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.

The treatment of psychosis depends on the specific diagnosis (such as schizophrenia, bipolar disorder or substance intoxication). The first-line psychiatric treatment for many psychotic disorders is antipsychotic medication, which can reduce the positive symptoms of psychosis in about 7 to 14 days.

The choice of which antipsychotic to use is based on benefits, risks, and costs. It is debatable whether, as a class, typical or atypical antipsychotics are better. Tentative evidence supports that amisulpride, olanzapine, risperidone and clozapine may be more effective for positive symptoms but result in more side effects. Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages. There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people. Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia), but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people.

Most people on antipsychotics get side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects while some atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain. Risperidone has a similar rate of extrapyramidal symptoms to haloperidol.

Psychological treatments such as acceptance and commitment therapy (ACT) are possibly useful in the treatment of psychosis, helping people to focus more on what they can do in terms of valued life directions despite challenging symptomology.

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.

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.

There are few treatments for many types of hallucinations. However, for those hallucinations caused by mental disease, a psychologist or psychiatrist should be alerted, and treatment will be based on the observations of those doctors. Antipsychotic and atypical antipsychotic medication may also be utilized to treat the illness if the symptoms are severe and cause significant distress. For other causes of hallucinations there is no factual evidence to support any one treatment is scientifically tested and proven. However, abstaining from hallucinogenic drugs, stimulant drugs, managing stress levels, living healthily, and getting plenty of sleep can help reduce the prevalence of hallucinations. In all cases of hallucinations, medical attention should be sought out and informed of one's specific symptoms.

An open study of cognitive behavior therapy has aimed to help patients reinterpret their symptoms in a nonthreatening way, leading to an improvement on several standardized measures. A standardized treatment for DPD based on cognitive behavioral principles was published in The Netherlands in 2011.

Primary depersonalization disorder is mostly refractory to current treatments. The disorder lacks effective treatment in part because it has been neglected within the field of psychiatry, which, in turn, is partly because funding has mainly been allocated to the search for cures of other illnesses, like alcoholism. However, recognizing and diagnosing the condition may in itself have therapeutic benefits, considering many patients express their problems as baffling and unique to them, but are in fact: one, recognized and described by psychiatry; and two, those affected by it are not the only individuals to be affected from the condition. A variety of psychotherapeutic techniques have been used to treat depersonalization disorder, such as cognitive behavioral therapy. Clinical pharmacotherapy research continues to explore a number of possible options, including selective serotonin reuptake inhibitors, tricyclic antidepressants, anticonvulsants, and opioid antagonists.

There are different types of treatments available for mood disorders, such as therapy and medications. Behaviour therapy, cognitive behaviour therapy and interpersonal therapy have all shown to be potentially beneficial in depression. Major depressive disorder medications usually include antidepressants, while bipolar disorder medications can consist of antipsychotics, mood stabilizers, anticonvulsants and/or lithium. Lithium specifically has been proven to reduce suicide and all causes of mortality in people with mood disorders. If mitochondrial dysfunction or mitochondrial diseases are the cause of mood disorders like bipolar disorder, then it has been hypothesized that N-acetyl-cysteine (NAC), acetyl-L-carnitine (ALCAR), S-adenosylmethionine (SAMe), coenzyme Q10 (CoQ10), alpha-lipoic acid (ALA), creatine monohydrate (CM), and melatonin could be potential treatment options.

Oneirophrenic patients are resistant to insulin and when injected with glucose, these patients take 30 to 50% longer to return to normal glycemia. The meaning of this finding is not known, but it has been hypothesized that it may be due to an insulin antagonist present in the blood during psychosis. However, There is currently no known treatment for oneiophrenia.

Generally, a person experiencing a psychedelic crisis can be helped either to resolve the impasse, to bypass it, or, failing that, to terminate the experience. A person's thoughts before taking or while under the influence of the psychedelic, often greatly influence the trip.

Medical treatment consists of supportive therapy and minimization of external stimuli. In some cases, sedation is used when necessary to control self-destructive behavior, or when hyperthermia occurs. Diazepam is the most frequently used sedative for such treatment, but other benzodiazepines such as lorazepam are also effective. Such sedatives will only decrease fear and anxiety, but will not subdue hallucinations. In severe cases, antipsychotics such as haloperidol can reduce or stop hallucinations. Haloperidol is effective against drug-induced psychosis caused by LSD and other tryptamines, amphetamines, ketamine and phencyclidine.

Often in those who have experienced their first episode of hypomania – generally without psychotic features – there may be a long or recent history of depression or a mix of hypomania combined with depression (known as mixed-state) prior to the emergence of manic symptoms. This commonly surfaces in the mid to late teens. Because the teenage years are typically an emotionally charged time of life, it is not unusual for mood swings to be passed off as normal hormonal teen behavior and for a diagnosis of bipolar disorder to be missed until there is evidence of an obvious manic or hypomanic phase.

Hypomania may also occur as a side effect of pharmaceuticals prescribed for conditions or diseases other than psychological states or mood disorders. In those instances, as in cases of drug-induced hypomanic episodes in unipolar depressives, the hypomania can almost invariably be eliminated by lowering medication dosage, withdrawing the drug entirely, or changing to a different medication if discontinuation of treatment is not possible.

Hypomania may also be triggered by the occurrence of a highly exciting event in the patient's situation, such as a substantial financial gain or recognition.

Hypomania can be associated with narcissistic personality disorder.

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.

The code F11.5 is reserved for opioid-induced psychosis, and F17.5 is reserved for tobacco-induced psychosis, but neither substance is traditionally associated with the induction of psychosis.

The code F15.5 also includes caffeine-induced psychosis, despite not being specifically listed in the DSM-IV. However, there is evidence that caffeine, in extreme acute doses or when severely abused for long periods of time, may induce psychosis.

Hypomania (literally "under mania" or "less than mania") is a mood state characterized by persistent disinhibition and elevation (euphoria). It may involve irritation, but less severely than full mania. According to DSM-V criteria, hypomania is distinct from mania in that there is no significant functional impairment; mania, by DSM-V definition, does include significant functional impairment and may have psychotic features.

Characteristic behaviors of persons experiencing hypomania are a notable decrease in the need for sleep, an overall increase in energy, unusual behaviors and actions, and a markedly distinctive increase in talkativeness and confidence, commonly exhibited with a flight of creative ideas. Other symptoms related to this may include feelings of grandiosity, distractibility, and hypersexuality. While hypomanic behavior often generates productivity and excitement, it can become troublesome if the subject engages in risky or otherwise inadvisable behaviors, and/or the symptoms manifest themselves in trouble with everyday life events. When manic episodes are separated into stages of a progression according to symptomatic severity and associated features, hypomania constitutes the first stage of the syndrome, wherein the cardinal features (euphoria or heightened irritability, pressure of speech and activity, increased energy, decreased need for sleep, and flight of ideas) are most plainly evident.

Only a small proportion of those with co-occurring disorders actually receive treatment for both disorders. Therefore, it was argued that a new approach is needed to enable clinicians, researchers and managers to offer adequate assessment and evidence-based treatments to patients with dual pathology, who cannot be adequately and efficiently managed by cross-referral between psychiatric and addiction services as currently configured and resourced. In 2011, it was estimated that only 12.4% of American adults with co-occurring disorders were receiving both mental health and addictions treatment. Clients with co-occurring disorders face challenges accessing treatment, as they may be excluded from mental health services if they admit to a substance abuse problem, and vice versa.

There are multiple approaches to treating concurrent disorders. Partial treatment involves treating only the disorder that is considered primary. Sequential treatment involves treating the primary disorder first, and then treating the secondary disorder after the primary disorder has been stabilized. Parallel treatment involves the client receiving mental health services from one provider, and addictions services from another.

Integrated treatment involves a seamless blending of interventions into a single coherent treatment package developed with a consistent philosophy and approach among care providers. With this approach, both disorders are considered primary. Integrated treatment can improve accessibility, service individualization, engagement in treatment, treatment compliance, mental health symptoms, and overall outcomes. The Substance Abuse and Mental Health Services Administration in the United States describes integrated treatment as being in the best interests or clients, programs, funders, and systems. Green suggested that treatment should be integrated, and a collaborative process between the treatment team and the patient. Furthermore, recovery should to be viewed as a marathon rather than a sprint, and methods and outcome goals should be explicit.

Although many patients may reject medications as antithetical to substance-abuse recovery and side effects, they can be useful to reduce paranoia, anxiety, and craving. Medications that have proven effective include opioid replacement therapies, such as lifelong maintenance on methadone or buprenorphine, to minimize risk of relapse, fatality, and legal trouble amongst opioid addicts, as well as helping with cravings, baclofen for alcoholics, opioid addicts, cocaine addicts, and amphetamine addicts, to help eliminate drug cravings, and clozapine, the first atypical antipsychotic, which appears to reduce illicit drug use amongst stimulant addicts. Clozapine can cause respiratory arrest when combined with alcohol, benzodiazepines, or opioids, so it is not recommended to use in these groups.

Catatonia is a state of psycho-motor immobility and behavioral abnormality manifested by stupor. It was first described in 1874 by Karl Ludwig Kahlbaum, in ("Catatonia or Tension Insanity").

Though catatonia has historically been related to schizophrenia (catatonic schizophrenia), it is now known that catatonic symptoms are nonspecific and may be observed in other mental disorders and neurological conditions. In the fifth edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM), catatonia is not recognized as a separate disorder, but is associated with psychiatric conditions such as schizophrenia (catatonic type), bipolar disorder, post-traumatic stress disorder, depression and other mental disorders, narcolepsy, as well as drug abuse or overdose (or both). It may also be seen in many medical disorders including infections (such as encephalitis), autoimmune disorders, focal neurologic lesions (including strokes), metabolic disturbances, alcohol withdrawal and abrupt or overly rapid benzodiazepine withdrawal. In the fifth edition of the DSM, it is written that a variety of medical conditions may cause catatonia, especially neurological conditions: encephalitis, cerebrovascular disease, neoplasms, head injury. Moreover, metabolic conditions: homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, hypercalcaemia.

It can be an adverse reaction to prescribed medication. It bears similarity to conditions such as encephalitis lethargica and neuroleptic malignant syndrome. There are a variety of treatments available; benzodiazepines are a first-line treatment strategy. Electroconvulsive therapy is also sometimes used. There is growing evidence for the effectiveness of NMDA receptor antagonists for benzodiazepine-resistant catatonia. Antipsychotics are sometimes employed but require caution as they can worsen symptoms and have serious adverse effects.

Chronic hallucinatory psychosis is a psychosis subtype, classified under "Other nonorganic psychosis" by the . Other abnormal mental symptoms in the early stages are, as a rule, absent. The patient is most usually quiet and orderly, with a good memory.

It has often been a matter of the greatest difficulty to decide under which heading of the recognized classifications individual members of this group should be placed. As the hallucinations give rise to slight depression, some might possibly be included under melancholia. In others, paranoia may develop. Others, again, might be swept into the widespread net of dementia praecox. This state of affairs cannot be regarded as satisfactory, for they are not truly cases of melancholia, paranoia, dementia praecox or any other described affection.

This disease, as its name suggests, is a hallucinatory case, for it is its main feature. These may be of all senses, but auditory hallucinations are the most prominent. At the beginning, the patient may realize that the hallucination is a morbid phenomenon and unaccountable. They may claim to hear a "voice" speaking, though there is no one in the flesh actually doing so. Such a state of affairs may last for years and possibly, though rarely, for life, and the subject would not be deemed insane in the ordinary sense of the word.

It's probable, however, that this condition forms the first stage of the illness, which eventually develops on definite lines. What usually happens is the patient seeks an explanation for the hallucinations. As none is forthcoming he/she tries to account for their presence and the result is a delusion, and, most frequently, a delusion of persecution. Also, it needs to be noted that the delusion is a comparatively late arrival and is the logical result of the hallucinations.

Psychosis manifests as disorientation, visual hallucinations and/or haptic hallucinations. It is a state in which a person's mental capacity to recognize reality, communicate, and relate to others is impaired, thus interfering with the capacity to deal with life demands. While there are many types of psychosis, substance-induced psychosis can be pinpointed to specific chemicals.

There are symptoms that are mechanism-based that are associated with hallucinations. These include superficial pressure and stabbing pain. Others include a burning-like sensation or electric shock feeling. Human studies of these symptoms remain mostly unclear unlike similar studies in animals.

There have been no clinical trials to show that any psychological or pharmacological intervention is effective in preventing sleepwalking episodes. Despite this, a wide range of treatments have been used with sleepwalkers. Psychological interventions have included psychoanalysis, hypnosis, scheduled or anticipatory waking, assertion training, relaxation training, managing aggressive feelings, sleep hygiene, classical conditioning (including electric shock), and play therapy. Pharmacological treatments have included an anticholinergic (biperiden), antiepileptics (carbamazepine, valproate), an antipsychotic (quetiapine), benzodiazepines (clonazepam, diazepam, flurazepam, imipramine, and triazolam), melatonin, a selective serotonin reuptake inhibitor (paroxetine), a barbiturate (sodium amytal) and herbs.

There is no evidence about whether waking sleepwalkers is harmful or not, though the sleepwalker is likely to be disoriented if awakened because sleepwalking occurs during the deepest stage of sleep.

Unlike other sleep disorders, sleepwalking is not associated with daytime behavioral or emotional problems—this may be because the sleepwalker's sleep is not disturbed—unless they are woken, they are still in a sleep state while sleepwalking.

Maintaining the safety of the sleepwalker and others and seeking treatment for other sleep problems is recommended. Reassurance is recommended if sleepwalking is not causing any problems. However, if it causes distress or there is risk of harm, hypnosis and scheduled waking are recommended as treatments.

Oneirophrenia was studied in the 1950s by the neurologist and psychiatrist Ladislas J. Meduna (1896–1964), also known as the discoverer of one of the forms of shock therapy, using the drug metrazol. Although oneirophrenia was recognized as a specific condition in the 1950's, it was not studied in depth until the 1960s. During its beginning stages oneriophrenia was studied very closely with schizophrenia as an acute form due to the relationship between their symptoms. It wasn't until greater research that oneirophrenia became its own mental disease.

Palinopsia from cerebrovascular accidents generally resolves spontaneously, and treatment should be focused on the vasculopathic risk factors. Palinopsia from neoplasms, AVMs, or abscesses require treatment of the underlying condition, which usually also resolves the palinopsia. Palinopsia due to seizures generally resolves after correcting the primary disturbance and/or treating the seizures. In persistent hallucinatory palinopsia, a trial of an anti-epileptic drug can be attempted. Anti-epileptics reduce cortical excitability and could potentially treat palinopsia caused by cortical deafferentation or cortical irritation. Patients with idiopathic hallucinatory palinopsia should have close follow-up.

A paranoid reaction may be caused from a decline in brain circulation as a result of high blood pressure or hardening of the arterial walls.

Drug-induced paranoia, associated with amphetamines, methamphetamine and similar stimulants has much in common with schizophrenic paranoia; the relationship has been under investigation since 2012. Drug-induced paranoia has a better prognosis than schizophrenic paranoia once the drug has been removed. For further information, see Stimulant psychosis and Substance-induced psychosis.

Based on data obtained by the Dutch NEMISIS project in 2005, there was an association between impaired hearing and the onset of symptoms of psychosis, which was based on a five-year follow up. Some older studies have actually declared that a state of paranoia can be produced in patients that were under a hypnotic state of deafness. This idea however generated much skepticism during its time.

Benzodiazepines, such as alprazolam, clonazepam, lorazepam and diazepam, can cause both depression and mania.

Benzodiazepines are a class of medication commonly used to treat anxiety, panic attacks and insomnia, and are also commonly misused and abused. Those with anxiety, panic and sleep problems commonly have negative emotions and thoughts, depression, suicidal ideations, and often have comorbid depressive disorders. While the anxiolytic and hypnotic effects of benzodiazepines disappear as tolerance develops, depression and impulsivity with high suicidal risk commonly persist. Unfortunately, these symptoms are “often interpreted as an exacerbation or as a natural evolution of previous disorders and the chronic use of sedatives is overlooked.” Benzodiazepines do not prevent the development of depression, can exacerbate preexisting depression, can cause depression in those with no history of it, and can lead to suicide attempts. Risk factors for attempted and completed suicide while using benzodiazepines include high dose prescriptions (even in those not misusing the medications), benzodiazepine intoxication, and underlying depression.

The long-term use of benzodiazepines may have a similar effect on the brain as alcohol, and are also implicated in depression. As with alcohol, the effects of benzodiazepine on neurochemistry, such as decreased levels of serotonin and norepinephrine, are believed to be responsible for the increased depression. Additionally, benzodiazepines can indirectly worsen mood by worsening sleep (i.e., benzodiazepine-induced sleep disorder). Like alcohol, benzodiazepines can put people to sleep but, while asleep, they disrupt sleep architecture: decreasing sleep time, delaying time to REM sleep, and decreasing deep sleep (the most restorative part of sleep for both energy and mood). Just as some antidepressants can cause or worsen anxiety in some patients due to being activating, benzodiazepines can cause or worsen depression due to being a central nervous system depressant—worsening thinking, concentration and problem solving (i.e., benzodiazepine-induced neurocognitive disorder). However, unlike antidepressants, in which the activating effects usually improve with continued treatment, benzodiazepine-induced depression is unlikely to improve until after stopping the medication.

In a long-term follow-up study of patients dependent on benzodiazepines, it was found that 10 people (20%) had taken drug overdoses while on chronic benzodiazepine medication despite only two people ever having had any pre-existing depressive disorder. A year after a gradual withdrawal program, no patients had taken any further overdoses.

Just as with intoxication and chronic use, benzodiazepine withdrawal can also cause depression. While benzodiazepine-induced depressive disorder may be exacerbated immediately after discontinuation of benzodiazepines, evidence suggests that mood significantly improves after the acute withdrawal period to levels better than during use. Depression resulting from withdrawal from benzodiazepines usually subsides after a few months but in some cases may persist for 6–12 months.