of the disorders can serve as a valuable guide in the topical diagnosis of tumors and other pathological processes. Central disturbances of the sense of smell always act as a basal symptom when the mediobasal parts of the anterior cranial fossa are affected (decreased sense of smell, its loss) or the mediobasal parts of the brain (impaired odor recognition, olfactory hallucinations), which is based on the clinical manifestations and anatomy of the olfactory analyzer. Central disturbances of smell always occur on the affected side up to the cortical part of the analyzer, in contrast to damage to all other cranial nerves. In this case, in contrast to neuritis of the olfactory nerve, other neurological and otoneurological symptoms from the central nervous system are added (mental disorders, Foster-Kennedy syndrome, changes in vestibular reactions, diencephalic-hypothalamic symptom complex, damage to the oculomotor innervation, visual disturbances, epileptic seizures that begin with olfactory hallucinations).

Lesions of the central olfactory formations in the anterior and middle cranial fossae give rise to different symptoms. Pathological processes in the anterior cranial fossa. With pathology in the anterior cranial fossa, unilateral or bilateral hypo- or anosmia occurs. In the case of germination or compression of the initial parts of the olfactory pathway (olfactory nerves, bulbs, tracts) by a tumor of the anterior cranial fossa, unilateral homolateral complete (if the olfactory pathways are pressed to the base of the skull) or incomplete (if they are pressed into the substance of the brain) loss of odor perception is noted. Loss of smell also occurs in patients after neurosurgical interventions in the anterior cranial fossa, for example, during frontal osteoplastic trepanation to approach the basal-frontal parts of the brain, the olfactory nerves are torn off, and patients experience loss of smell.

Pathological processes in the area of ​​the middle cranial fossa lead to damage to further parts of the olfactory pathways and their associative connections, which in turn leads to a predominant impairment of odor recognition, olfactory hallucinations, the adaptation time is reduced, and the readaptation time is extended. The appearance of cortical olfactory disorders in the form of persistent olfactory hallucinations and impaired recognition of odors indicates damage to the mediobasal structures of the temporal lobe by a neoplasm. The appearance of unilateral cortical olfactory disorders in a pituitary tumor indicates parasellar growth of the tumor, the possibility of germination of large vascular collectors - the cavernous sinus, which serves as an unfavorable prognostic symptom. Despite the characteristic topography of craniopharyngeomas, olfactory disorders in various forms are less common in them than expected, which is probably due to their cystic nature and soft consistency, and in childhood - to compensation of focal symptoms due to the divergence of cranial sutures. Increased sensitivity to odors against the background of general hyperpathy to any other stimuli (tactile, sound, visual) is accompanied by deep subcortical tumors affecting the visual thalamus. In such patients, with any irritation, a pronounced protective motor-affective reaction occurs; a pronounced form of this syndrome is a prognostically unfavorable sign, usually indicating a deep intracerebral location of the tumor and a decompensated stage of the disease.

If the olfactory pathways are damaged, anosmia to odorous substances with olfactory action may be observed. Damage to the cortical centers of smell leads to impaired recognition of odors of all odorous substances (olfactive, trigeminal, glossopharyngeal). When studying thresholds, a significant difference is revealed between the threshold of perception and the threshold of recognition of odorous substances, initially with olfactory action, and subsequently with mixed action. Recognition thresholds are particularly affected. Damage to the olfactory bulb is characterized by a decrease in adaptation time, and damage to the olfactory cortex is characterized by a violation of olfactory memory, preservation of normal thresholds to olfactory substances acting on the trigeminal and glossopharyngeal nerves. Damage to the cortical olfactory centers is characterized by a complete inability to identify odors, the so-called amnestic, or cortical, anosmia.

Central disturbances of the sense of smell are characterized by the addition of a wide variety of and numerous symptoms from the central nervous system, in contrast to peripheral damage to the olfactory nerve, in which, apart from disturbances of smell, there are no other neurological symptoms. When the anterior cranial fossa is affected, a violation of the sense of smell is most often combined with changes in the psyche of the frontal type, reflexes of oral automatism (sucking reflex, Marinescu-Radovic symptom), less often with a grasping reflex, anisoreflexia of tendon reflexes, symptoms of pyramidal insufficiency, Foster-Kennedy symptom (visual atrophy). nerve on the side of the lesion in the presence of congestion in the fundus on the opposite side).

When cortical olfactory structures are damaged in the middle cranial fossa, a diencephalic-hypothalamic syndrome occurs with sleep disturbance and autonomic functions, changes in vestibular experimental reactions of the diencephalic or diencephalic-subcortical type with inhibition of experimental nystagmus and a sharp increase in vestibulo-vegetative, less often sensory and motor reactions; central visual disturbances (chiasmal and tractus visual syndrome), changes in oculomotor innervation, epileptic seizures starting with olfactory hallucinations.

If the initial growth of the tumor is localized in parts of the brain that are not related to the olfactory, and affects the olfactory formations in the process of spread, then olfactory disorders arise later, and the first manifestations may be a wide variety of symptoms from the central nervous system. When the olfactory parts of the brain are directly affected, smell disturbances are one of the early symptoms.

Manifestations of central olfactory disorders depend not only on the location, but also on the nature of the lesion. In case of brain tumors, symptoms of loss of smell (hyposmia, anosmia, impaired recognition of smells) predominate; symptoms of irritation and olfactory hallucinations are less common. Reduction and loss of smell occurs with meningiomas of the olfactory fossa, gliomas of the frontal lobes of the brain, less commonly, tumors of the pituitary gland, tumors of the tubercle of the sella, craniopharyngeomas with growth forward, towards the anterior cranial fossa. Impaired odor recognition and olfactory hallucinations are observed in gliomas of the mediobasal parts of the temporal lobe, craniopharyngiomas with parasellar growth, and pituitary tumors. In the latter, this symptom is prognostically unfavorable. Deep tumors growing into the optic thalamus are accompanied by hyperosmia, which occurs against the background of a general increase in sensitivity to any irritation, and patients experience a pronounced protective motor-affective reaction. In 25% of cases of tumors of the posterior cranial fossa, smell disturbances are observed, caused by atrophy of the cortical part of the analyzer due to hydrocephalus, pressing of the olfactory tracts to the base of the skull due to hypertension, and herniation of the hippocampal gyri. Quite late, olfactory disorders manifest themselves as a dislocation craniobasal symptom with parasagittal tumors of the parietal and posterior frontal region, especially with meningiomas, as well as with occlusion in the posterior cranial fossa.

Closed craniocerebral injury. With a closed craniocerebral injury, neurogenic disturbances of the sense of smell clearly depend on the degree of its severity: with a mild degree of dysosmia, as a rule, they do not develop, with a moderate degree they occur in 15% and with a severe degree - in 48%. With mild traumatic brain injury, there are no neurogenic disorders of smell, with the exception of facial bruises, when in the acute period there is a slight decrease in the sense of smell associated with post-traumatic swelling of the nasal mucosa, i.e., having a conductive genesis. Uncomplicated fractures of the nasal bones, as a rule, are not accompanied by persistent impairment of the sense of smell; Characteristic is the occurrence of partial or complete anosmia immediately after a nasal injury. With a closed severe craniocerebral injury, regardless of the location of the bruise and fissure, contusional softening foci often arise, localized in the mediobasal regions of the frontal and temporal lobes of the brain, where the primary and secondary olfactory formations are located, which explains the frequent olfactory disorders in this pathology.

Open head injuries. Impaired sense of smell in open craniocerebral injuries with cracks in the anterior cranial fossa, as a rule, manifests itself in the form of its prolapse. Especially often, thin and delicate olfactory threads are affected by trauma. Moreover, injuries to any area accompanied by bilateral loss of smell are more often penetrating, that is, accompanied by damage to the dura mater.

Inflammatory processes of basal localization (arachnoiditis, arachnoencephalitis) in the acute period are often accompanied by symptoms of irritation: increased olfactory sensitivity, phase phenomena, olfactory hallucinations. All these symptoms are very changeable and dynamic. Subarachnoid hemorrhages due to rupture of arterial aneurysms are predominantly localized in the medio-temporo-frontal basal areas. Subsequently developing arachnoiditis disrupts the primary and secondary central olfactory formations.

Olfaction disorders can also occur when the trigeminal and glossopharyngeal nerves, which play an auxiliary role in the act of smell, are damaged. The literature describes a patient who experienced sharp pain along all branches of the trigeminal nerve, with a pronounced impairment in the recognition of olfactory-trigeminal odors, on the basis of which a tumor of the Gasserian ganglion was suspected, which was subsequently identified at surgery. A decreased sense of smell may be a manifestation of damage to the trigeminal nerve on the trigeminal side. The trigeminal nerve is not a specific olfactory nerve, but it enhances the olfactory sensation. The sense of smell is more severely reduced when the trigeminal and facial nerves are completely switched off, since the facial nerve, innervating the muscles that dilate the nostrils, helps sniff the smell. However, even with a complete anatomical break of the olfactory nerve, patients still feel odorous substances acting mainly on the trigeminal and glossopharyngeal nerve. Impaired odor recognition manifests itself in the absence of discrimination between even the most opposite odors in quality. At the same time, patients feel all odors.

Speaking about the manifestations of a violation of the sense of smell, it is necessary to remember that all olfactory projection zones are included in the limbic system of the brain - the anatomical and physical substrate of various emotional reactions of learning, memory and vital functions (nutrition, reproduction, regulation of metabolism, etc.) In connection with Violations of the content of neuroactive substances in various parts of the brain in neurodegenerative diseases cause dysfunction of the olfactory system. Such diseases include Alzheimer's disease, Huntington's chorea, Korsakoff's syndrome, Creutzfeldt-Jakob disease, etc. In Alzheimer's disease, the number of nerve cells in the accessory olfactory bulb and in the anterior olfactory nucleus decreases. Decreased cholinesterase in the olfactory tubercle and impaired sense of smell in Down's disease indicate involvement of the olfactory system. Patients with hypothyroid symptoms suffer from hyposmia. Korsakov's syndrome is accompanied by various changes in the sense of smell associated with organic atrophic disorders of the brain, localized in the area of ​​the mediodorsal thalamus and neocortical projections. Parkinson's disease, which reduces the amount of dopamine in the areas of the brain associated with smell, also leads to a decrease in olfactory abilities. The only disease in which a person's olfactory sensitivity sharply increases is Addison's disease, which is associated with irritation of the hypothalamic-pituitary structures. Examples demonstrating a connection between the human olfactory and reproductive systems include Kallmann syndrome, olfactogenital syndrome, and Turner syndrome.

Changes in the sense of smell observed in various emotional states and human diseases, pregnancy, are closely related to a variety of neuroactive substances that the olfactory system is rich in (neurotransmitters, neurohormones, regulatory peptides, metabolites, enzymes). All of them can regulate olfactory function at all levels of the system and participate in the transmission of information about odors at the level of the olfactory bulb.

Cortical disturbances of the sense of smell can also occur in functional disorders of the nervous system - functional, neurotic anosmia. Olfactory disorders often accompany neuroses. The likelihood of manifestations of emotional-olfactory integration increases when the brain is exposed to an additional pathogenic factor. It is assumed that the olfactory analyzer is partially ready when the neighboring structural elements of the horn of Ammon suffer. Functional anosmia should be considered when there is good nasal passage, but no sense of smell. The diagnosis is made based on the entire complex of symptoms in the absence of organic damage to the cerebral cortex. The history of patients with psychogenic anosmia does not always indicate psychogenic trauma; often the upper respiratory tract infection itself acts as a stress factor.

In schizophrenia, olfactory disorders manifest themselves in the form of impaired identification and differentiation of odors: agnosmia, pseudosmia and phantosmia; they indicate disturbances in the cortical part of the olfactory analyzer, as well as damage to the secondary olfactory centers and their associative connections. Senile anosmia (anosmia senilis) is not classified as a functional anosmia; it occurs due to atrophy of the mucous membrane even with a preserved olfactory nerve, or due to atrophy of a peripheral neuron, and the presence of degenerative-atrophic changes in the cortical-subcortical olfactory formations cannot be ruled out.

The diagnosis of dysosmia is established based on an analysis of the patient’s complaints, a multifaceted objective examination, including endoscopy of the leg cavity and nasopharynx, X-ray examination of the paranasal sinuses, and assessment of olfactory function. A significant role in the diagnosis of olfactory disorders is assigned to the results of rhinoscopy with a careful study of the state of the olfactory zone and assessment of nasal breathing. If necessary, X-rays of the skull, tomography of the sphenoid sinus and cribriform plate, computed tomography, taste testing, electroencephalography, and examination by a gastroenterologist, psychoneurologist, and dentist are performed. The study of olfactory function is carried out using subjective and objective olfactometry methods.

Etiological factor. Olfactory disorders are polyetiological. Congenital reduction and absence of smell is extremely rare and is more often associated with underdevelopment of the neuroepithelium and olfactory bulbs or with their complete absence. Congenital anomalies of the nose and paranasal sinuses play an important role in the etiology of respiratory hypo- and anosmia, when the flow of air to the olfactory cleft is disrupted.

The conductive form of olfactory disorders, according to foreign literature, accounts for up to 90% of dysosmia, and according to domestic authors - 35.7%. The cause of conductive disorders of smell is local changes in the nasal cavity, leading to restriction of air flow to the olfactory zone: deformation of the nasal septum, swelling and hypertrophy of the mucous membrane of the nasal turbinates, tumors and polyps of the nasal cavity, atresia and synechia of the nasal cavity, choanae and nasopharynx, etc. n. Olfactory dysfunction of varying degrees is observed in acute, allergic, vasomotor rhinitis, sinusitis, adenoiditis, nasal polyps, tumors of the nose and paranasal sinuses, infectious granulomas. This group of olfactory disorders should also include severe hyposmia in tracheotomized and laryngectomized patients. In almost all diseases of the nasal cavity that occur with obstruction of its lumen, preventing the flow of air and odors to the olfactory epithelium, the olfactory function suffers. Depending on the degree of difficulty in accessing the olfactory cleft of inhaled air containing odorous substances, either hyposmia (when access is difficult) or anosmia (when access is completely stopped) develops. In case of sinusitis, in addition to the mechanical obstructive factor, hyposmia is caused by a violation of the pH of the secretion of Bowman's glands, which acts as a solvent for odorous substances; when the process becomes chronic, metaplasia of the epithelium of the nasal cavity and paranasal sinuses occurs, which leads to damage to the olfactory receptor apparatus. In 70% of patients with diseases of the nose and paranasal sinuses, hyposmia is detected.

Much less often, the reason for limiting the contact of an odorous substance with the receptor cells of the neuroepithelium is insufficiency of the secretion of Bowman's glands and dryness of the mucous membrane of the olfactory area in subatrophic rhinitis, ozena, atrophic form of scleroma, atrophy of the mucous membrane in chronic iron deficiency and vitamin B12 deficiency anemia, and therefore odorous substances cannot dissolve in the mucous membrane of this part of the nose. However, in most cases, the olfactory neuroepithelium is early involved in the atrophic process, so pure forms of olfactory disorders of this type are very rare.

Central dysosmia is varied; they are divided into damage to the primary olfactory formations in the medio-basal parts of the anterior cranial fossa, manifested by hypo- and anosmia on the side of the pathological process, and damage to the secondary olfactory formations in the temporo-basal parts of the middle cranial fossa, which manifests itself in impaired recognition of odors and olfactory hallucinations.
Damage to the receptor apparatus of the olfactory analyzer accounts for about 90% of cases of perceptual dysosmia, damage to the olfactory nerve is 5% and damage to the central parts is 5%.

The most common causes of perceptual dysosmia at the receptor level: trauma to the olfactory zone, inflammatory process, traumatic brain injury, drug intoxication, allergic reaction, genetic mutation, deficiency of vitamins A and B12, intoxication with salts of heavy metals, viral damage, less often psycho-emotional stress, long-term use alcohol, smoking, chronic sinusitis and others. In these cases, a decrease in receptor sensitivity is explained by changes in protein structures with subsequent suppression of receptor regulation.

Damage to the olfactory nerve is most often associated with infectious diseases, metabolic disorders, tumors, demyelinating processes, intoxication, and damage during surgical interventions. Morphological and electrophysiological studies conducted by domestic and foreign scientists have shown that when individual components of the olfactory analyzer are damaged, all its structures are involved in the process, providing a single holistic response to the introduction of an infectious agent or to traumatic damage. Thus, the ability of neurotropic viruses, in particular the influenza virus, to move from the nasal cavity along the perineural tract into the cranial cavity has been established. With influenza, olfactory disorders are very widespread, and this explains the fact that the olfactory analyzer is the only analyzer of central origin that directly communicates with the external environment and is affected by the respiratory route of penetration of a neurotropic virus. If the olfactory receptor layer is damaged, this inevitably leads to degenerative changes in the olfactory bulbs, and vice versa. The causes of central olfactory disorders include brain tumors, traumatic brain injuries, cerebrovascular accidents, demyelinating processes, genetic and infectious diseases, metabolic disorders, Alzheimer's disease and others.

Principles of treatment. Treatment is aimed at sanitizing the nasal cavity and sinuses, restoring nasal breathing and sense of smell, its main goal is to eliminate the causes of the disease. It is generally accepted that successful treatment of patients with olfactory dysfunctions depends primarily on their etiology and correct diagnosis.

A difficult problem is the treatment of perceptual olfactory disorders. The most often used is complex drug therapy using drugs that improve nerve conduction (neostigmine methyl sulfate, galantamine), cerebral circulation (vinpocetine, cinnarizine), B vitamins; anti-inflammatory (antibiotics, glucocorticoids, intravenous infusion of methenamine with glucose), as well as dehydrating and desensitizing therapy. In the acute period of neuritis of the olfactory nerve, it is recommended to insufflate into the nasal cavity a mixture of powders of antibacterial drugs, which are well absorbed by the mucous membrane and reach the olfactory nerve through the perineural spaces.

It has been established that the most effective is complex treatment of patients with acute and subacute dysosmia using antihypoxic drugs administered intravenously, in combination with classical acupuncture for perceptual dysosmia and endonasal exposure of the olfactory area to a helium-neon laser for mixed dysosmia. The course of classical reflexology consists of 10 daily sessions, as well as the 2nd and 3rd courses (after 1 or 3 months). A course of laser therapy includes 10 procedures; if necessary, treatment is repeated after 1 and 2 months. For hyperosmia and cacosmia, it is recommended, if possible, to eliminate causative factors (neurasthenia, vegetative-vascular dystonia, hysteria, diseases of the central nervous system, sanitation of foci of chronic infection). General restorative therapy and endonasal novocaine blockades are indicated. Proper nutrition and avoiding the simultaneous intake of incompatible foods are important in treatment.

In the treatment of perceptual functional disorders of smell after surgery and previous respiratory infections, great importance is given to sanatorium-resort treatment using all resort factors and acupuncture, with the high effectiveness of the latter. Psychological support for this category of patients is also important.

Different treatment tactics for conductive forms of olfactory dysfunction. Rhinogenic hypo- and anosmia are eliminated by treating the causative disease, usually surgically, in order to restore nasal breathing and ensure free passage of air through the olfactory fissure into the olfactory zone of the nose. More often, nasal polypotomy, submucosal resection of the nasal septum, partial conchotomy, etc. are indicated. The most rational surgical interventions in the nasal cavity and paranasal sinuses are gentle, submucosal endonasal operations that involve preserving the mucous membrane, the optimal width and configuration of the nasal cavity: they do not interfere with the sense of smell and other physiological functions of the nose, prevent the formation of synechiae, etc. Such operations are most effective for improving the sense of smell. The functional effectiveness of endonasal surgical interventions is increased by the use of techniques such as resection-reimplantation of the nasal septum in case of its curvature, which impairs the function of nasal breathing and sense of smell; rhinoseptoplasty for deformation of the external nose, combined with a deviated nasal septum; submucosal electrocautery for hypertrophic rhinitis.

In case of hyposmia that occurs against the background of acute and chronic rhinosinusitis, it is advisable to use antioxidants and biostimulating serum in complex treatment to enhance reparative processes in dystrophically altered areas of the olfactory sensory epithelium. For olfactory disorders associated with allergic rhinitis and rhinosinusitis, glucocorticoids are used topically, including in the form of injections under the mucous membrane of the middle nasal passage. For diseases of the paranasal sinuses of a non-allergic nature and for disorders of smell that arose after an upper respiratory tract infection, the effectiveness of the use of topical glucocorticoids is noted, and in the absence of effect, the prescription of drugs of this group in a systemic short course. The positive result of this therapy is associated with a decrease in edema and inflammation of the mucous membrane of the olfactory cleft and a decrease in the viscosity of nasal secretions, which facilitates the penetration of the odorant to the olfactory neuroepithelium. The absence of any effect from systemic hormonal therapy in patients with olfactory disorders arising after an upper respiratory tract infection indicates damage to the olfactory receptor apparatus.

The complex of therapeutic measures for dystrophic changes in the mucous membrane of the upper respiratory tract in combination with damage to the receptor section of the olfactory analyzer includes vitamins, glucocorticoids, biostimulants, and agents that have a positive effect on tissue trophism. A well-known balneotherapeutic agent - deresined naphthalan - has a similar direction of action. One of its main active principles is polycyclic naphthalan hydrocarbons - derivatives of, which is part of cholesterol, ergosterol, folliculin, corpus luteum hormones, testosterone, bile acids, vitamin D. Biologically active components include aromatic hydrocarbons, nitrogenous bases, naphthenic acids, features cyclopentane. The therapeutic effect is also due to the content of numerous microelements in naphthalan: molybdenum, boron, lithium, rubidium, cobalt. Naftalan promotes tissue regeneration, causes local vasodilation, and improves blood circulation. The course of treatment is 10-14 days.
For mixed forms of dysosmia, treatment is complex: surgical methods are combined with conservative ones.

Treatment of functional (psychogenic) anosmia should be comprehensive in both acute and chronic cases. Psychotherapy should be carried out at the same time. When performing certain manipulations (blockade, lubrication, etc.) and operations, it is necessary to reinforce your actions with verbal suggestion in order to restore the perception and intelligibility of odors.

In most cases, the sense of smell can be restored. The prognosis depends on the form and cause of the smell disorder. With a long-term, over three years, perceptual impairment of smell and with bacterial and allergic rhinosinusitis lasting more than 10-15 years, restoration of the sense of smell is almost impossible due to irreversible changes in the structures of the olfactory analyzer and depends on the underlying disease.