Multiple guidelines recommend that delirium should be diagnosed when it presents to healthcare services. Much evidence suggest, however, that delirium is greatly underdiagnosed. Higher rates of detection of delirium in general settings (for the ICU see below) can be assisted by the use of validated delirium screening tools. Many such tools have been published. They differ in duration, complexity, need for training, and so on. Examples of tools in use in clinical practice are: Delirium Observation Screening Scale, the Nursing Delirium Screening Scale (Nu-DESC), the Confusion Assessment Method, the Recognizing Acute Delirium As part of your Routine (RADAR) tool and the 4 "A"s Test or 4AT.

In the ICU, international guidelines recommend that every patient gets checked for delirium every day (usually twice or more a day) using a validated clinical tool. The two most widely used are the Confusion Assessment Method for the ICU (CAM-ICU) and the Intensive Care Delirium Screening Checklist (ICDSC). There are translations of these tools in over 20 languages and they are used globally in many thousands of ICUs, and instructional videos and myriad implementation tips are available. It is not as important which tool is used as that the patient gets monitored. Without using one of these tools, 75% of ICU delirium is missed by the practicing team, which leaves the patient without any likely active interventions to help reduce the duration of his/her delirium.

The most salient component of the definition of delirium that nurses and other healthcare professionals use at the bedside is whether or not the patient can pay attention and follow simple commands (see videos and literature). The advent of daily monitoring for delirium, made easy by the CAM-ICU and other assessment tools, as well as proper documentation, had led to important changes in the culture of ICUs and rounds in that the entire team can now discuss the brain and how it is doing in terms of being “on” (not delirious) or “off” (delirious) and then focus on the several most likely causes of delirium in any specific patient. Thus, it is not the monitoring itself that changes the patient’s clinical course, but rather it is this combination of monitoring and then relaying the information on rounds in the ICU that makes such a huge difference in awareness of this form of organ dysfunction and then enables a difference to be made in clinical outcomes.

Other medical conditions that can resemble excited delirium are panic attack, hyperthermia, diabetes, head injury, delirium tremens, and hyperthyroidism.

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.

Psychosis is first and foremost a diagnosis of exclusion. So a new-onset episode of psychosis "cannot" be considered a symptom of a psychiatric disorder until other relevant and known causes of psychosis are properly excluded, or ruled out. Many clinicians improperly perform, or entirely miss this step, introducing avoidable diagnostic error and misdiagnosis.

An initial assessment includes a comprehensive history and physical examination by a physician, psychiatrist, psychiatric nurse practitioner or psychiatric physician assistant. Biological tests should be performed to exclude psychosis associated with or caused by substance use, medication, toxins, surgical complications, or other medical illnesses.

Delirium should be ruled out, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, indicating other underlying factors, including medical illnesses. Excluding medical illnesses associated with psychosis is performed by using blood tests to measure:

- Thyroid-stimulating hormone to exclude hypo- or hyperthyroidism,

- Basic electrolytes and serum calcium to rule out a metabolic disturbance,

- Full blood count including ESR to rule out a systemic infection or chronic disease, and

- Serology to exclude syphilis or HIV infection.

Other investigations include:

- EEG to exclude epilepsy, and an

- MRI or CT scan of the head to exclude brain lesions.

Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should be ruled out, particularly for first-episode psychosis. Both substance- and medication-induced psychosis can be excluded to a high level of certainty, using a

- Urinalysis and a

- Full serum toxicology screening.

Because some dietary supplements may also induce psychosis or mania, but cannot be ruled out with laboratory tests, a psychotic individual's family, partner, or friends should be asked whether the patient is currently taking any dietary supplements.

Common mistakes made when diagnosing people who are psychotic include:

- Not properly excluding delirium,

- Not appreciating medical abnormalities (e.g., vital signs),

- Not obtaining a medical history and family history,

- Indiscriminate screening without an organizing framework,

- Missing a toxic psychosis by not screening for substances "and" medications

- Not asking family or others about dietary supplements,

- Premature diagnostic closure, and

- Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.

Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatric differential diagnosis using a person's family history, incorporating information from the person with psychosis, and information from family, friends, or significant others.

Types of psychosis in psychiatric disorders may be established by formal rating scales. The Brief Psychiatric Rating Scale (BPRS) assesses the level of 18 symptom constructs of psychosis such as hostility, suspicion, hallucination, and grandiosity. It is based on the clinician's interview with the patient and observations of the patient's behavior over the previous 2–3 days. The patient's family can also answer questions on the behavior report. During the initial assessment and the follow-up, both positive and negative symptoms of psychosis can be assessed using the 30 item Positive and Negative Symptom Scale (PANSS).

According to the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th Edition), Cotard delusion falls under the category of somatic delusions, those that involve bodily functions or sensations. (Citation needed. DSM-5 does not specifically reference Cotard syndrome.)

There are no further diagnostic criteria for Cotard syndrome within the DSM-5, and identification of the syndrome relies heavily on clinical interpretation.

Cotard delusion should not be confused with Delusional Disorders as defined by the DSM-5, which involve a different spectrum of symptoms that are less severe and have lesser detrimental effect on functioning.

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.

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.

One study from as early as 1895 reported that approximately 10% of the population experiences hallucinations. A 1996-1999 survey of over 13,000 people reported a much higher figure, with almost 39% of people reporting hallucinatory experiences, 27% of which daytime hallucinations, mostly outside the context of illness or drug use. From this survey, olfactory (smell) and gustatory (taste) hallucinations seem the most common in the general population.

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.

Diagnosis is mainly based on symptoms. In a person with delirium tremens it is important to rule out other associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.

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 evidence for the effectiveness of early interventions to prevent psychosis appeared inconclusive. Whilst early intervention in those with a psychotic episode might improve short term outcomes, little benefit was seen from these measures after five years. However, there is evidence that cognitive behavioral therapy (CBT) may reduce the risk of becoming psychotic in those at high risk, and in 2014 the UK National Institute for Health and Care Excellence (NICE) recommended preventive CBT for people at risk of psychosis.

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.

Definitions vary, but currently it is defined as one continuous, unremitting seizure lasting longer than five minutes, or recurrent seizures without regaining consciousness between seizures for greater than five minutes. Previous definitions used a 30-minute time limit.

NCSE is believed to be under-diagnosed.

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

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.

Psychomotor agitation is a set of signs and symptoms that stem from mental tension and anxiety. The signs are unintentional and purposeless motions; the symptoms are emotional distress and restlessness. Typical manifestations include pacing around a room, wringing the hands, uncontrolled tongue movement, pulling off clothing and putting it back on, and other similar actions. In more severe cases, the motions may become harmful to the individual, such as ripping, tearing, or chewing at the skin around one's fingernails, lips, or other body parts to the point of bleeding. Psychomotor agitation is typically found in major depressive disorder or obsessive-compulsive disorder, and sometimes the manic phase in bipolar disorder, though it can also be a result of an excess intake of stimulants. It can also be caused by severe hyponatremia. The middle-aged and the elderly are more at risk to express it.

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.

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.

Metabolic studies are useful, but they are not able identify neural activity within a specific region to specific cognitive processes. Functionality can only be identified at the most general level: Metabolism in cortical and subcortical regions that may contribute to cognitive processes.

At present, there is no established relation between cerebral metabolic rates of glucose or oxygen as measured by PET and patient outcome. The decrease of cerebral metabolism occurs also when patients are treated with anesthetics to the point of unresponsiveness. Lowest value (28% of normal range) have been reported during propofol anesthesia. Also deep sleep represents a phase of decreased metabolism (down to 40% of the normal range)

In general, quantitative PET studies and the assessment of cerebral metabolic rates depends on many assumptions.

PET for example requires a correction factor, the lumped constant, which is stable in healthy brains. There are reports, that a global decrease of this constant emerges after a traumatic brain injury.

But not only the correction factors change due to TBI.

Another issue is the possibility of anaerobic glycolysis that could occur after TBI. In such a case the glucose levels measured by the PET are not tightly connected to the oxygen consumption of the patient's brain.

Third point regarding PET scans is the overall measurement per unit volume of brain tissue. The imaging can be affected by the inclusion of metabolically inactive spaces e.g. cerebrospinal fluidin the case of gross hydrocephalus, which artificially lowers the calculated metabolism.

Also the issue of radiation exposure must be considered in patients with already severely damaged brains and preclude longitudinal or follow-up studies.

Between 10 and 30% of people who have status epilepticus die within 30 days. The great majority of these people have an underlying brain condition causing their status seizure such as brain tumor, brain infection, brain trauma, or stroke. However, people with diagnosed epilepsy who have a status seizure also have an increased risk of death if their condition is not stabilized quickly, their medication and sleep regimen adapted and adhered to, and stress and other stimulant (seizure trigger) levels controlled.

However, with optimal neurological care, adherence to the medication regimen, and a good prognosis (no other underlying uncontrolled brain or other organic disease), the person—even people who have been diagnosed with epilepsy—in otherwise good health can survive with minimal or no brain damage, and can decrease risk of death and even avoid future seizures.

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.

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.