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.

Botulinum toxin injections also act upon acetylcholine to reduce dystonia symptoms. The neurotoxin is active in presynaptic terminals and blocks exocytosis of acetylcholine into the synaptic cleft which reduces muscle activity. Botulinum may also have a role in inhibiting glutamate and changing muscle movement. Studies have also shown possible axon transport of this neurotoxin as well as its function as a pain reliever without affect on overactive muscle movement in myoclonus dystonia patients.

Anticholinergics like benzatropine alleviate dystonia symptoms by blocking reuptake of acetylcholine. Acetylcholine is involved in the pathophysiology of dystonia within the basal ganglia, although its exact role has not been determined. Acetylcholine is involved with dopamine and glutamate pathways in the basal ganglia, in addition to presynaptic muscarinic receptors which are involved in motor control. Acetylcholine is usually overactive in dystonia patients and blocking of this neurotransmitter would reduce contortion of the upper body, but can produce side effects of drowsiness, confusion and memory issues in adults.

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.

Before prescribing medication for these conditions which often resolve spontaneously, recommendations have pointed to improved skin hygiene, good hydration via fluids, good nutrition, and installation of padded bed rails with use of proper mattresses. Pharmacological treatments include the typical neuroleptic agents such as fluphenazine, pimozide, haloperidol and perphenazine which block dopamine receptors; these are the first line of treatment for hemiballismus. Quetiapine, sulpiride and olanzapine, the atypical neuroleptic agents, are less likely to yield drug-induced parkinsonism and tardive dyskinesia. Tetrabenazine works by depleting presynaptic dopamine and blocking postsynaptic dopamine receptors, while reserpine depletes the presynaptic catecholamine and serotonin stores; both of these drugs treat hemiballismus successfully but may cause depression, hypotension and parkinsonism. Sodium valproate and clonazepam have been successful in a limited number of cases. Stereotactic ventral intermediate thalamotomy and use of a thalamic stimulator have been shown to be effective in treating these conditions.

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.

The medical treatment of essential tremor at the Movement Disorders Clinic at Baylor College of Medicine begins with minimizing stress and tremorgenic drugs along with recommending a restricted intake of beverages containing caffeine as a precaution, although caffeine has not been shown to significantly intensify the presentation of essential tremor. Alcohol amounting to a blood concentration of only 0.3% has been shown to reduce the amplitude of essential tremor in two-thirds of patients; for this reason it may be used as a prophylactic treatment before events during which one would be embarrassed by the tremor presenting itself. Using alcohol regularly and/or in excess to treat tremors is highly unadvisable, as there is a purported correlation between tremor and alcoholism. Alcohol is thought to stabilize neuronal membranes via potentiation of GABA receptor-mediated chloride influx. It has been demonstrated in essential tremor animal models that the food additive 1-octanol suppresses tremors induced by harmaline, and decreases the amplitude of essential tremor for about 90 minutes.

Two of the most valuable drug treatments for essential tremor are propranolol, a beta blocker, and primidone, an anticonvulsant. Propranolol is much more effective for hand tremor than head and voice tremor. Some beta-adrenergic blockers (beta blockers) are not lipid-soluble and therefore cannot cross the blood–brain barrier (propranolol being an exception), but can still act against tremors; this indicates that this drug’s mechanism of therapy may be influenced by peripheral beta-adrenergic receptors. Primidone’s mechanism of tremor prevention has been shown significantly in controlled clinical studies. The benzodiazepine drugs such as diazepam and barbiturates have been shown to reduce presentation of several types of tremor, including the essential variety. Controlled clinical trials of gabapentin yielded mixed results in efficacy against essential tremor while topiramate was shown to be effective in a larger double-blind controlled study, resulting in both lower Fahn-Tolosa-Marin tremor scale ratings and better function and disability as compared to placebo.

It has been shown in two double-blind controlled studies that injection of botulinum toxin into muscles used to produce oscillatory movements of essential tremors, such as forearm, wrist and finger flexors, may decrease the amplitude of hand tremor for approximately three months and that injections of the toxin may reduce essential tremor presenting in the head and voice. The toxin also may help tremor causing difficulty in writing, although properly adapted writing devices may be more efficient. Due to high incidence of side effects, use of botulinum toxin has only received a C level of support from the scientific community.

Deep brain stimulation toward the ventral intermediate nucleus of the thalamus and potentially the subthalamic nucleus and caudal zona incerta nucleus have been shown to reduce tremor in numerous studies. That toward the ventral intermediate nucleus of the thalamus has been shown to reduce contralateral and some ipsilateral tremor along with tremors of the cerebellar outflow, head, resting state and those related to hand tasks; however, the treatment has been shown to induce difficulty articulating thoughts (dysarthria), and loss of coordination and balance in long-term studies. Motor cortex stimulation is another option shown to be viable in numerous clinical trials.

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.

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.

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.

PKD patients usually show a good response to anticonvulsants. Most commonly used medications are sodium blockers, carbamazepine and phenytoin. During a drug-testing study, patients reported a decreasing response to the latter use of anticonvulsants and switched to carbamazepine or phenytoin. Refraining from established triggers such as sudden movement has been shown to lessen attacks occurrences. Avoidance of predisposing factors such as stress, excitement, and fatigue also help manage attacks.

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.

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.

Anticholinergic drugs are used to control neuroleptic-induced EPS, although akathisia may require beta blockers or even benzodiazepines. If the EPS are induced by an antipsychotic, EPS may be reduced by dose titration or by switching to an atypical antipsychotic, such as aripiprazole, ziprasidone, quetiapine, olanzapine, risperidone, or clozapine. These medications possess an additional mode of action that is believed to negate their effect on the nigrostriatal pathway, which means they are associated with fewer extrapyramidal side-effects than "conventional" antipsychotics (chlorpromazine, haloperidol, etc.), although some research has shown that second generation neuroleptics cause EPS at the same rate as the first generation drugs.

Commonly used medications for EPS are anticholinergic agents such as benztropine (Cogentin), diphenhydramine (Benadryl), and trihexyphenidyl (Artane). Another common course of treatment includes dopamine agonist agents such as pramipexole. These medications reverse the symptoms of extrapyramidal side effects caused by antipsychotics or other drugs that either directly or indirectly inhibit dopaminergic neurotransmission.

Studies are yet to be undertaken on the optimum dosage of the causative drugs to reduce their side effects (extrapyramidal symptoms (EPS)).

Baclofen, diazepam and dantrolene remain the three most commonly used pharmacologic agents in the treatment of spastic hypertonia. Baclofen is generally the drug of choice for spinal cord types of spasticity, while sodium dantrolene is the only agent which acts directly on muscle tissue. Tizanidine is also available. Phenytoin with chlorpromazine may be potentially useful if sedation does not limit their use. Ketazolam, not yet available in the United States, may be a significant addition to the pharmacologic armamentarium. Intrathecal administration of antispastic medications allows for high concentrations of drug near the site of action, which limits side effects.

Recent research indicates that the biomolecule taurine may be effective for hypertonia, perhaps through its benzodiazepine-like modulation of the inhibitory neurotransmitter GABA or the neuromuscular effects of increasing intracellular calcium levels.

Methylphenidate, commonly used to treat ADHD, has been used in conjunction with levodopa to treat hypokinesia in the short term. The two work together to increase dopamine levels in the striatum and prefrontal cortex. Methylphenidate mainly inhibits dopamine and noradrenaline reuptake by blocking presynaptic transporters, and levodopa increases the amount of dopamine, generally improving hypokinesic gait. Some patients, however, have adverse reactions of nausea and headache to the treatment and the long-term effects of the drug treatment still need to be assessed.

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.

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.

New treatments include increasing the number of dopamine cells by transplanting stem cells into the basal ganglia or stimulating endogenous stem cell production and movement to the basal ganglia. The successful integration of stem cells can relieve hypokinetic symptoms and decrease the necessary dose of dopaminergic drugs. However, a variety of complications, including possible tumor formation, inappropriate cell migration, rejection of cells by the immune system, and cerebral hemorrhage are possible, causing many physicians to believe the risks outweigh the possible benefits.

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.

Valbenazine has been approved by the FDA for tardive dyskinesia. Tetrabenazine, which is a dopamine depleting drug, is sometimes used to treat tardive dyskinesia and other movement disorders. However, it is only approved to treat chorea associated with Huntington's disease. The related VMAT2 inhibitor, reserpine, has also been tried in one small randomised double-blind placebo-controlled trial as a treatment for TD with success, as has α-methyldopa. Ondansetron has shown some benefit in experimental studies on tardive dyskinesia and a variety of anti-Parkinsonian medications are used such as donepezil, baclofen, and pramipexole. Clonidine may also be useful in the treatment of TD, although dose-limiting hypotension and sedation may hinder its usage. Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia. Benzodiazepines are an effective treatment for TD, however their use is limited by the development of tolerance which requires ever increasing doses of the benzodiazepines to be used to attenuate TD symptoms. The most popular benzodiazepine for the treatment of TD is clonazepam. Vitamin B6 has been reported to be an effective treatment for TD in two randomised double-blind placebo-controlled trials.

In males, the branched-chain amino acid formula Tarvil, containing the amino acids valine, isoleucine, and leucine in a 3:3:4 ratio was reported as beneficial for motor symptoms in a small, non-blinded study.

The most common drug used to treat AHC is flunarizine. Flunarizine functions by acting as a calcium channel blocker. Other drugs, in order of frequency of use are benzodiazepines, carbamazapine, barbiturates, and valproic acid. Flunarizine is prescribed for the purpose of reducing the severity of AHC attacks and the number of episodes, though it rarely stops attacks altogether. Minimizing the attacks may help reduce damage to the body from hemiplegic attacks and improve long-term outcomes as far as mental and physical disabilities are concerned.

Experts differ in their confidence in flunarizine's effectiveness. Some studies have found it to be very effective in reducing the duration, severity, and frequency of hemiplegic attacks. It is generally considered the best treatment available, but this drug is thought by some to be of little benefit to AHC patients. Many patients suffer adverse effects without seeing any improvement. Flunarizine also causes problems because it is difficult for patients to obtain, as it is not readily available in the United States.

There are two lines of treatment for Pisa syndrome. The first line entails discontinuation or reduction in dose of the antipsychotic drug(s). The second line of treatment is an anticholinergic medication. A pharmacological therapy for Pisa syndrome caused by prolonged use of antipsychotic drugs has not been established yet.