The development of conduct disorder is not immutable or predetermined. A number of interactive risk and protective factors exist that can influence and change outcomes, and in most cases conduct disorder develops due to an interaction and gradual accumulation of risk factors. In addition to the risk factors identified under cause, several other variables place youth at increased risk for developing the disorder, including child physical abuse and prenatal alcohol abuse and maternal smoking during pregnancy. Protective factors have also been identified, and most notably include high IQ, being female, positive social orientations, good coping skills, and supportive family and community relationships.

However, a mere correlation between a particular risk factor and a later developmental outcome (such as conduct disorder) cannot be taken as definitive evidence for a causal link. Co-variation between two variables can arise, for instance, if they represent age-specific expressions of similar underlying genetic factors. For example, the tendency to smoke during pregnancy (SDP) is subject to substantial genetic influence (D'Onofrio et al., 2007), as is conduct disorder. Thus, the genes that dispose the mother to SDP may also dispose the child to CD following mitotic transmission. Indeed, Rice et al. (2009) found that in mother-fetus pairs that were not genetically related (by virtue of in-vitro fertilisation), no link between SDP and later conduct problems arose. Thus, the distinction between causality and correlation is an important consideration.

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.

Negative parenting practices and parent–child conflict may lead to antisocial behavior, but they may also be a reaction to the oppositional and aggressive behaviors of children. Factors such as a family history of mental illnesses and/or substance abuse as well as a dysfunctional family and inconsistent discipline by a parent or guardian can lead to the development of behavior disorders.

Insecure parent–child attachments can also contribute to ODD. Often little internalization of parent and societal standards exists in children with conduct problems. These weak bonds with their parents may lead children to associate with delinquency and substance abuse.

Family instability and stress can also contribute to the development of ODD. Although the association between family factors and conduct problems is well established, the nature of this association and the possible causal role of family factors continues to be debated.

Low socioeconomic status is associated with poor parenting, specifically with inconsistent discipline and poor parental monitoring, which are then associated with an early onset of aggression and antisocial behaviors.

Externalizing problems are reported to be more frequent among minority-status youth, a finding that is likely related to economic hardship, limited employment opportunities, and living in high-risk urban neighborhoods.

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.

ODD has an estimated lifetime prevalence of 10.2% (11.2% for males, 9.2% for females).

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.

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.

The prognosis of SCT is unknown. In contrast, much is known about the adolescent and adult outcomes of children having ADHD. Those with SCT symptoms typically show a later onset of their symptoms than do those with ADHD, perhaps by as much as a year or two later on average. They have as much or more difficulty with academic tasks and far fewer social difficulties than do people having ADHD. They do not have the same risks for oppositional defiant disorder, conduct disorder, or social aggression and thus may have different life course outcomes compared to children with ADHD-HI and Combined subtypes who have far higher risks for these other "externalizing" disorders.

However, unlike ADHD, there are no longitudinal studies of children with SCT that can shed light on the developmental course and adolescent or adult outcomes of these individuals.

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.

In addition to genetics, some environmental factors might play a role in causing ADHD. Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it. Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD. Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive. Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.

Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71). There is an association between long term but not short term use of acetaminophen during pregnancy and ADHD. At least 30% of children with a traumatic brain injury later develop ADHD and about 5% of cases are due to brain damage.

Some studies suggest that in a small number of children, artificial food dyes or preservatives may be associated with an increased prevalence of ADHD or ADHD-like symptoms but the evidence is weak and may only apply to children with food sensitivities. The United Kingdom and the European Union have put in place regulatory measures based on these concerns. In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.

Research does not support popular beliefs that ADHD is caused by eating too much refined sugar, watching too much television, parenting, poverty or family chaos; however, they might worsen ADHD symptoms in certain people.

Impulsive behavior, and especially impulsive violence predisposition has been correlated to a low brain serotonin turnover rate, indicated by a low concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). This substrate appears to act on the suprachiasmatic nucleus in the hypothalamus, which is the target for serotonergic output from the dorsal and median raphe nuclei playing a role in maintaining the circadian rhythm and regulation of blood sugar. A tendency towards low 5-HIAA may be hereditary. A putative hereditary component to low CSF 5-HIAA and concordantly possibly to impulsive violence has been proposed. Other traits that correlate with IED are low vagal tone and increased insulin secretion. A suggested explanation for IED is a polymorphism of the gene for tryptophan hydroxylase, which produces a serotonin precursor; this genotype is found more commonly in individuals with impulsive behavior.

IED may also be associated with lesions in the prefrontal cortex, with damage to these areas, including the amygdala, increasing the incidence of impulsive and aggressive behavior and the inability to predict the outcomes of an individual's own actions. Lesions in these areas are also associated with improper blood sugar control, leading to decreased brain function in these areas, which are associated with planning and decision making. A national sample in the United States estimated that 16 million Americans may fit the criteria for IED.

An 8-year follow up of children diagnosed with ADHD (combined type) found that they often have difficulties in adolescence, regardless of treatment or lack thereof. In the USA, fewer than 5% of individuals with ADHD get a college degree, compared to 28% of the general population aged 25 years and older. The proportion of children meeting criteria for ADHD drops by about half in the three years following the diagnosis and this occurs regardless of treatments used. ADHD persists into adulthood in about 30–50% of cases. Those affected are likely to develop coping mechanisms as they mature, thus compensating to some extent for their previous symptoms. Children with ADHD have a higher risk of unintentional injuries, and greater mortality rates.

Two epidemiological studies of community samples approximated the lifetime prevalence of IED to be 4–6%, depending on the criteria set used. A Ukrainian study found comparable rates of lifetime IED (4.2%), suggesting that a lifetime prevalence of IED of 4–6% is not limited to American samples. One-month and one-year point prevalences of IED in these studies were reported as 2.0% and 2.7%, respectively. Extrapolating to the national level, 16.2 million Americans would have IED during their lifetimes and as many as 10.5 million in any year and 6 million in any month.

Among a "clinical" population, a 2005 study found the lifetime prevalence of IED to be 6.3%.

Prevalence appears to be higher in men than in women.

Of US subjects with IED, 67.8% had engaged in direct interpersonal aggression, 20.9% in threatened interpersonal aggression, and 11.4% in aggression against objects. Subjects reported engaging in 27.8 high-severity aggressive acts during their worst year, with 2–3 outbursts requiring medical attention. Across the lifespan, the mean value of property damage due to aggressive outbursts was $1603.

A study in the March 2016 "Journal of Clinical Psychiatry" suggests a relationship between infection with the parasite "Toxoplasma gondii" and psychiatric aggression such as IED.

Recent studies indicate that the symptoms of SCT in children form two dimensions: daydreamy-spacey and sluggish-lethargic, and that the former are more distinctive of the disorder from ADHD than the latter. This same pattern was recently found in the first study of adults with SCT by Barkley and also in more recent studies of college students. These studies indicated that SCT is probably not a subtype of ADHD but a distinct disorder from it. Yet it is one that overlaps with ADHD in 30–50% of cases of each disorder, suggesting a pattern of comorbidity between two related disorders rather than subtypes of the same disorder. Nevertheless, SCT is strongly correlated with ADHD inattentive and combined subtypes. According to a Norwegian study, "SCT correlated significantly with inattentiveness, regardless of the subtype of ADHD."

The rate in school age children is thought to be about 1.5%, compared with an estimated 5.3% for ADHD.

Epidemiological data are limited, but reactive attachment disorder appears to be very uncommon. The prevalence of RAD is unclear but it is probably quite rare, other than in populations of children being reared in the most extreme, deprived settings such as some orphanages. There is little systematically gathered epidemiologic information on RAD. A cohort study of 211 Copenhagen children to the age of 18 months found a prevalence of 0.9%.

Attachment disorders tend to occur in a definable set of contexts such as within some types of institutions, in the presence of repeated changes of primary caregiver or of extremely neglectful identifiable primary caregivers who show persistent disregard for the child's basic attachment needs, but not all children raised in these conditions develop an attachment disorder. Studies undertaken on children from Eastern European orphanages from the mid-1990s showed significantly higher levels of both forms of RAD and of insecure patterns of attachment in the institutionalized children, regardless of how long they had been there. It would appear that children in institutions like these are unable to form selective attachments to their caregivers. The difference between the institutionalized children and the control group had lessened in the follow-up study three years later, although the institutionalized children continued to show significantly higher levels of indiscriminate friendliness. However, even among children raised in the most deprived institutional conditions the majority did not show symptoms of this disorder.

A 2002 study of children in residential nurseries in Bucharest, in which the DAI was used, challenged the current DSM and ICD conceptualizations of disordered attachment and showed that inhibited and disinhibited disorders could coexist in the same child.

There are two studies on the incidence of RAD relating to high risk and maltreated children in the U.S. Both used ICD, DSM and the DAI. The first, in 2004, reported that children from the maltreatment sample were significantly more likely to meet criteria for one or more attachment disorders than children from the other groups, however this was mainly the proposed new classification of disrupted attachment disorder rather than the DSM or ICD classified RAD or DAD. The second study, also in 2004, attempted to ascertain the prevalence of RAD and whether it could be reliably identified in "maltreated" rather than "neglected" toddlers. Of the 94 maltreated toddlers in foster care, 35% were identified as having ICD RAD and 22% as having ICD DAD, and 38% fulfilled the DSM criteria for RAD. This study found that RAD could be reliably identified and also that the inhibited and disinhibited forms were not independent. However, there are some methodological concerns with this study. A number of the children identified as fulfilling the criteria for RAD did in fact have a preferred attachment figure.

It has been suggested by some within the field of attachment therapy that RAD may be quite prevalent because severe child maltreatment, which is known to increase risk for RAD, is prevalent and because children who are severely abused may exhibit behaviors similar to RAD behaviors. The APSAC Taskforce consider this inference to be flawed and questionable. Severely abused children may exhibit similar behaviors to RAD behaviors but there are several far more common and demonstrably treatable diagnoses which may better account for these difficulties. Further, many children experience severe maltreatment and do not develop clinical disorders. Resilience is a common and normal human characteristic. RAD does not underlie all or even most of the behavioral and emotional problems seen in foster children, adoptive children, or children who are maltreated and rates of child abuse and/or neglect or problem behaviors are not a benchmark for estimates of RAD.

There are few data on comorbid conditions, but there are some conditions that arise in the same circumstances in which RAD arises, such as institutionalization or maltreatment. These are principally developmental delays and language disorders associated with neglect. Conduct disorders, oppositional defiant disorder, anxiety disorders, post-traumatic stress disorder and social phobia share many symptoms and are often comorbid with or confused with RAD. Attachment disorder behaviors amongst institutionalized children are correlated with attentional and conduct problems and cognitive levels but nonetheless appear to index a distinct set of symptoms and behaviors.

According to Professor Emily Simonoff of the Institute of Psychiatry, Psychology and Neuroscience, "childhood hyperactivity and conduct disorder showed equally strong prediction of antisocial personality disorder (ASPD) and criminality in early and mid-adult life. Lower IQ and reading problems were most prominent in their relationships with childhood and adolescent antisocial behaviour."

Once the patient and family have been educated about the nature, management and treatment of the disorder and a decision has been made to treat, the European ADHD Guidelines group recommends medication rather than behavioral training as the first treatment approach; and the UK's National Institute for Health and Clinical Excellence recommends medication as first line treatment for those with hyperkinesis/severe ADHD, and the provision of group parent-training in all cases of ADHD.

The AACAP guidelines state that children with reactive attachment disorder are presumed to have grossly disturbed internal models for relating to others. However, the course of RAD is not well studied and there have been few efforts to examine symptom patterns over time. The few existing longitudinal studies (dealing with developmental change with age over a period of time) involve only children from poorly run Eastern European institutions.

Findings from the studies of children from Eastern European orphanages indicate that persistence of the inhibited pattern of RAD is rare in children adopted out of institutions into normative care-giving environments. However, there is a close association between duration of deprivation and severity of attachment disorder behaviors. The quality of attachments that these children form with subsequent care-givers may be compromised, but they probably no longer meet criteria for inhibited RAD. The same group of studies suggests that a minority of adopted, institutionalized children exhibit persistent indiscriminate sociability even after more normative caregiving environments are provided. Indiscriminate sociability may persist for years, even among children who subsequently exhibit preferred attachment to their new caregivers. Some exhibit hyperactivity and attention problems as well as difficulties in peer relationships. In the only longitudinal study that has followed children with indiscriminate behavior into adolescence, these children were significantly more likely to exhibit poor peer relationships.

Studies of children who were reared in institutions have suggested that they are inattentive and overactive, no matter what quality of care they received. In one investigation, some institution-reared boys were reported to be inattentive, overactive, and markedly unselective in their social relationships, while girls, foster-reared children, and some institution-reared children were not. It is not yet clear whether these behaviors should be considered as part of disordered attachment.

There is one case study on maltreated twins published in 1999 with a follow-up in 2006. This study assessed the twins between the ages of 19 and 36 months, during which time they suffered multiple moves and placements. The paper explores the similarities, differences and comorbidity of RAD, disorganized attachment and post traumatic stress disorder. The girl showed signs of the inhibited form of RAD while the boy showed signs of the indiscriminate form. It was noted that the diagnosis of RAD ameliorated with better care but symptoms of post traumatic stress disorder and signs of disorganized attachment came and went as the infants progressed through multiple placement changes. At age three, some lasting relationship disturbance was evident.

In the follow-up case study when the twins were aged three and eight years, the lack of longitudinal research on maltreated as opposed to institutionalized children was again highlighted. The girl's symptoms of disorganized attachment had developed into controlling behaviors—a well-documented outcome. The boy still exhibited self-endangering behaviors, not within RAD criteria but possibly within "secure base distortion", (where the child has a preferred familiar caregiver, but the relationship is such that the child cannot use the adult for safety while gradually exploring the environment). At age eight the children were assessed with a variety of measures including those designed to access representational systems, or the child's "internal working models". The twins' symptoms were indicative of different trajectories. The girl showed externalizing symptoms (particularly deceit), contradictory reports of current functioning, chaotic personal narratives, struggles with friendships, and emotional disengagement with her caregiver, resulting in a clinical picture described as "quite concerning". The boy still evidenced self-endangering behaviors as well as avoidance in relationships and emotional expression, separation anxiety and impulsivity and attention difficulties. It was apparent that life stressors had impacted each child differently. The narrative measures used were considered helpful in tracking how early attachment disruption is associated with later expectations about relationships.

One paper using questionnaires found that children aged three to six, diagnosed with RAD, scored lower on empathy but higher on self-monitoring (regulating your behavior to "look good"). These differences were especially pronounced based on ratings by parents, and suggested that children with RAD may systematically report their personality traits in overly positive ways. Their scores also indicated considerably more behavioral problems than scores of the control children.

Similar to adult personality disorders there are multiple causes and causal interactions for personality development disorders. In clinical practice it is important to view the disorder multi-perspectively and from an individual perspective. Biological and neurological causes need to be observed just as much as psychosocial factors. Looking at the disorder from only one perspective (e.g. (s)he had a bad childhood) often results in ignorance of important other factors or causal interactions. This might be one of the main reasons why traditional treatment methods often fail with these disorders. Only a multi-perspective view can provide for a multi-dimensional treatment approach which seems to be the key for these disorders.

The diagnosis personality development disorder should only be given carefully and after a longer period of evaluation. Also a thorough diagnostic evaluation is necessary. Parents should be questioned separately and together with the child or adolescent to evaluate the severity and duration of the problems. In addition standardized personality tests might be helpful. It is also useful to ask the family what treatment approaches they have already tried so far without success.

Emotional and behavioral disorders (EBD; sometimes called emotional disturbance or serious emotional disturbance) refer to a disability classification used in educational settings that allows educational institutions to provide special education and related services to students that have poor social or academic adjustment that cannot be better explained by biological abnormalities or a developmental disability.

The classification is often given to students that need individualized behavior supports to receive a free and appropriate public education, but would not be eligible for an individualized education program under another disability category of the Individuals with Disabilities Education Act (IDEA).

Complications of late Parkinson's disease may include a range of impulse-control disorders, including eating, buying, compulsive gambling and sexual behavior. One study found that 13.6% of Parkinson's patients exhibited at least one form of ICD. There is a significant co-occurrence of pathological gambling and personality disorder, and is suggested to be caused partly by their common "genetic vulnerability". The degree of heritability to ICD is similar to other psychiatric disorders including substance abuse disorder. There has also been found a genetic factor to the development of ICD just as there is for substance abuse disorder. The risk for subclinical PG in a population is accounted for by the risk of alcohol dependence by about 12-20% genetic and 3-8% environmental factors. There is a high rate of comorbidity between ADHD and other impulse-control disorders.

Research into genetic associations in antisocial personality disorder is suggestive that ASPD has some or even a strong genetic basis. Prevalence of ASPD is higher in people related to someone afflicted by the disorder. Twin studies, which are designed to discern between genetic and environmental effects have reported significant genetic influences on antisocial behavior and conduct disorder.

In the specific genes that may be involved, one gene that has seen particular interest in its correlation with antisocial behavior is the gene that encodes for Monoamine oxidase A (MAO-A), an enzyme that breaks down monomamine neurotransmitters such as serotonin and norephinephrine. Various studies examining the gene's relationship to behavior have suggested that variants of the gene that results in less MAO-A being produced, such as the 2R and 3R alleles of the promoter region have associations with aggressive behavior in men. The association is also found influenced by negative experience in early life, with children possessing a low-activity variant (MAOA-L) with who experienced such maltreatment being more likely to develop antisocial behavior than those with the high-activity variants (MAOA-H). Even when environmental interactions (e.g. emotional abuse) are controlled for, a small association between MAOA-L and aggressive and antisocial behavior remains.

The gene that encodes for the serotonin transporter (SCL6A4), a gene that is heavily researched for its associations with other mental disorders, is another gene of interest in antisocial behavior and personality traits. Genetic associations studies have suggested that the short "S" allele is associated with impulsive antisocial behavior and ASPD in the inmate population. However, research into psychopathy find that the long "L" allele is associated with the Factor 1 traits of psychopathy, which describes its core affective (e.g. lack of empathy, fearlessness) and interpersonal (e.g. grandiosity, manipulativeness) personality disturbances. This is suggestive of two different forms, one associated more with impulsive behavior and emotional dysregulation, and the other with predatory aggression and affective disturbance, of the disorder.

Various other gene candidates for ASPD have been identified by a genome-wide association study published in 2016. Several of these gene candidates are shared with attention-deficit hyperactivity disorder, with which ASPD is comorbid.

A personality development disorder is an inflexible and pervasive pattern of inner experience and behavior in children and adolescents, that markedly deviates from the expectations of the individual's culture. Personality development disorder is not recognized as a mental disorder in any of the medical manuals, such as the ICD-10 or the DSM-IV, neither is it part of the proposed revision of this manual, the DSM-5. DSM-IV allows the diagnosis of personality disorders in children and adolescents only as an exception.

This diagnosis is currently proposed by a few authors in Germany. The term personality "development" disorder is used to emphasize the changes in personality development which might still take place and the open outcome during development. Personality development disorder is considered to be a childhood risk factor or early stage of a later personality disorder in adulthood.

Adults usually show personality patterns over a long duration of time. Children and adolescents however still show marked changes in personality development. Some of these children and adolescents have a hard time developing their personalities in an ordinary way. DSM-IV states, for example, that children and adolescents are at higher risk to develop an antisocial personality disorder if they showed signs of conduct disorder and attention deficit disorder before the age of 10. This led Adam & Breithaupt-Peters (2010) to the idea that these children and adolescents need to be looked at more carefully. The therapy which these children and adolescents need might be more intense and maybe even different from looking at the disorders traditionally. The concept of personality development disorders also focuses on the severity of the disorder and the poor prognosis. An early diagnosis might help to get the right treatment at an early stage and thus might help to prevent a personality disorder outcome in adulthood.

The IDEA requires that a student must exhibit one or more of the following characteristics over a long duration, and to a marked degree that adversely affects their educational performance, to receive an EBD classification:

- Difficulty to learn that cannot be explained by intellectual, sensory, or health factors.

- Difficulty to build or maintain satisfactory interpersonal relationships with peers and teachers.

- Inappropriate types of behavior (acting out against self or others) or feelings (expresses the need to harm self or others, low self-worth, etc.) under normal circumstances.

- A general pervasive mood of unhappiness or depression.

- A tendency to develop physical symptoms or fears associated with personal or school problems.

The term "EBD" includes students diagnosed with schizophrenia, but does not apply to students who are "socially maladjusted", unless it is determined that they also meet the criteria for an EBD classification.