Anosmia can be diagnosed by doctors by using acetylcysteine tests. Doctors will begin with a detailed elicitation of history. Then the doctor will ask for any related injuries in relation to anosmia which could include upper respiratory infections or head injury. Psychophysical Assessment of order and taste identification can be used to identify anosmia. A nervous system examination is performed to see if the cranial nerves are damaged. The diagnosis 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. Occasionally, after accidents, there is a change in a patient's sense of smell. Particular smells that were present before are no longer present. On occasion, after head traumas, there are patients who have unilateral anosmia. The sense of smell should be tested individually in each nostril.

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 is unaware of the deficit. It may also lead to reduction of appetite.

Diagnosing a patient can be difficult as they are often frustrated from ineffective therapy and being told they have mental illnesses. Some patients actually have trouble deciding whether they have a taste or smell problem. In this case asking questions about food choices will help determine whether a patient has a smell or taste disorder. It is important to identify whether the distortion applies to an inhaled odorant or if an odor exists without the stimulus. The distortion of an odorant is presented in two types: the stimuli are different from what one remembers and in the second, everything has a similar smell. A clinical history can also help determine what kind of disorder one has because events such as respiratory infection and head trauma are usually indications of parosmia where as phantosmias usually have no history of such events and occur spontaneously. Unfortunately there are no accurate diagnostic tests or methods for dysosmia. Evaluation must be done through questionnaires and medical history.

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. However, the treatment is not permanent and may have to be repeated after a short while. Together with medication, pressure of the upper area of the nose must be mitigated through aeration and drainage.

Anosmia caused by a nasal polyp may be treated by steroidal treatment or removal of the polyp.

There have also been cases where the use of acupuncture have successfully treated anosmia.

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.

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

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.

The most challenging task for the examiner is to determine and obtain the correct symptoms and associate them with one of the olfactory disorders, as there are several of them and they are related to each other.

The first step the examiner usually takes is to investigate if the problem is olfactory or gustatory related. As it may be that the patient releases certain bodily odors that are causing them to have this perception.

If the examiner is able to confirm that the problem is olfactory related, the next step is to determine which olfactory disorder the patient suffers from. The following is a list of possible olfactory disorders:

- anosmia

- dysosmia

- hyperosmia

- hyposmia

- parosmia or troposmia

- phantosmia

The second step is very difficult for both the examiner and the patient as the patient has some difficulty describing their perception of the phantom odor. Furthermore, the patient is in a position of stress and anxiety thus it is crucial that the examiner be patient.

After determining the nature of the disorder, and confirming phantosmia, the examiner must then have the patient describe their perception of the phantom odor. In many cases, patients have described the odor to be that of something burning and rotten and have described it to be unpleasant and foul.

The third step for the examiner is to determine the health history of the patient to take note of head trauma, accidents, upper respiratory infections, allergic rhinitis or chronic rhinitis. Although these may be events that have resulted in the phantom odor, studies conducted by Zilstrof have found that the majority of phantosmia patients have no previous history of head trauma and upper respiratory infections.

One method used to establish parosmia is the University of Pennsylvania Smell Identification Test, or UPSIT. "Sniffin' Sticks" are another method that can be used to properly diagnose parosmia. These different techniques can also help deduce whether a specific case of parosmia can be attributed to just one stimulating odor or if there is a group of stimulating odors that will generate the displaced smell. One case study performed by Frasnelli "et al." offers a situation where certain smells, specifically coffees, cigarettes, onions, and perfumes, induced a "nauseating" odor for the patient, one which was artificial but unable to be aptly related to another known smell. In another case study cited in the same paper, one woman had parosmia in one nostril but not the other. Medical examinations and MRIs did not reveal any abnormalities; however the parosmia in this case was degenerative and only got worse with time. The authors do comment, however, that cases of parosmia can predict regeneration of olfactory senses.

Due to the rareness of the disorder there is no well-defined treatment. Sometimes the patients are just told to live with the disorder or the patients end up performing "stereotypical methods" that might help in reducing the severity of the odor. This might include forced crying, bending over holding knees while holding breath, rinsing the nose with saline water and gagging. All these behaviours at the end fail to resolve the hallucination. Various treatments like prophylactic have been suggested but more research is needed for its confirmation. Also, due to being a poorly understood disorder, and having analogies to some psychiatric conditions, some patients are told that they have a mental illness. It is also usual for these patients to have suicidal thoughts as they are not provided with much support or hope from many physicians.

One of the surgical treatments proposed has included olfactory bulb ablation through a bifrontal craniotomy approach. But a counter-argument by Leopold, Loehrl and Schwob (2002) has stated that this ablation process results in a bilateral permanent anosmia and includes risks associated with a craniotomy. According to them, the use of transnasal endoscopic exhibition of olfactory epithelium is a safe and effective treatment for patients with unremitting Phantosmia with the olfactory function being potentially spared.

It is also cautioned that the surgery is challenging one and is associated with major risks, and that it should be restricted to expertise centres.

On the other hand, many cases have also reported that the strength of their symptoms have decreased with time. (Duncan and Seidan, 1995)

A case involving long term phantosmia has been treated with the use of an anti depressive medication by the common name Venlafaxine. The brand name of the drug is Effexor. The relation between mood disorders and phantosmia is unknown, and is a widely researched area. In many cases, the symptoms of phantosmia have been reduced by the use of anti seizure and anti depressants that act on the central and peripheral neurons.

The most commonly used treatment method is the removal of the olfactory epithelium or the bulb by means of surgery to alleviate the patient from the symptoms.

Other traditional methods include the use of topical anesthetics (Zilstorff-Pederson, 1995) and use of sedatives.

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.

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.

Both taste and smell disorders are diagnosed by an otolaryngologist, a doctor of the ear, nose, throat, head, and neck. An otolaryngologist can determine the extent of your taste disorder by measuring the lowest concentration of a taste quality that you can detect or recognize. You may also be asked to compare the tastes of different substances or to note how the intensity of a taste grows when a substance’s concentration is increased.

Scientists have developed taste testing in which the patient responds to different chemical concentrations. This may involve a simple “sip, spit, and rinse” test, or chemicals may be applied directly to specific areas of the tongue.

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.

Due to its non-specific nature, diagnosing CSE requires a multidisciplinary "Solvent Team" typically consisting of a neurologist, occupational physician, occupational hygienist, neuropsychologist, and sometimes a psychiatrist or toxicologist. Together, the team of specialists together assesses the patient's history of exposure, symptoms, and course of symptom development relative to the amount and duration of exposure, presence of neurological signs, and any existing neuropsychological impairment.

Furthermore, CSE must be diagnosed "by exclusion". This means that all other possible causes of the patient’s symptoms must first be ruled out beforehand. Because screening and assessing for CSE is a complex and time-consuming procedure requiring several specialists of multiple fields, few cases of CSE are formally diagnosed in the medical field. This may, in part, be a reason for the syndrome’s lack of recognition. The solvents responsible for neurological effects dissipate quickly after an exposure, leaving only indirect evidence of their presence, in the form of temporary or permanent impairments.

Brain imaging techniques that have been explored in research have shown little promise as alternative methods to diagnose CSE. Neuroradiology and functional imaging have shown mild cortical atrophy, and effects in dopamine-mediated frontostriatal circuits in some cases. Examinations of regional cerebral blood flow in some imaging techniques have also shown some cerebrovascular abnormalities in patients with CSE, but the data were not different enough from healthy patients to be considered significant. The most promising brain imaging technique being studied currently is functional magnetic resonance imaging (fMRI) but as of now, no specific brain imaging techniques are available to reliably diagnose CSE.

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.

Introduced by a working group from the World Health Organization (WHO) in 1985, WHO diagnostic criteria states that CSE can occur in three stages, organic affective syndrome (type I), mild chronic toxic encephalopathy (type II), and severe chronic toxic encephalopathy (type III). Shortly after, a workshop in Raleigh-Durham, NC (United States) released a second diagnostic criterion which recognizes four stages as symptoms only (type 1), sustained personality or mood swings (type 2A), impairment of intellectual function (type 2B), and dementia (type 3). Though not identical, the WHO and Raleigh criteria are relatively comparable. WHO type I and Raleigh types 1 and 2A are believed to encompass the same stages of CSE, and WHO type II and Raleigh type 2B both involve deficiencies in memory and attention. No other international classifications for CSE have been proposed, and neither the WHO nor Raleigh criteria have been uniformly accepted for epidemiological studies.

The diagnosis is often one of exclusion found during the workup of delayed puberty.

A paper published in 2012 by Prof. Jacques Young highlights a typical example of the diagnostic work up involved in a suspected case of KS/CHH.

One of the biggest problems in the diagnosis of KS and other forms of CHH is the ability to distinguish between a normal constitutional delay of puberty and KS or CHH.

The main biochemical parameters in men are low serum testosterone and low levels of the gonadotropins LH and FSH, and in women low serum oestrogen and low levels of LH and FSH.

For both males and females with constitutional delay of puberty, endogenous puberty will eventually commence without treatment. However a delay in treatment in a case of KS/HH will delay the physical development of the patient and can cause severe psychological damage. The "wait and see" approach applied to "late bloomers" is probably counterproductive to the needs of the patient whereas a step-by-step approach with hormone replacement therapy used with slowly increasing doses can be used as a diagnostic tool.

Post natal diagnosis of KS / CHH before the age of 6 months is sometimes possible. The normal post natal hormonal surge of gonadotropins along with testosterone or oestrogen is absent in babies with KS / CHH. This lack of detectable hormones in the blood can be used as a diagnostic indicator, especially in male infants.

Normally testicular enlargement is the key sign for the onset of puberty in boys however the use of nighttime LH sampling can help predict the onset of puberty.

In females diagnosis is sometimes further delayed as other causes of amenorrhoea normally have to be investigated first before a case of KS/CHH is considered. KS/CHH can still occur in females in cases when menstruation has begun but stopped after one or two menstrual bleeds. A study of GnRH deficient women in 2011 showed that 10% had experienced one or two bleeds before the onset of amenorrhoea.

In males, treatment with age-appropriate levels of testosterone can be used to distinguish between a case of KS/CHH from a case of delayed puberty. If just delayed the testosterone can "kick-start" endogenous puberty, as demonstrated by testicular enlargement, whereas in the case of KS/CHH there will be no testicular enlargement while on testosterone therapy alone. If no puberty is apparent, especially no testicular development, then a review by a reproductive endocrinologist may be appropriate. Dr Richard Quinton, a leading UK expert on KS/CHH, suggests that if puberty is not apparent by the age of 16 then the patient should be referred for endocrinological review.

A full endocrine workup will be required to measure the levels of the other pituitary hormones, especially prolactin, to check that the pituitary gland is working correctly. There can be other general health issues such as being overweight or having an underlying chronic or acute illness which could cause a delay of puberty. This makes it essential for a patient to get a full endocrine review to distinguish between a case of KS/CHH and another cause for the pubertal delay.

Bone age can be assessed using hand and wrist X-rays. If the bone age is significantly lower than the chronological age of the patient, this could suggest delayed puberty unless there is another underlying reason for the discrepancy.

A karyotype may be performed to rule out Klinefelter syndrome and Turner syndrome, although the hormones levels would also rule out both these relatively common reasons for hypogonadism.

A magnetic resonance imaging (MRI) scan can be used to determine whether the olfactory bulb is present and to check for any physical irregularities of the pituitary gland or hypothalamus.

A standard smell test can be used to check for anosmia, but it must be remembered that even in total anosmia various substances (such as menthol and alcohol) can still be detected by direct stimulation of the trigeminal nerve.

Genetic screening can be carried out, but in light of the unknown genes involved in the majority of KS and CHH cases, a negative result will not rule out a possible diagnosis.

A review paper published in 2014 highlighted the need for doctors to be aware of the possible diagnosis of KS / HH if pubertal delay is found alongside associated "red flag" symptoms. The symptoms listed in the paper were split into two categories; reproductive symptoms associated with the lack of mini puberty seen between birth and six months of age and non-reproductive symptoms which are associated with specific forms of HH. As with other review papers the authors also warned against the "wait and see" approach when puberty appears to be delayed.

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.

The third indicator is the presence of clues to specific disorders of the reproductive system.

- Malnutrition or anorexia nervosa severe enough to delay puberty will give other clues as well.

- Poor growth would suggest the possibility of coeliac disease, hypopituitarism or Turner syndrome.

- Reduced sense of smell (hyposmia) or no sense of smell (anosmia) suggests Kallmann syndrome.

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.

Diagnostic criteria have been proposed for ORS:

- Persistent (> six months), false belief that one emits an offensive odor, which is not perceived by others. There may be degrees of insight (i.e. the belief may or may not be of delusional intensity).

- This pre-occupation causes clinically significant distress (depression, anxiety, shame), social and occupational disability, or may be time-consuming (i.e. preoccupies the individual at least one hour per day).

- The belief is not a symptom of schizophrenia or other psychotic disorder, and not due to the effects of medication or recreational drug abuse, or any other general medical condition.

The first is simply degree of lateness: although no recommended age of evaluation cleanly separates pathologic from physiologic delay, a delay of 2–3 years or more warrants evaluation.

- In girls, no breast development by 13 years, or no menarche by 3 years after breast development (or by 16).

- In boys, no testicular enlargement by 14 years, or delay in development for 5 years or more after onset of genitalia enlargement.

A delay of two standard deviations has been proposed as a standard.

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

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.

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.