Somatization disorder is estimated to occur in 0.2% to 2% of females, and 0.2% of males.

There are cultural differences in the prevalence of somatization disorder. For example, somatization disorder and symptoms were found to be significantly more common in Puerto Rico. In addition the diagnosis is also more prevalent among African Americans and those with less than a high school education or lower socioeconomic status.

There is usually co-morbidity with other psychological disorders, particularly mood disorders or anxiety disorders. Research also showed comorbidity between somatization disorder and personality disorders, especially antisocial, borderline, narcissistic, histrionic, avoidant, and dependent personality disorder.

About 10-20 percent of female first degree relatives also have somatization disorder and male relatives have increased rates of alcoholism and sociopathy.

Socioeconomic status has also been looked at as a potential cause for personality disorders. There is a strong association with low parental/neighborhood socioeconomic status and personality disorder symptoms. In a recent study comparing parental socioeconomic status and a child's personality, it was seen that children who were from higher socioeconomic backgrounds were more altuistic, less risk seeking, and had overall higher IQs. These traits correlate with a low risk of developing personality disorders later on in life. In a study looking at female children who were detained for disciplinary actions found that psychological problems were most negatively associated with socioeconomic problems. Furthermore, social disorganization was found to be inversely correlated with personality disorder symptoms.

Currently, genetic research for the understanding of the development of personality disorders is severely lacking. However, there are a few possible risk factors currently in discovery. Researchers are currently looking into genetic mechanisms for traits such as aggression, fear and anxiety, which are associated with diagnosed individuals. More research is being conducted into disorder specific mechanisms.

Reported prevalence of STPD in community studies ranges from 0.6% in a Norwegian sample, to 4.6% in an American sample. A large American study found a lifetime prevalence of 3.9%, with somewhat higher rates among men (4.2%) than women (3.7%). It may be uncommon in clinical populations, with reported rates of 0% to 1.9%.

Together with other Cluster A personality disorders, it is also very common among homeless people.

A University of Colorado Colorado Springs study comparing personality disorders and Myers-Briggs Type Indicator types found that the disorder had a significant correlation with the Introverted (I), Intuitive (N), Thinking (T), and Perceiving (P) preferences.

Externalizing disorders are frequently comorbid or co-occurring with other disorders. Individuals who have the co-occurrence of more than one externalizing disorder have homotypic comorbidity, whereas individuals who have co-occurring externalizing and Internalizing disorders have heterotypic comorbidity. It is not uncommon for children with early externalizing problems to develop both internalizing and further externalizing problems across the lifespan.

While the cause of conduct disorder is complicated by an intricate interplay of biological and environmental factors, identifying underlying mechanisms is crucial for obtaining accurate assessment and implementing effective treatment. These mechanisms serve as the fundamental building blocks on which evidence-based treatments are developed. Despite the complexities, several domains have been implicated in the development of conduct disorder including cognitive variables, neurological factors, intraindividual factors, familial and peer influences, and wider contextual factors. These factors may also vary based on the age of onset, with different variables related to early (e.g., neurodevelopmental basis) and adolescent (e.g., social/peer relationships) onset.

Although somatization disorder has been studied and diagnosed for more than a century, there is debate and uncertainty regarding its pathophysiology. Most current explanations focus on the concept of a misconnection between the mind and the body. Genetics probably contributes a very small amount to development of the disorder.

One of the oldest explanations for somatization disorder advances the theory that it is a result of the body's attempt to cope with emotional and psychological stress. The theory states that the body has a finite capacity to cope with psychological, emotional, and social distress, and that beyond a certain point symptoms are experienced as physical, principally affecting the digestive, nervous, and reproductive systems. There are many different feedback systems where the mind affects the body; for instance, headaches are known to be associated with psychological factors, and stress and the hormone cortisol are known to have a negative impact on immune functions. This might explain why somatization disorders are more likely in people with irritable bowel syndrome, and why patients with SSD are more likely to have a mood or anxiety disorder. There is also a much increased incidence of SSD in women with a history of physical, emotional or sexual abuse.

Another hypothesis for the cause of somatization disorder is that people with the disorder have heightened sensitivity to internal physical sensations and pain. A biological sensitivity to somatic feelings could predispose a person to developing SSD. It is also possible that a person's body might develop increased sensitivity of nerves associated with pain and those responsible for pain perception, as a result of chronic exposure to stressors.

Cognitive theories explain somatization disorder as arising from negative, distorted, and catastrophic thoughts and reinforcement of these cognitions. Catastrophic thinking could lead a person to believe that slight ailments, such as mild muscle pain or shortness of breath, are evidence of a serious illness such as cancer or a tumor. These thoughts can then be reinforced by supportive social connections. A spouse who responds more to his or her partner's pain cues makes it more likely that he or she will express greater pain. Children of parents who are preoccupied or overly attentive to the somatic complaints of their children are more likely to develop somatic symptoms. Severe cognitive distortions can make a person with SSD limit the behaviors he or she engages in, and cause increased disability and impaired functioning.

Elements of the family and social environment may also play a role in the development and maintenance of conduct disorder. For instance, antisocial behavior suggestive of conduct disorder is associated with single parent status, parental divorce, large family size, and young age of mothers. However, these factors are difficult to tease apart from other demographic variables that are known to be linked with conduct disorder, including poverty and low socioeconomic status. Family functioning and parent-child interactions also play a substantial role in childhood aggression and conduct disorder, with low levels of parental involvement, inadequate supervision, and unpredictable discipline practices reinforcing youth's defiant behaviors.

Peer influences have also been related to the development of antisocial behavior in youth, particularly peer rejection in childhood and association with deviant peers. Peer rejection is not only a marker of a number of externalizing disorders, but also a contributing factor for the continuity of the disorders over time. Hinshaw and Lee (2003) also explain that association with deviant peers has been thought to influence the development of conduct disorder in two ways: 1) a “selection” process whereby youth with aggressive characteristics choose deviant friends, and 2) a “facilitation” process whereby deviant peer networks bolster patterns of antisocial behavior. In a separate study by Bonin and colleagues, parenting programs were shown to positively affect child behavior and reduce costs to the public sector.

Data from the 2001–02 National Epidemiologic Survey on Alcohol and Related Conditions indicates a prevalence rate of 2.36% in the American general population. It appears to occur with equal frequency in males and females. In one study, it was seen in 14.7% of psychiatric outpatients.

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.

Genetic

Schizotypal personality disorder is widely understood to be a "schizophrenia spectrum" disorder. Rates of schizotypal personality disorder are much higher in relatives of individuals with schizophrenia than in the relatives of people with other mental illnesses or in people without mentally ill relatives. Technically speaking, schizotypal personality disorder may also be considered an "extended phenotype" that helps geneticists track the familial or genetic transmission of the genes that are implicated in schizophrenia. But there is also a genetic connection of STPD to mood disorders and depression in particular.

Social and environmental

There is now evidence to suggest that parenting styles, early separation, trauma/maltreatment history (especially early childhood neglect) can lead to the development of schizotypal traits. Neglect or abuse, trauma, or family dysfunction during childhood may increase the risk of developing schizotypal personality disorder. Over time, children learn to interpret social cues and respond appropriately but for unknown reasons this process does not work well for people with this disorder.

Schizotypal personality disorders are characterized by a common attentional impairment in various degrees that could serve as a marker of biological susceptibility to STPD. The reason is that an individual who has difficulties taking in information may find it difficult in complicated social situations where interpersonal cues and attentive communications are essential for quality interaction. This might eventually cause the individual to withdraw from most social interactions, thus leading to asociality.

ADHD often precedes the onset of ODD, and approximately half of children with ADHD, Combined Type also have ODD. ODD is a risk factor for CD and frequently precedes the onset of CD symptoms. Children with an early onset of CD symptoms, with at least one symptom before age 10 years, are at risk for more severe and persistent antisocial behavior continuing into adulthood. Youth with early-onset conduct problems are particularly at risk for ASPD (note that an onset of CD prior to age 15 is part of the diagnostic criteria for ASPD), whereas CD is typically limited to adolescence when youth's CD symptoms begin during adolescence.

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.

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.

Empirical studies have found that the prognosis for conversion disorder varies widely, with some cases resolving in weeks, and others enduring for years or decades. There is also evidence that there is no cure for Conversion Disorder, and that although patients may go into remission, they can relapse at any point. Furthermore, many patients who are 'cured' continue to have some degree of symptoms indefinitely.

In the opinion of Allen Frances, chair of the DSM-IV task force, the DSM-5's somatic symptom disorder brings with it a risk of mislabeling a sizable proportion of the population as mentally ill. “Millions of people could be mislabeled, with the burden falling disproportionately on women, because they are more likely to be casually dismissed as ‘catastrophizers’ when presenting with physical symptoms.”

Information on the frequency of conversion disorder in the West is limited, in part due to the complexities of the diagnostic process. In neurology clinics, the reported prevalence of unexplained symptoms among new patients is very high (between 30 and 60%). However, diagnosis of conversion typically requires an additional psychiatric evaluation, and since few patients will see a psychiatrist it is unclear what proportion of the unexplained symptoms are actually due to conversion. Large scale psychiatric registers in the US and Iceland found incidence rates of 22 and 11 newly diagnosed cases per 100,000 person-years, respectively. Some estimates claim that in the general population, between 0.011% and 0.5% of the population have conversion disorder.

Panic disorder typically begins during early adulthood; roughly half of all people who have panic disorder develop the condition before age 24, especially those subjected to traumatic experiences. However, some sources say that the majority of young people affected for the first time are between the ages of 25 and 30. Women are twice as likely as men to develop panic disorder and it occurs more often in people with above average intelligence.

Panic disorder can continue for months or years, depending on how and when treatment is sought. If left untreated, it may worsen to the point where one's life is seriously affected by panic attacks and by attempts to avoid or conceal the condition. In fact, many people have had problems with personal relationships or employment while struggling to cope with panic disorder. Some people with panic disorder may conceal their condition because of the stigma of mental illness. In some individuals, symptoms may occur frequently for a period of months or years, then many years may pass without symptoms. In some cases, the symptoms persist at the same level indefinitely. There is also some evidence that many individuals (especially those who develop symptoms at an early age) may experience symptom cessation later in life (e.g. past age 50).

In 2000, the World Health Organization found prevalence and incidence rates for panic disorder to be very similar across the globe. Age-standardized prevalence per 100,000 ranged from 309 in Africa to 330 in East Asia for men and from 613 in Africa to 649 in North America, Oceania, and Europe for women.

Being a personality disorder, which are usually chronic and long-lasting mental conditions, avoidant personality disorder is not expected to improve with time without treatment. It is a poorly studied personality disorder and in light of prevalence rates, societal costs, and the current state of research, AvPD qualifies as a neglected disorder.

Psychotherapy, more specifically, cognitive behavioral therapy (CBT), is the most widely used form of treatment for Somatic symptom disorder. In 2016, a randomized 12-week study suggested steady and significant improvement in health anxiety measures with cognitive behavioral therapy compared to the control group.

CBT can help in some of the following ways:

- Learn to reduce stress

- Learn to cope with physical symptoms

- Learn to deal with depression and other psychological issues

- Improve quality of life

- Reduce preoccupation with symptom

Moreover, brief psychodynamic interpersonal psychotherapy (PIT) for patients with multisomatoform disorder has shown its long-term efficacy for improving the physical quality of life in patients with multiple, difficult-to-treat, medically unexplained symptoms.

Antidepressant medication has also been used to treat some of the symptoms of depression and anxiety that are common among people who have somatic symptom disorder. Medications will not cure somatic symptom disorder, but can help the treatment process when combined with CBT.

It is possible for this disorder to progress over time. A patient suffering from the disorder can improve the condition with treatments. There are several types of therapies that may improve the condition, but depending on a patient’s experience of the disorder or the cause of the disorder, treatments will vary.

- Psychotherapy including behaviour therapy, Gestalt therapy, Adlerian therapy, psychoanalytic therapy and existential therapy.

- Pharmacotherapy through medications including antidepressants.

Dependent personality disorder occurs in about 0.6% of the general population. The disorder is diagnosed more often in females than males; however, research suggests that this is largely due to behavioural differences in interviews and self-reporting rather than a difference in prevalence between the sexes. A 2004 twin study suggests a heritability of 0.81 for developing dependent personality disorder. Because of this, there is significant evidence that this disorder runs in families. Children and adolescents with a history of anxiety disorders and physical illnesses are more susceptible to acquiring this disorder.

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".

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.

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.