Those suffering from post-schizophrenic depression are also commonly at risk for suicidal tendencies. There is a trend correlated between suicide and post-schizophrenic depression according to Mulholland and Cooper's research in "The Symptoms of Depression in Schizophrenia and its Management." Furthermore, depression and schizophrenia have both been studied individually to try to determine if there is a correlation, and research has indicated that there is a very strong tendency for people with depression or schizophrenia to attempt suicide. Statistically, out of all patients suffering from schizophrenia, "10%...commit suicide. Depressed patients with schizophrenia are at a particularly high risk for suicide the first few months after diagnosis and after hospital discharge." Risk factors increasing the chance of suicide are, from highest to lowest, previous depressive orders, previous suicide attempts, drug abuse, and several other factors. Surprisingly, the suicide risk actually decreased with the presence of hallucinations. "The ICD-10 Classification of MEntal and Behavioural Disorders" officially recognizes suicide as being a prominent aspect of post-schizophrenic depression. Because of this drastic increase in suicide, it can be difficult to study post-schizophrenic depression as many of its victims tragically take their own lives.

There is no clear cause to how certain patients with schizophrenia develop post-schizophrenic depression while others may surpass this stage. However, there are a few theories as to possible causes. Those suffering from post-schizophrenic depression often suffer from social isolation due to their illness, which may increase depression levels. There is strong evidence of stigma-related isolation against those suffering from mental illnesses in a variety of societies, especially those with schizophrenia as they are often viewed as dangerous and unpredictable. Because of this isolation and studies linking social isolation and depression, it is possible that patients under these stigmas eventually develop post-schizophrenic depression. Depression in patients with schizophrenia may also be caused by substance abuse, which is fairly common among those suffering from schizophrenia, as depressants such as alcohol and cannabis can relax the patient. Furthermore, with what little information is currently known about post-schizophrenic depression, the onset may be caused by not giving patients with schizophrenia antipsychotic medications. After being taken off of antipsychotic medication, schizophrenic patients' antidepressant medication had to be increased, while those under antipsychotic medication reported suffering fewer depressive symptoms, further giving reason to believe that a lack of antipsychotic medication in earlier stages of schizophrenia may lead to post-schizophrenic depression. However, some psychology professionals still push for the reduction of neuroleptic drugs, as there is a popular belief that post-schizophrenic depression is caused by neuroleptic treatment. Therapists are also believed to engage the depression in people with schizophrenia, having given too much psychotherapy after the patient had overcome their schizophrenic symptoms. Schizophrenia itself should not be overlooked as a key player in causing post-schizophrenic depression, though. A study done over a two-year time period shadowing patients with schizophrenia and monitoring their depression was unable to locate possible triggers such as the ones previously listed, so it is possible the nature of schizophrenia itself is the primary cause of post-schizophrenic depression.

The exact cause of cyclothymia is unknown. It is known that major depression, bipolar disorder, and cyclothymia often occur together within families. There may be a genetic component to cyclothymia: In one study, it was found that an individual is 2–3 times more likely to have the disorder if an identical twin is affected.

It is also believed that a person suffering with PTSD may experience similar shifts in mood based on how many flashbacks they've been dealing with.

Cyclothymia (), also called cyclothymic disorder, is a type of chronic mood disorder widely considered to be a more chronic but milder or subthreshold form of bipolar disorder. Cyclothymia is characterized by numerous mood swings, with periods of hypomanic symptoms that do not meet criteria for a manic episode, alternating with periods of mild or moderate symptoms of depression that do not meet criteria for a major depressive episode.

An individual with cyclothymia may feel stable at a baseline level but experience a noticeable shift to an emotional high during subthreshold hypomanic episodes of elation or euphoria, with symptoms similar to those of mania but less severe, and often cycle to emotional lows with moderate depressive symptoms. To meet the diagnostic criteria for cyclothymia, a person must experience this alternating pattern of emotional highs and lows for a period of at least two years with no more than two consecutive symptom-free months. For children and adolescents, the duration must be at least one year.

The diagnosis of cyclothymia is rare compared to other mood disorders. Diagnosis of cyclothymia entails the absence of any major depressive episode, manic episode or mixed episode, which would qualify the individual for diagnosis of other mood disorders. When a major episode manifests after an initial diagnosis of cyclothymia, the individual may qualify for a diagnosis of bipolar I or bipolar II disorder. Although estimates vary greatly, 15–50% of cases of cyclothymia later advance to the diagnostic criteria for bipolar I and/or bipolar II disorder (with cyclothymic features). Although the emotional highs and lows of cyclothymia are less extreme than those of bipolar disorder and generally do not cause the same conditions, the symptomatology, longitudinal course, family history and treatment response of cyclothymia are consistent with bipolar spectrum.

Lifetime prevalence of cyclothymic disorder is 0.4–1%. Frequency appears similar in men and women, though women more often seek treatment. People with cyclothymia during periodic hypomania (euphoria) tend to feel an inflated self-worth, self-confidence and elation, often with rapid speech, racing thoughts, not much need to sleep, increased aggression and impulsive behavior, showing little regard for consequences of decisions—but may sometimes be somewhat, fully or hyper-productive for a period of several days at a time.

Men and women are diagnosed in equal numbers with depersonalization disorder. A 1991 study on a sample from Winnipeg, Manitoba estimated the prevalence of depersonalization disorder at 2.4% of the population. A 2008 review of several studies estimated the prevalence between 0.8% and 1.9%. This disorder is episodic in about one-third of individuals, with each episode lasting from hours to months at a time. Depersonalization can begin episodically, and later become continuous at constant or varying intensity.

Onset is typically during the teenage years or early 20s, although some report being depersonalized as long as they can remember, and others report a later onset. The onset can be acute or insidious. With acute onset, some individuals remember the exact time and place of their first experience of depersonalization. This may follow a prolonged period of severe stress, a traumatic event, an episode of another mental illness, or drug use. Insidious onset may reach back as far as can be remembered, or it may begin with smaller episodes of lesser severity that become gradually stronger. Patients with drug-induced depersonalization do not appear to be a clinically separate group from those with a non-drug precipitant.

Pseudoneurotic schizophrenia is a postulated mental disorder categorized by the presence of two or more symptoms of mental illness such as anxiety, hysteria, and phobic or obsessive-compulsive neuroses. It is often acknowledged as a personality disorder. Patients generally display salient anxiety symptoms that disguise an underlying psychotic disorder.

In the 1940s, psychiatrists Paul Hoch and Philip Polatin created the term pseudoneurotic schizophrenia. This mental illness, however, is no longer acknowledged as a clinical entity. In 1972 it went on to be called borderline personality disorder, a term coined by Otto Friedmann Kernberg, which referred to an expansive range of issues.

Pseudoneurotic schizophrenia is in the Russian adapted version of the ICD-10 (code F21.3).

When pseudoneurotic schizophrenia was still being utilized as a diagnostic term, doctors were expected to be able to magically cure patients. Patients usually had very little understanding of themselves and the complexity of their illness. They were willing to employ any process in order to maintain mental stability. Their perception of mental stability, however, was also impaired, which made it much more difficult to make proper, helpful medication prescriptions.

Patients would often misuse medication in order to receive attention from their families. They would describe the dosage and effects of the medicine in some strange demeanor to demonstrate that their illness was physical rather than psychological. In like manner, taking medication also kept doctors concerned about the possibility of the patient developing substance dependence and/or drug addiction. Patients used this to get attention and sympathy from others.

The cause (etiology) of RBD is unknown, but recent findings may suggest a link between RBD and bipolar disorders, pointing to the importance of genetic factors. A small sub-group of patients with RBD has temporal lobe epilepsy.

Another theory is that there may be shared risk factors that can lead to both substance abuse and mental illness. Mueser hypothesizes that these may include factors such as social isolation, poverty, lack of structured daily activity, lack of adult role responsibility, living in areas with high drug availability, and association with people who already misuse drugs.

Other evidence suggests that traumatic life events, such as sexual abuse, are associated with the development of psychiatric problems and substance abuse.

The lifetime prevalence of RBD has been estimated at 2.6 to 10.0%, and the one-year prevalence at 5.0-8.2%. The World Health Organization project on "Psychological problems in general health care", which was based on primary care samples, reported a one-year prevalence of 3.7 – 9.9%. However none of these studies differentiate between RBD with and without a history of other mood disorders (e.g. major depression). DSM-IV field trial estimated the life-time of RBD only to be about 2%.

Risk factors for mental illness include genetic inheritance, such as parents having depression, or a propensity for high neuroticism or "emotional instability".

In depression, parenting risk factors include parental unequal treatment, and there is association with high cannabis use.

In schizophrenia and psychosis, risk factors include migration and discrimination, childhood trauma, bereavement or separation in families, and abuse of drugs, including cannabis, and urbanicity.

In anxiety, risk factors may include family history (e.g. of anxiety), temperament and attitudes (e.g. pessimism), and parenting factors including parental rejection, lack of parental warmth, high hostility, harsh discipline, high maternal negative affect, anxious childrearing, modelling of dysfunctional and drug-abusing behaviour, and child abuse (emotional, physical and sexual).

Environmental events surrounding pregnancy and birth have also been implicated. Traumatic brain injury may increase the risk of developing certain mental disorders. There have been some tentative inconsistent links found to certain viral infections, to substance misuse, and to general physical health.

Social influences have been found to be important, including abuse, neglect, bullying, social stress, traumatic events and other negative or overwhelming life experiences. For bipolar disorder, stress (such as childhood adversity) is not a specific cause, but does place genetically and biologically vulnerable individuals at risk for a more severe course of illness. The specific risks and pathways to particular disorders are less clear, however. Aspects of the wider community have also been implicated, including employment problems, socioeconomic inequality, lack of social cohesion, problems linked to migration, and features of particular societies and cultures.

Neither antidepressants nor antipsychotics have been found to be useful, Additionally antipsychotics can worsen symptoms of depersonalisation. To date, no clinical trials have studied the effectiveness of benzodiazepines. Tentative evidence supports naloxone and naltrexone.

A combination of an SSRI and a benzodiazepine has been proposed to be useful for DPD patients with anxiety.

Modafinil used alone has been reported to be effective in a subgroup of individuals with depersonalization disorder (those who have attentional impairments, under-arousal and hypersomnia). However, clinical trials have not been conducted.

In the mental health field, schizophasia or word salad is language that is confused and often repetitious, symptomatic of various mental illnesses.

It is usually associated with a manic presentation of bipolar affective disorder and other symptoms of serious mental illnesses, such as psychosis, including schizophrenia. It is characterized by an apparently confused usage of words with no apparent meaning or relationship attached to them. In this context, it is considered to be a symptom of a formal thought disorder. In some cases schizophasia can be a sign of asymptomatic schizophrenia; e.g. the question "Why do people believe in God?" could elicit a response consisting of a series of words commonly associated with religion or prayer but strung together with no regard to language rules.

Schizophasia should be contrasted with another symptom of cognitive disruption and cognitive slippage involving certain idiosyncratic arrangements of words. With this symptom, the language may or may not be grammatically correct depending on the severity of the disease and the particular mechanisms which have been impacted by the disease.

The American diagnostic codes, from the "DSM-IV", do not specifically code for this disorder although they include it as a symptom under the diagnosis of schizophrenia.

MD is supposed to be a common clinical phenomenon. According to some authors, masked depression is as frequent as overt depression. Although masked depression can be found at any age, it has been observed more commonly after mid-life.

Making the diagnosis and the management of MD in clinical practice are complicated by the fact that he who has got MD is unaware of his mental illness.

Patients with MD are reluctant to associate their physical symptoms with an affective disorder and refuse mental health care. As a rule, these patients attribute their disturbances to physical illness, seek medical care for them, and report only somatic complaints to their physicians, with the consequence that many of such depressions are not recognized or are misdiagnosed and mistreated Estimates of depressed patients who are correctly identified and treated range from 5% to 60%. Recent data show that about 10% of people who consult a physician for any reason originally suffer from affective disorders disguised by physical symptoms.

The alleviation of dysphoria theory suggests that people with severe mental illness commonly have a negative self-image, which makes them vulnerable to using psychoactive substances to alleviate these feelings. Despite the existence of a wide range of dysphoric feelings (anxiety, depression, boredom, and loneliness), the literature on self-reported reasons for use seems to lend support for the experience of these feelings being the primary motivator for drug and alcohol misuse.

About 8% of children and adolescents suffer from depression. Research suggests that the prevalence of young depression sufferers in Western cultures ranges from 1.9% to 3.4% among primary school children and 3.2% to 8.9% among adolescents. Studies have also found that among children diagnosed with a depressive episode, there is a 70% rate of recurrence within five years. Furthermore, 50% of children with depression will have a recurrence at least once during their adulthood. While there is no gender difference in depression rates up until age 15, after that age the rate among women doubles compared to men. However, in terms of recurrence rates and symptom severity, there is no gender difference. In an attempt to explain these findings, one theory asserts that pre-adolescent women, on average, have more risk factors for depression than men. These risk factors then combine with the typical stresses and challenges of adolescent development to trigger the onset of depression.

Like their adult counterparts, children and adolescent depression sufferers are at an increased risk of attempting or committing suicide. Suicide is the third leading cause of death among 15-19 year olds. Adolescent males may be at an even higher risk of suicidal behavior if they also present with a conduct disorder. In the 1990s, the National Institute of Mental Health (NIMH) found that up to 7% of adolescents who develop major depressive disorder may commit suicide as young adults. Such statistics demonstrate the importance of interventions by family and friends, as well as the importance of early diagnosis and treatment by medical staff, to prevent suicide among depressed or at-risk youth.

Dementia praecox (a "premature dementia" or "precocious madness") is a disused psychiatric diagnosis that originally designated a chronic, deteriorating psychotic disorder characterized by rapid cognitive disintegration, usually beginning in the late teens or early adulthood. Over the years, the term "dementia praecox" was gradually replaced by "schizophrenia", which remains in current diagnostic use.

The term "dementia praecox" was first used in 1891 by Arnold Pick (1851–1924), a professor of psychiatry at Charles University in Prague. His brief clinical report described the case of a person with a psychotic disorder resembling hebephrenia. German psychiatrist Emil Kraepelin (1856–1926) popularised it in his first detailed textbook descriptions of a condition that eventually became a different disease concept and relabeled as schizophrenia. Kraepelin reduced the complex psychiatric taxonomies of the nineteenth century by dividing them into two classes: manic-depressive psychosis and dementia praecox. This division, commonly referred to as the Kraepelinian dichotomy, had a fundamental impact on twentieth-century psychiatry, though it has also been questioned.

The primary disturbance in dementia praecox was seen to be a disruption in cognitive or mental functioning in attention, memory, and goal-directed behaviour. Kraepelin contrasted this with manic-depressive psychosis, now termed bipolar disorder, and also with other forms of mood disorder, including major depressive disorder. He eventually concluded that it was not possible to distinguish his categories on the basis of cross-sectional symptoms.

Kraepelin viewed dementia praecox as a progressively deteriorating disease from which no one recovered. However, by 1913, and more explicitly by 1920, Kraepelin admitted that while there may be a residual cognitive defect in most cases, the prognosis was not as uniformly dire as he had stated in the 1890s. Still, he regarded it as a specific disease concept that implied incurable, inexplicable madness.

Neurocognitive disorders can have numerous causes: genetics, brain trauma, stroke, and heart issues. The main causes are neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease because they affect or deteriorate brain functions. Other diseases and conditions that cause NDCs include vascular dementia, frontotemporal degeneration, Lewy body disease, prion disease, normal pressure hydrocephalus, and dementia/neurocognitive issues due to HIV infection. They may also include dementia due to substance abuse or exposure to toxins.

Neurocongnitive disorder may also be caused by brain trauma, including concussions and Traumatic Brain Injuries, as well as post-traumatic stress and alcoholism. This is referred to as amnesia, and is characterized by damage to major memory encoding parts of the brain such as the hippocampus. Difficulty creating recent term memories is called anterograde amnesia and is caused by damage to the hippocampus part of the brain, which is a major part of the memory process. Retrograde amnesia is also caused by damage to the hippocampus, but the memories that were encoded or in the process of being encoded in long term memory are erased

Correlations of mental disorders with drug use include cannabis, alcohol and caffeine, use of which appears to promote anxiety. For psychosis and schizophrenia, usage of a number of drugs has been associated with development of the disorder, including cannabis, cocaine, and amphetamines. There has been debate regarding the relationship between usage of cannabis and bipolar disorder.

Delirium can be caused by the worsening of previous medical conditions, substance abuse or withdrawal, mental illness, severe pain, immobilization, sleep deprivation and hypnosis.

Other common causes that may increase the risk of delirium include infections of urinary tract, skin and stomach, pneumonia, old age, and poor nutrition.

Somatic manifestations of MD are distinguished by an extreme diversity and include headaches, back pain, abdominal pain etc. Pathological behaviour masking depression may take the form of compulsive gambling, compulsive work, changes in arousal or orgasmic function, decreased libido or, on the contrary, impulsive sexual behaviour, alcoholism, drug addiction and more.

Depressive Disorder Not Otherwise Specified (DD-NOS) is designated by the code "311" in the DSM-IV for depressive disorders that are impairing but do not fit any of the officially specified diagnoses. According to the DSM-IV, DD-NOS encompasses "any depressive disorder that does not meet the criteria for a specific disorder." In the DSM-5, it is called unspecified depressive disorder.

Examples of disorders in this category include those sometimes described as minor depressive disorder and recurrent brief depression.

"Depression" refers to a spectrum of disturbances in mood that vary from mild to severe and from short periods to constant illness. DD-NOS is diagnosed if a patients symptoms fail to meet the criteria more common depressive disorders such as major depressive disorder or dysthymia. Although DD-NOS shares similar symptoms to dysthymia, dysthymia is classified by a period of at least 2 years of constantly recurring depressed mood, where as DD-NOS is classified by much shorter periods of depressed moods.

For most people who suffer the condition, their life will be significantly affected. DD-NOS can make many aspects of a person's daily life difficult to manage, inhibiting their ability to enjoy the things that used to make them happy. Sufferers of the disorder tend to isolate themselves from their friends and families, lose interest in some activities, and experience behavioural changes and sleeping disorders. Some sufferers also experience suicidal tendencies or suicide attempts. In addition to having these symptoms, a diagnosis of DD-NOS will only be made if the symptoms cause significant distress or impairment in social, occupational, or other important areas of functioning. For the diagnosis to be accurate, a psychiatrist is required to spend extensive time with the patient.

Symptoms of the disorder may arise due to several reasons. These include:

- Distress due to medical conditions

- Environmental effects and situations

However, the effects of drugs or medication or bereavement are not classified under the diagnosis.

A person will not be diagnosed with the condition if they have or have had any of the following: a major depressive episode, manic episode, mixed episode or hypomanic episode.

A diagnosis of the disorder will look like: "Depressive Disorder NOS 311".

Disorders that cause injury or damage to the brain and contribute to OBS include, but are not limited to:

- Alcoholism

- Alzheimer's Disease

- Attention deficit/hyperactivity disorder

- Autism

- Concussion

- Encephalitis

- Epilepsy

- Fetal alcohol syndrome

- Hypoxia

- Parkinson's disease

- Intoxication/overdose caused by drug abuse including alcoholism

- Sedative hypnotic dependence and drug abuse

- Intracranial hemorrhage/trauma

- Korsakoff Syndrome

- Mastocytosis

- Meningitis

- Psychoorganic syndrome

- Stroke/transient ischemic attack (TIA)

- Withdrawal from drugs, especially sedative hypnotics, e.g. alcohol or benzodiazepines

Other conditions that may be related to organic brain syndrome include: clinical depression, neuroses, and psychoses, which may occur simultaneously with the OBS.

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.