NMS is a medical emergency and can lead to death if untreated. The first step is to stop the antipsychotic medication and treat the hyperthermia aggressively, such as with cooling blankets or ice packs to the axillae and groin. Supportive care in an intensive care unit capable of circulatory and ventilatory support is crucial. The best pharmacological treatment is still unclear. Dantrolene has been used when needed to reduce muscle rigidity, and more recently dopamine pathway medications such as bromocriptine have shown benefit.

Amantadine is another treatment option due to its dopaminergic and anticholinergic effects.

Apomorphine may be used however its use is supported by little evidence. Benzodiazepines may be used to control . Highly elevated blood myoglobin levels can result in kidney damage, therefore aggressive intravenous hydration with diuresis may be required. When recognized early NMS can be successfully managed; however, up to 10% of cases can be fatal.

Should a patient subsequently require an antipsychotic, trialing a low dose of a low-potency atypical antipsychotic is recommended.

Non-selective beta-blockers are the most effective in reducing the frequency and severity of PSH episodes. They help decrease the effect of circulating catecholamines and lower metabolic rates, which are high in patients during PSH episodes. Beta-blockers also help in reducing fever, diaphoresis, and in some cases dystonia. Propanolol is a common beta-blocker administered due to the fact that it penetrates the blood-brain barrier relatively well. Typically it is administered in doses of twenty milligrams to sixty milligrams every four to six hours in the treatment of PSH.

The two most common medications used in the treatment of paroxysmal sympathetic hyperactivity are morphine sulfate and beta-blockers. Morphine is useful in helping halt episodes that have started to occur. Beta-blockers are helpful in preventing the occurrence of 'sympathetic storms'. Other drugs that have been used and have in some cases been helpful are dopamine agonists, other various opiates, benzodiazepines, clonidine, and baclofen. Chlorpromazine and haloperidol, both dopamine antagonists, in some cases have worsened PSH symptoms. These drugs are in use currently for treatment; exact pathways are not known and wide-range helpfulness is speculative.

The prognosis is best when identified early and treated aggressively. In these cases NMS is not usually fatal. In previous studies the mortality rates from NMS have ranged from 20%–38%; however, in the last two decades, mortality rates have fallen below 10% due to early recognition and improved management. Re-introduction to the drug that originally caused NMS to develop may also trigger a recurrence, although in most cases it does not.

Memory impairment is a consistent feature of recovery from NMS, and usually temporary, though in some cases, may become persistent.

As with other neuroleptic-induced tardive syndromes, there is no definite treatment for tardive dysphrenia. The continuing to take the drug or changing the dosage of the atypical antipsychotic drug in use, or augmenting it with a typical antipsychotic, can alleviate symptoms temporarily. However, these solutions carry the risk of worsening or perpetuating the iatrogenesis in the long term.

Some patients could gradually benefit from changing to a dopamine D2 receptor partial agonist agent like clozapine. These drugs do not induce up-regulation, instead acting as a prophylactic.

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.

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.

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.

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.

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)).

In the past, the prophylactic use of dantrolene was recommended for MH-susceptible patients undergoing general anesthesia. However, multiple retrospective studies have demonstrated the safety of trigger-free general anesthesia in these patients in the absence of prophylactic dantrolene administration. The largest of these studies looked at the charts of 2214 patients who underwent general or regional anesthesia for an elective muscle biopsy. About half (1082) of the patients were muscle biopsy positive for MH. Only five of these patients exhibited signs consistent with MH, four of which were treated successfully with dantrolene, and the remaining one recovered with only symptomatic therapy. After weighing its questionable benefits against its possible adverse effects (including nausea, vomiting, muscle weakness and prolonged duration of action of nondepolarizing neuromuscular blocking agents), experts no longer recommend the use of prophylactic dantrolene prior to trigger-free general anesthesia in MH-susceptible patients.

Case reports and small randomized studies suggest benzodiazepines, propranolol, and anticholinergics may help treat acute akathisia, but are much less effective in treating chronic akathisia. Taylor et al. found success in lowering the dose of antipsychotic medication as an initial response to drug-induced akathisia, which should be done gradually, if possible. To minimize the risk of akathisia from antipsychotics, the clinician is advised to be conservative when increasing dosages.

One study showed vitamin B to be effective for the treatment of neuroleptic-induced akathisia.

Additional pharmacologic interventions found to have antiakathisia effects (especially for neuroleptic-induced akathisia) include ß-adrenergic antagonists (e.g., propranolol), benzodiazepines (e.g., lorazepam), anticholinergics (e.g., benztropine), and serotonin antagonists (e.g., cyproheptadine) as an alternative.

Initial treatment is aimed at providing symptomatic relief. Benzodiazepines are the first line of treatment, and high doses are often required. A test dose of intramuscular lorazepam will often result in marked improvement within half an hour. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.

Electroconvulsive therapy (ECT) is an effective treatment for catatonia. Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.

Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine are used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. Topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors.

Dantrolene is a muscle relaxant that appears to work directly on the ryanodine receptor to prevent the release of calcium. After the widespread introduction of treatment with dantrolene, the mortality of malignant hyperthermia fell from 80% in the 1960s to less than 5%. Dantrolene remains the only drug known to be effective in the treatment of MH. It is recommended that each hospital keeps a minimum stock of 36 dantrolene vials (720 mg) sufficient for a 70-kg person.

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.

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 evidence-based criteria for treating SPS, and there have been no large controlled trials of treatments for the condition. The rarity of the disease complicates efforts to establish guidelines.

GABA agonists, usually diazepam but sometimes other benzodiazepines, are the primary treatment for SPS. Drugs that increase GABA activity alleviate muscle stiffness caused by a lack of GABAergic tone. They increase pathways that are dependent upon GABA and have muscle relaxant and anticonvulsant effects, often providing symptom relief. Because the condition worsens over time, patients generally require increased dosages, leading to more side effects. For this reason, gradual increase in dosage of benzodiazepines is indicated. Baclofen, a GABA agonist, is generally used when individuals taking high doses of benzodiazepines have high side effects. In some cases it has shown improvements in electrophysiological and muscle stiffness when administered intravenously. Intrathecal baclofen administration may not have long-term benefits though, and there are potential serious side effects.

Treatments that target the autoimmune response are also used. Intravenous immunoglobin is the best second-line treatment for SPS. It often decreases stiffness and improves quality of life and startle reflex. It is generally safe, but there are possible serious side effects and it is expensive. The European Federation of Neurological Societies suggests it be used when disabled patients do not respond well to diazepam and baclofen. Steroids, rituximab, and plasma exchange have been used to suppress the immune system in SPS patients, but the efficacy of these treatments is unclear. Botulinum toxin has been used to treat SPS, but it does not appear to have long-term benefits and has potential serious side effects. In paraneoplastic cases, tumors must be managed for the condition to be contained. Opiates are sometimes used to treat severe pain, but in some cases they exacerbate symptoms.

Drug treatment is indicated for patients with severe disabling chorea. It is treated with haloperidol, chlorpromazine alone or in combination with diazepam, and also pimozide, which is another neuroleptic drug which may have fewer adverse effects than haloperidol. Valproic acid, chloral hydrate, risperidone, or phenobarbital can also be used.

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 underlying cause must be removed. Mild hyperthemia caused by exertion on a hot day may be adequately treated through self-care measures, such as increased water consumption and resting in a cool place. Hyperthermia that results from drug exposure requires prompt cessation of that drug, and occasionally the use of other drugs as counter measures. Antipyretics (e.g., acetaminophen, aspirin, other nonsteroidal anti-inflammatory drugs) have no role in the treatment of heatstroke because antipyretics interrupt the change in the hypothalamic set point caused by pyrogens; they are not expected to work on a healthy hypothalamus that has been overloaded, as in the case of heatstroke. In this situation, antipyretics actually may be harmful in patients who develop hepatic, hematologic, and renal complications because they may aggravate bleeding tendencies.

When body temperature is significantly elevated, mechanical cooling methods are used to remove heat and to restore the body's ability to regulate its own temperatures. Passive cooling techniques, such as resting in a cool, shady area and removing clothing can be applied immediately. Active cooling methods, such as sponging the head, neck, and trunk with cool water, remove heat from the body and thereby speed the body's return to normal temperatures. Drinking water and turning a fan or dehumidifying air conditioning unit on the affected person may improve the effectiveness of the body's evaporative cooling mechanisms (sweating).

Sitting in a bathtub of tepid or cool water (immersion method) can remove a significant amount of heat in a relatively short period of time. It was once thought that immersion in very cold water is counterproductive, as it causes vasoconstriction in the skin and thereby prevents heat from escaping the body core. However, a British analysis of various studies stated: "this has never been proven experimentally. Indeed, a recent study using normal volunteers has shown that cooling rates were fastest when the coldest water was used." The analysis concluded that cool water immersion is the most-effective cooling technique for exertional heat stroke. No superior cooling method has been found for non-exertional heat stroke. Thus, aggressive ice-water immersion remains the gold standard for life-threatening heat stroke.

When the body temperature reaches about 40 °C, or if the affected person is unconscious or showing signs of confusion, hyperthermia is considered a medical emergency that requires treatment in a proper medical facility. In a hospital, more aggressive cooling measures are available, including intravenous hydration, gastric lavage with iced saline, and even hemodialysis to cool the blood.

5-HT receptor antagonists are very effective antiemetics and constitute a great advance in the management of CINV. These drugs block one or more of the nerve signals that cause nausea and vomiting. During the first 24 hours after chemotherapy, the most effective approach appears to be blocking the 5-HT nerve signal. Approved 5-HT inhibitors include dolasetron (Anzemet), granisetron (Kytril, Sancuso), and ondansetron (Zofran). Their antiemetic effect due to blockade of 5HT3 receptor on vagal afferent in the gut. in addition they also block 5-HT3 receptors in CTZ and STN. The newest 5-HT inhibitor, palonosetron (Aloxi), also prevents delayed nausea and vomiting, which can occur during the 2–5 days after treatment. Since some patients have trouble swallowing pills, these drugs are often available by injection, as orally disintegrating tablets, or as transdermal patches.

Olanzapine, as well as several other neuroleptic drugs, have also has been investigated for the control of CINV. A 2007 study demonstrated Olanzapine's successful potential for this use, achieving a complete response in the acute prevention of nausea and vomiting in 100% of patients treated with moderately and highly emetogenic chemotherapy, when used in combination with palonosetron and dexamethasone. Neuroleptic agents are now indicated for rescue treatment and the control of breakthrough nausea and vomiting.

Some studies and patient groups say that the use of cannabinoids derived from cannabis during chemotherapy greatly reduces the associated nausea and vomiting, and enables the patient to eat. Synthesized tetrahydrocannabinol (also one of the main active substances in marijuana) is marketed as Marinol and may be practical for this application. Natural medical cannabis is also used and recommended by some oncologists, though its use is regulated and it is not legal in all jurisdictions. However, Marinol was less effective than megestrol acetate in helping cancer patients regain lost appetites. A phase III study found no difference in effects of an oral cannabis extract or THC on appetite and quality of life (QOL) in patients with cancer-related anorexia-cachexia syndrome (CACS) to placebo.

Dexamethasone, a corticosteroid, is often used alongside other antiemetic drugs, as it has synergistic action with many of them, although its specific antiemetic mechanism of action is not fully understood. Metoclopramide, a dopamine D receptor antagonist with possible other mechanisms, is an older drug that is sometimes used, either on its own or in combination with others. Histamine blockers such as diphenhydramine or meclozine may be used in rescue treatment. Lorazepam and diazepam may sometimes be used to relieve anxiety associated with CINV before administration of chemotherapy, and are also often used in the case of rescue treatment.

Prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time. However, with diseases of chronic psychosis such as schizophrenia, this strategy must be balanced with the fact that increased dosages of neuroleptics are more beneficial in preventing recurrence of psychosis. If tardive dyskinesia is diagnosed, the causative drug should be discontinued. Tardive dyskinesia may persist after withdrawal of the drug for months, years or even permanently. Some studies suggest that physicians should consider using atypical antipsychotics as a substitute to typical antipsychotics for patients requiring medication. These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia.

Recent studies have tested the use of melatonin, high dosage vitamins, and different antioxidants in concurrence with antipsychotic drugs (often used to treat schizophrenia) as a way of preventing and treating tardive dyskinesia. Although further research is needed, studies reported a much lower percentage of individuals developing tardive dyskinesia than the current prevalence rate for those taking antipsychotic drugs.

Pharmaceutical management, as with Parkinson's disease, involves striking a balance between treating the motor, emotive, and cognitive symptoms. Motor symptoms appear to respond somewhat to the medications used to treat Parkinson's disease (e.g. levodopa), while cognitive issues may improve with medications for Alzheimer's disease such as donepezil. Medications used in the treatment of ADHD (e.g. methylphenidate) might improve cognition or daytime sleepiness; however, medications for both Parkinson's disease and ADHD increase levels of the chemical dopamine in the brain, so increase the risk of hallucinations with those classes of pharmaceuticals.

Treatment of the movement and cognitive portions of the disease may worsen hallucinations and psychosis, while treatment of hallucinations and psychosis with antipsychotics may worsen parkinsonian or ADHD symptoms in DLB, such as tremor or rigidity and lack of concentration or impulse control. Physicians may find the use of cholinesterase inhibitors represents the treatment of choice for cognitive problems and donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) may be recommended as a means to help with these problems and to slow or prevent the decline of cognitive function. DLB may be more responsive to donepezil than Alzheimer's disease. Memantine also may be useful. Levocarb may help with movement problems, but in some cases, as with dopamine agonists, may tend to aggravate psychosis in people with DLB. Clonazepam may help with rapid eye movement behavior disorder; table salt or antihypotensive medications may help with fainting and other problems associated with orthostatic hypotension. Botulinum toxin injections in the parotid glands may help with sialorrhea. Other medications, especially stimulants such as the ADHD drug methylphenidate (Ritalin) and modafinil, may improve daytime alertness, but as with the antiparkinsonian drug Levocarb, antihyperkinetics such as Ritalin increase the risk of psychosis. Experts advise extreme caution in the use of antipsychotic medication in people with DLB because of their sensitivity to these agents. When these medications must be used, atypical antipsychotics are preferred to typical antipsychotics; a very low dose should be tried initially and increased slowly, and patients should be carefully monitored for adverse reactions to the medications.

Due to hypersensitivity to neuroleptics, preventing DLB patients from taking these medications is important. People with DLB are at risk for neuroleptic malignant syndrome, a life-threatening illness, because of their sensitivity to these medications, especially the older typical antipsychotics, such as haloperidol. Other medications, including medications for urinary incontinence and the antihistamine medication diphenhydramine (Benadryl), also may worsen confusion.

No cure for dementia with Lewy bodies is known. Treatment may offer symptomatic benefit, but remains palliative in nature. Current treatment modalities are divided into pharmaceutical and caregiving.