Delirium arises through the interaction of a number of predisposing and precipitating factors. A predisposing factor might be any biological, psychological or social factor that increases an individual’s susceptibility to delirium. An individual with multiple predisposing factors is said to have "high baseline vulnerability". A precipitating factor is any biological, psychological or social factor that can trigger delirium. The division of causes into "predisposing" and "precipitating" is useful in order to assess an individual’s risk of suffering from delirium, and in guiding the management of delirium – however there may be a significant degree of overlap between the two categories.

Delirium most commonly affects the old age and those of ill health. Health results from physical and socioeconomic assets, and opposing factors come from physical and socioeconomic deficits. Individuals with significant predisposing factors don't compensate for physical or social stressors ("precipitating factors"). In such an individual, a single or mild precipitating factor could be sufficient to trigger an episode of delirium. Conversely, delirium may only result in a healthy individual if they suffer serious or multiple precipitating factors. It is important to note that the factors affecting those of an individual can change over time, thus an individual’s risk of delirium is in a state of flux.

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.

The most important predisposing factors are listed below:

- Older age

- Cognitive impairment / dementia

- Physical comorbidity (biventricular failure, cancer, cerebrovascular disease)

- Psychiatric comorbidity (e.g., depression)

- Sensory impairment (vision, hearing)

- Functional dependence (e.g., requiring assistance for self-care and/or mobility)

- Dehydration / malnutrition

- Drugs and drug-dependence.

- Alcohol dependence

The pathophysiology of excited delirium has been unclear, but likely involves multiple factors. These may include positional asphyxia, hyperthermia, drug toxicity, and/or catecholamine-induced fatal cardiac arrhythmias.

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 symptoms of sedative/hypnotic toxidrome include ataxia, blurred vision, coma, confusion, delirium, deterioration of central nervous system functions, diplopia, dysesthesias, hallucinations, nystagmus, paresthesias, sedation, slurred speech, and stupor. Apnea is a potential complication. Substances that may cause this toxidrome include anticonvulsants, barbiturates, benzodiazepines, gamma-Hydroxybutyric acid, Methaqualone, and ethanol. While most sedative-hypnotics are anticonvulsant, some such as GHB and methaqualone instead lower the seizure threshold, and so can cause paradoxical seizures in overdose.

The symptoms of a sympathomimetic toxidrome include anxiety, delusions, diaphoresis, hyperreflexia, mydriasis, paranoia, piloerection, and seizures. Complications include hypertension, and tachycardia. Substances that may cause this toxidrome include salbutamol, amphetamines, cocaine, ephedrine (Ma Huang), methamphetamine, phenylpropanolamine (PPA's), and pseudoephedrine. It may appear very similar to the anticholinergic toxidrome, but is distinguished by hyperactive bowel sounds and sweating.

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.

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.

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.

There is evidence that trauma during childhood increases the risk of developing psychosis. One meta-analysis found that 60-70% of those who experience psychosis have experienced childhood trauma (abuse and neglect). The relationship appears to be causal and cumulative one, meaning the more adverse childhood events experienced the greater the likelihood of developing psychosis of one kind of another.

The underlying neurophysiology and psychopathology of Cotard syndrome might be related to problems of delusional misidentification. Neurologically, the Cotard delusion (negation of the Self) is thought to be related to the Capgras delusion (people replaced by impostors); each type of delusion is thought to result from neural misfiring in the fusiform face area of the brain (which recognizes faces) and in the amygdalae (which associate emotions to a recognized face).

The neural disconnection creates in the patient a sense that the face they are observing is not the face of the person to whom it belongs; therefore, that face lacks the familiarity (recognition) normally associated with it. This results in derealization, or a disconnection from the environment. If the observed face is that of a person known to the patient, they experience that face as the face of an impostor (the Capgras delusion). If the patient sees their own face, they might perceive no association between the face and their own sense of Self—which results in the patient believing that they do not exist (the Cotard delusion).

Cotard's syndrome is usually encountered in people afflicted with a psychosis (e.g., schizophrenia ), neurological illness, mental illness, clinical depression, derealization, brain tumor, and with migraine headache. The medical literature indicate that the occurrence of Cotard's delusion is associated with lesions in the parietal lobe. As such, the Cotard-delusion patient presents a greater incidence of brain atrophy—especially of the median frontal lobe—than do the people in the control groups.

The Cotard delusion also has resulted from a patient's adverse physiological response to a drug (e.g., aciclovir) and to its prodrug precursor (e.g., valaciclovir). The occurrence of Cotard delusion symptoms was associated with a high serum-concentration of 9-Carboxymethoxymethylguanine (CMMG), the principal metabolite of the drug aciclovir. As such, the patient with weak kidneys (impaired renal function) continued risking the occurrence of delusional symptoms, despite the reduction of the dose of aciclovir. Hemodialysis resolved the patient's delusions (of negating the Self) within hours of treatment, which suggests that the occurrence of Cotard-delusion symptoms might not always be cause for psychiatric hospitalization of the patient.

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.

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.

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.

Delirium tremens (DTs) is a rapid onset of confusion usually caused by withdrawal from alcohol. When it occurs, it is often three days into the withdrawal symptoms and lasts for two to three days. Physical effects may include shaking, shivering, irregular heart rate, and sweating. People may also see or hear things other people do not. Occasionally, a very high body temperature or seizures may result in death. Alcohol is one of the most dangerous drugs from which to withdraw.

Delirium tremens typically only occurs in people with a high intake of alcohol for more than a month. A similar syndrome may occur with benzodiazepine and barbiturate withdrawal. Withdrawal from stimulants such as cocaine does not have major medical complications. In a person with delirium tremens it is important to rule out other associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.

Prevention is by treating withdrawal symptoms. If delirium tremens occurs, aggressive treatment improves outcomes. Treatment in a quiet intensive care unit with sufficient light is often recommended. Benzodiazepines are the medication of choice with diazepam, lorazepam, chlordiazepoxide, and oxazepam all commonly used. They should be given until a person is lightly sleeping. The antipsychotic haloperidol may also be used. The vitamin thiamine is recommended. Mortality without treatment is between 15% and 40%. Currently death occurs in about 1% to 4% of cases.

About half of people with alcoholism will develop withdrawal symptoms upon reducing their use. Of these, three to five percent develop DTs or have seizures. The name delirium tremens was first used in 1813; however, the symptoms were well described since the 1700s. The word "delirium" is Latin for "going off the furrow," a plowing metaphor. It is also called shaking frenzy and Saunders-Sutton syndrome. Nicknames include the shakes, barrel-fever, blue horrors, bottleache, bats, drunken horrors, elephants, gallon distemper, quart mania, and pink spiders, among others.

A very large number of medical conditions can cause psychosis, sometimes called "secondary psychosis". Examples include:

- disorders causing "delirium" ("toxic psychosis"), in which consciousness is disturbed

- neurodevelopmental disorders and chromosomal abnormalities, including velocardiofacial syndrome

- neurodegenerative disorders, such as Alzheimer's disease, dementia with Lewy bodies, and Parkinson's disease

- focal neurological disease, such as stroke, brain tumors, multiple sclerosis, and some forms of epilepsy

- malignancy (typically via masses in the brain, paraneoplastic syndromes, or drugs used to treat cancer)

- infectious and postinfectious syndromes, including infections causing delirium, viral encephalitis, HIV/AIDS, malaria, Lyme disease, syphilis

- endocrine disease, such as hypothyroidism, hyperthyroidism, adrenal failure, Cushing's syndrome, hypoparathyroidism and hyperparathyroidism; sex hormones also affect psychotic symptoms and sometimes childbirth can provoke psychosis, termed puerperal psychosis

- inborn errors of metabolism, such as Succinic semialdehyde dehydrogenase deficiency, porphyria and metachromatic leukodystrophy

- nutritional deficiency, such as vitamin B deficiency

- other acquired metabolic disorders, including electrolyte disturbances such as hypocalcemia, hypernatremia, hyponatremia, hypokalemia, hypomagnesemia, hypermagnesemia, hypercalcemia, and hypophosphatemia, but also hypoglycemia, hypoxia, and failure of the liver or kidneys

- autoimmune and related disorders, such as systemic lupus erythematosus (lupus, SLE), sarcoidosis, Hashimoto's encephalopathy, and anti-NMDA-receptor encephalitis Patients with these conditions may be, 'slipping through the net'.

- poisoning, by therapeutic drugs (see below), recreational drugs (see below), and a range of plants, fungi, metals, organic compounds, and a few animal toxins

- some sleep disorders, including hallucinations in narcolepsy (in which REM sleep intrudes into wakefulness)

Psychosis can even be caused by familiar ailments such as flu or mumps.

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.

Women with a history of bipolar disorder, schizophrenia, prior episode of postpartum psychosis, or a family history of postpartum psychosis are at high risk; about 25-50% of women in this group will have postpartum psychosis. around 37% of women with bipolar disorder have a severe postpartum episode. Women with a prior episode of postpartum psychosis have about a 30% risk of having another episode in the next pregnancy. For a woman with no history of mental illness who has a close relative (a mother or sister) who had postpartum psychosis, the risk is about 3%. There may be a genetic component; while mutations in chromosome 16 and in specific genes involved in serotoninergic, hormonal, and inflammatory pathways have been identified, none had been confirmed as of 2014.

Family history of affective psychosis, prenatal depression, and autoimmune thyroid dysfunction also increase the risk of postpartum psychosis.

About half of women who experience postpartum psychosis had no risk factors. Many other potential factors like pregnancy and delivery complications, caesarean section, sex of the baby, length of pregnancy, changes in psychiatric medication, and psychosocial factors have been researched and no clear association has been found; the only clear risk factor identified as of 2014 was that postpartum psychosis happens more often to women giving birth for the first time, than to women having second or subsequent deliveries, but the reason for that was not known. There may be a role for hormonal changes that occur following delivery, in combination with other factors; there may be a role changes in the immune system as well.

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.

Chronic abuse of methylphenidate can also lead to psychosis. Psychotic symptoms from methylphenidate can include hearing voices, visual hallucinations, urges to harm oneself, severe anxiety, mania, grandiosity, paranoid delusions, confusion, increased aggression, and irritability.

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.

The cause of alcoholic hallucinosis is unclear. It seems to be highly related to the presence of dopamine in the limbic system with the possibility of other systems. There are many symptoms that could possibly occur before the hallucinations begin. Symptoms include headache, dizziness, irritability, insomnia, and indisposition. Typically, alcoholic hallucinosis has a sudden onset.

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

Causes include:

- Schizophrenia

- Bipolar disorder

- Excited delirium

- Post-traumatic stress disorder (PTSD)

- Panic attacks

- Anxiety disorder

- Obsessive-compulsive disorder (OCD)

- Alcohol withdrawal

- Claustrophobia

- Dementia

- Parkinson's disease

- Traumatic brain injury

- Alzheimer's disease

- Acute intermittent porphyria

- Hereditary coproporphyria

- Variegate porphyria

- Side effects of drugs like cocaine or methylphenidate

- Side effects of antipsychotics like haloperidol