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.

Not all individuals with ET require treatment, but there are many treatment options depending on symptom severity. Caffeine and stress should be avoided, and good sleep is recommended.

When symptoms are sufficiently troublesome to warrant treatment, the first medication choices are beta blockers such as propranolol or alternately, nadolol and timolol. Atenolol and pindolol are not effective for tremor. The anti-epileptic primidone is also effective for ET.

Second-line or third-line medications can be added if the first-line medications do not control the tremor. Second-line medications are the anti-epileptics topiramate, gabapentin (as monotherapy) and levetiracetam, or benzodiazepines like alprazolam. Third-line medications are clozapine and mirtazapine.

Theophylline has been used by some practitioners to treat ET, even though it may also induce tremor. However, its use is debated due to conflicting data on its efficacy. There is some evidence that low doses may lead to improvement.

Ethanol has shown superior efficacy to that of benzodiazepines in small trials. It improves tremor in small doses and its effects are usually noticeable within 20 minutes for 3–5 hours, but occasionally appears a rebound tremor augmentation later.

When medications do not control the tremor or the person does not tolerate medication, botulinum toxin, deep brain stimulation or occupational therapy can be helpful. The electrodes for deep brain stimulation are usually placed in the "tremor center" of the brain, the ventral intermediate nucleus of the thalamus.

Additionally, MRI-guided high intensity focused ultrasound is a non-surgical treatment option for people with essential tremor who have not seen improvement with medication and refused or are not valid candidates for other techniques, such as deep brain stimulation. MRI-guided high intensity focused ultrasound does not achieve healing but can improve the quality of life. However, its safety, efficacy and long-term effects are not yet established. Temporary and permanent adverse side effects have been documented, and also the reappearance of tremors. Possible adverse events include gait difficulties, balance disturbances, paresthesias, headache, hemorrhage in the treated area (which requiries emergency treatment), tissue damage in other areas, skin burns with ulcerations, skin retraction, scars and blood clots. This procedure is contraindicated in pregnant women, persons who have a non-MRI compatible implanted metallic devices, allergy to MR contrast agents, cerebrovascular disease, abnormal bleeding, hemorrhage and/or blood clotting disorders, advanced kidney disease or on dialysis, heart conditions, severe hypertension, ethanol or substance abuse, among others. The US Food and Drug Administration ("FDA") approved Insightec’s Exablate Neuro system to treat essential tremor in 2016.

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.

Reducing the types of movements that trigger or worsen dystonic symptoms provides some relief, as does reducing stress, getting plenty of rest, moderate exercise, and relaxation techniques. Various treatments focus on sedating brain functions or blocking nerve communications with the muscles via drugs, neuro-suppression, or denervation. All current treatments have negative side-effects and risks.

A "geste antagoniste" is a physical gesture or position (such as touching one's chin) which serves to temporarily interrupt dystonia, it is also known as a "sensory trick". Patients may be aware of the presence of a geste antagoniste which provides some relief from their symptoms. Therapy for dystonia can involve prosthetics which provide passive simulation of the stimulation.

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.

Patients must have early consultation with craniofacial and orthopaedic surgeons, when craniofacial, clubfoot, or hand correction is indicated to improve function or aesthetics. Operative measures should be pursued cautiously, with avoidance of radical measures and careful consideration of the abnormal muscle physiology in Freeman–Sheldon syndrome. Unfortunately, many surgical procedures have suboptimal outcomes, secondary to the myopathy of the syndrome.

When operative measures are to be undertaken, they should be planned for as early in life as is feasible, in consideration of the tendency for fragile health. Early interventions hold the possibility to minimise developmental delays and negate the necessity of relearning basic functions.

Due to the abnormal muscle physiology in Freeman–Sheldon syndrome, therapeutic measures may have unfavourable outcomes. Difficult endotracheal intubations and vein access complicate operative decisions in many DA2A patients, and malignant hyperthermia (MH) may affect individuals with FSS, as well. Cruickshanks et al. (1999) reports uneventful use of non-MH-triggering agents. Reports have been published about spina bifida occulta in anaesthesia management and cervical kyphoscoliosis in intubations.

Treatment can include pharmaceutical or surgical means. The drug carbamazepine (Tegretol) has been used successfully. Other drugs used with variable success include gabapentin and, recently, memantine. Successful surgery options include superior oblique tenectomy accompanied by inferior oblique myectomy. However, "Overall, the bulk of the ophthalmic literature would agree with the viewpoint that invasive craniotomy surgical procedures should be justified only by the presence of intractable and absolutely unbearable symptoms."

Samii et al. and Scharwey and Samii described a patient who had superior oblique myokymia for 17 years. The interposition of a Teflon pad between the trochlear nerve and a compressing artery and vein at the nerve's exit from the midbrain led to a remission lasting for a follow-up of 22 months.

Patients and their parents must receive psychotherapy, which should include marriage counselling. Mitigation of lasting psychological problems, including depression secondary to chronic illness and posttraumatic stress disorder (PTSD), can be very successfully addressed with early interventions. This care may come from the family physician, or other attending physician, whoever is more appropriate; specialist care is generally not required. Lewis and Vitulano (2003) note several studies suggesting predisposal for psychopathology in paediatric patients with chronic illness. Esch (2002) advocates preventive psychiatry supports to facilitate balance of positive and negative stressors associated with chronic physical pathology. Patients with FSS should have pre-emptive and ongoing mixed cognitive therapy-psychodynamic psychotherapy for patients with FSS and cognitive-behavioural therapy (CBT), if begun after onset of obvious pathology.

Adler (1995) cautioned the failure of modern medicine to implement the biopsychosocial model, which incorporates all aspects of a patient’s experience in a scientific approach into the clinical picture, often results in chronically-ill patients deferring to non-traditional and alternative forms of therapy, seeking to be understood as a whole, not a part, which may be problematic among patients with FSS.

Furthermore, neuropsychiatry, physiological, and imaging studies have shown PTSD and depression to be physical syndromes, in many respects, as they are psychiatric ones in demonstrating limbic system physiological and anatomy disturbances. Attendant PTSD hyperarousal symptoms, which additionally increase physiological stress, may play a part in leading to frequent MH-like hyperpyrexia and speculate on its influence on underlying myopathology of FSS in other ways. PTSD may also bring about developmental delays or developmental stagnation, especially in paediatric patients.

With psychodynamic psychotherapy, psychopharmacotherapy may need to be considered. Electroconvulsive therapy (ECT) is advised against, in light of abnormal myophysiology, with predisposal to MH.

There is no cure available for Weaver syndrome. However, with multidisciplinary management such as neurological, pediatric, orthopedic, and psychomotor care and genetic counseling, symptoms can be managed. Surgery may be used to correct any skeletal issues. Physical and occupational therapy are considered an option to help with muscle tone. Also, speech therapy is often recommended for speech related problems.

There is no cure for this syndrome. Treatment is supportive and symptomatic. All children with Mowat–Wilson syndrome required early intervention with speech therapy, occupational therapy and physical therapy.

Treatment is symptomatic. There is no standard course of treatment for Sotos syndrome.

RBD is treatable. Medications are prescribed for RBD based on symptoms. Low doses of clonazepam is most effective with a 90% success rate. How this drug works to restore REM atonia is unclear: It is thought to suppress muscle activity, rather than directly restoring atonia. Melatonin is also effective and can also be prescribed as a more natural alternative. For those with Parkinson's and RBD, Levodopa is a popular choice. Pramipexole is another drug which can be an effective treatment option. Recent evidence has shown melatonin and clonazepam to be comparably effective in treatment of RBD with patients who received melatonin treatment reporting fewer side effects. In addition, patients with neurodegenerative diseases such as Parkinson's disease reported more favorable outcomes with melatonin treatment.

In addition to medication, it is wise to secure the sleeper's environment in preparation for episodes by removing potentially dangerous objects from the bedroom and either place a cushion round the bed or moving the mattress to the floor for added protection against injuries. Some extreme sufferers sleep in a sleeping bag zipped up to their neck, and wear mittens so they can't unzip it until they awake in the morning.

Patients are advised to maintain a normal sleep schedule, avoid sleep deprivation, and keep track of any sleepiness they may have. Treatment includes regulating neurologic symptoms and treating any other sleep disorders that might interfere with sleep. Sleep deprivation, alcohol, certain medications, and other sleep disorders can all increase RBD and should be avoided if possible.

With appropriate treatment and management, patients with Weaver syndrome appear to do well, both physically and intellectually, throughout their life and have a normal lifespan. Their adult height is normal as well.

The twins require the use of wheelchairs for mobility and are unable to speak without the assistance of electronic speaking aids. They experience persistent and painful muscle spasms which are worsened by emotional distress. They are currently living with their parents, with the assistance of hospice workers. Doctors continue to administer tests to the twins in search of a treatment.

Sotos syndrome is not a life-threatening disorder and patients may have a normal life expectancy. Developmental delays may improve in the school-age years; however, coordination problems may persist into adulthood, along with any learning disabilities and/or other physical or mental issues.

Geniospasm is movement disorder of the mentalis muscle.

It is a benign genetic disorder linked to chromosome 9q13-q21 where there are episodic involuntary up and down movements of the chin and lower lip. The movements consist of rapid fluttering or trembling at about 8 Hz superimposed onto a once per three seconds movement of higher amplitude and occur symmetrically in the V shaped muscle. The tongue and buccal floor muscles may also be affected but to a much lesser degree.

The movements are always present but extreme episodes may be precipitated by stress, concentration or emotion and commence in early childhood.

The condition is extremely rare and in a study in 1999 only 23 families in the world were known to be affected, although it may be under-reported. Inheritance is aggressively autosomal dominant. In at least two studies the condition appeared spontaneously in the families.

The condition responds very well to regular botulinus toxin injections into the mentalis muscle which paralyse the muscle but cause no impairment of facial expression or speech.

If binocular vision is present and head position is correct, treatment is not obligatory.

Treatment is required for: visual symptoms, strabismus, or incorrect head position.

Acquired cases that have active inflammation of the superior oblique tendon may benefit from local corticosteroid injections in the region of the trochlea.

The goal of surgery is to restore free ocular rotations. Various surgical techniques have been used:

- Harold Brown advocated that the superior oblique tendon be stripped. A procedure named sheathotomy. The results of such a procedure are frequently unsatisfactory because of reformation of scar tissue.

- Tenotomy of the superior oblique tendon (with or with out a tendon spacer) has also been advocated. This has the disadvantage that it frequently produces a superior oblique paresis.

- Weakening of the inferior oblique muscle of the affected eye may be needed to compensate for iatrogenic fourth nerve palsy.

During surgery, a traction test is repeated until the eye rotations are free and the eye is anchored in an elevated adducted position for about two weeks after the surgery. This maneuver is intended to prevent the reformation of scar tissue in the same places. Normalization of head position may occur but restoration of full motility is seldom achieved. A second procedure may be required.

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.

Treatment is symptomatic, often addressing indicators associated with peripheral pulmonary artery stenosis. Laryngotracheal calcification resulting in dyspnea and forceful breathing can be treated with bronchodilators including the short and long-acting β2-agonists, and various anticholinergics. Prognosis is good, yet life expectancy depends on the severity and extent of diffuse pulmonary and arterial calcification.

Although essential tremor is often mild, people with severe tremor have difficulty performing many of their routine activities of daily living. ET is generally progressive in most cases (sometimes rapidly, sometimes very slowly), and can be disabling in severe cases.

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.

Paroxysmal tonic upgaze (PTU) of childhood is a rare and distinctive neuro-ophthalmological syndrome characterized by episodes of sustained upward deviation of the eyes. Symptoms normally appear in babies under one year of age and are characterized by an upward stare or gaze, with the eyes rolled back, while the chin is typically held low.

Babies suffering from PTU may exhibit normal or slightly jerky side-to-side eye movement, nausea, irritability, frequent sleep, developmental and language delays, vertigo and loss of muscle tone.

The condition is generally regarded as having a benign outcome, in the sense that it improves, rather than worsens over time. The average age of recovery is at about 2.5 years.

PTU was first described in 1988. As of 2002, approximately fifty cases had been diagnosed. Because the condition is so rare, the majority of physicians have never seen it, and thus may not recognize it. Videotaping a child both in and out of the upgaze state can be vital for reaching a diagnosis.

The medication that may be prescribed to someone who has a mental breakdown is based upon the underlying causes, which are sometimes more serious mental disorders. Antidepressants are given to treat depression. Anxiolytics are used for those with anxiety disorders. Antipsychotics are used for schizophrenia and mood stabilizers help with bipolar disorder. Depending upon what caused a person’s mental breakdown, any of these treatments can be helpful for them.

There are several different kinds of therapy that a patient can receive. The most common type of therapy is counseling. This is where the patient is able to talk about whatever is on their mind without worrying about any judgments. Psychotherapy is a very common type of therapy that addresses the current problems in someone’s life and helps them to deal with them. Past experiences may also be explored in this type of therapy. In psychoanalysis therapy, the main focus is a patient’s past experiences so that they can confront these issues and prevent breakdowns in the future. Cognitive behavioral therapy explores how a person behaves and what they are thinking and feeling. If there is anything negative in these three different categories, then this therapy will try to turn them around into positives. Hypnotherapy is where hypnosis is performed and used to help the patient relax. Hypnosis can also be used to figure out why a person acts or feels a certain way, by examining past events that may have caused the breakdown. Expressive therapy focuses on how the patient is able to express their feelings. If the patient has a hard time doing this, expression through the arts is highly recommended. There is also aromatherapy, which consists of herbs to help the patient relax and to try to relieve stress. Yoga and massage may also be included in this therapy that will help the muscles to relax. Meditation is also often recommended. All of these therapies help a person to relax and de-stress and also help to prevent future breakdowns.

Although the cause of writer's cramp is not well known, it was historically believed to be the result of excessive fine motor activity, possibly complicated by a tense or otherwise inappropriate writing technique. More recently, Karin Rosenkranz et al. have suggested that this is not necessarily the case. Musician's cramp (a similar focal dystonia which affects some 1% of instrumentalists) has historically been grouped together with writer's cramp because of this and their common task-specificity. Rosenkranz et al. have more recently identified significant differences between the two populations, however. No matter exactly how it arises, researchers generally agree that these types of focal dystonia are the result of a basal ganglia and/or sensorimotor cortex malfunction in the brain.

Early symptoms may include loss of precision muscle coordination (sometimes first manifested in declining penmanship, frequent small injuries to the hands, dropped items and a noticeable increase in dropped or chipped dishes), cramping pain with sustained use and trembling. Significant muscle pain and cramping may result from very minor exertions like holding a book and turning pages. It may become difficult to find a comfortable position for arms and legs with even the minor exertions associated with holding arms crossed causing significant pain similar to restless leg syndrome. Affected persons may notice trembling in the diaphragm while breathing, or the need to place hands in pockets, under legs while sitting or under pillows while sleeping to keep them still and to reduce pain. Trembling in the jaw may be felt and heard while lying down, and the constant movement to avoid pain may result in the grinding and wearing down of teeth, or symptoms similar to TMD. The voice may crack frequently or become harsh, triggering frequent throat clearing. Swallowing can become difficult and accompanied by painful cramping. Patients may also present with varying degree of disability and symptoms, such as experiencing more difficulty writing down-stroke as compared to writing upstroke.

Electrical sensors (EMG) inserted into affected muscle groups, while painful, can provide a definitive diagnosis by showing pulsating nerve signals being transmitted to the muscles even when they are at rest. The brain appears to signal portions of fibers within the affected muscle groups at a firing speed of about 10 Hz causing them to pulsate, tremble and contort. When called upon to perform an intentional activity, the muscles fatigue very quickly and some portions of the muscle groups do not respond (causing weakness) while other portions over-respond or become rigid (causing micro-tears under load). The symptoms worsen significantly with use, especially in the case of focal dystonia, and a "mirror effect" is often observed in other body parts: use of the right hand may cause pain and cramping in that hand as well as in the other hand and legs that were not being used. Stress, anxiety, lack of sleep, sustained use and cold temperatures can worsen symptoms.

Direct symptoms may be accompanied by secondary effects of the continuous muscle and brain activity, including disturbed sleep patterns, exhaustion, mood swings, mental stress, difficulty concentrating, blurred vision, digestive problems and short temper. People with dystonia may also become depressed and find great difficulty adapting their activities and livelihood to a progressing disability. Side effects from treatment and medications can also present challenges in normal activities.

In some cases, symptoms may progress and then plateau for years, or stop progressing entirely. The progression may be delayed by treatment or adaptive lifestyle changes, while forced continued use may make symptoms progress more rapidly. In others, the symptoms may progress to total disability, making some of the more risky forms of treatment worth considering in the future.

"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.