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.

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.

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.

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.

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.

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 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.

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).