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.

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.

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.

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilization of either a mood stabilizer (valproate, lithium, or carbamazepine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). Although hypomanic episodes may respond to a mood stabilizer alone, full-blown episodes are treated with an atypical antipsychotic (often in conjunction with a mood stabilizer, as these tend to produce the most rapid improvement).

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilize the patient's mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabilizer to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine, which is another anticonvulsant. Clonazepam (Klonopin) is also used. Sometimes atypical antipsychotics are used in combination with the previous mentioned medications as well, including olanzapine (Zyprexa) which helps treat hallucinations or delusions, Asenapine (Saphris, Sycrest), aripiprazole (Abilify), risperidone, ziprasidone, and clozapine which is often used for people who do not respond to lithium or anticonvulsants.

Verapamil, a calcium-channel blocker, is useful in the treatment of hypomania and in those cases where lithium and mood stabilizers are contraindicated or ineffective. Verapamil is effective for both short-term and long-term treatment.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilizers in these patients.

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.

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.

The medication that may be prescribed to someone who has a mental breakdown is based upon the underlying causes, which are sometimes more serious mental disorders. Antidepressants are given to treat depression. Anxiolytics are used for those with anxiety disorders. Antipsychotics are used for schizophrenia and mood stabilizers help with bipolar disorder. Depending upon what caused a person’s mental breakdown, any of these treatments can be helpful for them.

There are several different kinds of therapy that a patient can receive. The most common type of therapy is counseling. This is where the patient is able to talk about whatever is on their mind without worrying about any judgments. Psychotherapy is a very common type of therapy that addresses the current problems in someone’s life and helps them to deal with them. Past experiences may also be explored in this type of therapy. In psychoanalysis therapy, the main focus is a patient’s past experiences so that they can confront these issues and prevent breakdowns in the future. Cognitive behavioral therapy explores how a person behaves and what they are thinking and feeling. If there is anything negative in these three different categories, then this therapy will try to turn them around into positives. Hypnotherapy is where hypnosis is performed and used to help the patient relax. Hypnosis can also be used to figure out why a person acts or feels a certain way, by examining past events that may have caused the breakdown. Expressive therapy focuses on how the patient is able to express their feelings. If the patient has a hard time doing this, expression through the arts is highly recommended. There is also aromatherapy, which consists of herbs to help the patient relax and to try to relieve stress. Yoga and massage may also be included in this therapy that will help the muscles to relax. Meditation is also often recommended. All of these therapies help a person to relax and de-stress and also help to prevent future breakdowns.

Oneiroid syndrome, from the Ancient Greek "" ("oneiros", meaning "dream") and "" ("eidos", meaning "form, likeness"), is dream-like fantastic derangement of consciousness with illusions and hallucinations, catatonic symptoms and kaleidoscopic quality of psychopathological experiences. It's an element of the catatonic form of schizophrenia and presents with a dream-like or nightmare-like state as a background of intensive psychopathological experiences.

Oneiroid states were first described by the German physician Wilhelm Mayer-Gross in 1924. Mayer-Gross's 1924 habilitation on "Self-descriptions of Confusional States: the Oneiroid Form of Experience" () is considered the first monograph about oneiroid state. In this monograph the psychopathological method was used (German psychiatrists called that the "phenomenological method" – phänomenologische Methode).

The oneiroid syndrome, known to European and Russian psychiatrists, but all but forgotten in the USA.

Later in 1961 the Bulgarian psychiatrist S.T. Stoyanov studied the dynamics and the course of the oneiroid syndrome in "periodic", or recurrent schizophrenia (ICD-10).

According to this research the syndrome has six stages in its course:

1. initial general-somatic and vegetative disorder

2. delusional mood

3. affective-delusional depersonalisation and derealisation

4. fantastic-delusional and affective depersonalisation and derealisation

5. illusional depersonalisation and derealisation, and

6. catatonic-oneiroid state in the culmination.

In most of the cases of the oneiroid syndrome there were crude pathological changes in the electroencephalography (EEG).

The prognosis of oneiroid catatonia is optimal, in comparison with lucid catatonia.

Mania, also known as manic syndrome, is a state of abnormally elevated arousal, affect, and energy level, or "a state of heightened overall activation with enhanced affective expression together with lability of affect." Although mania is often conceived as a "mirror image" to depression, the heightened mood can be either euphoric or irritable; indeed, as the mania intensifies, irritability can be more pronounced and result in violence, or anxiety.

The symptoms of mania include heightened mood (either euphoric or irritable); flight of ideas and pressure of speech; and increased energy, decreased need for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states; in full-blown mania, however, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behavior.

Mania is a syndrome of multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, as multiple sclerosis; certain medications, as prednisone; or certain substances of abuse, as cocaine or anabolic steroids. In current DSM-5 nomenclature, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterized as either mild, moderate, or severe, with specifiers with regard to certain symptomatic features (e.g. catatonia, psychosis). Mania, however, may be divided into three stages: hypomania, or stage I; acute mania, or stage II; and delirious mania, or stage III. This "staging" of a manic episode is, in particular, very useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardized tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic bipolar person needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have "gone manic" severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

There is limited evidence that the hypnotic drug zolpidem has an effect. The results of the few scientific studies that have been published so far on the effectiveness of zolpidem have been contradictory.

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.

For those whose sleepwalking episodes turn to be hazardous, a door alarm may offer a measure of protection. There are various kinds of door alarms that can attach to a bedroom door and when the door is opened, the alarm sounds off. The intention is that the sound will fully awaken the person and interrupt the sleepwalking episode, or if the sleepwalker lives with others, the sound will prompt them to check on the person.

Sleepwalkers should aim to have their bedrooms on the first floor of a home, apartment, dorm, hotel, etc.

Also, sleepwalkers should not have easily accessible weapons (loaded guns, knives) in the bedroom or any room of the house for that matter. If there are weapons, they should be locked away with keys secluded from the sleepwalker.

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.

In the United States, it is estimated that there may be between 15,000 and 40,000 patients who are in a persistent vegetative state, but due to poor nursing home records exact figures are hard to determine.

Rapport, Todd, Lumley, and Fisicaro suggest that the closest DSM-IV diagnostic category to nervous breakdown is Adjustment Disorder with Mixed Anxiety and Depressed Mood (Acute). Adjustment disorders and nervous breakdowns are both acute reactions to stress that resolve after removal of the stressor. However, DSM-IV excludes from adjustment disorders cases secondary to bereavement, which contributes to approximately 6–8% of nervous breakdowns.

Nervous breakdowns may share some features of acute stress disorder and post-traumatic stress disorder, in that these each occur in response to an external stressor, and may be marked with sleep disturbance, diminished concentration, and mood lability. However, the symptoms of nervous breakdown do not include the constellation of re-experienced trauma, dissociation, avoidance, and numbing of general responsiveness that are associated with the other two disorders, and the types of stressors linked to a nervous breakdown are generally less extreme.

Nervous breakdowns may share many features of mixed anxiety-depressive disorder (MADD). However, the definition of MADD suggests a chronic condition, in contrast to the acute, short-term nature of a nervous breakdown.

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.

It was reported in 1998 that there were 25 families in the world known to carry the gene for FFI: eight German, five Italian, four American, two French, two Australian, two British, one Japanese, and one Austrian. In the Basque Country there were 16 family cases of the 178N mutation between 1993 and 2005 related to two families whose common origin is located in the eighteenth century. In 2011, another family was added to the list when researchers found the first man in the Netherlands with FFI. While he had lived in the Netherlands for 19 years, he was of Egyptian descent. There are other prion diseases that are similar to FFI and could be related but are missing the D178N gene mutation.

Only nine cases of sporadic fatal insomnia have ever been diagnosed . In sFI, there is no mutation in "PRNP"-prion gene in D178N, but all have methionine homozygosity at codon 129.

In late 1983, Italian neurologist/sleep expert Dr. Ignazio Roiter received a patient at the University of Bologna hospital's sleep institute. The man, known only as Silvano, decided in a rare moment of consciousness to be recorded for future studies and to donate his brain for research in hopes of finding a cure for future victims. As of 2017, no cure or treatment has yet been found for FFI. Gene therapy has been thus far unsuccessful. While it is not currently possible to reverse the underlying illness, there is some evidence that treatments that focus solely upon the symptoms may improve quality of life.

It has been proven that sleeping pills and barbiturates are unhelpful; on the contrary, in 74% of cases, they have been shown to worsen the clinical manifestations and hasten the course of the disease.

One of the most notable cases is that of Michael (Michel A.) Corke, a music teacher from New Lenox, Illinois (born in Watseka, Illinois). He began to have trouble sleeping before his 40th birthday in 1991; following these first signs of insomnia, his health and state of mind quickly deteriorated as his condition worsened. Eventually, sleep became completely unattainable, and he was soon admitted to University of Chicago Hospital with a misdiagnosis of clinical depression due to multiple sclerosis. Medical professionals Dr. Raymond Roos and Dr. Anthony Reder, at first unsure of the nature of his illness, initially diagnosed multiple sclerosis; in a bid to provide temporary relief in the later stages of the disease, physicians attempted to induce a coma with the use of sedatives, to no avail as his brain still failed to shut down completely. Corke died in 1993, a month after his 42nd birthday, by which time he had been completely sleep-deprived for six months.

One person was able to exceed the average survival time by nearly one year with various strategies, including vitamin therapy and meditation, using different stimulants and hypnotics, and even complete sensory deprivation in an attempt to induce sleep at night and increase alertness during the day. He managed to write a book and drive hundreds of miles in this time but nonetheless, over the course of his trials, the person succumbed to the classic four-stage progression of the illness.

In the late 2000s, a mouse model was made for FFI. These mice expressed a humanized version of the PrP protein that also contains the D178N FFI mutation. These mice appear to have progressively fewer and shorter periods of uninterrupted sleep, damage in the thalamus, and early deaths, similar to humans with FFI.

As of 2016, studies are investigating whether doxycycline may be able to slow or even prevent the development of the disease.

There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent diarrhea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and others. Some experts advise parenteral thiamine should be given to all at-risk patients in the emergency room.

In the clinical diagnosis should be remembered that early symptoms are nonspecific, and it has been stated that WE may present nonspecific findings. There is consensus to provide water-soluble vitamins and minerals after gastric operations.

In some countries certain foods have been supplemented with thiamine, and have reduced WE cases. Improvement is difficult to quantify because they applied several different actions. Avoiding alcohol and having adequate nutrition reduces one of the main risk factors in developing Wernicke-Korsakoff syndrome.

Most current treatments for aboulia are pharmacological, including the use of antidepressants. However, antidepressant treatment is not always successful and this has opened the door to alternative methods of treatment. The first step to successful treatment of aboulia, or any other DDM, is a preliminary evaluation of the patient's general medical condition and fixing the problems that can be fixed easily. This may mean controlling seizures or headaches, arranging physical or cognitive rehabilitation for cognitive and sensorimotor loss, or ensuring optimal hearing, vision, and speech. These elementary steps also increase motivation because improved physical status may enhance functional capacity, drive, and energy and thereby increase the patient's expectation that initiative and effort will be successful.

There are 5 steps to pharmacological treatment:

1. Optimize medical status.

2. Diagnose and treat other conditions more specifically associated with diminished motivation (e.g., apathetic hyperthyroidism, Parkinson's disease).

3. Eliminate or reduce doses of psychotropics and other agents that aggravate motivational loss (e.g., SSRIs, dopamine antagonists).

4. Treat depression efficaciously when both DDM and depression are present.

5. Increase motivation through use of stimulants, dopamine agonists, or other agents such as cholinesterase inhibitors.

Postpartum PTSD was first described in 1978. Since then over 60 papers have been published. After excessively painful labours, or those with a disturbing loss of control, fear of stillbirth or complications requiring emergency Caesarean section, some mothers suffer nightmares, and intrusive images and memories ('flashbacks'), similar to those occurring after other harrowing experiences. They can last for months. Some avoid further pregnancy (secondary tocophobia), and those who become pregnant again may experience a return of symptoms, especially in the last trimester. Rates up to 5.9% of deliveries have been reported. There is some evidence that early counseling reduces these symptoms. Enduring symptoms require specific psychological treatment.

Most symptoms will improve quickly if deficiencies are treated early. Memory disorder may be permanent.

In patients suspected of WE, thiamine treatment should be started immediately. Blood should be immediately taken to test for thiamine, other vitamins and minerals levels. Following this an immediate intravenous or intramuscular dose of thiamine should be administered two or three times daily. Thiamine administration is usually continued until clinical improvement ceases.

Considering the diversity of possible causes and several surprising symptomatologic presentations, and because there is low assumed risk of toxicity of thiamine, because the therapeutic response is often dramatic from the first day, some qualified authors indicate parenteral thiamine if WE is suspected, both as a resource for diagnosis and treatment. The diagnosis is highly supported by the response to parenteral thiamine, but is not sufficient to be excluded by the lack of it. Parenteral thiamine administration is associated with a very small risk of anaphylaxis.

Alcohol abusers may have poor dietary intakes of several vitamins, and impaired thiamine absorption, metabolism, and storage; they may thus require higher doses.

If glucose is given, such as in hypoglycaemic alcoholics, thiamine must be given concurrently. If this is not done, the glucose will rapidly consume the remaining thiamine reserves, exacerbating this condition.

The observation of edema in MR, and also the finding of inflation and macrophages in necropsied tissues, has led to successful administration of antiinflammatories.

Other nutritional abnormalities should also be looked for, as they may be exacerbating the disease. In particular, magnesium, a cofactor of transketolase which may induce or aggravate the disease.

Other supplements may also be needed, including: cobalamin, ascorbic acid, folic acid, nicotinamide, zinc, phosphorus (dicalcium phosphate) and in some cases taurine, especially suitable when there cardiocirculatory impairment.

Patient-guided nutrition is suggested. In patients with Wernicke-Korsakoff syndrome, even higher doses of parenteral thiamine are recommended. Concurrent toxic effects of alcohol should also be considered.

The word comes from the Greek "tokos", meaning parturition. Early authors like Ideler wrote about this fear, and, in 1937, Binder drew attention to a group of women who sought sterilization because of tocophobia. In the last 40 years there have been a series of papers published mainly from Scandinavia. Tocophobia can be primary (before the first child is born) or secondary (typically after extremely traumatic deliveries). Elective Caesarean section is one solution, but psychotherapy can also help these women to give birth vaginally.

Anticholinergic drugs have been reported to be extremely effective in 40% of the patients with the Pisa syndrome. Patients with Pisa syndrome that is resistant to anticholinergic drugs is mostly resolved by the reduction of the administration of the antipsychotic drugs as previously mentioned. While the specific pathology underlying idiopathic Pisa syndrome is unknown, the administration of anticholinergic drugs has provided resolution in known cases.