Intramuscular midazolam, lorazepam, or another benzodiazepine can be used to both sedate agitated patients, and control semi-involuntary muscle movements in cases of suspected akathisia.

Droperidol, haloperidol, or other typical antipsychotics can decrease the duration of agitation caused by acute psychosis, but should be avoided if the agitation is suspected to be akathisia, which can be potentially worsened. Also using promethazine may be useful.

In those with psychosis causing agitation there is a lack of support for the use of benzodiazepines, although they can prevent side effects associated with dopamine antagonists.

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.

The treatment for delirium with medications depends on its cause. Antipsychotics, particularly haloperidol, are the most commonly used drugs for delirium and the most studied. Evidence is weaker for the atypical antipsychotics, such as risperidone, olanzapine and quetiapine. British professional guidelines by the National Institute for Health and Clinical Excellence advise haloperidol or olanzapine. Antipsychotics however are not supported for the treatment or prevention of delirium among those who are in hospital.

Benzodiazepines themselves can cause delirium or worsen it, and there is no reliable evidence for use in non-alcohol-related delirium. If delirium is due to alcohol withdrawal or benzodiazepine withdrawal or if antipsychotics are contraindicated (e.g. in Parkinson's disease or neuroleptic malignant syndrome), then benzodiazepines are recommended. Similarly, people with dementia with Lewy bodies may have significant side-effects to antipsychotics, and should either be treated with a small dose or not at all.

The antidepressant trazodone is occasionally used in the treatment of delirium, but it carries a risk of oversedation, and its use has not been well studied.

Delirium tremens due to alcohol withdrawal can be treated with benzodiazepines. High doses may be necessary to prevent death. Amounts given are based on the symptoms. Typically the person is kept sedated with benzodiazepines, such as diazepam, lorazepam, chlordiazepoxide, or oxazepam.

In some cases antipsychotics, such as haloperidol may also be used. Older drugs such as paraldehyde and clomethiazole were formerly the traditional treatment but have now largely been superseded by the benzodiazepines.

Acamprosate is occasionally used in addition to other treatments, and is then carried on into long term use to reduce the risk of relapse. If status epilepticus occurs it is treated in the usual way. It can also be helpful to control environmental stimuli, by providing a well-lit but relaxing environment for minimizing distress and visual hallucinations.

Alcoholic beverages can also be prescribed as a treatment for delirium tremens, but this practice is not universally supported.

High doses of thiamine often by the intravenous route is also recommended.

Treatment initially may include ketamine or midazolam and haloperidol injected into a muscle to sedate the person. Rapid cooling may be required in those with high body temperature. Other supportive measures such as intravenous fluids and sodium bicarbonate may be useful.

Treatment consists of supportive care during the acute intoxication phase: maintaining hydration, body temperature, blood pressure, and heart rate at acceptable levels until the drug is sufficiently metabolized to allow vital signs to return to baseline. Typical and atypical antipsychotics have been shown to be helpful in the early stages of treatment. This is followed by abstinence from psychostimulants supported with counseling or medication designed to assist the individual preventing a relapse and the resumption of a psychotic state.

Discontinuation syndrome is often prevented by taking medication as directed, and when discontinuing, doing so gradually. When discontinuing an antidepressant with a short half-life, switching to a drug with a longer half-life (e.g. fluoxetine or citalopram) and then discontinuing from that drug can decrease the likelihood and severity of symptoms.

Treatment is dependent on the severity of the discontinuation reaction and whether or not further antidepressant treatment is warranted. In cases where further antidepressant treatment is required then the only step required is restarting the antidepressant; this is usually the case following patient noncompliance with the drug. If antidepressants are no longer required, treatment depends on symptom severity. Mild reactions may only require reassurance. Moderate cases may require symptom management. If symptoms of discontinuation are severe, or do not respond to symptom management, the antidepressant can be reinstated and then withdrawn more cautiously. In rare but severe cases, hospitalization may be required.

Treatment of delirium involves two main strategies: first, treatment of the underlying presumed acute cause or causes; secondly, optimising conditions for the brain. This involves ensuring that the person with delirium has adequate oxygenation, hydration, nutrition, and normal levels of metabolites, that drug effects are minimised, constipation treated, pain treated, and so on. Detection and management of mental stress is also important. Therefore, the traditional concept that the treatment of delirium is 'treat the cause' is not adequate; people with delirium require a highly detailed and expert analysis of all the factors which might be disrupting brain function.

Non medication treatments are the first measure in delirium, unless there is severe agitation that places the person at risk of harming oneself or others. Avoiding unnecessary movement, involving family members, having recognizable faces at the bedside, having means of orientation available (such as a clock and a calendar) may be sufficient in stabilizing the situation. If this is insufficient, verbal and non-verbal de-escalation techniques may be required to offer reassurances and calm the person experiencing delirium. Only if this fails, or if de-escalation techniques are inappropriate, is pharmacological treatment indicated.

“The T-A-DA method (tolerate, anticipate, don't agitate)” can be an effective management technique for older people with delirium. All unnecessary attachments are removed (IVs, catheters, NG tubes) which allows for greater mobility. Patient behavior is tolerated even if it is not considered normal as long as it does not put the patient or other people in danger. This technique requires that patients are isolated in a specific area designated for patients of old age dealing with symptoms of delirium. Patient behavior is anticipated so care givers can plan required care. Patients are treated to reduce agitation. Reducing agitation may mean that patients are not reoriented if reorientation causes agitation.

Physical restraints are occasionally used as a last resort with patients in a severe delirium. Restraint use should be avoided as it can increase agitation and risk of injury. In order to avoid the use of restraints some patients may require constant supervision.

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.

Treatment is effective in about 80% of identified cases, when treatment is provided. Effective management requires a biopsychosocial approach, combining pharmacotherapy and psychotherapy. Therapy generally results in improved quality of life, enhanced functional capacity, possible improvement in medical health status, increased longevity, and lower health care costs. Improvement should be evident as early as two weeks after the start of therapy, but full therapeutic effects may require several months of treatment. Psychotherapy and medication are the two primary treatment approaches.Therapy for older patients should be continued for longer periods than are typically used in younger patients.

Pharmacotherapy for acute episodes of depression usually is effective and free of complications. Underuse or misuse of antidepressants and prescribing inadequate dosages are the most common mistakes physicians make when treating elderly patients for depression. Only 10 to 40 percent of depressed elderly patients are given medication. Antidepressants, in general, may also work by playing a neuroprotective role in how they relieve anxiety and depression. It's thought that antidepressants may increase the effects of brain receptors that help nerve cells keep sensitivity to glutamate which is an organic compound of a nonessential amino acid. This increased support of nerve cells lowers glutamate sensitivity, providing protection against the glutamate overwhelming and exciting key brain areas related to depression. Antidepressant medications are often the first treatment choice for adults with moderate or severe depression, sometimes along with psychotherapy. Although antidepressants may not cure depression, they can lead to remission, which is the disappearance or nearly complete reduction of depression symptoms.

The most common treatment for reducing bipolar II disorder symptoms is medication, usually in the form of mood stabilizers. However, treatment with mood stabilizers may produce a flat affect in the patient, which is dose-dependent. Concurrent use of SSRI antidepressants may help some with bipolar II disorder, though these medications should be used with caution because it is believed that they may cause a hypomanic switch.

The pharmaceutical management of bipolar II disorder is not generally supported by strong evidence, with limited randomised controlled trials (RCTs) published in the literature. Some medications used are:

- Lithium - There is strong evidence that lithium is effective in treating both the depressive and hypomanic symptoms in bipolar II. In addition, its action as a mood stabilizer can be used to decrease the risk of hypomanic switch in patients treated with antidepressants.

- Anticonvulsants - there is evidence that lamotrigine decreases the risk of relapse in rapid cycling bipolar II. It appears to be more effective in bipolar II than bipolar I, suggesting that lamotrigine is more effective for the treatment of depressive rather than manic episodes. Doses ranging from 100–200 mg have been reported to have the most efficacy, while experimental doses of 400 mg have rendered little response. A large, multicentre trial comparing carbamazepine and lithium over two and a half years found that carbamazepine was superior in terms of preventing future episodes of bipolar II, although lithium was superior in individuals with bipolar I. There is also some evidence for the use of valproate and topiramate, although the results for the use of gabapentin have been disappointing.

- Antidepressants - there is evidence to support the use of SSRI and SNRI antidepressants in bipolar II. Indeed, some sources consider them to be one of the first line treatments. However, antidepressants also pose significant risks, including a switch to mania, rapid cycling, and dysphoria and so many psychiatrists advise against their use for bipolar. When used, antidepressants are typically combined with a mood stabilizer.

- Antipsychotics - there is good evidence for the use of quetiapine, and it has been approved by the FDA for this indication. There is also some evidence for the use of risperidone, although the relevant trial was not placebo controlled and was complicated by the use of other medications in some of the patients.

- Dopamine agonists - there is evidence for the efficacy of pramipexole from one RCT.

If there is evidence of overdose or it is suspected, the patient should be given gastric lavage, activated charcoal, or both; this could make the difference between life and death in a close situation. It can however aggravate the patient which should be taken into account.

The first line treatments are diazepam and a non-selective beta blocker; other antihypertensive drugs may also be used. It is important to note that not all benzodiazepines and beta blockers are safe to use in an adrenergic storm; for instance, alprazolam and propranolol; alprazolam weakly agonizes dopamine receptors and causes catecholamine release while propranolol mildly promotes some catecholamine release - each worsening the condition.

Adrenergic storms are often idiopathic in nature; however if there is an underlying condition, then that must be addressed after bringing the heart rate and blood pressure down.

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.

Treatment typically includes three things: the treatment of acute hypomania, the treatment of acute depression, and the prevention of the relapse of either hypomania or depression. The main goal is to make sure that patients do not harm themselves.

Symptoms can last for more than 4 weeks and typically resolve within a day of restoring the medication.

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.

Involutional melancholia is classically treated with antidepressants and mood elevators.

Electroconvulsive therapy may also be used. Mid-century, there was a consensus that the technique indeed 'yields the best results in the long-lasting depressions of the change of life, the so-called "involutional melancholias", which before this form of treatment was introduced often required years of hospitalization'. The 21st century also records 'an excellent and rapid clinical response found in melancholia of recent onset...in older rather than younger patients' with ECT

Treatment of mixed states is typically based upon administration of mood stabilizing medication, which may include anticonvulsants such as valproic acid; atypical antipsychotics such as olanzapine, aripiprazole, and ziprasidone; or first-generation antipsychotics such as haloperidol. There is question of lithium's efficacy for treatment of mixed states due to conflicting conclusions drawn from various trials and research. Mood stabilizers work to reduce the manic symptoms associated with the mixed state, but they are not considered particularly effective for improving concurrent depressive symptoms.

Immediate treatment of drug induced OGC can be achieved with intravenous antimuscarinic benzatropine or procyclidine; which usually are effective within 5 minutes, although may take as long as 30 minutes for full effect. Further doses of procyclidine may be needed after 20 minutes. Any causative new medication should be discontinued. Also can be treated with 25 mg diphenhydramine.

Treatment of any kind of complex visual hallucination requires an understanding of the different pathologies in order to correctly diagnose and treat. If a person is taking a pro-hallucinogenic medication, the first step is to stop taking it. Sometimes improvement will occur spontaneously and pharmacotherapy is not necessary. While there is not a lot of evidence of effective pharmacological treatment, antipsychotics and anticonvulsants have been used in some cases to control hallucinations. Since peduncular hallucinosis occurs due to an excess of serotonin, modern antipsychotics are used to block both dopamine and serotonin receptors, preventing the overstimulation of the lateral geniculate nucleus. The drug generically called carbamazepine increases GABA, which prevents the LGN from firing, thereby increasing the inhibition of the LGN. Regular antipsychotics as well as antidepressants can also be helpful in reducing or eliminating peduncular hallucinosis.

More invasive treatments include corrective surgery such as cataract surgery, laser photocoagulation of the retina, and use of optical correcting devices. Tumor removal can also help to relieve compression in the brain, which can decrease or eliminate peduncular hallucinosis. Some hallucinations may be due to underlying cardiovascular disease, so in these cases the appropriate treatment includes control of hypertension and diabetes. As described, the type of treatment varies widely depending on the causation behind the complex visual hallucinations.

Clonidine may be used in combination with benzodiazepines to help some of the symptoms. There is insufficient evidence to support the use of baclofen for alcohol withdrawal syndrome.

Antipsychotics, such as haloperidol, are sometimes used in addition to benzodiazepines to control agitation or psychosis. Antipsychotics may potentially worsen alcohol withdrawal as they lower the seizure threshold. Clozapine, olanzapine, or low-potency phenothiazines (such as chlorpromazine) are particularly risky; if used, extreme caution is required.

While intravenous ethanol could theoretically be used, evidence to support this use, at least in those who are very sick, is insufficient.

The use of lithium and quetiapine (Seroquel) have both shown to be particularly valuable, though several other medications of the anticonvulsants and atypical antipsychotics classes may also be helpful.

- Lithium – Lithium has been shown to help stabilize the mood of patients suffering from cyclothymia and as well as bipolar disorders. It also aids in the prevention of acute suicidal and manic episodes. Dosage must be carefully monitored as lithium has a plethora of side effects.

- Atypical antipsychotics – (e.g., quetiapine (Seroquel), also olanzapine (Zyprexa), and risperidone (Risperdal).

- Anticonvulsants – (e.g., valproic acid, lamotrigine (Lamictal), and valproate semisodium (Depakote)).

- Electroconvulsive therapy – Through a systematic review done by Versiani, Cheriaux, and Landeira-Fernandez, it was determined that the efficacy and safety of ECT in patients with bipolar disorder had been poorly investigated and the evidence had methodological limitations.

There are three medications used to help prevent a return to drinking: disulfiram, naltrexone, and acamprosate. They are used after withdrawal has occurred.

There is limited evidence that caffeine, in high doses or when chronically abused, may induce psychosis in normal individuals and worsen pre-existing psychosis in those diagnosed with schizophrenia.