The lifetime prevalence of dissociative disorders varies from 10% in the general population to 46% in psychiatric inpatients. Diagnosis can be made with the help of structured interviews such as the Dissociative Disorders Interview Schedule (DDIS) and the Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D), or with the Dissociative Experiences Scale (DES) which is a self-assessment questionnaire. Some diagnostic tests have also been adapted and/or developed for use with children and adolescents such as the Children's Version of the Response Evaluation Measure (REM-Y-71), Child Interview for Subjective Dissociative Experiences, Child Dissociative Checklist (CDC), Child Behavior Checklist (CBCL) Dissociation Subscale, and the Trauma Symptom Checklist for Children Dissociation Subscale.

There are problems with classification, diagnosis and therapeutic strategies of dissociative and conversion disorders which can be understood by the historic context of hysteria. Even current systems used to diagnose DD such as the DSM-IV and ICD-10 differ in the way the classification is determined. In most cases mental health professionals are still hesitant to diagnose patients with Dissociative Disorder, because before they are considered to be diagnosed with Dissociative Disorder these patients have more than likely been diagnosed with major depression, anxiety disorder, and most often post-traumatic disorder.

An important concern in the diagnosis of dissociative disorders is the possibility that the patient may be feigning symptoms in order to escape negative consequences. Young criminal offenders report much higher levels of dissociative disorders, such as amnesia. In one study it was found that 1% of young offenders reported complete amnesia for a violent crime, while 19% claimed partial amnesia. There have also been incidences in which people with dissociative identity disorder provide conflicting testimonies in court, depending on the personality that is present.

Individual differences in women's estrogen cycles may be related to the expression of BPD symptoms in female patients. A 2003 study found that women's BPD symptoms were predicted by changes in estrogen levels throughout their menstrual cycles, an effect that remained significant when the results were controlled for a general increase in negative affect.

There is a strong correlation between child abuse, especially child sexual abuse, and development of BPD. Many individuals with BPD report a history of abuse and neglect as young children, but causation is still debated. Patients with BPD have been found to be significantly more likely to report having been verbally, emotionally, physically, or sexually abused by caregivers of either gender. They also report a high incidence of incest and loss of caregivers in early childhood. Individuals with BPD were also likely to report having caregivers of both sexes deny the validity of their thoughts and feelings. Caregivers were also reported to have failed to provide needed protection and to have neglected their child's physical care. Parents of both sexes were typically reported to have withdrawn from the child emotionally and to have treated the child inconsistently. Additionally, women with BPD who reported a previous history of neglect by a female caregiver and abuse by a male caregiver were significantly more likely to experience sexual abuse by a non-caregiver.

It has been suggested that children who experience chronic early maltreatment and attachment difficulties may go on to develop borderline personality disorder. Writing in the psychoanalytic tradition, Otto Kernberg argues that a child's failure to achieve the developmental task of and failure to overcome splitting might increase the risk of developing a borderline personality. A child's inability to tolerate delayed gratification at age four does not predict later development of BPD.

Dissociative disorders (DD) are widely believed to have roots in traumatic childhood experience (abuse or loss), but symptomology often goes unrecognized or is misdiagnosed in children and adolescents. There are several reasons why recognizing symptoms of dissociation in children is challenging: it may be difficult for children to describe their internal experiences; caregivers may miss signals or attempt to conceal their own abusive or neglectful behaviors; symptoms can be subtle or fleeting; disturbances of memory, mood, or concentration associated with dissociation may be misinterpreted as symptoms of other disorders.

In addition to developing diagnostic tests for children and adolescents (see above), a number of approaches have been developed to improve recognition and understanding of dissociation in children. Recent research has focused on clarifying the neurological basis of symptoms associated with dissociation by studying neurochemical, functional and structural brain abnormalities that can result from childhood trauma. Others in the field have argued that recognizing disorganized attachment (DA) in children can help alert clinicians to the possibility of dissociative disorders.

Clinicians and researchers also stress the importance of using a developmental model to understand both symptoms and the future course of DDs. In other words, symptoms of dissociation may manifest differently at different stages of child and adolescent development and individuals may be more or less susceptible to developing dissociative symptoms at different ages. Further research into the manifestation of dissociative symptoms and vulnerability throughout development is needed. Related to this developmental approach, more research is required to establish whether a young patient’s recovery will remain stable over time.

Dissociative disorder not otherwise specified (DDNOS) is a mental health diagnosis for pathological dissociation that matches the DSM-5 criteria for a dissociative disorder, but does not fit the full criteria for any of the specifically identified subtypes, which include dissociative identity disorder, dissociative amnesia, and depersonalization/derealization disorder. The International Statistical Classification of Diseases and Related Health Problems (ICD-10) refers to the diagnosis as "Other dissociative and conversion disorders".

Examples of DDNOS include chronic and recurrent syndromes of mixed dissociative symptoms, identity disturbance due to prolonged and intense coercive persuasion, disorders similar to dissociative identity disorder, acute dissociative reactions to stressful events, and dissociative trance.

DDNOS is the most common dissociative disorder and is diagnosed in 40% of dissociative disorder cases. It is often co-morbid with other mental illnesses such as complex posttraumatic stress disorder, major depressive disorder, generalized anxiety disorder, personality disorders, substance abuse disorders and eating disorders.

Little is known about prognosis of untreated DID. It rarely, if ever, goes away without treatment, but symptoms may resolve from time to time or wax and wane spontaneously. Patients with mainly dissociative and posttraumatic symptoms face a better prognosis than those with comorbid disorders or those still in contact with abusers, and the latter groups often face lengthier and more difficult treatment. Suicidal ideation, failed suicide attempts, and self-harm also occur. Duration of treatment can vary depending on patient goals, which can extend from elimination of all alters to merely reducing inter-alter amnesia, but generally takes years.

There is little systematic data on the prevalence of DID. It occurs more commonly in young adults and declines with age. Reported rates in the community vary from 1% to 3% with higher rates among psychiatric patients. It is 5 to 9 times more common in females than males during young adulthood, though this may be due to selection bias as males who could be diagnosed with DID may end up in the criminal justice system rather than hospitals. In children rates among females and males are approximately the same (5:4). DID diagnoses are extremely rare in children; much of the research on childhood DID occurred in the 1980s and 1990s and does not address ongoing controversies surrounding the diagnosis.

Though the condition has been described in non-English speaking nations and non-Western cultures, these reports all occur in English-language journals authored by international researchers who cite Western scientific literature and are therefore not isolated from Western influences.

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.

Multiple complex developmental disorder is likely to be caused by a number of different various genetic factors. Each individual with MCDD is unique from one another and displays different symptoms. Various neuropsychological disorders can also be found in family members of people with MCDD.

The exact cause of depersonalization is unknown, although biopsychosocial correlations and triggers have been identified. Childhood interpersonal trauma – emotional abuse in particular – is a significant predictor of a diagnosis. The most common immediate precipitators of the disorder are severe stress; major depressive disorder and panic; and hallucinogen ingestion. People who live in highly individualistic cultures may be more vulnerable to depersonalization, due to threat hypersensitivity and an external locus of control.

One cognitive behavioral conceptualization is that misinterpreting normally transient dissociative symptoms as an indication of severe mental illness or neurological impairment leads to the development of the chronic disorder. This leads to a vicious cycle of heightened anxiety and symptoms of depersonalization and derealization.

Not much is known about the neurobiology of depersonalization disorder; however, there is converging evidence that the prefrontal cortex may inhibit neural circuits that normally form the substrate of emotional experience. A PET scan found functional abnormalities in the visual, auditory, and somatosensory cortex, as well as in areas responsible for an integrated body schema. In an fMRI study of DPD patients, emotionally aversive scenes activated the right ventral prefrontal cortex. Participants demonstrated a reduced neural response in emotion-sensitive regions, as well as an increased response in regions associated with emotional regulation. In a similar test of emotional memory, depersonalization disorder patients did not process emotionally salient material in the same way as did healthy controls. In a test of skin conductance responses to unpleasant stimuli, the subjects showed a selective inhibitory mechanism on emotional processing.

Depersonalization disorder may be associated with dysregulation of the hypothalamic-pituitary-adrenal axis, the area of the brain involved in the "fight-or-flight" response. Patients demonstrate abnormal cortisol levels and basal activity. Studies found that patients with DPD could be distinguished from patients with clinical depression and posttraumatic stress disorder.

The symptoms are sometimes described by those with neurological diseases, such as amyotrophic lateral sclerosis, Alzheimer's, multiple sclerosis (MS), neuroborreliosis (Lyme disease), etc., that directly affect brain tissue.

It has been thought that depersonalization has been caused by a biological response to dangerous or life-threatening situations which causes heightened senses and emotional neutrality. If this response occurs in real-life, non-threatening situations, the result can be shocking to the individual.

Traumatic grief or complicated mourning are conditions where both trauma and grief coincide. There are conceptual links between trauma and bereavement since loss of a loved one is inherently traumatic. If a traumatic event was life-threatening, but did not result in death, then it is more likely that the survivor will experience post-traumatic stress symptoms. If a person dies, and the survivor was close to the person who died, then it is more likely that symptoms of grief will also develop. When the death is of a loved one, and was sudden or violent, then both symptoms often coincide. This is likely in children exposed to community violence.

For C-PTSD to manifest, the violence would occur under conditions of captivity, loss of control and disempowerment, coinciding with the death of a friend or loved one in life-threatening circumstances. This again is most likely for children and stepchildren who experience prolonged domestic or chronic community violence that ultimately results in the death of friends and loved ones. The phenomenon of the increased risk of violence and death of stepchildren is referred to as the Cinderella effect.

Depersonalization has been described by some as a desirable state, particularly by those that have experienced it under the influence of mood-altering recreational drugs. It is an effect of dissociatives and psychedelics, as well as a possible side effect of caffeine, alcohol, amphetamine, and cannabis. It is a classic withdrawal symptom from many drugs.

Benzodiazepine dependence, which can occur with long-term use of benzodiazepines, can induce chronic depersonalization symptomatology and perceptual disturbances in some people, even in those who are taking a stable daily dosage, and it can also become a protracted feature of the benzodiazepine withdrawal syndrome.

Lieutenant Colonel Dave Grossman, in his book "", suggests that military training artificially creates depersonalization in soldiers, suppressing empathy and making it easier for them to kill other human beings.

Graham Reed (1974) noted that depersonalization occurs in relation to the experience of falling in love.

A clear causal connection between drug use and psychotic spectrum disorders, including schizoaffective disorder, has been difficult to prove. In the specific case of marijuana or cannabis, however, evidence supports a link between earlier onset of psychotic illness and cannabis use. The more often cannabis is used, particularly in early adolescence, the more likely a person is to develop a psychotic illness, with frequent use being correlated with double the risk of psychosis and schizoaffective disorder. A 2009 Yale review stated that in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. While cannabis use is accepted as a contributory cause of schizoaffective disorder by many, it remains controversial, since not all young people who use cannabis later develop psychosis, but those who do use cannabis have an increased odds ratio of about 3.

There is evidence that the two major component cannabinoids in cannabis have different effects: tetrahydrocannabinol (THC), which causes a "high," may increase propensity to psychosis; while cannabidiol (CBD), which doesn't cause a "high" and may have neuroprotective effects—that is, reduce psychosis and have mood stabilizing effects.

About half of those with schizoaffective disorder use drugs or alcohol excessively. There is evidence that alcohol abuse via a kindling mechanism can occasionally cause the development of a chronic substance induced psychotic disorder, i.e. schizoaffective disorder. There is little evidence to suggest that psychotic individuals choose specific drugs to self-medicate; there is some support for the hypothesis that they use drugs to cope with unpleasant states such as depression, anxiety, boredom and loneliness.

Amphetamine, cocaine, and to a lesser extent alcohol, can result in psychosis that presents clinically like psychosis in schizoaffective disorder. It is well understood that methamphetamine and cocaine use can result in methamphetamine or cocaine-induced psychosis that may persist even when users remain abstinent. Alcohol-induced psychosis can also persist during abstinence, though it appears to do so at a lower rate, than when it is being abused.

Although it is not generally believed to be a cause of the illness, people with schizoaffective disorder use nicotine at much greater rates than the general population.

The cause of sleepwalking is not known. A number of, as yet unproven, hypotheses are suggested for why it might occur. These include a delay in the maturity of the central nervous system, increased slow wave sleep, sleep deprivation, fever, and excessive tiredness.

There may be a genetic component to sleepwalking. One study found that sleepwalking occurred in 45% of children who have one parent who sleepwalked, and in 60% of children if both parents sleepwalked. Thus, heritable factors may predispose an individual to sleepwalking, but expression of the behavior may also be influenced by environmental factors. Genetic studies using common fruit flies as experimental models reveal a link between night sleep and brain development mediated by evolutionary conserved transcription factors such as AP-2

Sleepwalking may be inherited as an autosomal dominant disorder with reduced penetrance. Genome-wide multipoint parametric linkage analysis for sleepwalking revealed a maximum logarithm of the odds score of 3.14 at chromosome 20q12-q13.12 between 55.6 and 61.4 cM.

Medications, primarily in four classes—benzodiazepine receptor agonists and other GABA modulators, antidepressants and other serotonergic agents, antipsychotics, and β-blockers— have been associated with sleepwalking. The best evidence of medications causing sleepwalking is for Zolpidem and sodium oxybate—all other reports are based on associations noted in case reports.

A number of conditions, such as Parkinson's Disease, are thought to trigger sleepwalking in people without a previous history of sleepwalking.

Depersonalization is also a direct symptom of Lyme disease as well as other tick-borne diseases. If depersonalization is suspected a blood-test is required in search of anti-bodies.

The disorder is extraordinarily rare. While individuals of all backgrounds have been reported with the disorder, there is a higher inclination towards males (75% or more). The average age of those with Ganser syndrome is 32 and it stretches from ages 15 to 62 years old. It has been reported in children.

The disorder is apparently most common in men and prisoners, although prevalence data and familial patterns are not established.

A combination of genetic and environmental factors are believed to play a role in the development of schizoaffective disorder.

Viewed broadly then, biological and environmental factors interact with a person's genes in ways which may increase or decrease the risk for developing schizoaffective disorder; exactly how this happens (the biological mechanism) is not yet known. Schizophrenia spectrum disorders, of which schizoaffective disorder is a part, have been increasingly linked to advanced paternal age at the time of conception, a known cause of genetic mutations. The physiology of people diagnosed with schizoaffective disorder appears to be similar, but not identical, to that of those diagnosed with schizophrenia and bipolar disorder; however, human neurophysiological function in normal brain and mental disorder syndromes is not fully understood.

Complex post-traumatic stress disorder (C-PTSD; also known as complex trauma disorder) is a psychological disorder thought to occur as a result of repetitive, prolonged trauma involving harm or abandonment by a caregiver or other interpersonal relationships with an uneven power dynamic. C-PTSD is associated with sexual, emotional or physical abuse or neglect in childhood, intimate partner violence, victims of kidnapping and hostage situations, indentured servants, victims of slavery, sweatshop workers, prisoners of war, victims of bullying, concentration camp survivors, and defectors of cults or cult-like organizations. Situations involving captivity/entrapment (a situation lacking a viable escape route for the victim or a perception of such) can lead to C-PTSD-like symptoms, which include prolonged feelings of terror, worthlessness, helplessness, and deformation of one's identity and sense of self.

Some researchers argue that C-PTSD is distinct from, but similar to PTSD, somatization disorder, dissociative identity disorder, and borderline personality disorder, with the main distinction being that it distorts a person's core identity, especially when prolonged trauma occurs during childhood development . It was first described in 1992 by Judith Herman in her book "Trauma & Recovery" and an accompanying article. Though peer-reviewed journals have published papers on C-PTSD, the category is not yet adopted by either the American Psychiatric Association's (APA) "Diagnostic and Statistical Manual of Mental Disorders", 5th Edition (DSM-5), or in the World Health Organization's (WHO) "International Statistical Classification of Diseases and Related Health Problems", 10th Edition (ICD-10). However, it is proposed for the ICD-11, to be finalized in 2018.

The DSM-IV-TR states that the fugue may have a duration from days to months, and recovery is usually rapid. However, some cases may be refractory. An individual usually has only one episode.

Some treatments for internalizing disorders include antidepressants, electroconvulsive therapy, and psychotherapy.

The lifetime prevalence of sleepwalking is estimated to be 4.6%–10.3%. A meta-analysis of 51 studies, that included more than 100,000 children and adults, found that sleepwalking is more common in children with an estimated 5%, compared with 1.5% of adults, sleepwalking at least once in the previous 12 months. The rate of sleepwalking does not vary across ages during childhood.

Hospitalization may be necessary during the acute phase of symptoms, and psychiatric care if the patient is a danger to self or others. A neurological consult is advised to rule out any organic cause.

Multiple complex developmental disorder (MCDD) is a research category, proposed to involve several neurological and psychological symptoms where at least some symptoms are first noticed during early childhood and persist throughout life. It was originally suggested to be a subtype of autistic spectrum disorders (PDD) with co-morbid schizophrenia or another psychotic disorder; however, there is some controversy that not everyone with MCDD meets criteria for both PDD and psychosis. The term "multiplex developmental disorder" was coined by Donald J. Cohen in 1986.

Dissociative fugue, formerly fugue state or psychogenic fugue, is a dissociative disorder. It is a rare psychiatric disorder characterized by reversible amnesia for personal identity, including the memories, personality, and other identifying characteristics of individuality. The state can last days, months or longer. Dissociative fugue usually involves unplanned travel or wandering, and is sometimes accompanied by the establishment of a new identity. It is a facet of dissociative amnesia, according to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

After recovery from fugue, previous memories usually return intact. Because of this, there is not normally any treatment necessary for people who have been in fugue states. Additionally, an episode of fugue is not characterized as attributable to a psychiatric disorder if it can be related to the ingestion of psychotropic substances, to physical trauma, to a general medical condition, or to dissociative identity disorder, delirium, or dementia. Fugues are precipitated by a series of long-term traumatic episodes. It is most commonly associated with childhood victims of sexual abuse who learn over time to dissociate memory of the abuse (dissociative amnesia).

An internalizing disorder is one type of emotional and behavioral disorder, along with externalizing disorders, and low incidence disorders. One who suffers from an internalizing disorder will keep their problems to themselves, or internalize the problems.