In some cases Meige's syndrome can be reversed when it is caused by medication. It has been theorized that it is related to cranio-mandibular orthopedic misalignment, a condition that has been shown to cause a number of other movement disorders (Parkinon's, tourettes, and torticollis). This theory is supported by the fact that the trigeminal nerve is sensory for blink reflex, and becomes hypertonic with craniomandibular dysfunction. Palliative treatments are available, such as botulinum toxin injections.

The main symptoms involve involuntary blinking and chin thrusting. Some patients may experience excessive tongue protrusion, squinting, light sensitivity, muddled speech, or uncontrollable contraction of the platysma muscle. Some Meige's patients also have "laryngeal dystonia" (spasms of the larynx). Blepharospasm may lead to embarrassment in social situations, and oromandibular dystonia can affect speech, making it difficult to carry on the simplest conversations. This can cause difficulty in both personal and professional contexts, and in some cases may cause patients to withdraw from social situations.

The condition tends to affect women more frequently than men.

There is no cure for torsion dystonia. However, there are several medical approaches that can be taken in order to lessen the symptoms of the disease. The treatment must be patient specific, taking into consideration all of the previous and current health complications. The doctor that creates the treatment must have intimate knowledge of the patients’ health and create a treatment plan that covers all of the symptoms focusing on the most chronic areas.

The first step for most with the disorder begins with some form of physical therapy in order for the patient to gain more control over the affected areas. The therapy can help patients with their posture and gain control over the areas of their body that they have the most problems with.

The second step in the treatment process is medication. The medications focus on the chemicals released by neurotransmitters in the nervous system, which control muscle movement. The medications on the market today are anticholinergics, benzodiazepines, baclofen, dopaminergic agents/dopamine-depleting agents, and tetrabenazine. Each medication is started on a low dosage and gradually increased to higher doses as the disease progresses and the side effects are known for the individual.

A more site-specific treatment is the injection of botulinum toxin. It is injected directly into the muscle and works much the same way the oral medications do—by blocking neurotransmitters. The injections are not a treatment for the disease, but are a means to control its symptoms.

A fourth option in the treatment for the symptoms of torsion dystonia is surgery. Surgery is performed only if the patient does not respond to the oral medications or the injections. The type of surgery performed is specific to the type of dystonia that the patient has.

In the past, dopamine blocking agents have been used in the treatment of spasmodic torticollis. Treatment was based on the theory that there is an imbalance of the neurotransmitter dopamine in the basal ganglia. These drugs have fallen out of fashion due to various serious side effects: sedation, parkinsonism, and tardive dyskinesia.

Other oral medications can be used in low doses to treat early stages of spasmodic torticollis. Relief from spasmodic torticollis is higher in those patients who take anticholinergic agents when compared to other oral medications. Many have reported complete management with gabapentin alone or in combination with another drug such as clonazepam. 50% of patients who use anticholinergic agents report relief, 21% of patients report relief from clonazepam, 11% of patients report relief from baclofen, and 13% from other benzodiazepines.

Higher doses of these medications can be used for later stages of spasmodic torticollis; however, the frequency and severity of side effects associated with the medications are usually not tolerated. Side effects include dry mouth, cognitive disturbance, drowsiness, diplopia, glaucoma and urinary retention.

The most commonly used treatment for spasmodic torticollis is the use of botulinum toxin injection in the dystonic musculature. Botulinum toxin type A is most often used; it prevents the release of acetylcholine from the presynaptic axon of the motor end plate, paralyzing the dystonic muscle. By disabling the movement of the antagonist muscle, the agonist muscle is allowed to move freely. With botulinum toxin injections, patients experience relief from spasmodic torticollis for approximately 12 to 16 weeks. There are several type A preparations available worldwide; however Botox and Dysport are the only preparations approved by the U.S. Food and Drug Administration (FDA) for clinical use in the United States.

Some patients experience or develop immunoresistance to botulinum toxin type A and must use botulinum toxin type B. Approximately 4% to 17% of patients develop botulinum toxin type A antibodies. The only botulinum toxin type B accessible in the United States is Myobloc. Treatment using botulinum toxin type B is comparable to type A, with an increased frequency of the side effect dry mouth.

Common side effects include pain at the injection site (up to 28%), dysphagia due to the spread to adjacent muscles (11% to 40%), dry mouth (up to 33%), fatigue (up to 17%), and weakness of the injected or adjacent muscle (up to 56%). A Cochrane review published in 2016 reported moderate-quality evidence that a single Botulinum toxin-B treatment session could improve cervical dystonia symptoms by 10% to 20%, although with an increased risk of dry mouth and swallowing difficulties.

Surgery, such as the denervation of selected muscles, may also provide some relief; however, the destruction of nerves in the limbs or brain is not reversible and should be considered only in the most extreme cases. Recently, the procedure of deep brain stimulation (DBS) has proven successful in a number of cases of severe generalised dystonia. DBS as treatment for medication-refractory dystonia, on the other hand, may increase the risk of suicide in patients. However, reference data of patients without DBS therapy are lacking.

Oromandibular dystonia is a form of focal dystonia affecting the mouth, jaw and tongue, and in this disease it is hard to speak. It is associated with bruxism.

Botulinum toxin has been used in treatment.

Since the root of the problem is neurological, doctors have explored sensorimotor retraining activities to enable the brain to "rewire" itself and eliminate dystonic movements. The work of several doctors such as Nancy Byl and Joaquin Farias has shown that sensorimotor retraining activities and proprioceptive stimulation can induce neuroplasticity, making it possible for patients to recover substantial function that was lost due to Cervical Dystonia, oromandibular dystonia and dysphonia.

Some causes of blepharospasm have been identified; however, the causes of many cases of blepharospasm remain unknown, although some educated guesses are being made. Some blepharospasm patients have a history of dry eyes and/or light sensitivity, but others report no previous eye problems before onset of initial symptoms.

Some drugs can induce blepharospasm, such as those used to treat Parkinson's disease, as well as sensitivity to hormone treatments, including estrogen-replacement therapy for women going through menopause. Blepharospasm can also be a symptom of acute withdrawal from benzodiazepines. In addition to blepharospasm being a benzodiazepine withdrawal symptom, prolonged use of benzodiazepines can induce blepharospasm and is a known risk factor for the development of blepharospasm.

Blepharospasm may also come from abnormal functioning of the brain basal ganglia. Simultaneous dry eye and dystonias such as Meige's syndrome have been observed. Blepharospasms can be caused by concussions in some rare cases, when a blow to the back of the head damages the basal ganglia.

Multiple sclerosis can cause blepharospasm.

To date, there is no single, universal treatment that has been found to cure myoclonus dystonia. However, there are several treatment methods that have been found to be effective for helping to reduce the symptoms associated with the syndrome.

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.

Blepharospasm is any abnormal contraction or twitch of the eyelid. In most cases, symptoms last for a few days then disappear without treatment, but sometimes the twitching is chronic and persistent, causing lifelong challenges. In those rare cases, the symptoms are often severe enough to result in functional blindness. The person's eyelids feel like they are clamping shut and will not open without great effort. People have normal eyes, but for periods of time are effectively blind due to their inability to open their eyelids. In contrast, the reflex blepharospasm is due to any pain in and around the eye.

It is of two types: essential and reflex blepharospasm. The benign essential blepharospasm is a focal dystonia—a neurological movement disorder involving involuntary and sustained contractions of the muscles around the eyes. The term "essential" indicates that the cause is unknown, but fatigue, stress, or an irritant are possible contributing factors.

Although there is no cure botulinum toxin injections may help temporarily. A surgical procedure known as myectomy may also be useful. It is a fairly rare disease, affecting only one in every 20,000 people in the United States. The word is from Greek: βλέφαρον / blepharon, eyelid, and σπασμός / spasmos, "spasm," an uncontrolled muscle contraction.

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.

Reducing the dosage of the antipsychotic drugs resulted in gradual improvement in the abnormal posture. In some cases, discontinuing the use of those drugs resulted in complete disappearance of the syndrome. The time it took for the improvement and the disappearance of the syndrome depended on the type of drug being administered or the specific cause of the syndrome itself.

Studies and evidence from clinical practice show that 85–90% of cases of congenital torticollis are resolved with conservative treatment. It is possible that torticollis will resolve spontaneously but chance of relapse is possible.

Most pharmacological treatments work poorly, but the best treatment is a low dosage of clonazepam, a muscle relaxant. Patients may also benefit from other benzodiazepines, phenobarbital, and other anticonvulsants such as valproic acid. Affected individuals have reported garlic to be effective for softening the attacks, but no studies have been done on this.

Anticholinergic drugs have been reported to be extremely effective in 40% of the patients with the Pisa syndrome. Patients with Pisa syndrome that is resistant to anticholinergic drugs is mostly resolved by the reduction of the administration of the antipsychotic drugs as previously mentioned. While the specific pathology underlying idiopathic Pisa syndrome is unknown, the administration of anticholinergic drugs has provided resolution in known cases.

Although dystonias may be induced by chemical exposure/ingestion, brain injury, or hereditary/genetic predisposition, the task-specific focal dystonias such as writer's cramp are a unique challenge to diagnose and treat. Some cases may respond to chemical injections - botulinum toxin (botox) is often cited, though it is not helpful in all cases. Behavioral retraining attempts may include writing devices, switching hands, physical therapy, biofeedback, constraint-induced motion therapy, and others. Some writing instruments allow variations of pressure application for use. None of these are effective in all cases, however. The work of Dr. Joaquin Farias has shown that proprioceptive stimulation can induce neuroplasticity, making it possible for patients to recover substantial function that was lost from focal dystonia.

Anticholinergics such as Artane can be prescribed for off-label use, as some sufferers have had success.

This condition is often treated with injections of botox, a commercially prepared form of botulinum toxin. Botox reduces the symptoms of the disorder but it is not a cure for dystonia. Since the root of the problem is neurological, doctors have explored sensorimotor retraining activities to enable the brain to "rewire" itself and eliminate dystonic movements. The work of several doctors such as Nancy Byl and Joaquin Farias has shown that sensorimotor retraining activities and proprioceptive stimulation can induce neuroplasticity, making it possible for patients to recover substantial function that was lost to focal dystonia.

Anticholinergics such as Artane can be prescribed for off-label use, as some sufferers have had success.

Bass guitarist and instructor Scott Devine said that he wears a glove while playing bass guitar because of the condition. He finds that the glove stops the involuntary finger movements. He says it works for him but does not suggest that it may work for everyone with the condition.

Consumption of alcohol has also been found to be an effective agent for temporarily easing the severity of the tremors associated with myoclonus dystonia. Alcohol causes an increase in GABA transmission between interneurons and Purkinje cells. This then reduces the transmission of glutamate at granule cell-Purkinje cell synapses, which decreases muscle movements. This treatment only alleviates the strength of the tremors for a short duration and does not change how often tremors will occur. Doctors inform patients of risks associated with the use of alcohol for myoclonus dystonia due to the high susceptibility for alcohol abuse and dependency. Alcoholism itself causes tremors in the hands and degeneration of the Purkinje cells and other parts of the cerebral cortex, counteracting alcohol's original corrective effects.

Initially, the condition is treated with physical therapies, such as stretching to release tightness, strengthening exercises to improve muscular balance, and handling to stimulate symmetry. A TOT collar is sometimes applied. Early initiation of treatment is very important for full recovery and to decrease chance of relapse.

A 1969 study of torsion dystonia patients found an average IQ 10 points higher than controls matched for age, sex and ethnic background.

Different medications are tried in an effort to find a combination that is effective for a specific person. Not all people will respond well to the same medications. Medications that have had positive results in some include: diphenhydramine, benzatropine and atropine. anti-Parkinsons agents (such as ropinirole and bromocriptine), and muscle relaxants (such as diazepam).

- Anticholinergics

Medications such as anticholinergics (benztropine), which act as inhibitors of the neurotransmitter acetylcholine, may provide some relief. In the case of an acute dystonic reaction, diphenhydramine is sometimes used (though this drug is well known as an antihistamine, in this context it is being used primarily for its anticholinergic role).. See also Procyclidine.

- Baclofen

A baclofen pump has been used to treat patients of all ages exhibiting muscle spasticity along with dystonia. The pump delivers baclofen via a catheter to the thecal space surrounding the spinal cord. The pump itself is placed in the abdomen. It can be refilled periodically by access through the skin. Baclofen can also be taken in tablet form

- Botulin toxin injection

Botulinum toxin injections into affected muscles have proved quite successful in providing some relief for around 3–6 months, depending on the kind of dystonia. Botox or Dysport injections have the advantage of ready availability (the same form is used for cosmetic surgery) and the effects are not permanent. There is a risk of temporary paralysis of the muscles being injected or the leaking of the toxin into adjacent muscle groups, causing weakness or paralysis in them. The injections have to be repeated, as the effects wear off and around 15% of recipients will develop immunity to the toxin. There is a Type A and a Type B toxin approved for treatment of dystonia; often, those that develop resistance to Type A may be able to use Type B.

- Muscle relaxants

Clonazepam, an anti-seizure medicine, is also sometimes prescribed. However, for most, their effects are limited and side-effects like mental confusion, sedation, mood swings, and short-term memory loss occur.

- Parkinsonian drugs

Dopamine agonists: One type of dystonia, dopamine-responsive dystonia, can be completely treated with regular doses of L-DOPA in a form such as Sinemet (carbidopa/levodopa). Although this does not remove the condition, it does alleviate the symptoms most of the time. (In contrast, dopamine antagonists can sometimes cause dystonia.)

Ketogenic Diet

A Ketogenic diet consisting of 70% fats (focusing on medium chain triglycerides and unsaturated fats), 20% protein and 10% carbohydrates (any sugar) has shown strong promise as a treatment for Dystonia.

PED patients usually avoid prolonged, continuous exertion to prevent occurrence of attacks. Use of anticonvulsants such as benzodiazepines show little to no success in PED patients. A few cases have shown that patients were able to lessen their attacks with a high carbohydrate snack. A new approach to managing PED is the ketogenic diet, which alters the primary cerebral energy metabolism from glucose to ketone bodies. Reports have shown that the ketonic diet protects against seizures in epilepsy. In PED, it is probable that ketones will provide sufficient energy for the basal ganglia, which is normally deficient in patients with PED.

Current research at the University of Utah is investigating whether sodium oxybate, also known as Gamma-Hydroxybutyric acid is an effective treatment for AHC. Thus far, only a small number of patients have been sampled, and no conclusive results are yet available. While some success has been had thus far with the drug, AHC patients have been known to respond well initially to other drugs, but then the effectiveness will decline over time. Currently, sodium oxybate is used as a narcolepsy-cataplexy treatment, though in the past it has been used controversially in nutritional supplements. This drug was chosen to test because of a possible link between the causes of narcolepsy-cataplexy and AHC.

Treatment for PKND is more difficult than other Paroxysmal Dyskinesias. The majority of patients experience some relief from low dosages of clonazepam, a muscle relaxant and anticonvulsant. Similar to PKD, avoidance of stress, excitement, and fatigue will lower the frequency of PNKD attacks. Many patients also avoid known methyglyoxal containing foods and beverages such as alcohol, coffee, tea, and chocolate.