The effects of drug-related dysgeusia can often be reversed by stopping the patient's regimen of the taste altering medication. In one case, a forty-eight-year-old woman who was suffering from hypertension was being treated with valsartan. Due to this drug's inability to treat her condition, she began taking a regimen of eprosartan, an angiotensin II receptor antagonist. Within three weeks, she began experiencing a metallic taste and a burning sensation in her mouth that ceased when she stopped taking the medication. When she began taking eprosartan on a second occasion, her dysgeusia returned. In a second case, a fifty-nine-year-old man was prescribed amlodipine in order to treat his hypertension. After eight years of taking the drug, he developed a loss of taste sensation and numbness in his tongue. When he ran out of his medication, he decided not to obtain a refill and stopped taking amlodipine. Following this self-removal, he reported experiencing a return of his taste sensation. Once he refilled his prescription and began taking amlodipine a second time, his taste disturbance reoccurred. These two cases suggest that there is an association between these drugs and taste disorders. This link is supported by the "de-challenge" and "re-challenge" that took place in both instances. It appears that drug-induced dysgeusia can be alleviated by reducing the drug's dose or by substituting a second drug from the same class.

In addition to the aforementioned treatments, there are also many management approaches that can alleviate the symptoms of dysgeusia. These include using non-metallic silverware, avoiding metallic or bitter tasting foods, increasing the consumption of foods high in protein, flavoring foods with spices and seasonings, serving foods cold in order to reduce any unpleasant taste or odor, frequently brushing one's teeth and utilizing mouthwash, or using sialogogues such as chewing sugar-free gum or sour-tasting drops that stimulate the productivity of saliva. When taste is impeded, the food experience can be improved through means other than taste, such as texture, aroma, temperature, and color.

Another treatment option is the topical solution of cocaine HCl which also provides relief for a short time period by acting as an anesthetic and desensitizing the nasal neurons. The topical solution is applied on the nostril. This topical solution can have several side effects as it has been found that some patients suffering from troposmia started to show symptoms of phantosmia after its use. Other patients have lost complete function of the nostril where the drug was applied.

This antidepressant medication is a serotonin norepinephrine reuptake inhibitor (SNRI). In the case study of a 52-year-old female suffering from phantosmia for 27 years, a dose of 75 mg a day relieved and eliminated her symptoms. The drug was prescribed initially in order to treat her depression.

Even though dysosmia often goes away on its own over time, there are both medical and surgical treatments for dysosmia for patients that want immediate relief. Medical treatments include the use of topical nasal drops and oxymetazoline HCL, which give an upper nasal block so that the air flow can't reach the olfactory cleft. Other medications suggested include sedatives, anti-depressants, and anti-epileptic drugs. The medications may or may not work and for some patients, the side effects may not be tolerable. Most patients benefit from medical treatment but for some surgical treatment is required. Options include a bifrontal craniotomy and an excision of the olfactory epithelium, which cuts all of the fila olfactoria. According to some studies, transnasal endoscopic excision of the olfactory epithelium has been described as a safe and effective phantosmia treatment. The bifrontal craniotomy results in permanent anosmia and both surgeries are accompanied with the risks associated with general surgery.

There is no agreed treatment protocol. In most reported cases of ORS the attempted treatment was antidepressants, followed by antipsychotics and various psychotherapies. Little data are available regarding the efficacy of these treatments in ORS, but some suggest that psychotherapy yields the highest rate of response to treatment, and that antidepressants are more efficacious than antipsychotics (response rates 78%, 55% and 33% respectively). According to one review, 43% of cases which showed overall improvement required more than one treatment approach, and in only 31% did the first administered treatment lead to some improvement.

Pharmacotherapies that have been used for ORS include antidepressants, (e.g. selective serotonin reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors), antipsychotics, (e.g. blonanserin, lithium, chlorpromazine), and benzodiazepines. The most common treatment used for ORS is SSRIs. Specific antidepressants that have been used include clomipramine.

Psychotherapies that have been used for ORS include cognitive behavioral therapy, eye movement desensitization and reprocessing.

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.

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.

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

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.

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

Since the conversion of dihydroxyphenylserine (Droxidopa; trade name: Northera; also known as L-DOPS, L-threo-dihydroxyphenylserine, L-threo-DOPS and SM-5688), to norepinephrine bypasses the dopamine beta-hydroxylation step of catecholamine synthesis, L-Threo-DOPS is the ideal therapeutic agent. In humans with DβH deficiency, L-Threo-DOPS, a synthetic precursor of noradrenaline, administration has proven effective in dramatic increase of blood pressure and subsequent relief of postural symptoms.

L-DOPS continues to be studied pharmacologically and pharmacokinetically and shows an ability to increase the levels of central nervous system norepinephrine by a significant amount. This is despite the fact that L-DOPS has a relative difficulty crossing the blood-brain barrier when compared to other medications such as L-DOPA. When used concurrently, there is evidence to show that there is increased efficacy as they are both intimately involved and connected to the pathway in becoming norepinephrine.

There is hope and evidence that L-DOPS can be used much more widely to help other conditions or symptoms such as pain, chronic stroke symptoms, and progressive supranuclear palsy, amongst others. Clinically, L-DOPS has been already shown to be helpful in treating a variety of other conditions related to hypotension including the following:

- Diabetes induced orthostatic hypotension

- Dialysis-induced hypotension

- Orthostatic intolerance

- Familial amyloidotic polyneuropathy

- Spinal Cord Injury related hypotension

Empirical evidence of mild effectiveness has been reported using mineralocorticoids or adrenergic receptor agonists as therapies.

Other medications that can bring relief to symptoms include:

- phenylpropanolamine- due to pressor response to vascular α-adrenoceptors

- indomethacin

Vitamin C (ascorbic acid) is also a required cofactor for the Dopamine beta hydroxylase enzyme. Recent research has shown that vitamin C rapidly catalyzes the conversion of dopamine to norepinephrine through stimulation of the dopamine beta hydroxylase enzyme.

There no standardized effective treatment strategies for the condition. Severe fatal respiratory failure can develop; long-term treatment with macrolides such as clarithromycin, erythromycin and azithromycin has been empirically applied for the treatment of primary ciliary dyskinesia in Japan, though controversial due to the effects of the medications.

There is no cure for the condition. Management is through therapy.

Like diagnosis, treating CSE is difficult due to how vaguely defined it is, as well as lack of data on the mechanism of CSE effects on neural tissue. There is no existing treatment that is effective at completely recovering any neurological or physical function lost due to CSE. This is believed to be because of the limited regeneration capabilities in the central nervous system. Furthermore, existing symptoms of CSE can potentially worsen with age. Some symptoms of CSE, such as depression and sleep issues, can be treated separately, and therapy is available to help patients adjust to any disabilities. Current treatment for CSE involves treating accompanying psychopathology, symptoms, and preventing further deterioration.

CGD is relatively unresponsive to antidepressants or interpersonal psychotherapy; however, recent studies support the use of CG-targeted psychotherapy (similar to PTSD-targeted psychotherapy). Other methods of psycho-pharmacological treatment are under investigation.

With time the symptoms of ARFID can lessen and can eventually disappear without treatment. However, in some cases treatment will be needed as the symptoms persist into adulthood. The most common type of treatment for ARFID is some form of cognitive-behavioral therapy. Working with a clinician can help to change behaviors more quickly than symptoms may typically disappear without treatment. Also hypnotherapy may be used. In that it lessens the anxiety associated with food.

There are support groups for adults with ARFID.

Untreated individuals with DβH deficiency should avoid hot environments, strenuous exercise, standing still, and dehydration.

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 aim for hormone replacement therapy (HRT) for both men and women is to ensure that the level of circulating hormones (testosterone for men and oestrogen/progesterone for women) is at the normal physiological level for the age of the patient. At first the treatment will produce most of the physical and psychological changes seen at puberty, with the major exception that there will be no testicular development in men and no ovulation in women.

After the optimum physical development has been reached HRT for men will continue to ensure that the normal androgen function is maintained; such as libido, muscle development, energy levels, hair growth, and sexual function. In women, a variety of types of HRT will either give a menstruation cycle or not as preferred by the patient. HRT is very important in both men and women to maintain bone density and to reduce the risk of early onset osteoporosis.

The fertility treatments used for both men and women would still include hormone replacement in their action.

There are a range of different preparations available for HRT for both men and women; a lot of these, especially those for women are the same used for standard HRT protocols used when hormone levels fall in later life or after the menopause.

For males with KS / CHH the types of delivery method available include daily patches, daily gel use, daily capsules, sub cutaneous or intramuscular injections or six monthly implants. Different formulations of testosterone are used to ensure both the anabolic and androgenic effects of testosterone are achieved.

Testosterone undecanoate is commonly used worldwide, though less so in the US, for treating male KS / CHH patients and has proved to be effective in maintaining good testosterone levels with an increased injection period of up to 12 weeks.

The precise treatment method used and interval between injections will vary from patient to patient and may need to be adjusted to maintain a physiological normal level of testosterone over a longer period of time to prevent the mood swings or adverse effects that can occur if testosterone levels are too high or low. Some treatments may work better with some patients than others so it might be a case of personal choice as which one to use.

As an alternative human chorionic gonadotrophin (hCG) can also be used to stimulate natural testosterone production. It acts in the same way as LH; stimulating the Leydig cells in the testes to produce testosterone. hCG can be used as pre-cursor to male fertility treatments but it can be used in isolation just for testosterone production.

There are no specialist HRT treatments available just for women with KS/HH but there are multitude of different HRT products on the market including oral contraceptives and standard post-menopause products. Pills are popular but patches are also available. It may take some trial and error to find the appropriate HRT for the patient depending on how her body reacts to the particular HRT. Specialist medical advice will be required to ensure the correct levels of oestrogen and progesterone are maintained each month, depending on whether the patient requires continuous HRT (no-bleed) or a withdrawal option to create a "menstrual" type bleed. This withdrawal bleed can be monthly or over longer time periods depending on the type of medication used.

Treatment for KS and other forms of HH can be divided into hormone replacement therapy and fertility treatments.

Children can benefit from a four stage in-home treatment program based on the principles of systematic desensitization. The four stages of the treatment are record, reward, relax and review.

- In the record stage, children are encouraged to keep a log of their typical eating behaviors without attempting to change their habits as well as their cognitive feelings.

- The reward stage involves systematic desensitization. Children create a list of foods that they might like to try eating some day. These foods may not be drastically different from their normal diet, but perhaps a familiar food prepared in a different way. Because the goal is for the children to try new foods, children are rewarded when they sample new foods.

- The relaxation stage is most important for those children that suffer severe anxiety when presented with unfavorable foods. Children learn to relax to reduce the anxiety that they feel. Children work through a list of anxiety-producing stimuli and can create a story line with relaxing imagery and scenarios. Often these stories can also include the introduction of new foods with the help of a real person or fantasy person. Children then listen to this story before eating new foods as a way to imagine themselves participating in an expanded variety of foods while relaxed.

- The final stage, review, is important to keep track of the child's progress. It is important to include both one-on-one sessions with the child, as well as with the parent in order to get a clear picture of how the child is progressing and if the relaxation techniques are working.

Congenital myasthenic syndromes (CMS) is "often difficult to diagnose because of a broad differential diagnosis and lack of specific laboratory findings. Identification of the underlying mutation is critical, as certain mutations lead to treatment-responsive conditions while others do not." Whole exome sequencing (WES) is often used as a diagnostic tool that allows for the "initiation of specific treatment".

Treatment depends on the form (category) of the disease. Although symptoms are similar to myasthenia gravis, treatments used in MG are not useful in CMS. MG is treated with immunosuppressants, but CMS is not an autoimmune disorder. Instead, CMS is genetic and responds to other forms of drug treatments.

A form of presynaptic CMS is caused by an insufficient release of acetylcholine (ACh) and is treated with cholinesterase inhibitors.

Postsynaptic fast-channel CMS (ACh receptors do not stay open long enough) is treated with cholinesterase inhibitors and 3,4-diaminopyridine. In the U.S., the more stable phosphate salt formulation of 3,4-diaminopyridine (amifampyridine phosphate) is under development as an orphan drug for CMS and is available to eligible patients at no cost under an expanded access program by Catalyst Pharmaceuticals.

Postsynaptic slow-channel CMS is treated with quinidine or fluoxetine, which plugs the ACh receptor.

Ephedrine has been tested on patients in clinical trials and appears to be an effective treatment for DOK7 CMS. Most patients tolerate this type of treatment and improvements in strength can be impressive. Further research must be done in order to determine the long-term response of ephedrine as well as the most effective dosage regimen. Ephedrine can lead to a profound improvement in muscle strength and an even more impressive effect on day-to-day function. The effect of ephedrine is delayed and the improvement occurs over a period of months. Ephedrine was given at doses between 15 and 90 mg/day and as a result, muscle strength improved

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.

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