There is currently no cure for FD and death occurs in 50% of the affected individuals by age 30. There are only two treatment centers, one at New York University Hospital and one at the Sheba Medical Center in Israel. One is being planned for the San Francisco area.

The survival rate and quality of life have increased since the mid-1980s mostly due to a greater understanding of the most dangerous symptoms. At present, FD patients can be expected to function independently if treatment is begun early and major disabilities avoided.

A major issue has been aspiration pneumonia, where food or regurgitated stomach content would be aspirated into the lungs causing infections. Fundoplications (by preventing regurgitation) and gastrostomy tubes (to provide nonoral nutrition) have reduced the frequency of hospitalization.

Other issues which can be treated include FD crises, scoliosis, and various eye conditions due to limited or no tears.

An FD crisis is the body's loss of control of various autonomic nervous system functions including blood pressure, heart rate, and body temperature. Both short-term and chronic periodic high or low blood pressure have consequences and medication is used to stabilize blood pressure.

Although the FD-causing gene has been identified and it seems to have tissue specific expression, there is no definitive treatment at present.

Treatment of FD remains preventative, symptomatic and supportive. FD does not express itself in a consistent manner. The type and severity of symptoms displayed vary among patients and even at different ages on the same patients. So patients should have specialized individual treatment plans. Medications are used to control vomiting, eye dryness, and blood pressure. There are some commonly needed treatments including:

1. Artificial tears: using eye drops containing artificial tear solutions (methylcellulose)

2. Feeding: Maintenance of adequate nutrition, avoidance of aspiration; thickened formula and different shaped nipples are used for baby.

3. Daily chest physiotherapy (nebulization, bronchodilators, and postural drainage): for Chronic lung disease from recurrent aspiration pneumonia

4. Special drug management of autonomic manifestations such as vomiting: intravenous or rectal diazepam (0.2 mg/kg q3h) and rectal chloral hydrate (30 mg/kg q6h)

5. Protecting the child from injury (coping with decreased taste, temperature and pain perception)

6. Combating orthostatic hypotension: hydration, leg exercise, frequent small meals, a high-salt diet, and drugs such as fludrocortisone.

7. Treatment of orthopedic problems (tibial torsion and spinal curvature)

8. Compensating for labile blood pressures

There is no cure for Familial Dysautonomia.

Pharmacological methods of treatment include fludrocortisone, midodrine, somatostatin, erythropoietin, and other vasopressor agents. However, often a patient with pure autonomic failure can mitigate his or her symptoms with far less costly means. Compressing the legs and lower body, through crossing the legs, squatting, or the use of compression stockings can help. Also, ingesting more water than usual can increase blood pressure and relieve some symptoms.

Depending on subtype, many patients find that acetazolamide therapy is useful in preventing attacks. In some cases, persistent attacks result in tendon shortening, for which surgery is required.

Smoking is the number one cause of Reinke's edema. Other factors include gastroesophageal reflux, hypothyroidism and chronic overuse of the voice. Smoking is the only risk factor that may lead to cancer. Additionally, the combination of several risk factors increase the likelihood of an individual developing Reinke's edema. For example, an individual who smokes and also has gastric reflux would have an increased susceptibility for developing Reinke's edema over time.

Reinke's edema is commonly diagnosed in middle-aged females with a history of smoking (aged 50 years or older). Because males have lower pitched voices than females, males are less likely to observe a significant changes in the voice, and are therefore less likely to seek treatment. Females also report more physical discomfort due to Reinke's edema. The risk of Reinke's edema increases with age and also with prolonged exposure to smoking. Additionally, individuals in professions that require constant use of the voice, such as singers, teachers, and radio hosts, may be at an increased risk for developing the disease.

Because the disease is heavily linked to smoking, there is no established way to screen for Reinke's edema. Similarly, the only way to prevent Reinke's edema is to avoid smoking. By adopting a non-smoking lifestyle after being diagnosed with Reinke's edema, it is possible to stop the disease's progression, although it is not possible to reverse it. Therefore, it is critical to maintain a non-smoking lifestyle even after surgery, because the fluid can re-emerge. In fact, in many cases surgeons will not perform surgery without the guarantee that the individual will stop smoking.

The first step in treating Reinke’s edema is to eliminate or control those risk factors that are causing the disease. This includes the cessation of smoking, the control of gastric reflux using antacids and/or Proton Pump Inhibitors (PPIs), and the discontinuation of activities that cause vocal distress. Those experiencing a hoarseness of the voice may choose to undergo voice therapy to improve the voice’s quality and range. Most cases of Reinke’s edema are caused by the long term usage of cigarettes. In this case, it is important to make lifestyle changes to stop smoking. While this will not resolve or improve the edema, the cessation of smoking will halt the disease's progression.

If the elimination of risk factors is not sufficient to improve the patient’s symptoms, surgery may be required. The most common type of surgery performed today for Reinke's edema is called surgical microlaryngoscopy. Most procedures follow the microflap technique set in place by Hirano. During surgery, an incision is made into the vocal cord using either microscissors or a CO laser. A flap of mucosa is lifted and the affected tissue is removed using suction or a microdebrider. The flap is then re-draped and trimmed to the appropriate size.

Most cases of Reinke’s Edema are bilateral - effecting both vocal cords - rather than unilateral. In the case of bilateral edema, the surgeon must choose whether to operate each side of the vocal cord in two separate surgeries or to operate both sides in a single surgery. The complication associated with removing tissue from both sides in a single surgery is that the raw, cut ends of the vocal cords may form an anterior glottis web, in which the two sides grow together in a continuous sheet. Other complications of surgery include tissue scarring due to damage to the vocal ligament during the incision and vocal cord stiffening due to over-suctioning of the superficial lamina propria (Reinke’s space).

While surgical microlarynscopy has its associated risks, if left untreated, Reinke’s edema can lead to a variety of long-term complications. Besides dysphonia (impaired speech), the most serious of these complications is airway obstruction due to severe inflammation of the vocal cords. The risk of complications has decreased drastically with the creation of new tools, such as the CO laser for surgical microlaryngoscopy. Before the Hirano microflap method was developed in 1895, vocal stripping was the most common procedure used to correct Reinke's Edema. Vocal stripping was often performed without magnification and with a monocular laryngoscope, instead of a binocular scope. This led to major complications such as vocal ligament scarring.

Women are more likely than men to undergo surgery due to a greater change in vocal pitch and quality. Surgery is capable of restoring the voice, with the condition that smoking is not resumed after surgery. Post-operative voice therapy is also advised to restore the voice's strength. Reinke's edema is not a fatal pathology unless the tissue becomes precancerous.

There is currently no cure for SCA 6; however, there are supportive treatments that may be useful in managing symptoms.

Pure autonomic failure (PAF), also known as Bradbury-Eggleston syndrome or idiopathic orthostatic hypotension, is a form of dysautonomia that first occurs in middle age or later in life; men are affected more often than women.

The list of treatments mentioned in various sources for presbylarynx includes the following list. Always seek professional medical advice about any treatment or change in treatment plans.

- Voice therapy

Foix–Alajouanine syndrome is a disorder caused by an arteriovenous malformation of the spinal cord. The patients present with symptoms indicating spinal cord involvement (paralysis of arms and legs, numbness and loss of sensation and sphincter dysfunction), and pathological examination reveals disseminated nerve cell death in the spinal cord and abnormally dilated and tortuous vessels situated on the surface of the spinal cord. Surgical treatment can be tried in some cases. If surgical intervention is contraindicated, corticosteroids may be used.

The condition is named after Charles Foix and Théophile Alajouanine.

Vestibulocochlear dysfunction progressive familial, known also as familial progressive vestibulocochlear dysfunction is an autosomal dominant disease that results in sensorineural hearing loss and vestibular areflexia. Patients report feelings of vague dissiness, blurred vision, dysequilibrium in the dark, and progressive hearing impairment.

Cobb syndrome is a rare congenital disorder characterized by visible skin lesions with underlying spinal angiomas or arteriovenous malformations (AVMs). The skin lesions of Cobb syndrome typically are present as port wine stains or angiomas, but reports exist of angiokeratomas, angiolipomas, and lymphangioma circumscriptum. The intraspinal lesions may be angiomas or AVMs and occur at levels of the spinal cord corresponding to the affected skin dermatomes. They may in turn produce spinal cord dysfunction and weakness or paralysis.

The disorder was first described by Berenbruch in 1890, but became widely known only after Cobb's report in 1915. Cobb syndrome is thought to be more common in males and have no racial predilection, but only a few dozen cases are known. It is believed to be due to a sporadic mutation, since parents of affected children usually have no evidence of the disease.

There are a number of potential treatments for spasmodic dysphonia, including botox, surgery and voice therapy. A number of medications have also been tried including anticholinergics (such as benztropine) which have been found to be effective in 40-50% of people, but which are associated with a number of side effects.

No specific treatment is known that would prevent, slow, or reverse HSP. Available therapies mainly consist of symptomatic medical management and promoting physical and emotional well-being. Therapeutics offered to HSP patients include:

- Baclofen – a voluntary muscle relaxant to relax muscles and reduce tone. This can be administered orally or intrathecally. (Studies in HSP )

- Tizanidine – to treat nocturnal or intermittent spasms (studies available )

- Diazepam and clonazepam – to decrease intensity of spasms

- Oxybutynin chloride – an involuntary muscle relaxant and spasmolytic agent, used to reduce spasticity of the bladder in patients with bladder control problems

- Tolterodine tartate – an involuntary muscle relaxant and spasmolytic agent, used to reduce spasticity of the bladder in patients with bladder control problems

- Botulinum toxin – to reduce muscle overactivity (existing studies for HSP patients)

- Antidepressants (such as selective serotonin re-uptake inhibitors, tricyclic antidepressants and monoamine oxidase inhibitors) – for patients experiencing clinical depression

- Physical therapy – to restore and maintain the ability to move; to reduce muscle tone; to maintain or improve range of motion and mobility; to increase strength and coordination; to prevent complications, such as frozen joints, contractures, or bedsores.

Bogart–Bacall syndrome (BBS) is a voice disorder that is caused by abuse or overuse of the vocal cords.

People who speak or sing outside their normal vocal range can develop BBS; symptoms are chiefly an unnaturally deep or rough voice, or dysphonia, and vocal fatigue. The people most commonly afflicted are those who speak in a low-pitched voice, particularly if they have poor breath and vocal control. The syndrome can affect both men and women.

In 1988 an article was published, describing a discrete type of vocal dysfunction which results in men sounding like Humphrey Bogart and women sounding like Lauren Bacall. BBS is now the medical term for an ongoing hoarseness that often afflicts actors, singers or TV/radio voice workers who routinely speak in a very low pitch.

Treatment usually involves voice therapy by a speech language pathologist.

Botulinum toxin (Botox) is often used to improve some symptoms of spasmodic dysphonia. Whilst the level of evidence for its use is limited, it remains a popular choice for many patients due to the predictability and low chance of long term side effects. It results in periods of some improvement. The duration of benefit averages 10–12 weeks before the patient returns to baseline. Repeat injection is required to sustain good vocal production.

The disease is an inherited autosomal dominant disease, but the physiological cause of the dysfunction is still unclear. An acidophyllic mucopolysaccharide-containing substance was discovered, especially in cochleas, maculas, and crista ampullaris of patients with DFNA9 (a chromosome locus), as well as severe degeneration of vestibular and cochlear sensory axons and dendrites. It is suggested that the mucopolysaccharide deposit could cause strangulation of nerve endings.

The maculas and crista ampullaris are what allow for non-visual sensation of head movements. The crista ampullaris resides in the semicircular canals of the inner ear and detects angular acceleration, while the maculas are housed within the vestibule of the inner ear and detect linear acceleration. When affected, these organs can lead to vertigo and nausea because the body would always feel off-balance.

Episodic ataxia (EA) is an autosomal dominant disorder characterized by sporadic bouts of ataxia (severe discoordination) with or without myokymia (continuous muscle movement). There are seven types recognised but the majority are due to two recognized entities. Ataxia can be provoked by stress, startle, or heavy exertion such as exercise. Symptoms can first appear in infancy. There are at least 6 loci for EA, of which 4 are known genes. Some patients with EA also have migraine or progressive cerebellar degenerative disorders, symptomatic of either familial hemiplegic migraine or spinocerebellar ataxia. Some patients respond to acetazolamide though others do not.

There is no known prevention of spinocerebellar ataxia. Those who are believed to be at risk can have genetic sequencing of known SCA loci performed to confirm inheritance of the disorder.

Surgical intervention is usually given to those individuals who have increased instability of their cervical spine, which cannot be resolved by conservative management alone. Further indications for surgery include a neurological decline in spinal cord function in stable patients as well as those who require cervical spinal decompression.

In many cases, individuals with CCS can experience a reduction in their neurological symptoms with conservative management. The first steps of these intervention strategies include admission to an intensive care unit (ICU) after initial injury. After entering the ICU, early immobilization of the cervical spine with a neck collar would be placed on the patient to limit the potential of further injury. Cervical spine restriction is maintained for approximately six weeks until the individual experiences a reduction in pain and neurological symptoms. Inpatient rehabilitation is initiated in the hospital setting, followed by outpatient physical therapy and occupational therapy to assist with recovery.

An individual with a spinal cord injury may have many goals for outpatient occupational and physiotherapy. Their level of independence, self-care, and mobility are dependent on their degree of neurological impairment. Rehabilitation organization and outcomes are also based on these impairments. The physiatrist, along with the rehabilitation team, work with the patient to develop specific, measurable, action-oriented, realistic, and time-centered goals.

With respect to physical therapy interventions, it has been determined that repetitive task-specific sensory input can improve motor output in patients with central cord syndrome. These activities enable the spinal cord to incorporate both supraspinal and afferent sensory information to help recover motor output. This occurrence is known as "activity dependent plasticity". Activity dependant plasticity is stimulated through such activities as: locomotor training, muscle strengthening, voluntary cycling, and functional electrical stimulation (FES) cycling

Medical often works in conjunction with behavioral approaches. A pulmonary or ENT (otolaryngologist) specialist will screen for and address any potential underlying pathology that may be associated with VCD. Managing GERD has also been found to relieve laryngospasm, a spasm of the vocal cords that makes breathing and speaking difficult.

Non-invasive positive pressure ventilation can be used if a patient's vocal cords adduct (close) during exhalation. Mild sedatives have also been employed to reduce anxiety as well as reduce acute symptoms of VCD. Benzodiazepines are an example of one such treatment, though they have been linked to a risk of suppression of the respiratory drive. While Ketamine, a dissociative anesthetic, does not suppress respiratory drive, it has been thought to be associated with laryngospasms.

For more severe VCD cases, physicians may inject botulinum toxin into the vocal (thyroarytenoid) muscles to weaken or decrease muscle tension. Nebulized Lignocaine can also been used in acute cases and helium-oxygen inhalation given by face mask has been used in cases of respiratory distress.

Voice disorders are medical conditions involving abnormal pitch, loudness or quality of the sound produced by the larynx and thereby affecting speech production. These include:

- Puberphonia

- Chorditis

- Vocal fold nodules

- Vocal fold cysts

- Vocal cord paresis

- Reinke's edema

- Spasmodic dysphonia

- Foreign accent syndrome

- Bogart–Bacall syndrome

- Laryngeal papillomatosis

- Laryngitis

Liver transplantation has proven to be effective for ATTR familial amyloidosis due to Val30Met mutation.

Alternatively, a European Medicines Agency approved drug Tafamidis or Vyndaqel now exists which stabilizes transthyretin tetramers comprising wild type and different mutant subunits against amyloidogenesis halting the progression of peripheral neuropathy and autonomic nervous system dysfunction.

Currently there are two ongoing clinical trials undergoing recruitment in the United States and worldwide to evaluate investigational medicines that could possibly treat TTR.

Psychological interventions including psychotherapy, cognitive behavioural therapy (CBT), Biofeedback, and teaching self-hypnosis are also suggested to treat VCD. Intervention is generally targeted at making the client aware of stressors that may trigger VCD symptoms, to implement strategies to reduce stress and anxiety, and to teach techniques for coping with their symptoms.

CBT can focus on bringing awareness to negative thought patterns and help reframe them by focusing on problem solving strategies. Psychologists may also use relaxation to reduce distress when a patient is experiencing symptoms. Biofeedback can be a helpful addition to psychotherapy. The aim of Biofeedback is to educate the client on what happens to the vocal cords during breathing and to help them learn to control their symptoms.

Choosing an intervention strategy needs to be assessed by a multidisciplinary team and individualized therapy planned carefully, keeping the characteristics of each patient in mind.