The treatment options for hypohidrosis and anhidrosis is limited. Those with hypohidrosis should avoid drugs that can aggravate the condition (see medication-causes). They should limit activities that raise the core body temperature and if exercises are to be performed, they should be supervised and be performed in a cool, sheltered and well-ventilated environment. In instances where the cause is known, treatment should be directed at the primary pathology. In autoimmune diseases, such as Sjogren syndrome and systemic sclerosis, treatment of the underlying disease using immunosuppressive drugs may lead to improvement in hypohidrosis. In neurological diseases, the primary pathology is often irreversible. In these instances, prevention of further neurological damage, such as good glycaemic control in diabetes, is the cornerstone of management. In acquired generalized anhidrosis, spontaneous remission may be observed in some cases. Numerous cases have been reported to respond effectively to systemic corticosteroids. Although an optimum dose and regime has not been established, pulse methylprednisolone (up to 1000 mg ⁄ day) has been reported to have good effect.

Even though there is no way to cure the disease itself, there are ways to dampen the symptoms. These include medical help in form of pills, and using heavy lotions and oils.

To maintain the good health of the skin after the symptoms have dampened the person with the disease are advised to go on normally with their lives but to take precautions while showering. This is to take shorter, colder baths than usual to not stress the skin. It is also known to help to use bar-soap, instead of a liquid body wash.

Treatment of AIGA almost always consists of steroid pulse therapy or high-dose oral steroids and is not consistently effective. Much remains unclear regarding the reasons for recurrent anhidrosis.

A number of treatments are available. The most successful non-invasive procedure is cognitive behavioural therapy (CBT), which attempts to alleviate the anxiety felt by sufferers.

In extreme cases a surgical procedure known as endoscopic transthoracic sympathicotomy (ETS) is available. Pioneered by surgeons in Sweden, this procedure has recently become increasingly controversial due to its many potential adverse effects. Patients who have undergone the procedure frequently complain of compensatory sweating and fatigue, with around 5% reconsidering getting the treatment. ETS is now normally only considered in extreme cases where other treatments have been ineffective.

There is no standard medical or surgical treatment for acrocyanosis, and treatment, other than reassurance and avoidance of cold, is usually unnecessary. The patient is reassured that no serious illness is present. A sympathectomy would alleviate the cyanosis by disrupting the fibers of the sympathetic nervous system to the area. However, such an extreme procedure would rarely be appropriate. Treatment with vasoactive drugs is not recommended but traditionally is mentioned as optional. However, there is little, if any, empirical evidence that vasoactive drugs (α-adrenergic blocking agents or calcium channel blockers) are effective.

The primary remedy for miliaria is to wear lighter clothing, move to a cooler climate, or otherwise avoid overheating one's body. The immediate treatment of the involved skin areas involves the use of a soothing ointment such as calamine lotion.

Medical assistance should be sought for the first episode of a rash with the appearance of miliaria. The differential diagnosis includes several conditions that an experienced practitioner should be able to recognise and may require treatment distinct from the usual measures taken for miliaria. In most cases the rash of miliaria will resolve without intervention. However, severe cases can last for weeks and cause significant disability. General measures should be recommended for all patients, including moving to an air-conditioned environment if possible, avoiding sweat-provoking activities and occlusive clothing, and taking frequent cool showers.

It has been suggested that the use of topical antibacterials (including antibacterial soaps) may shorten the duration of symptoms in miliaria rubra even in the absence of obvious superinfection. Other topical agents that may reduce the severity of symptoms include anti-itch preparations such as calamine or menthol- or camphor-based preparations, and topical steroid creams. However, caution should be used with oil-based preparations (ointments and oily creams as opposed to water-based or aqueous lotions) that may increase blockage to the sweat glands and prolong duration of illness. Other agents have been investigated including supplemental vitamin A and C and vitamin A based medications, but it is worth noting that there is little scientific evidence supporting any of the above treatments in reducing the duration of symptoms or frequency of complications.

In most cases, doctors will recommend that any pimple-like blisters that may form should have the fluid drained out of them (either through in-office procedure or at home in a sterile environment) to avoid the rash from spreading underneath the skin, leading to an increased state of dermatitis. Left untreated, the blisters may spread and take on an increased red appearance, with the fluid inside increasing in viscosity. It is recommended by physicians to sanitize the infected area and then drain the blisters with a sterilized needle or lancet.

In most tropical areas the local dispensaries sell prickly heat powder, a talc admixture containing drying milk proteins (Labilin) and Triclosan to fight the infection. These include cooling menthol to help alleviate difficulty getting to sleep. This is an effective treatment—the powder stays on the skin longer and treats bacteria dispersed into bed linens, providing a reasonably dry refuge area for healing. Miliaria often covers large areas, and generous use of Cortisone may be contraindicated for reasons stated on package warnings. Regular talcum powder will not reduce the rash but can alleviate burning and itching.

In cases where the rash has developed into open blisters or pustular lesions a doctor should be consulted since more aggressive, medically monitored treatment may be required.

Sweating causes lesions to form, but lesions aggravated by sweat usually return to "normal" fairly quicklyavoiding sweat is not a reason to avoid exercise. Minor outbreaks can be controlled with prescription strength topical cortisone creams. More severe eruptions usually clear up after treatment for one to three months with Accutane or tetracycline. If these fail or the outbreak is severe, PUVA phototherapy treatments, antifungal pills and cortisone injections are alternatives.

Some research has suggested a correlation of Grover's disease with mercury toxicity in which case Dimercaptosuccinic acid might help.

Normally, exfoliation is restricted to a particular area and normal skin will replace the exfoliated parts, so no treatment is needed. Since keratolysis exfoliativa is caused by friction, detergents, and solvents, these factors should be avoided. Creams, especially those with silicone and lactic acid are also helpful. In severe cases, photochemotherapy is an option.

There are many treatments available for dyshidrosis. However, few of them have been developed or tested specifically on the condition.

- Barriers to moisture and irritants, including barrier creams and gloves.

- Topical steroids - while useful, can be dangerous long-term due to the skin-thinning side-effects, which are particularly troublesome in the context of hand dyshidrosis, due to the amount of toxins and bacteria the hands typically come in contact with.

- Potassium permanganate dilute solution soaks - also popular, and used to 'dry out' the vesicles, and kill off superficial "Staphylococcus aureus", but it can also be very painful. Undiluted it may cause significant burning.

- Dapsone (diamino-diphenyl sulfone), an antibacterial, has been recommended for the treatment of dyshidrosis in some chronic cases.

- Antihistamines: Fexofenadine up to 180 mg per day.

- Alitretinoin (9-cis-retinoic acid) has been approved for prescription in the UK. It is specifically used for chronic hand and foot eczema. It is made by Basilea of Switzerland (BAL 4079).

- Systemic steroids can be taken orally to treat especially acute and severe cases of dyshidrosis.

Prickly heat can be prevented by avoiding activities that induce sweating, using air conditioning to cool the environment, wearing light clothing and in general, avoiding hot and humid weather. Frequent cool showers or cool baths with mild soap can help to prevent heat rash.

The usual treatment of a standardised Adie syndrome is to prescribe reading glasses to correct for impairment of the eye(s). Pilocarpine drops may be administered as a treatment as well as a diagnostic measure. Thoracic sympathectomy is the definitive treatment of diaphoresis, if the condition is not treatable by drug therapy.

Pitted keratolysis can be reduced and eventually stopped by regularly applying a liberal amount of antiperspirant body powder to the inside of the shoes and socks of the sufferer. Regular powder application will greatly reduce foot perspiration and keep the plantar surface of the foot dry therefore creating an environment hostile to the Corynebacterium.

While there is no cure for acrocyanosis, patients otherwise have excellent prognosis. Unless acrocyanosis results from another condition (e.g. malignancy, antiphospholipid syndrome, atherosclerosis, acute ischemic limb, bacterial endocarditis), there is no associated increased risk of disease or death, and there are no known complications. Aside from the discoloration, there are no other symptoms: no pain, and no loss of function. Patients can expect to lead normal lives. In secondary acrocyanosis treatment of the primary condition defines outcomes.

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.

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.

Mild cases of hemifacial spasm may be managed with sedation or carbamazepine (an anticonvulsant drug). Microsurgical decompression and botulinum toxin injections are the current main treatments used for hemifacial spasm.

Botulinum toxin is highly effective in the treatment of hemifacial spasm. It has a success rate equal to that of surgery, but repeated injections may be required every 3 to 6 months. The injections are administered as an outpatient or office procedure. Whilst side effects occur, these are never permanent. Repeated injections over the years remain highly effective. Whilst the toxin is expensive, the cost of even prolonged courses of injections compares favourably with the cost of surgery. Patients with HFS should be offered a number of treatment options. Very mild cases or those who are reluctant to have surgery or Botulinum toxin injections can be offered medical treatment, sometimes as a temporary measure. In young and fit patients microsurgical decompression and Botulinum injections should be discussed as alternative procedures. In the majority of cases, and especially in the elderly and the unfit, Botulinum toxin injection is the treatment of first choice. Imaging procedures should be done in all unusual cases of hemifacial spasm and when surgery is contemplated. Patients with hemifacial spasm were shown to have decreased sweating after botulinum toxin injections. This was first observed in 1993 by Khalaf Bushara and David Park. This was the first demonstration of nonmuscular use of BTX-A. Bushara further showed the efficacy of botulinum toxin in treating hyperhidrosis (excessive sweating). BTX-A was later approved for the treatment of excessive underarm sweating. This is technically known as severe primary axillary hyperhidrosis – excessive underarm sweating with an unknown cause which cannot be managed by topical agents (see focal hyperhidrosis).

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

There is no known cure for neuromyotonia, but the condition is treatable. Anticonvulsants, including phenytoin and carbamazepine, usually provide significant relief from the stiffness, muscle spasms, and pain associated with neuromyotonia. Plasma exchange and IVIg treatment may provide short-term relief for patients with some forms of the acquired disorder. It is speculated that the plasma exchange causes an interference with the function of the voltage-dependent potassium channels, one of the underlying issues of hyper-excitability in autoimmune neuromyotonia. Botox injections also provide short-term relief. Immunosuppressants such as Prednisone may provide long term relief for patients with some forms of the acquired disorder.

Hypohidrosis is diminished sweating in response to appropriate stimuli. While hyperhidrosis is a socially troubling but benign condition, hypohidrosis can lead to hyperthermia, heat exhaustion, heat stroke and potentially death. An extreme case of hypohydrosis in which there is a complete absence of sweating and the skin is dry is termed anhidrosis.

In most cases exfoliation resolves spontaneously and no lasting damage is seen. On the other hand, some patients experience cracking and even bleeding in extreme cases.

Proper treatment of autonomic dysreflexia involves administration of anti-hypertensives along with immediate determination and removal of the triggering stimuli. Often, sitting the patient up and dangling legs over the bedside can reduce blood pressures below dangerous levels and provide partial symptom relief. Tight clothing and stockings should be removed. Straight catheterization of the bladder every 4 to 6 hrs, or relief of a blocked urinary catheter tube may resolve the problem. The rectum should be cleared of stool impaction, using anaesthetic lubricating jelly. If the noxious precipitating trigger cannot be identified, drug treatment is needed to decrease elevating intracranial pressure until further studies can identify the cause.

Drug treatment includes the rapidly acting vasodilators, including sublingual nitrates or oral clonidine. Ganglionic blockers are also used to control sympathetic nervous system outflow. Topical nitropaste is a convenient and safe treatment—an inch or two can be applied to the chest wall, and wiped off when blood pressures begin to normalize. Autonomic dysreflexia is abolished temporarily by spinal or general anaesthesia. These treatments are used during obstetric delivery of a woman with autonomic dysreflexia.

In most of the reported cases, the treatment options were very similar. Plasmapheresis alone or in combination with steroids, sometimes also with thymectomy and azathioprine, have been the most frequently used therapeutic approach in treating Morvan’s Syndrome. However, this does not always work, as failed response to steroids and to subsequently added plasmapheresis have been reported. Intravenous immunoglobulin was effective in one case.

In one case, the dramatic response to high-dose oral prednisolone together with pulse methylprednisolone with almost complete disappearance of the symptoms within a short period should induce consideration of corticosteroids.

In another case, the subject was treated with haloperidol (6 mg/day) with some improvement in the psychomotor agitation and hallucinations, but even high doses of carbamazepine given to the subject failed to improve the spontaneous muscle activity. Plasma Exchange (PE) was initiated, and after the third such session, the itching, sweating, mental disturbances, and complex nocturnal behavior improved and these symptoms completely disappeared after the sixth session, with improvement in insomnia and reduced muscle twitching. However, one month after the sixth PE session, there was a progressive worsening of insomnia and diurnal drowsiness, which promptly disappeared after another two PE sessions.

In one case there high dose steroid treatment resulted in a transient improvement, but aggressive immuno-suppressive therapy with cyclophosphamide was necessary to control the disease and result in a dramatic clinical improvement.

In another case, the subject was treated with prednisolone (1 mg/kg body weight) with carbamazepine, propanolol, and amitriptyline. After two weeks, improvement with decreased stiffness and spontaneous muscle activity and improved sleep was observed. After another 7–10 days, the abnormal sleep behavior disappeared completely.

In another case, symptomatic improvement with plasmapheresis, thymectomy, and chronic immunosuppression provide further support for an autoimmune or paraneoplastic basis.

Although thymectomy is believed to be a key element in the proposed treatment, there is a reported case of Morvan’s Syndrome presenting itself post-thymectomy.

Body odor may be reduced or prevented or even aggravated by using deodorants, antiperspirants, disinfectants, underarm liners, triclosan, special soaps or foams with antiseptic plant extracts such as ribwort and liquorice, chlorophyllin ointments and sprays topically, and chlorophyllin supplements internally. Although body odor is commonly associated with hygiene practices, its presentation can be affected by changes in diet as well as the other factors.

Adie's syndrome is not life-threatening or disabling. As such, there is no mortality rate relating to the condition; however, loss of deep tendon reflexes is permanent and may progress over time.