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.

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.

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.

It is very difficult to treat an intention tremor. The tremor may disappear for a while after a treatment has been administered and then return. This situation is addressed with a different treatment. First, individuals will be asked if they use any of the drugs known to cause tremors. If so, they are asked to stop taking the medication and then evaluated after some time to determine if the medication was related to the onset of the tremor. If the tremor persists, treatment that follows may include drug therapy, lifestyle changes, and more invasive forms of treatment, such as surgery and thalamic deep brain stimulation.

Intention tremors are known to be very difficult to treat with pharmacotherapy and drugs. Although there is no established pharmacological treatment for an intention tremor, several drugs have been found to have positive effects on intention tremors and are used as treatment by many health professionals. Isoniazid, buspirone hydrochloride, glutethimide, carbamazepine, clonazepam, topiramate, zofran, propranolol and primidone have all seen moderate results in treating intention tremor and can be prescribed treatments. Isoniazid inhibits γ-aminobutyric acid-aminotransferase, which the first step in enzymatic breakdown of GABA, thus increasing GABA, the major inhibitory neurotransmitter in the central nervous system. This causes a reduction in cerebellar ataxias. Another neurotransmitter targeted by drugs that has been found to alleviate intention tremors is serotonin. The agonist buspirone hydrochloride, which decreases serotonin's function in the central nervous system, has been viewed as an effective treatment of intention tremors.

Physical therapy has had great results in reducing tremors but usually does not cure them. Relaxation techniques, such as meditation, yoga, hypnosis, and biofeedback, have seen some results with tremors. Wearing wrist weights which weigh down one's hands as they make movements, masking much of the tremor, is a proven home remedy. This is not a treatment, since wearing the weights does not have any lasting effects when they are not on. However, they do help the individual cope with the tremor immediately.

A more radical treatment that is used in individuals who do not respond to drug therapy, physical therapy, or any other treatment listed above, with moderate to severe intention tremors, is surgical intervention. Deep brain stimulation and surgical lesioning of the thalamic nuclei has been found to be an effective long-term treatment with intention tremors.

Deep brain stimulation treats intention tremors but does not help related diseases or disorders such as dyssynergia and dysmetria. Deep brain stimulation involves the implantation of a device called a neurostimulator, sometimes called a 'brain pacemaker'. It sends electrical impulses to specific parts of the brain, changing brain activity in a controlled manner. In the case of an intention tremor, the thalamic nuclei is the region targeted for treatment. This form of treatment causes reversible changes and does not cause any permanent lesions. Since it is reversible, deep brain stimulation is considered fairly safe: Reduction in tremor amplitude is almost guaranteed and sometimes resolved. Some individuals with multiple sclerosis have seen sustained benefits in MS progress.

Thalamotomy is another surgical treatment where lesions of the thalamus nucleus are created to disrupt the tremor circuit. Thalamotomy has been used to treat many forms of tremors, including those that arise from trauma, multiple sclerosis, stroke, and those whose cause it unknown. This is a very invasive, high-risk treatment with many negative effects, such as multiple sclerosis worsening, cognitive dysfunction, worsening of dysarthria, and dysphagia. Immediate positive effects are seen in individuals treated with a thalamotomy procedure. However, the tremor often comes back; it is not a complete treatment. Thalamotomy is in clinical trials to determine the validity of the treatment of intention tremors with all its high risks.

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.

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.

Research has focused on finding a pharmacological treatment that is specific for intention tremor. Limited success has been seen in treating intention tremor with drugs effective at treating essential tremor. Clinical trials of levetiracetam, typically used to treat epilepsy, and pramipexole, used to treat resting tremor, were completed in 2009-2010 to establish their effectiveness in treating kinetic tremor. A clinical trial for riluzole, typically used to treat amyotrophic lateral sclerosis, was completed at the Sapienza University of Rome to evaluate its effectiveness of treating cerebellar ataxia and kinetic tremor.

Medications remain the basis of therapy in many cases. Symptomatic drug therapy is available for several forms of tremor:

- Parkinsonian tremor drug treatment involves L-DOPA and/or dopamine-like drugs such as pergolide, bromocriptine and ropinirole; They can be dangerous, however, as they may cause symptoms such as tardive dyskinesia, akathisia, clonus, and in rare instances tardive (late developing) psychosis. Other drugs used to lessen parkinsonian tremor include amantadine and anticholinergic drugs like benztropine

- Essential tremor may be treated with beta blockers (such as propranolol and nadolol) or primidone, an anticonvulsant

- Cerebellar tremor symptoms may decrease with the application of alcohol (ethanol) or benzodiazepine medications, both of which carry some risk of dependence and/or addiction

- Rubral tremor patients may receive some relief using L-DOPA or anticholinergic drugs. Surgery may be helpful

- Dystonic tremor may respond to diazepam, anticholinergic drugs, and intramuscular injections of botulinum toxin. Botulinum toxin is also prescribed to treat voice and head tremors and several movement disorders

- Primary orthostatic tremor sometimes is treated with a combination of diazepam and primidone. Gabapentin provides relief in some cases

- Enhanced physiological tremor is usually reversible once the cause is corrected. If symptomatic treatment is needed, beta blockers can be used

Eliminating tremor “triggers” such as caffeine and other stimulants from the diet is often recommended.

Essential tremor may benefit from slight doses of ethanol, but the potential negative consequences of regular ethanol intake need to be taken into account. Beta blockers have been used as an alternative to alcohol in sports such as competitive dart playing and carry less potential for addiction.

Physical therapy and occupational therapy may help to reduce tremor and improve coordination and muscle control for some patients. A physical therapist and/or occupational therapist will evaluate the patient for tremor positioning, muscle control, muscle strength, and functional skills. Teaching the patient to brace the affected limb during the tremor or to hold an affected arm close to the body is sometimes useful in gaining motion control. Coordination and balancing exercises may help some patients. Some occupational therapists recommend the use of weights, splints, other adaptive equipment, and special plates and utensils for eating.

Treatment of a Holmes tremor can fail or is delayed because there are only a few diagnostic tools available. The treatment of choice is complete removal of the tumor. Removing the tumor can result in elimination or better control of the tremors. Other treatment options involve coping strategies such as avoiding movements or actions that worsen tremors. Patients suffering from Holmes tremors can also benefit from using larger utensil handles and wrist weights. There are also some pharmacological treatments, but they are not very effective.

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.

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.

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.

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.

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.

Tolcapone inhibits the activity COMT, an enzyme which degrades dopamine. It has been used to complement levodopa; however, its usefulness is limited by possible complications such as liver damage. A similarly effective drug, entacapone, has not been shown to cause significant alterations of liver function. Licensed preparations of entacapone contain entacapone alone or in combination with carbidopa and levodopa.

Several dopamine agonists that bind to dopamine receptors in the brain have similar effects to levodopa. These were initially used as a complementary therapy to levodopa for individuals experiencing levodopa complications (on-off fluctuations and dyskinesias); they are now mainly used on their own as first therapy for the motor symptoms of PD with the aim of delaying the initiation of levodopa therapy and so delaying the onset of levodopa's complications. Dopamine agonists include bromocriptine, pergolide, pramipexole, ropinirole, piribedil, cabergoline, apomorphine and lisuride.

Though dopamine agonists are less effective than levodopa at controlling PD motor symptoms, they are usually effective enough to manage these symptoms in the first years of treatment. Dyskinesias due to dopamine agonists are rare in younger people who have PD but, along with other complications, become more common with older age at onset. Thus dopamine agonists are the preferred initial treatment for younger onset PD, and levodopa is preferred for older onset PD.

Dopamine agonists produce significant, although usually mild, side effects including drowsiness, hallucinations, insomnia, nausea, and constipation. Sometimes side effects appear even at a minimal clinically effective dose, leading the physician to search for a different drug. Agonists have been related to impulse control disorders (such as compulsive sexual activity, eating, gambling and shopping) even more strongly than levodopa. They tend to be more expensive than levodopa.

Apomorphine, a non-orally administered dopamine agonist, may be used to reduce off periods and dyskinesia in late PD. It is administered by intermittent injections or continuous subcutaneous infusions. Since secondary effects such as confusion and hallucinations are common, individuals receiving apomorphine treatment should be closely monitored. Two dopamine agonists that are administered through skin patches (lisuride and rotigotine) and are useful for people in the initial stages and possibly to control off states in those in the advanced state.

There is no cure for XDP and medical treatment offers only temporary relief. Some authors have reported benzodiazepines and anticholinergic agents in the early stages of the disease. Botulinum toxin injections have been used to relieve focal dystonia. Deep brain stimulation has shown promise in the few cases treated surgically.

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.

Lesionsing is the intentional destruction of neuronal cells in a particular area used for therapeutic purposes. Though this seems dangerous, vast improvements have been achieved in patients with movement disorders. The exact process generally involves unilateral lesioning in the sensorimotor territory of the GPi. This process is called pallidotomy. It is believed that the success of pallidotomies in reducing the effects of movement disorders may result from the interruption of abnormal neuronal activity in the GPi. This ablation technique can be viewed as simply removing a faulty piece of a circuit. With the damaged piece of the circuit removed, the healthy area of the circuit can continue normal function.

Treatment for hyperthermia includes reducing muscle overactivity via sedation with a benzodiazepine. More severe cases may require muscular paralysis with vecuronium, intubation, and artificial ventilation. Suxamethonium is not recommended for muscular paralysis as it may increase the risk of cardiac dysrhythmia from hyperkalemia associated with rhabdomyolysis. Antipyretic agents are not recommended as the increase in body temperature is due to muscular activity, not a hypothalamic temperature set point abnormality.

Medication is often not necessary in children as symptoms usually alleviate spontaneously as the child ages. However, because the disorder may affect wakeful behavior, many adults who continue to suffer from RMD may seek treatment. Benzodiazepines or tricyclic antidepressants have been considered as therapeutic options in managing the disorder. Infantile and adolescent RMD respond well to low doses of clonazepam. Prescription medications such as ropinirole or pramipexole given to restless legs syndrome patients do not show any clinical improvement in many patients with RMD.

Management is based primarily on stopping the usage of the precipitating drugs, the administration of serotonin antagonists such as cyproheptadine, and supportive care including the control of agitation, the control of autonomic instability, and the control of hyperthermia. Additionally, those who ingest large doses of serotonergic agents may benefit from gastrointestinal decontamination with activated charcoal if it can be administered within an hour of overdose. The intensity of therapy depends on the severity of symptoms. If the symptoms are mild, treatment may only consist of discontinuation of the offending medication or medications, offering supportive measures, giving benzodiazepines for myoclonus, and waiting for the symptoms to resolve. Moderate cases should have all thermal and cardiorespiratory abnormalities corrected and can benefit from serotonin antagonists. The serotonin antagonist cyproheptadine is the recommended initial therapy, although there have been no controlled trials demonstrating its efficacy for serotonin syndrome. Despite the absence of controlled trials, there are a number of case reports detailing apparent improvement after people have been administered cyproheptadine. Animal experiments also suggest a benefit from serotonin antagonists. Cyproheptadine is only available as tablets and therefore can only be administered orally or via a nasogastric tube; it is unlikely to be effective in people administered activated charcoal and has limited use in severe cases. Additional pharmacological treatment for severe case includes administering atypical antipsychotic drugs with serotonin antagonist activity such as olanzapine. Critically ill people should receive the above therapies as well as sedation or neuromuscular paralysis. People who have autonomic instability such as low blood pressure require treatment with direct-acting sympathomimetics such as epinephrine, norepinephrine, or phenylephrine. Conversely, hypertension or tachycardia can be treated with short-acting antihypertensive drugs such as nitroprusside or esmolol; longer acting drugs such as propranolol should be avoided as they may lead to hypotension and shock. The cause of serotonin toxicity or accumulation is an important factor in determining the course of treatment. Serotonin is catabolized by monoamine oxidase in the presence of oxygen, so if care is taken to prevent an unsafe spike in body temperature or metabolic acidosis, oxygenation will assist in dispatching the excess serotonin. The same principle applies to alcohol intoxication. In cases of serotonin syndrome caused by monoamine oxidase inhibitors oxygenation will not help to dispatch serotonin. In such instances, hydration is the main concern until the enzyme is regenerated.

There is no known cure for MSA and management is primarily supportive.

Ongoing care from a neurologist specializing in "movement disorders" is recommended as the complex symptoms of MSA are often not familiar to less-specialized health care professionals.

One particularly serious problem, the drop in blood pressure upon standing up (with risk of fainting and thus injury from falling) often responds to fludrocortisone, a synthetic mineralocorticoid. Another common drug treatment is midodrine (an alpha-agonist). Non-drug treatments include "head-up tilt" (elevating the head of the whole bed by about 10 degrees), salt tablets or increasing salt in the diet, generous intake of fluids, and pressure (elastic) stockings. Avoidance of triggers of low blood pressure (such as hot weather, alcohol, and dehydration) are crucial.

Hospice/homecare services can be very useful as disability progresses.

Levodopa (L-Dopa), a drug used in the treatment of Parkinson's disease, improves parkinsonian symptoms in a small percentage of MSA patients. A recent trial reported that only 1.5% of MSA patients experienced a less than 50% improvement when taking levodopa, and even this was a transient effect lasting less than one year. Poor response to L-Dopa has been suggested as a possible element in the differential diagnosis of MSA from Parkinson's disease.

A November, 2008 study conducted in Europe failed to find an effect for the drug riluzole in treating MSA or PSP.

The medical management of FXTAS aims to reduce the level of disability and minimize symptoms. Presently, there are many gaps in the research on the management of FXTAS, as the disorder was first described in the literature in 2001. There is no treatment modality aimed at reversing the pathogenesis of FXTAS. However, there are a variety of drug therapies that are being utilized in the management of FXTAS symptoms, although there is a lack of randomized control trials assessing the efficacy these therapies and support is limited to anecdotal evidence. Therefore, many of the treatments are based on what has been helpful in disorders with similar clinical presentations.

There is no cure for FXTAS. Current treatment includes medications for alleviating symptoms of tremor, ataxia, mood changes, anxiety, cognitive decline, dementia, neuropathic pain, or fibromyalgia. Neurological rehabilitation has not been studied for patients with FXTAS but should also be considered as a possible form of therapy. Additionally, occupational and physical therapy may help to improve performance of functional tasks.