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 suffering from 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 & 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 performed 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 hence correlating the use of Amiodarone to the development of anosmia.

Anosmia can have a number of harmful effects. Patients 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. The common view 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.

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 olfaction may lead to the loss of libido, though this usually does not apply to congenital anosmics.

Often people who have congenital anosmia 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 study done on patients suffering from anosmia found that when testing both nostrils, there was no anosmia revealed; however, when testing each nostril individually, tests showed that the sense of smell was usually affected in only one of the nostrils as opposed to both. This demonstrated that unilateral anosmia is not uncommon in anosmia patients.

The frequency of phantosmia is rare in comparison with the frequency of parosmia. Parosmia has been estimated to be in 10-60% of patients with olfactory dysfunction and from studies, it has been shown that it can last anywhere from 3 months to 22 years. Smell and taste problems result in over 200,000 visits to physicians annually in the US. Lately, it has been thought that phantosmia might co-occur with Parkinson's disease. However, its potential to be a premotor biomarker for Parkinson's is still up for debate as not all patients with Parkinson's disease have olfactory disorders

Smell disorders can result in the inability to detect environmental dangers such as gas leaks, toxins, or smoke. In addition to safety, nutritional and eating habits can also be affected. There is a loss of appetite because of unpleasant flavor and fear of failing to recognize and consuming spoiled food. A decreased or distorted sense of smell therefore results in a decreased quality of life. Distortions are believed to have a greater negative impact on people than the complete loss of smell because they are constantly reminded of the disorder and the distortions have a greater effect on eating habits.

Local damage and inflammation that interferes with the taste buds or local nervous system such as that stemming from radiation therapy, glossitis, tobacco use, and denture use also cause ageusia. Other known causes include loss of taste sensitivity from aging (causing a difficulty detecting salty or bitter taste), anxiety disorder, cancer, renal failure and liver failure.

A longitudinal study on pregnant females found that 76% of pregnant females experienced significant changes in gustation and olfaction perception. This was found to be caused and linked to their pregnancy. The study concluded that 67% of the pregnant females had reported a higher level of sensitivity to smell, 17% suffered from an olfactory distortion and 14% suffered from phantosmia; these distortions were very minimal towards the last stages of pregnancy and in the majority were not present post partum. Furthermore, 26% of these participants also claimed that they also experienced an increased sensitivity to foods that were bitter and a decreased sensitivity to salt. These findings suggest that pregnant females experience distorted smell and taste perception during pregnancy. It has also been found that 75% of women alter their diets during pregnancy. Further research is being conducted to determine the mechanism behind food cravings during pregnancy.

Phantosmia is most likely to occur in women between the ages of 15 and 30 years. The time of the first hallucination(s) lasts from anywhere from five to twenty minutes. It has also been found that the second hallucination will occur approximately a month later in the same manner as the first. Over time, the length of the hallucination will begin to increase.

Deficiency of vitamin B (niacin) and zinc can cause problems with the endocrine system, which may cause taste loss or alteration. Disorders of the endocrine system, such as Cushing's syndrome, hypothyroidism and diabetes mellitus, can cause similar problems. Ageusia can also be caused by medicinal side-effects from antirheumatic drugs such as penicillamine, antiproliferative drugs such as cisplatin, ACE inhibitors, and other drugs including azelastine, clarithromycin, terbinafine, and zopiclone.

Merciful anosmia is a condition in which the person is unaware of the foul smell emanating from his own nose. This condition is seen in atrophic rhinitis. In atrophic rhinitis, the turbinates, venous sinusoids, seromucinous glands and nerves undergo atrophy, resulting in a foul smelling discharge. As the nerve fibres sensing smell are also atrophied, the patient is unable to appreciate the foul smell.

Fortunately for patients afflicted with parosmia, symptoms usually decrease with time. Although there are instances of parosmia affecting patients for years at a time, this is certainly not the majority of cases. There have been experiments done to treat parosmia with L-Dopa, but besides that there are no current treatments other than inducing anosmia or hyposmia to the point where the odors are negligible.

Hyposmia is a reduced ability to smell and to detect odors. A related condition is anosmia, in which no odors can be detected. Some of the causes of olfaction problems are allergies, nasal polyps, viral infections and head trauma. It is estimated that up to 4 million people in the United States have hyposmia or the related anosmia.

Hyposmia might be a very early sign of Parkinson's disease. Hyposmia is also an early and almost universal finding in Alzheimer's disease and dementia with Lewy bodies. Lifelong hyposmia could be caused by Kallmann syndrome.

There are numerous diseases that parosmia is associated with. In the case study cited above, Frasnelli "et al." examined five patients that endured parosmia or phantosmia, most as a result of upper respiratory tract infections (URTIs). It is hypothesized that URTIs can result in parosmia because of damage to olfactory receptor neurons (ORNs).

Exposure to harmful solvents has also been linked to parosmia and more specifically damaging ORNs.

Damage to these neurons could end in the inability to correctly encode a signal representing a particular odor, which would send an erroneous signal to the odor processing center, the olfactory bulb. This, in turn, leads to the signal activating a different trigger, i.e. a different smell, than the stimulating odor, and thus the patient cannot sync the input and output odors. Damage to ORNs describes a peripheral defect in the pathway, but there are also instances where damage to the processing center in the brain can lead to distorted odors as well.

Different types of head traumas could obviously lead to dysfunctions that relate to what the afflicted brain area controls. In humans, the olfactory bulb is located on the inferior side of the brain. Physical damage to this area would alter how the area processes information in a variety of ways, but there are also other types of diseases that can alter how this area works. If the part of the brain that interprets these input signals is damaged, then a distorted output is possible. This would also lead to parosmia. Temporal lobe epilepsy has also led to cases of parosmia, but these were only temporary; the onset of parosmia was a seizure and it typically lasted a week or two after.

Parosmia is also a known symptom for Parkinson's disease, though not ubiquitous for patients with it, and although the specific pathway is undetermined, the lack of dopamine has resulted in documented cases of parosmia and phantosmia.

Anosmia is the inability to perceive odor, or in other words a lack of functioning olfaction. Many patients may experience unilateral or bilateral anosmia.

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. The lack of the sense of smell at birth, usually due to genetic factors, is referred to as congenital anosmia.

The diagnosis of anosmia as well as the degree of impairment can now be tested much more efficiently and effectively than ever before thanks to "smell testing kits" that have been made available as well as screening tests which use materials that most clinics would readily have.

Many cases of congenital anosmia remain unreported and undiagnosed. Since the disorder is present from birth the individual may have little or no understanding of the sense of smell, hence are unaware of the deficit.

Degrees of vision loss vary dramatically, although the ICD-9 released in 1979 categorized them into three tiers: normal vision, low vision, and blindness. Two significant causes of vision loss due to sensory failures include media opacity and optic nerve diseases, although hypoxia and retinal disease can also lead to blindness. Most causes of vision loss can cause varying degrees of damage, from total blindness to a negligible effect. Media opacity occurs in the presence of opacities in the eye tissues or fluid, distorting and/or blocking the image prior to contact with the photoreceptor cells. Vision loss often results despite correctly functioning retinal receptors. Optic nerve diseases such as optic neuritis or retrobulbar neuritis lead to dysfunction in the afferent nerve pathway once the signal has been correctly transmitted from retinal photoreceptors.

Partial or total vision loss may affect every single area of a person's life. Though loss of eyesight may occur naturally as we age, trauma to the eye or exposure to hazardous conditions may also cause this serious condition. Workers in virtually any field may be at risk of sustaining eye injuries through trauma or exposure. A traumatic eye injury occurs when the eye itself sustains some form of trauma, whether a penetrating injury such as a laceration or a non-penetrating injury such as an impact. Because the eye is a delicate and complex organ, even a slight injury may have a temporary or permanent effect on eyesight.

When untreated, the prognosis for ORS is generally poor. It is chronic, lasting many years or even decades with worsening of symptoms rather than spontaneous remission. Transformation to another psychiatric condition is unlikely, although very rarely what appears to be ORS may later manifest into schizophrenia, psychosis, mania, or major depressive disorder. The most significant risk is suicide.

When treated, the prognosis is better. In one review, the proportion of treated ORS cases which reported various outcomes were assessed. On average, the patients were followed for 21 months (range: 2 weeks to 10 years). With treatment, 30% recovered (i.e. no longer experienced ORS odor beliefs and thoughts of reference), 37% improved and in 33% there was a deterioration in the condition (including suicide) or no change from the pre-treatment status.

Cases have been reported from many different countries around the world. It is difficult to estimate the prevalence of ORS in the general population because data are limited and unreliable, and due to the delusional nature of the condition and the characteristic secrecy and shame.

For unknown reasons, males appear to be affected twice as commonly as females. High proportions of ORS patients are unemployed, single, and not socially active. The average age reported is around 20–21 years, with almost 60% of cases occurring in subjects under 20 in one report, although another review reported an older average age for both males (29) and females (40).

Samter's triad goes by several other names:

A sufferer who has not yet experienced asthma or aspirin sensitivity might be diagnosed as having:

- Non-allergic rhinitis

- Non-allergic rhinitis with eosinophilia syndrome (NARES)

The olfactory system is the system related to the sense of smell (olfaction). Many fish activities are dependent on olfaction, such as: mating, discriminating kin, avoiding predators, locating food, contaminant avoidance, imprinting and homing. These activities are referred to as “olfactory-mediated.” Impairment of the olfactory system threatens survival and has been used as an ecologically relevant sub-lethal toxicological endpoint for fish within studies. Olfactory information is received by sensory neurons, like the olfactory nerve, that are in a covered cavity separated from the aquatic environment by mucus. Since they are in almost direct contact with the surrounding environment, these neurons are vulnerable to environmental changes. Fish can detect natural chemical cues in aquatic environments at concentrations as low as parts per billion (ppb) or parts per trillion (ppt).

Studies have shown that exposures to metals, pesticides, or surfactants can disrupt fish olfaction, which can impact their survival and reproductive success. Many studies have indicated copper as a source of olfactory toxicity in fishes, among other common substances. Olfactory toxicity can occur by multiple, complex Modes of Toxic Action.

Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. Aspirin is quickly converted in the body to salicylic acid, also known as 2-Hydroxybenzoic acid. Sommer "et al." reported a multi-center prospective randomized cross-over trial with 30 patients following a low-salicylate diet for 6 weeks. This study demonstrated a clinically significant decrease in both subjective and objective scoring of severity of disease, but made note of the challenge for patients in following what is a fairly stringent diet.

A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help. In a small study, aspirin-sensitive asthma patients taking 10 grams of fish oil daily reported relief of most symptoms after six weeks, however symptoms returned if the supplement was stopped.

It has been hypothesized that biofilm bacterial infections may account for many cases of antibiotic-refractory chronic sinusitis. Biofilms are complex aggregates of extracellular matrix and inter-dependent microorganisms from multiple species, many of which may be difficult or impossible to isolate using standard clinical laboratory techniques. Bacteria found in biofilms have their antibiotic resistance increased up to 1000 times when compared to free-living bacteria of the same species. A recent study found that biofilms were present on the mucosa of 75% of people undergoing surgery for chronic sinusitis.

IHH is divided into two syndromes: IHH with olfactory alterations or anosmia, Kallmann syndrome and IHH with normal smell (normosmic IHH).

Kallmann syndrome is responsible for approximately 50% of all cases of the condition. It is associated with mutations in "KAL1", "FGFR1/FGF8", "FGF17", "IL17RD", "PROKR2", "NELF", "CHD7"(which positively regulates GnRH secretion), HS6ST1, "FLRT3", "SPRY4", DUSP6, "SEMA3A", and "WDR11 (gene)", genes which are related to defects in neuronal migration.

Gene defects associated with IHH and normal smell include "PROKR2, FGFR1, FGF8, CHD7, DUSP6," and "WDR11", as in KS, but in addition

also mutations in "KISS1R", "TACR3", GNRH1/GNRHR, LEP/LEPR, HESX1, FSHB, and LHB.

GnRH insensitivity is the second most common cause of IHH, responsible for up to 20% of cases.

A minority of less than 5-10% is due to inactivating mutations in genes which positively regulate GnRH secretion such as ,"CHD7", "KISS1R", and "TACR3".

The causes of about 25% of all IHH cases are still unknown.

Isolated hypogonadotropic hypogonadism (IHH), also called idiopathic or congenital hypogonadotropic hypogonadism (CHH), as well as isolated or congenital gonadotropin-releasing hormone deficiency (IGD) constitutes a small subset of cases of hypogonadotropic hypogonadism (HH).

IHH is due to deficiency in or insensitivity to gonadotropin-releasing hormone (GnRH), where the function and anatomy of the anterior pituitary is otherwise normal, and secondary causes of HH are not present.

Based on recent theories on the role that fungus may play in the development of chronic sinusitis, antifungal treatments have been used, on a trial basis. These trials have had mixed results.

The disruption of olfaction and potential effects to survival and reproductive success at environmentally-relevant concentrations metals, pesticides or surfactants have implications for fish and salmon recovery because these are commonly found in western United States streams. Conventional, acute and chronic toxicity testing do not explicitly address nervous system function and underestimate thresholds for toxicity in salmonids. Since these effects are not explicitly looked at during studies they oftentimes can go unnoticed. Olfactory toxicity occurring at environmentally relevant concentrations can induce reduction to food odor attraction and predator scent or alarm response pheromones can cause major problems with survivorship. Olfactory toxicity can also affect the ability of anadromous fish to find their natal stream causing them to stray to other streams.

Reversal of symptoms have been reported in between 15% to 22% of cases. The causes of this reversal are still under investigation but have been reported in both males and females.

Reversal appears to be associated with 14 of the known gene defects linked to KS/CHH. The study suggests no obvious gene defect showing a tendency to allow reversal. There is a suggestion that the TAC3 and TACR3 mutations might allow for a slightly higher chance of reversal, but the numbers involved are too low to confirm this. The ANOS1 mutations appear to be least likely to allow reversal with to date only one recorded instance in medical literature. Even male patients who previous had micro-phallus or cryptorchidism have been shown to undergo reversal of symptoms.

The reversal might not be permanent and remission can occur at any stage; the paper suggests that this could be linked to stress levels. The paper highlighted a reversal case that went into remission but subsequently achieved reversal again, strongly suggesting an environmental link.

Reversal cases have been seen in cases of both KS and normosmic CHH but appear to be less common in cases of KS (where the sense of smell is also affected). A paper published in 2016 agreed with the theory that there is a strong environmental or epigenetic link to the reversal cases. The precise mechanism of reversal is unclear and is an area of active research.

Reversal would be apparent if testicular development was seen in men while on testosterone therapy alone or in women who menstruate or achieved pregnancy while on no treatment. To date there have been no recorded cases of the reversal of anosmia found in Kallmann syndrome cases.

The treatment, and therefore prognosis, varies depending upon the underlying tumour.