In January 2001, researchers at Fordham University and Massachusetts General Hospital simultaneously reported finding the genetic mutation that causes FD, a discovery that opens the door to many diagnostic and treatment possibilities.

Despite that it probably would not happen in the near future, some expect that stem-cell therapy will result. Eventually, treatment could be given in utero.

While that may be years ahead, genetic screening became available around April 2001, enabling Ashkenazi Jews to find out if they are carriers. Screening organization Dor Yeshorim offers to test as part of its panel, which also includes Tay-Sachs disease and cystic fibrosis.

In the meantime, more research into treatments is being funded by the foundations that exist. These foundations are organized and run by parents of those with FD. There is no governmental support beyond recognizing those diagnosed with FD as eligible for certain programs.

The outlook for patients with FD depends on the particular diagnostic category. Patients with chronic, progressive, generalized dysautonomia in the setting of central nervous system degeneration have a generally poor long-term prognosis. Death can occur from pneumonia, acute respiratory failure, or sudden cardiopulmonary arrest in such patients.

Parents and patients should generally be educated regarding daily eye care and early warning signs of corneal problems as well as the use of punctal cautery. This education has resulted in decreased corneal scarring and need for more aggressive surgical measures such as tarsorrhaphy, conjunctival flaps, and corneal transplants.

"See the equivalent section in the main migraine article."

People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.

Treatment for Romano–Ward syndrome can "deal with" the imbalance between the right and left sides of the sympathetic nervous system which may play a role in the cause of this syndrome. The imbalance can be temporarily abolished with a left stellate ganglion block, which shorten the QT interval. If this is successful, surgical ganglionectomy can be performed as a permanent treatment.Ventricular dysrhythmia may be managed by beta-adrenergic blockade (propranolol)

While the true causes of Tietze's syndrome are not well understood, it often results from a physical strain or minor injury, such as repeated coughing, sneezing, vomiting, or impacts to the chest. It has even been known to occur after hearty bouts of laughter. It can occur by over exerting or by an injury in the chest and breast.

Psychological stress can exacerbate Tietze's syndrome, but there is no evidence to suggest that it is a direct cause.

Patients who have had radiation therapy to the chest/breast will often experience this syndrome which can occur shortly after therapy or years later.

It is found more often in teens than adults.

Although patients will often mistake the pain of Tietze's syndrome for a myocardial infarction (heart attack), the syndrome does not progress to cause harm to any organs.

It is important to rule out a heart attack, as the symptoms may be similar. After assessment, providers often reassure patients that their symptoms are not associated with a heart attack, although they may need to treat the pain, which in some cases can be severe enough to cause significant but temporary disability to the patient.

IST has been treated both pharmacologically and invasively, with varying degrees of success. IST, in and of itself, is not indicative of higher rates of mortality, and non-treatment is an option chosen by many if they have minimal symptoms.

Some types of medication tried by cardiologists and other physicians include: beta blockers, selective sinus node I channel inhibitors (ivabradine), calcium channel blockers and antiarrhythmic agents. Some SSRI drugs are also occasionally tried and also treatments more commonly used to treat postural orthostatic tachycardia syndrome such as fludrocortisone. This approach is very much "trial-and-error". Patients with IST are often intolerant to beta blockers. A new selective sinus node inhibitor ivabradine is also being used to treat IST.

Invasive treatments include forms of catheter ablation such as sinus node modification (selective ablation of the sinus node), complete sinus node ablation (with associated implantation of a permanent artificial pacemaker) and AV node ablation in very resistant cases (creation of iatrogenic complete heart block, necessitating implantation of a permanent artificial pacemaker).

However invasive treatments can also make the symptoms worse, not cure it. Treatment should be chosen with care as the patient could become in need of a pacemaker or have more extensive symptoms.

About 20–30% of the population report to have experienced dizziness at some point in the previous year.

Romano–Ward syndrome is the major variant of "long QT syndrome". It is a condition that causes a disruption of the heart's normal rhythm. This disorder is a form of long QT syndrome, which is a heart condition that causes the cardiac muscle to take longer than usual to recharge between beats; if untreated, the irregular heartbeats can lead to fainting, seizures, or sudden death

Currently, some individuals with short QT syndrome have had implantation of an implantable cardioverter-defibrillator (ICD) as a preventive action, although it has not been demonstrated that heart problems have occurred before deciding to implant an ICD.

A recent study has suggested the use of certain antiarrhythmic agents, particularly quinidine, may be of benefit in individuals with short QT syndrome due to their effects on prolonging the action potential and by their action on the I channels. Some trials are currently under way but do not show a longer QT statistically.

Collapse is a sudden and often unannounced loss of postural tone (going weak), often but not necessarily accompanied by loss of consciousness.

If the episode was accompanied by a loss of consciousness, the term syncope is used. The main causes are cardiac (e.g. due to irregular heart beat, low blood pressure), seizures or a psychological cause. The main tool in distinguishing the causes is careful history on the events before, during and after the collapse, from the patient as well as from any possible witnesses. Other investigations may be performed to further strengthen the diagnosis, but many of these have a low yield.

Where an underlying neoplasm is the cause, treatment of this condition is indicated in order to reduce progression of symptoms. For cases without a known cause, treatment involves suppression of the immune system with corticosteroid treatment, intravenous immunoglobulin, immunosuppressive agents like Rituximab, Cellcept, or Imuran or plasmapheresis.

Prenatal screening is not typically done for FHM, however it may be performed if requested. As penetrance is high, individuals found to carry mutations should be expected to develop signs of FHM at some point in life.

The risk for untreated LQTS patients having events (syncopes or cardiac arrest) can be predicted from their genotype (LQT1-8), gender, and corrected QT interval.

- High risk (> 50%) - QTc > 500 ms, LQT1, LQT2, and LQT3 (males)

- Intermediate risk (30-50%) - QTc > 500 ms, LQT3 (females) or QTc < 500 ms, LQT2 (females) and LQT3

- Low risk (< 30%) - QTc < 500 ms, LQT1 and LQT2 (males)

A 1992 study reported that mortality for symptomatic, untreated patients was 20% within the first year and 50% within the first 10 years after the initial syncope.

Henri Gougerot and Alexandre Carteaud originally described the condition in 1927. The cause remains unknown, but the observation that the condition may clear with Minocycline turned attention to an infectious agent. "Actinomycete Dietzia" strain X was isolated from one individual. Other antibiotics found useful include azithromycin, fusidic acid, clarithromycin, erythromycin, tetracycline and cefdinir.

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.

In recent reports, left cardiac sympathetic denervation and bilateral thoracoscopic sympathectomy have shown promising results in individuals whose symptoms cannot be controlled by beta blockers.

This is a form of dysautonomia but differentiated from familial dysautonomia by a lack of familial dysautonomic symptoms such as loss of sense of pain and smell. While L-threo-DOPS has been described as being "very effective for restoring noradrenergic tone and correcting postural hypotension, response to treatment is variable and the long-term and functional outcome is unknown."

Researchers have put together retrospective data collections in order to better under the progression of this orphan disease. Most studies show a perinatal period marked by inadequacy of the ANS to control blood pressure, blood sugar, and body temperature. The experiences of orthostatic hypotension, exercise intolerance, and "traumatic morbidity related to falls and syncope" have been documented later in lives of people with this condition. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation, outcome of these diseases, their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies, a patient registry was established by the non-commercial International Working Group on Neurotransmitter Related Disorders (iNTD).

Most patients experience an improvement of their symptoms, but for some, OI can be gravely disabling and can be progressive in nature, particularly if it is caused by an underlying condition which is deteriorating. The ways in which symptoms present themselves vary greatly from patient to patient; as a result, individualized treatment plans are necessary.

OI is treated both pharmacologically and non-pharmacologically. Treatment does not cure OI; rather, it controls symptoms.

Physicians who specialize in treating OI agree that the single most important treatment is drinking more than two liters (eight cups) of fluids each day. A steady, large supply of water or other fluids reduces most, and for some patients all, of the major symptoms of this condition. Typically, patients fare best when they drink a glass of water no less frequently than every two hours during the day, instead of drinking a large quantity of water at a single point in the day.

For most severe cases and some milder cases, a combination of medications are used. Individual responses to different medications vary widely, and a drug which dramatically improves one patient's symptoms may make another patient's symptoms much worse. Medications focus on three main issues:

Medications that increase blood volume:

- Fludrocortisone (Florinef)

- Erythropoietin

- Hormonal contraception

Medications that inhibit acetylcholinesterase:

- Pyridostigmine

Medications that improve vasoconstriction:

- Stimulants: (e.g., Ritalin or Dexedrine)

- Midodrine (ProAmatine)

- Ephedrine and pseudoephedrine (Sudafed)

- Theophylline (low-dose)

- Selective serotonin reuptake inhibitors (SSRI's - Prozac, Zoloft, and Paxil)

Behavioral changes that patients with OI can make are:

- Avoiding triggers such as prolonged sitting, quiet standing, warm environments, or vasodilating medications

- Using postural maneuvers and pressure garments

- Treating co-existing medical conditions

- Increasing fluid and salt intake

- Physical therapy and exercise unless contraindicated by an underlying condition such as chronic fatigue syndrome where traditional exercise can worsen the condition

The cause of short QT syndrome is unclear at this time. A current hypothesis is that short QT syndrome is due to increased activity of outward potassium currents in phase 2 and 3 of the cardiac action potential. This would cause a shortening of the plateau phase of the action potential (phase 2), causing a shortening of the overall action potential, leading to an overall shortening of refractory periods and the QT interval.

In the families afflicted by short QT syndrome, mutations have been described in three genes, KvLQT1, the "human ether-a-go-go gene (HERG)", and KCNJ2.

Panayiotopoulos syndrome (named after C. P. Panayiotopoulos) is a common idiopathic childhood-related seizure disorder that occurs exclusively in otherwise normal children (idiopathic epilepsy) and manifests mainly with autonomic epileptic seizures and autonomic status epilepticus. An expert consensus has defined Panayiotopoulos syndrome as "a benign age-related focal seizure disorder occurring in early and mid-childhood. It is characterized by seizures, often prolonged, with predominantly autonomic symptoms, and by an EEG [electroencephalogram] that shows shifting and/or multiple foci, often with occipital predominance."

"See the equivalent section in the main migraine article."

People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.

Medications to treat CPVT include beta blockers and verapamil.

Flecainide inhibits the release of the cardiac ryanodine receptor–mediated Ca, and is therefore believed to medicate the underlying molecular cause of CPVT in both mice and humans.

Arrhythmia termination involves stopping a life-threatening arrhythmia once it has already occurred. One effective form of arrhythmia termination in individuals with LQTS is placement of an implantable cardioverter-defibrillator (ICD). Also, external defibrillation can be used to restore sinus rhythm. ICDs are commonly used in patients with fainting episodes despite beta blocker therapy, and in patients having experienced a cardiac arrest.

With better knowledge of the genetics underlying LQTS, more precise treatments hopefully will become available.

Orthostatic intolerance (OI) is the development of symptoms when standing upright which are relieved when reclining. There are many types of orthostatic intolerance. OI can be a subcategory of dysautonomia, a disorder of the autonomic nervous system occurring when an individual stands up.

There is a substantial overlap between syndromes of orthostatic intolerance on the one hand, and either chronic fatigue syndrome (CFS) or fibromyalgia (FM) on the other. It affects more women than men (female-to-male ratio is at least 4:1), usually under the age of 35.

Orthostatic intolerance occurs in humans because standing upright is a fundamental stressor and requires rapid and effective circulatory and neurologic compensations to maintain blood pressure, cerebral blood flow, and consciousness. When a human stands, approximately 750 mL of thoracic blood is abruptly translocated downward. People who suffer from OI lack the basic mechanisms to compensate for this deficit. Changes in heart rate, blood pressure, and cerebral blood flow that produce OI may be caused by abnormalities in the interactions between blood volume control, the cardiovascular system, the nervous system and circulation control system.