Certain diagnostic tools can also be used to help determine the extent of dysgeusia. Electrophysiological tests and simple reflex tests may be applied to identify abnormalities in the nerve-to-brainstem pathways. For example, the blink reflex may be used to evaluate the integrity of the trigeminal nerve–pontine brainstem–facial nerve pathway, which may play a role in gustatory function.

Structural imaging is routinely used to investigate lesions in the taste pathway. Magnetic resonance imaging allows direct visualization of the cranial nerves. Furthermore, it provides significant information about the type and cause of a lesion. Analysis of mucosal blood flow in the oral cavity in combination with the assessment of autonomous cardiovascular factors appears to be useful in the diagnosis of autonomic nervous system disorders in burning mouth syndrome and in patients with inborn disorders, both of which are associated with gustatory dysfunction. Cell cultures may also be used when fungal or bacterial infections are suspected.

In addition, the analysis of saliva should be performed, as it constitutes the environment of taste receptors, including transport of tastes to the receptor and protection of the taste receptor. Typical clinical investigations involve sialometry and sialochemistry. Studies have shown that electron micrographs of taste receptors obtained from saliva samples indicate pathological changes in the taste buds of patients with dysgeusia and other gustatory disorders.

In order to further classify the extent of dysgeusia and clinically measure the sense of taste, gustatory testing may be performed. Gustatory testing is performed either as a whole-mouth procedure or as a regional test. In both techniques, natural or electrical stimuli can be used. In regional testing, 20 to 50 µL of liquid stimulus is presented to the anterior and posterior tongue using a pipette, soaked filter-paper disks, or cotton swabs. In whole mouth testing, small quantities (2-10 mL) of solution are administered, and the patient is asked to swish the solution around in the mouth.

Threshold tests for sucrose (sweet), citric acid (sour), sodium chloride (salty), and quinine or caffeine (bitter) are frequently performed with natural stimuli. One of the most frequently used techniques is the "three-drop test." In this test, three drops of liquid are presented to the subject. One of the drops is of the taste stimulus, and the other two drops are pure water. Threshold is defined as the concentration at which the patient identifies the taste correctly three times in a row.

Suprathreshold tests, which provide intensities of taste stimuli above threshold levels, are used to assess the patient's ability to differentiate between different intensities of taste and to estimate the magnitude of suprathreshold loss of taste. From these tests, ratings of pleasantness can be obtained using either the direct scaling or magnitude matching method and may be of value in the diagnosis of dysgeusia. Direct scaling tests show the ability to discriminate among different intensities of stimuli and whether a stimulus of one quality (sweet) is stronger or weaker than a stimulus of another quality (sour). Direct scaling cannot be used to determine if a taste stimulus is being perceived at abnormal levels. In this case, magnitude matching is used, in which a patient is asked to rate the intensities of taste stimuli and stimuli of another sensory system, such as the loudness of a tone, on a similar scale. For example, the Connecticut Chemosensory Clinical Research Center asks patients to rate the intensities of NaCl, sucrose, citric acid and quinine-HCl stimuli, and the loudness of 1000 Hz tones. Assuming normal hearing, the results of this cross-sensory test show the relative strength of the sense of taste in relation to the loudness of the auditory stimulus. Although many of the tests are based on ratings using the direct scaling method, some tests do use the magnitude-matching procedure.

Other tests include identification or discrimination of common taste substances. Topical anesthesia of the tongue has been reported to be of use in the diagnosis of dysgeusia as well, since it has been shown to relieve the symptoms of dysgeusia temporarily. In addition to techniques based on the administration of chemicals to the tongue, electrogustometry is frequently used. It is based on the induction of gustatory sensations by means of an anodal electrical direct current. Patients usually report sour or metallic sensations similar to those associated with touching both poles of a live battery to the tongue. Although electrogustometry is widely used, there seems to be a poor correlation between electrically and chemically induced sensations.

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.

Measurement of urine for the ratio of trimethylamine to trimethylamine oxide is the standard screening test. A blood test is available to provide genetic analysis. The prominent enzyme responsible for TMA N-oxygenation is coded by the "FMO3" gene.

False positives can occur in the following conditions, where elevated TMA can be present in the urine without any underlying TMAU:

- Urinary tract infection

- Bacterial vaginosis

- Cervical cancer

- Advanced liver or kidney disease

A similar foul-smelling odor of the urine has also been associated with colonization of the urinary tract with a bacterium called "Aerococcus urinae", especially in children.

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.

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.

In response to a WHO call for papers at the 5th Paris Appeal Congress of Environmental Idiopathic Intolerance conference that took place in Belgium on the 18th of May, a report that was generally supportive quoted a number of international practitioners. This was provisionally accepted by the Spanish health ministry, and later found proven by a judge in the case of a plumber in the Province of Castellón

MCS is a diagnosis of exclusion, and the first step in diagnosing a potential MCS sufferer is to identify and treat all other conditions which are present and which often explain the reported symptoms. For example, depression, allergy, thyroid disorders, orthostatic syndromes, lupus, hypercalcemia, and anxiety need to be carefully evaluated and, if present, properly treated. The "gold standard" procedure for identifying a person who has MCS is to test response to the random introduction of chemicals the patient has self-identified as relevant. This may be done in a carefully designed challenge booth to eliminate the possibility of contaminants in the room. Chemicals and controls, sometimes called prompts, are introduced in a random method, usually scent-masked. The test subject does not know when a prompt is being given. Objective and subjective responses are measured. Objective measures, such as the galvanic skin response indicate psychological arousal, such as fear, anxiety, or anger. Subjective responses include patient self-reports. A diagnosis of MCS can only be justified when the subject cannot consciously distinguish between chemicals and controls, and when responses are consistently present with exposure to chemicals and consistently absent when prompted by a control.

A 1999 consensus statement recommends that MCS be diagnosed according to six standardized criteria:

1. Symptoms are reproducible with repeated (chemical) exposures

2. The condition has persisted for a significant period of time

3. Low levels of exposure (lower than previously or commonly tolerated) result in manifestations of the syndrome ("i.e." increased sensitivity)

4. The symptoms improve or resolve completely when the triggering chemicals are removed

5. Responses often occur to multiple chemically unrelated substances

6. Symptoms involve multiple-organ symptoms (runny nose, itchy eyes, headache, scratchy throat, ear ache, scalp pain, mental confusion or sleepiness, palpitations of the heart, upset stomach, nausea and/or diarrhea, abdominal cramping, aching joints).

The International Statistical Classification of Diseases and Related Health Problems (ICD), maintained by the World Health Organization, does not recognize multiple chemical sensitivity or environmental sensitivity as a valid diagnosis. The Australian Department of Health recognizes that sometimes debilitating symptoms are attributed to MCS but notes that diagnosis, treatment, and any underlying mechanism remain uncertain. The German Institute for Medical Documentation and Information recognizes MCS as a physical disease and is subsequentially recognized in Austria. The American Medical Association does not recognize MCS as an organic disease because of the lack of scientific evidence supporting a cause-and-effect relationship between very low level exposure and the symptoms of MCS. The American Academy of Allergy, Asthma, and Immunology, the California Medical Association, the American College of Physicians, and the International Society of Regulatory Toxicology and Pharmacology also do not recognize MCS. The US Occupational Safety and Health Administration (OSHA) indicates that MCS is highly controversial and that there is insufficient scientific evidence to explain the relationship between the suggested causes of MCS and its symptoms. OSHA recommends evaluation by a physician knowledgeable of the symptoms presented.

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

Normal olfactory acuity will usually return over time if the cause is environmental, even if it is untreated. The hyperosmic person may need to be removed from strong odorants for a period of time if the sensation becomes unbearable. Before they had been discontinued due to undesirable side effects, butyrophenones or thioridazine hydrochloride, both of which are dopamine antagonists, have been used to treat hyperosmia.

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.

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.

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.

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).

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.

There is no known cure or treatment for the disorder.

The metabolic and clinical manifestations of TMAU are generally regarded as benign, as there is no associated organ dysfunction. This

designation, and the fact that the condition is often unrecognised by doctors, can have important ramifications including missed or delayed diagnosis.

Affected individuals experience shame and embarrassment, fail to maintain relationships, avoid contact with people who comment on their condition, and are obsessive about masking the odour with hygiene products and even smoking. The malodorous aspect can have serious and destructive effects on schooling, personal life, career and relationships, resulting in social isolation, low self-esteem, depression, paranoid behaviour, and suicide. Delayed diagnosis, body odour and the lack of cure may lead to psychosocial issues. When the condition is suspected or known to occur in a family, genetic testing can be helpful in identifying the specific individuals who have or carry the disorder.

Ways of reducing the fishy odor may include:

- Avoiding foods such as egg yolks, legumes, red meats, fish, beans and other foods that contain choline, carnitine, nitrogen, sulfur and lecithin

- Taking low doses of antibiotics such as neomycin and metronidazole in order to reduce the amount of bacteria in the gut

- Using slightly acidic detergent with a pH between 5.5 and 6.5

Additionally, at least one study has suggested that daily intake of the supplements activated charcoal and copper chlorophyllin may improve the quality of life of individuals afflicted with TMAU by helping their bodies to oxidize and convert TMA to the odorless "N"-oxide (TMAO) metabolite. Study participants experienced subjective reduction in odor as well as objective reduction in TMA and increase in TMAO concentration measured in their urine. The study found that:

- 85% of test participants experienced complete loss of detectable "fishy" odor

- 10% experienced some reduction in detectable odor

- 5% did not experience any detectable odor reduction

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.

When accompanied by the combination of situs inversus (reversal of the internal organs), chronic sinusitis, and bronchiectasis, it is known as Kartagener syndrome (only 50% of primary ciliary dyskinesia cases include situs inversus).

Several diagnostic tests for this condition have been proposed. These include nasal nitric oxide levels, light microscopy of biopsies for ciliary beat pattern and frequency and electron microscopic examination of dynein arms. Genetic testing has also been proposed but this is difficult given that there are multiple genes involved.

There has not been extensive research into environmental causes of hyperosmia, but there are some theories of some possible causes.

In a study by Atianjoh et al., it has been found that amphetamines decrease levels of dopamine in the olfactory bulbs of rodents. On this basis, it has been hypothesized that amphetamine use may cause hyperosmia in rodents and humans, but further research is still needed. Anecdotal support for the belief that amphetamines may cause hyperosmia comes from Oliver Sacks's account of a patient with a heightened sense of smell after taking amphetamines.

It has been observed that the inhalation of hydrocarbons can cause hyperosmia, most likely due to the destruction of dopaminergic neurons in the olfactory bulb.

Methotrexate, administered in the treatment of psoriasis, has been known to cause hyperosmia, and may be more likely to do so in patients with a history of migraines. However, this is only an observation and not part of a study, therefore it is yet to be verified.

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.

One form of treatment is Cognitive behavioral therapy which promotes desensitization methods.

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.

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.