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.

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.

In general, alcohol abusers with withdrawal symptoms, such as alcoholic hallucinosis, have a deficiency of several vitamins and minerals and their bodies could cope with the withdrawal easier by taking nutritional supplements. Alcohol abuse can create a deficiency of thiamine, magnesium, zinc, folate and phosphate as well as cause low blood sugar. However, several tested drugs have shown the disappearance of hallucinations. Neuroleptics and benzodiazepines showed normalization. Common benzodiazepines are chlordiazepoxide and lorazepam. It has been shown that management has been effective with a combination of abstinence from alcohol and the use of neuroleptics. It is also possible to treat withdrawal before major symptoms start to happen in the body. Diazepam and chlordiazepoxide have proven to be effective in treating alcohol withdrawal symptoms such as alcoholic halluciniosis. With the help of these specific medications, the process of withdrawal is easier to go through, making alcoholic hallucinosis less likely to occur.

Episodes of delirium can be prevented by identifying hospitalized people at risk of the condition: those over 65, those with a known cognitive impairment, those with hip fracture, those with severe illness. Close observation for the early signs is recommended in those people.

Systematically addressing the common contributing factors (such as constipation, dehydration and polypharmacy), as well as providing a therapeutic environment (such as adequate lighting, minimizing noise, clear communication, minimizing relocation, signage, ways to tell the time, and helping the person to walk and be mobile) may prevent delirium. Rates with a number of interventions together decrease rates to 0.72 from baseline in the elderly.

It is thought that 30–40% of all cases of delirium could be prevented, and that high rates of delirium reflect negatively on the quality of care. Melatonin and other pharmacological agents have been studied for prevention of postoperative delirium, but evidence is not clear. In critically ill individuals avoidance or cautious use of benzodiazepines has been recommended to reduce the risk of delirium.

It is unclear if the medication donepezil, a cholinesterase inhibitor, reduces delirium following surgery. There is also no clear evidence to suggest that citicoline, Methylprednisolone, or antipsychotic medications prevent delirium.

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.

The condition is rare, with only 80 established cases reported in medical literature and incomplete evidence of a further 200.

For women taking psychiatric medication, the decision as to whether continue during pregnancy and whether to take them while breast feeding is difficult in any case; there is no data to guide this decision with respect to preventing postpartum psychosis. There is no data to guide a decision as to whether women at high risk for postpartum psychosis should take antipsychotic medicine to prevent it. For women at risk of postpartum psychosis, informing medical care-givers, and monitoring by a psychiatrist during pregnancy, in the perinatal period, and for a few weeks following delivery, is recommended.

For women with known bipolar disorder, taking medication during pregnancy roughly halves the risk of a severe postpartum episode, as does starting to take medication immediately after the birth.

In most cases hospital admission is necessary. Antipsychotic drugs and mood stabilizing drugs such as lithium are typically administered but is not clear if mood stabilizers can be titrated to a high enough level quickly enough to be effective. Electroconvulsive therapy may be considered, especially if there is a high risk of suicide.

Family support may be provided via a social worker.

The article "Cotard's syndrome: A Review" (2010) reports successful pharmacological treatments (mono-therapeutic and multi-therapeutic) using antidepressant, antipsychotic, and mood stabilizing drugs; likewise, with the depressed patient, electroconvulsive therapy (ECT) is more effective than pharmacotherapy. Cotard syndrome resulting from an adverse drug reaction to valacyclovir is attributed to elevated serum concentration of one of valacyclovir's metabolites, 9-carboxymethoxymethylguanine (CMMG). Successful treatment warrants cessation of the drug, valacyclovir. Hemodialysis was associated with timely clearance of CMMG and resolution of symptoms.

Menstrual psychosis is a debated form of psychosis with a brief, sudden onset related to the menstrual cycle. The symptoms associated to it are dramatic and include delirium, mania or mutism. Most psychiatrists do not recognise the condition. Only 80 established cases are reported in medical literature and most of them were described by 19th Century physicians. It is thought to be linked with postpartum psychosis. This journal has been published looking at the 'evidence' for menstrual psychosis'.

Treatment of secondary forms of delusional parasitosis are addressed by treating the primary associated psychological or physical condition. The primary form is treated much as other delusional disorders and schizophrenia. In the past, pimozide was the drug of choice when selecting from the typical antipsychotics. Currently, atypical antipsychotics such as olanzapine or risperidone are used as first line treatment.

However, it is also characteristic that sufferers will reject the diagnosis of delusional parasitosis by medical professionals, and very few are willing to be treated, despite demonstrable efficacy of treatment.

Alcoholic hallucinosis (or alcohol-related psychosis or alcohol-induced psychotic disorder) is a complication of alcohol withdrawal in alcoholics. Descriptions of the condition date back to at least 1907. They can occur during acute intoxication or withdrawal with the potential of having delirium tremens. Alcohol hallucinosis is a rather uncommon alcohol-induced psychotic disorder only being seen in chronic alcoholics who have many consecutive years of severe and heavy drinking during their lifetime. Alcoholic hallucinosis develops about 12 to 24 hours after the heavy drinking stops suddenly, and can last for days. It involves auditory and visual hallucinations, most commonly accusatory or threatening voices. The risk of developing alcoholic hallucinosis is increased by long-term heavy alcohol abuse and the use of other drugs.

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.

Excited delirium occurs most commonly in males with a history of serious mental illness or acute or chronic drug abuse, particularly stimulant drugs such as cocaine and MDPV. Alcohol withdrawal or head trauma may also contribute to the condition.

A majority of fatal case involved men.

People with excited delirium commonly have acute drug intoxication, generally involving PCP, methylenedioxypyrovalerone (MDPV), cocaine, or methamphetamine. Other drugs that may contribute to death are antipsychotics.

Cotard delusion is a rare mental illness in which the affected person holds the delusional belief that they are already dead, do not exist, are putrefying, or have lost their blood or internal organs. Statistical analysis of a hundred-patient cohort indicates that the denial of self-existence is a symptom present in 69% of the cases of Cotard's syndrome; yet, paradoxically, 55% of the patients present delusions of immortality.

In 1880, the neurologist Jules Cotard described the condition as "Le délire des négations" ("The Delirium of Negation"), a psychiatric syndrome of varied severity. A mild case is characterized by despair and self-loathing, while a severe case is characterized by intense delusions of negation and chronic psychiatric depression. The case of Mademoiselle X describes a woman who denied the existence of parts of her body and of her need to eat. She said that she was condemned to eternal damnation and therefore could not die a natural death. In the course of suffering "The Delirium of Negation", Mademoiselle X died of starvation.

The Cotard delusion is not mentioned in either the "Diagnostic and Statistical Manual of Mental Disorders" (DSM) or the tenth edition of the "International Statistical Classification of Diseases and Related Health Problems" (ICD-10) of the World Health Organization.

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.

Delusional parasitosis is divided into primary, secondary functional, and secondary organic groups.

Treatment of OBS varies with the causative disorder or disease. It is important to note that it is not a primary diagnosis and a cause needs to be sought out and treated.

Before delirium treatment, the cause must be established. Medication such as antipsychotics or benzodiazepines can help reduce the symptoms for some cases. For alcohol or malnourished cases, vitamin B supplements are recommended and for extreme cases, life-support can be used.

An organic brain syndrome (OBS), also known as an organic brain disease/disorder (OBD), an organic mental syndrome (OMS), or an organic mental disorder (OMD), is a syndrome or disorder of mental function whose cause is alleged to be known as organic (physiologic) rather than purely of the mind. These names are older and nearly obsolete general terms from psychiatry, referring to many physical disorders that cause impaired mental function. They are meant to exclude psychiatric disorders (mental disorders). Originally, the term was created to distinguish physical (termed "organic") causes of mental impairment from psychiatric (termed "functional") disorders, but during the era when this distinction was drawn, not enough was known about brain science (including neuroscience, cognitive science, neuropsychology, and mind-brain correlation) for this cause-based classification to be more than educated guesswork labeled with misplaced certainty, which is why it has been deemphasized in current medicine.

"Acute" organic brain syndrome is (by definition) a recently appearing state of mental impairment, as a result of intoxication, drug overdose, infection, pain, and many other physical problems affecting mental status. In medical contexts, "acute" means "of recent onset". As is the case with most acute disease problems, acute organic brain syndrome is often temporary, although this does not guarantee that it will not recur (happen again) or progress to become chronic, that is, long-term. A more specific medical term for the "acute" subset of organic brain syndromes is delirium.

"Chronic" organic brain syndrome is long-term. For example, some forms of chronic drug or alcohol dependence can cause organic brain syndrome due to their long-lasting or permanent toxic effects on brain function. Other common causes of chronic organic brain syndrome sometimes listed are the various types of dementia, which result from permanent brain damage due to strokes, Alzheimer's disease, or other damaging causes which are not reversible.

Though OBS was once a common diagnosis in the elderly, until the understanding of the various types of dementias it is related to a disease process and is not an inevitable part of aging. In some of the older literature, there was an attempt to separate organic brain syndrome from dementia, but this was related to an older world view in which dementia was thought to be a part of normal aging, and thus did not represent a special disease process. The later identification of various dementias as clear pathologies is an example of the types of pathological problems discovered to be associated with mental states, and is one of the areas which led to abandonment of all further attempts to clearly define and use OBS as a term.

There is no cure for neurocognitive disorder or the diseases that cause it. Antidepressants, antipsychotics, and other medications that treat memory loss and behavioral symptoms are available and may help to treat the diseases. Ongoing psychotherapy and psychosocial support for patients and families are usually necessary for clear understanding and proper management of the disorder and to maintain a better quality of life for everyone involved. Speech therapy has been shown to help with language impairment.

Studies suggest that diets with high Omega 3 content, low in saturated fats and sugars, along with regular exercise can increase the level of brain plasticity. Other studies have shown that mental exercise such a newly developed “computerized brain training programs” can also help build and maintain targeted specific areas of the brain. These studies have been very successful for those diagnosed with schizophrenia and can improve fluid intelligence, the ability to adapt and deal with new problems or challenges the first time encountered, and in young people, it can still be effective in later life.

A person with amnesia may slowly be able to recall their memories or work with an occupational therapist to learn new information to replace what was lost, or to use intact memories as a basis for taking in new information. If it is caused by an underlying cause such as Alzheimer's disease or infections, the cause may be treated but the amnesia may not be.

Delirium tremens is mainly caused by a long period of drinking being stopped abruptly. Withdrawal leads to a biochemical regulation cascade. It may also be triggered by head injury, infection, or illness in people with a history of heavy use of alcohol.

Another cause of delirium tremens is abrupt stopping of tranquilizer drugs of the barbiturate or benzodiazepine classes in a person with a relatively strong addiction to them. Because these tranquilizers' primary pharmacological and physiological effects stem from their manipulation of the GABA chemical and transmitter somatic system, the same neurotransmitter system affected by alcohol, delirium tremens can occur upon abrupt decrease of dosage in those who are heavily dependent. These DTs are much the same as those caused by alcohol and so is the attendant withdrawal syndrome of which they are a manifestation. That is the primary reason benzodiazepines are such an effective treatment for DTs, despite also being the cause of them in many cases. Because ethanol and tranquilizers such as barbiturates and benzodiazepines function as positive allosteric modulators at GABA receptors, the brain, in its desire to equalize an unbalanced chemical system, triggers the abrupt stopping of the production of endogenous GABA. This decrease becomes more and more marked as the addiction becomes stronger and as higher doses are needed to cause intoxication. In addition to having sedative properties, GABA is an immensely important regulatory neurotransmitter that controls the heart rate, blood pressure, and seizure threshold among myriad other important autonomic nervous subsystems.

Delirium tremens is most common in people who have a history of alcohol withdrawal, especially in those who drink the equivalent of of beer or of distilled beverage daily. Delirium tremens also commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years.

Waxy flexibility is a psychomotor symptom of catatonia as associated with schizophrenia, bipolar disorder, or other mental disorders which leads to a decreased response to stimuli and a tendency to remain in an immobile posture. Attempts to reposition the patient are met by "slight, even resistance", and after being repositioned the patient will typically remain in the new position. Waxy flexibility rarely occurs in cases of delirium. The presence of waxy flexibility along with at least two other catatonic symptoms such as stupor or negativism are enough to warrant a diagnosis of catatonia.

For instance, if one were to move the arm of someone with waxy flexibility, they would keep their arm where one moved it until it was moved again, as if it were made from wax. Further alteration of an individual's posture is similar to bending a candle. Although waxy flexibility has historically been linked to schizophrenia, there are also other disorders which it may be associated with, for example, mood disorder with catatonic behaviour.

Electroconvulsive therapy is often used as a treatment for catatonia. A study has found that catatonic patients suffering from waxy flexibility responded faster to electroconvulsive therapy, compared to patients with different catatonic symptoms.

If the patient is institutionalised, monitoring of behaviour and serum sodium levels is necessary. In treatment-resistant polydipsic psychiatric patients, regulation in the inpatient setting can be accomplished by use of a weight-water protocol. First, base-line weights must be established and correlated to serum sodium levels. Weight will normally fluctuate during the day, but as the water intake of the polydipsic goes up, the weight will naturally rise. The physician can order a stepped series of interventions as the weight rises. The correlation must be individualized with attention paid to the patient's normal weight and fluctuations, diet, comorbid disorders (such as a seizure disorder) and urinary system functioning. Progressive steps might include redirection, room restriction, and increasing levels of physical restraint with monitoring. Such plans should also include progressive increases in monitoring, as well as a level at which a serum sodium level is drawn.

The body's inflammatory response to surgery likely plays an important role, at least in elderly patients. Various research initiatives during recent years have evaluated whether actions taken before, during and after surgery can lessen the possible deleterious effects of inflammation. For example, anti-inflammatory agents can be given before surgery. During surgery, inflammation can be modulated by temperature control, use of regional rather than general anesthesia or the use of beta blockers. After surgery, optimal pain management and infection control is important. Several studies have shown variable-significance positive effects when a multidisciplinary, multifactorial approach to elderly patient is followed during pre, peri and post-operative care.

Animal studies indicate that volatile anaesthestics may augment the pathological processes of Alzheimer's Disease by affecting amyloid-beta processing. However, in young healthy mice, the volatile anesthetic isoflurane can also produce long-lasting memory impairment. This adverse effect is preventable by pre-administering the GABA(A)α5 inverse agonist L-655,708.