Мұрынның иіс сезу қабілетінің жоқтығы және оның себептері

Inability to smell
When anosmia is caused by inflammatory changes in the nasal passageways, it is treated simply by reducing inflammation. It can be caused by chronic meningitis and neurosyphilis that would increase intracranial pressure over a long period of time, and, in some cases, by ciliopathy, including ciliopathy due to primary ciliary dyskinesia. The term derives from the Neo Latin anosmia, based on Ancient Greek ἀν (an ) + ὀσμή (osmḗ 'smell'; another related term, hyperosmia, refers to an increased ability to smell). Some people may be anosmic for one particular odor, a condition known as "specific anosmia". The absence of the sense of smell from birth is known as congenital anosmia. In the United States, 3% of people aged over 40 are affected by anosmia.

Anosmia is the inability to smell. People with sudden onset anosmia may find food less appetizing, though congenital anosmics rarely complain about this, and none report a loss in weight. Loss of smell can also be dangerous because it hinders the detection of gas leaks, fire, and spoiled food. Misconceptions of anosmia as trivial can make it more difficult for a patient to receive the same types of medical aid as someone who has lost other senses, such as hearing or sight. Many experience one sided loss of smell, often as a result of minor head trauma. This type of anosmia is normally only detected if both of the nostrils are tested separately. Using this method of testing each nostril separately will often show a reduced or even completely absent sense of smell in either one nostril or both, something which is often not revealed if both nostrils are simultaneously tested. Losing an established and sentimental smell memory (e. g. the smell of grass, of the grandparents' attic, of a particular book, of loved ones, or of oneself) has been known to cause feelings of depression. Loss of the ability to smell may lead to the loss of libido, but this usually does not apply to those with olfactory dysfunction at birth. Often people who have loss of smell at birth report that they pretended to be able to smell as children because they thought that smelling was something that older/mature people could do, or did not understand the concept of smelling but did not want to appear different from others. When children get older, they often realize and report to their parents that they do not actually possess a sense of smell, often to the surprise of their parents.

A temporary loss of smell can be caused by a blocked nose or infection. In contrast, a permanent loss of smell may be caused by death of olfactory receptor neurons in the nose or by brain injury in which there is damage to the olfactory nerve or damage to brain areas that process smell (see olfactory system). The lack of the sense of smell at birth, usually due to genetic factors, is referred to as congenital anosmia. Family members of the patient with congenital anosmia are often found with similar histories; this suggests that the anosmia may follow an autosomal dominant pattern. Anosmia may very occasionally be an early sign of a degenerative brain disease such as Parkinson's disease and Alzheimer's disease. Another specific cause of permanent loss could be from damage to olfactory receptor neurons because of use of certain types of nasal spray; i. e., those that cause vasoconstriction of the nasal microcirculation. To avoid such damage and the subsequent risk of loss of smell, vasoconstricting nasal sprays should be used only when absolutely necessary and then for only a short amount of time. Non vasoconstricting sprays, such as those used to treat allergy related congestion, are safe to use for prescribed periods of time. Anosmia can also be caused by nasal polyps. These polyps are found in people with allergies, histories of sinusitis, and family history. Individuals with cystic fibrosis often develop nasal polyps. Amiodarone is a drug used in the treatment of arrhythmias of the heart. A clinical study demonstrated that the use of this drug induced anosmia in some patients. Although rare, there was a case in which a 66 year old male was treated with amiodarone for ventricular tachycardia. After the use of the drug he began experiencing olfactory disturbance, however after decreasing the dosage of amiodarone, the severity of the anosmia decreased accordingly, suggesting a relationship between use of amiodarone to the development of anosmia.

Chemosensory disturbances, including loss of smell or taste, are the predominant neurological symptom of COVID 19. As many as 80% of COVID 19 patients exhibit some change in chemesthesis, including smell. Loss of smell has also been found to be more predictive of COVID 19 than all other symptoms, including fever, cough or fatigue, based on a survey of 2 million participants in the UK and US. Google searches for "smell", "loss of smell", "anosmia", and other similar terms increased since the early months of the pandemic, and strongly correlated with increases in daily cases and deaths. Research into the mechanisms underlying these symptoms is currently ongoing. Many countries list anosmia as an official COVID 19 symptom, and some have developed "smell tests" as potential screening tools. In 2020, the Global Consortium for Chemosensory Research, a collaborative research organization of international smell and taste researchers, formed to investigate loss of smell and related chemosensory symptoms.

Though anosmia caused by brain damage cannot be treated, anosmia caused by inflammatory changes in the mucosa may be treated with glucocorticoids. Reduction of inflammation through the use of oral glucocorticoids such as prednisone, followed by long term topical glucocorticoid nasal spray, would easily and safely treat the anosmia. A prednisone regimen is adjusted based on the degree of the thickness of mucosa, the discharge of oedema and the presence or absence of nasal polyps. Anosmia caused by a nasal polyp may be treated by steroidal treatment or removal of the polyp. Although very early in development, gene therapy has restored a sense of smell in mice with congenital anosmia when caused by ciliopathy. In this case, a genetic condition had affected cilia in their bodies which normally enabled them to detect air borne chemicals, and an adenovirus was used to implant a working version of the IFT88 gene into defective cells in the nose, which restored the cilia and allowed a sense of smell.

In the United States 3% of people aged over 40 are affected by anosmia.