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.

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.

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

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.

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.

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.

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.

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."

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.

ASPD is seen in 3% to 30% of psychiatric outpatients. The prevalence of the disorder is even higher in selected populations, like prisons, where there is a preponderance of violent offenders. A 2002 literature review of studies on mental disorders in prisoners stated that 47% of male prisoners and 21% of female prisoners had ASPD. Similarly, the prevalence of ASPD is higher among patients in alcohol or other drug (AOD) abuse treatment programs than in the general population (Hare 1983), suggesting a link between ASPD and AOD abuse and dependence.

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).

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.

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.

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.

Communication deviance (CD) occurs when a speaker fails to effectively communicate meaning to their listener with confusing speech patterns or illogical patterns. These disturbances can range from vague linguistic references, contradictory statements to more encompassing non-verbal problems at the level of turn-taking. The term was originally introduced by Wynne and Singer in 1963 to describe a communication style found among parents who had children with schizophrenia. A recent meta-analysis reported that communication deviance is highly prevalent in parents of patients diagnosed with schizophrenia and adoption studies have reported significant associations between CD in the parent and thought disorder in the offspring, however, the mechanisms by which CD impacts on the offspring's cognition are still unknown.

The research of psychiatrists and psychoanalysts Lyman Wynne and Theodore Lidz on communication deviance and roles (e.g., pseudo-mutuality, pseudo-hostility, schism and skew) in families of people with schizophrenia also became influential with "systems-communications"-oriented theorists and therapists.

Functional weakness is weakness of an arm or leg due to the nervous system not working properly. It is not caused by damage or disease of the nervous system. Patients with functional weakness experience symptoms of limb weakness which can be disabling and frightening such as problems walking or a ‘heaviness’ down one side, dropping things or a feeling that a limb just doesn’t feel normal or ‘part of them’. Functional weakness may also be described as functional neurological symptom disorder (FNsD), Functional Neurological Disorder (FND) or functional neurological symptoms. If the symptoms are caused by a psychological trigger, it may be diagnosed as 'dissociative motor disorder' or conversion disorder (CD).

To the patient and the doctor it often looks as if there has been a stroke or have symptoms of multiple sclerosis. However, unlike these conditions, with functional weakness there is no permanent damage to the nervous system which means that it can get better or even go away completely.

The diagnosis should usually be made by a consultant neurologist so that other neurological causes can be excluded. The diagnosis should be made on the basis of positive features in the history and the examination (such as Hoover's sign). It is dangerous to make the diagnosis simply because tests are normal. Neurologists usually diagnose wrongly about 5% of the time (which is the same for many other conditions.)

Many patients with functional weakness suffer from not being believed. Although psychological factors can be important for a some patients, for the majority of individuals the cause of their weakness has a physical trigger such as a virus, injury or other medical condition. The symptoms of functional weakness are real, and are as disabling and distressing as Multiple Sclerosis or Parkinson's.

The most effective treatment is physiotherapy, however it is also helpful for patients to understand the diagnosis, and some may find CBT helps them to cope with the emotions associated with being unwell. For those with conversion disorder, psychological therapy is key to their treatment as it is emotional or psychological factors which are causing their symptoms.

Giveway weakness (also "give-away weakness", "collapsing weakness", etc.) refers to a symptom where a patient's arm, leg, can initially provide resistance against an examiner's touch, but then suddenly "gives way" and provides no further muscular resistance.

RA has been found among alcohol-dependent patients who suffer from Korsakoff's syndrome. Korsakoff's syndrome patients suffer from retrograde amnesia due to a thiamine deficiency (lack of vitamin B1). Also, chronic alcohol use disorders are associated with a decrease in volume of the left and right hippocampus.

These patients' regular diet consists mostly of hard alcohol intake, which lacks the necessary nutrients for healthy development and maintenance. Therefore, after a prolonged time consuming primarily alcohol, these people undergo memory difficulties and ultimately suffer from RA. However, some of the drawback of using Korsakoff patients to study RA is the progressive nature of the illness and the unknown time of onset.

RA can occur without any anatomical damage to the brain, lacking an observable neurobiological basis. Primarily referred to as psychogenic amnesia or psychogenic fugue, it often occurs due to a traumatic situation that individuals wish to consciously or unconsciously avoid through intrapsychic conflicts or unconscious repressions. The onset of psychogenic amnesia can be either global (i.e., individual forgets all history) or situation specific (i.e., individual is unable to retrieve memories of specific situations).

People experiencing psychogenic amnesia have impaired episodic memory, instances of wandering and traveling, and acceptance of a new identity as a result of inaccessible memories pertaining to their previous identity.

Recent research has begun to investigate the effects of stress and fear-inducing situations with the onset of RA. Long-term potentiation (LTP) is the process by which there is a signal transmission between neurons after the activation of a neuron, which has been known to play a strong role in the hippocampus in learning and memory. Common changes in the hippocampus have been found to be related to stress and induced LTP. The commonalities support the idea that variations of stress can play a role in producing new memories as well as the onset of RA for other memories. Also, the amygdala plays a crucial role in memory and can be affected by emotional stimuli, evoking RA.

Studies of specific cases, such as 'AMN', support evidence of traumatic experiences as a plausible cause of RA. AMN escaped a small fire in his house, did not inhale any smoke, and had no brain damage. Surprisingly, the next day, he was unable to recall autobiographical based knowledge. This case shows that RA can occur in the absence of structural brain damage.

After a traumatic head injury, emotional disturbances can occur at three different levels: neurological, reactionary, and long-term disturbances. Neurological disturbances can change emotional and motivational responses. Reactionary disturbances effect emotional and motivational responses as well, but they reflect failure to cope with environmental demands. Someone with this might withdraw from the environment that they are placed in because they no longer know how to handle the cognitive resources.

Feline hyperesthesia syndrome is an uncommon but recognized condition in cats, particularly Siamese, Burmese, Himalayan, and Abyssinian cats. It can affect cats of all ages, though it is most prevalent in mature animals. The disease can be somewhat difficult to detect as it is characterized by brief bursts of abnormal behavior, lasting around a minute or two. One of its symptoms is also found in dogs that have canine distemper disease (CD) caused by canine distemper virus (CDV).

Underwear fetishism is a sexual fetishism relating to undergarments, and refers to preoccupation with the sexual excitement of certain types of underwear, including panties, stockings, pantyhose, bras, or other items. Some people experience sexual excitement from wearing, while others get their excitement when observing or handling the underwear worn by another, or watching somebody putting underwear on/taking it off. Some may steal used underwear to get satisfaction. Not only does this include physical contact with the garment(s), or their wearers, but also includes arousal by printed or electronic image with depictions of underwear.

Underwear fetishism is not considered as paraphilia unless it causes distress or serious problems for the person or those associated with them.

Hyperkinesia, also known as hyperkinesis, refers to an increase in muscular activity that can result in excessive abnormal movements, excessive normal movements, or a combination of both. The word hyperkinesis comes from the Greek "hyper", meaning "increased," and "kinein", meaning "to move." Hyperkinesia is a state of excessive restlessness which is featured in a large variety of disorders that affect the ability to control motor movement, such as Huntington's disease. It is the opposite of hypokinesia, which refers to decreased bodily movement, as commonly manifested in Parkinson's disease. Many hyperkinetic movements are the result of improper regulation of the basal ganglia-thalamocortical circuitry. Overactivity of a direct pathway combined with decreased activity of an indirect pathway results in activation of thalamic neurons and excitation of cortical neurons, resulting in increased motor output. Often, hyperkinesia is paired with hypotonia, a decrease in muscle tone. Many hyperkinetic disorders are psychological in nature and are typically prominent in childhood. Depending on the specific type of hyperkinetic movement, there are different treatment options available to minimize the symptoms, including different medical and surgical therapies.

Hyperesthesia (or hyperaesthesia) is a condition that involves an abnormal increase in sensitivity to stimuli of the sense. "When a non-noxious stimulus causes the sensation of pain the area will be termed hyperaesthetic". Stimuli of the senses can include sound that one hears, foods that one tastes, textures that one feels, and so forth. Increased touch sensitivity is referred to as "tactile hyperesthesia", and increased sound sensitivity is called "auditory hyperesthesia". Tactile hyperesthesia may be a common symptom of many neurologic disorders such as herpes zoster, peripheral neuropathy and radiculopathies. In 1979, and then in 1994, Merskey, Bogduk, Noordenbos, Devor and others (a subcommittee of International Association for the Study of Pain) proposed, instead of hyperaesthesia, the concept of allodynia, meaning "other pain", defined as a pain resulting from a stimulus that does not normally provoke pain.

In psychology, Jeanne Siaud-Facchin uses the term by defining it as an "exacerbation des sens" that characterizes gifted children (and adults): for them, the sensory information reaches the brain much faster than the average, and the information is processed in a significantly shorter time.

People with epilepsy are at an increased risk of death. This increase is between 1.6 and 4.1 fold greater than that of the general population and is often related to: the underlying cause of the seizures, status epilepticus, suicide, trauma, and sudden unexpected death in epilepsy (SUDEP). Death from status epilepticus is primarily due to an underlying problem rather than missing doses of medications. The risk of suicide is increased between two and six times in those with epilepsy. The cause of this is unclear. SUDEP appears to be partly related to the frequency of generalized tonic-clonic seizures and accounts for about 15% of epilepsy related deaths. It is unclear how to decrease its risk. The greatest increase in mortality from epilepsy is among the elderly. Those with epilepsy due to an unknown cause have little increased risk. In the United Kingdom, it is estimated that 40–60% of deaths are possibly preventable. In the developing world, many deaths are due to untreated epilepsy leading to falls or status epilepticus.

Gluten-sensitive idiopathic neuropathies are apparently sporadic neuropathy of unknown cause in the absence of an alternative cause and where there is serological evidence of gluten sensitivity.