The psychological mechanism of conversion can be the most difficult aspect of a conversion diagnosis. Even if there is a clear antecedent trauma or other possible psychological trigger, it is still not clear exactly how this gives rise to the symptoms observed. Patients with medically unexplained neurological symptoms may not have any psychological stressor, hence the use of the term "functional neurological symptom disorder" in DSM-V as opposed to "conversion disorder", and DSM-V's removal of the need for a psychological trigger.

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.

For a child or adolescent to qualify for a diagnosis of ODD, behaviours must cause considerable distress for the family or interfere significantly with academic or social functioning. Interference might take the form of preventing the child or adolescent from learning at school or making friends, or placing him or her in harmful situations. These behaviours must also persist for at least six months. Effects of ODD can be greatly amplified by other disorders in comorbidity such as ADHD. Other common comorbid disorders include depression and substance use disorders.

ASPD commonly coexists with the following conditions:

When combined with alcoholism, people may show frontal function deficits on neuropsychological tests greater than those associated with each condition.

About 25-40% of youths diagnosed with conduct disorder qualify for a diagnosis of antisocial personality disorder when they reach adulthood. For those that do not develop ASPD, most still exhibit social dysfunction in adult life.

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

Conduct disorder is classified in the fourth edition of "Diagnostic and Statistical Manual of Mental Disorders" (DSM). It is diagnosed based on a prolonged pattern of antisocial behaviour such as serious violation of laws and social norms and rules in people younger than the age of 18. Similar criteria are used in those over the age of 18 for the diagnosis of antisocial personality disorder. No proposed revisions for the main criteria of conduct disorder exist in the "DSM-5"; there is a recommendation by the work group to add an additional specifier for callous and unemotional traits. According to DSM-5 criteria for conduct disorder, there are four categories that could be present in the child's behavior: aggression to people and animals, destruction of property, deceitfulness or theft, and serious violation of rules.

Almost all adolescents who have a substance use disorder have conduct disorder-like traits, but after successful treatment of the substance use disorder, about half of these adolescents no longer display conduct disorder-like symptoms. Therefore, it is important to exclude a substance-induced cause and instead address the substance use disorder prior to making a psychiatric diagnosis of conduct disorder.

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."

Despite recent initiatives to study psychopathology along dimensions of behavior and neurobiological indices, which would help refine a clearer picture of the development and treatment of externalizing disorders, the majority of research has examined specific mental disorders. Thus, best practices for many externalizing disorders are disorder-specific. For example, substance use disorders themselves are very heterogeneous and their best-evidenced treatment typically includes cognitive behavioral therapy, motivational interviewing, and a substance disorder-specific detoxification or psychotropic medication treatment component. The best-evidenced treatment for childhood conduct and externalizing problems more broadly, including youth with ADHD, ODD, and CD, is parent management training, a form of cognitive behavioral therapy. Additionally, individuals with ADHD, both youth and adults, are frequently treated with stimulant medications (or alternative psychotropic medications), especially if psychotherapy alone has not been effective in managing symptoms and impairment. Psychotherapy and medication interventions for individuals with severe, adult forms of antisocial behavior, such as antisocial personality disorder, have been mostly ineffective. An individual's comorbid psychopathology may also influences the course of treatment for an individual.

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.

ADHD is diagnosed by an assessment of a person's childhood behavioral and mental development, including ruling out the effects of drugs, medications and other medical or psychiatric problems as explanations for the symptoms. It often takes into account feedback from parents and teachers with most diagnoses begun after a teacher raises concerns. It may be viewed as the extreme end of one or more continuous human traits found in all people. Whether someone responds to medications does not confirm or rule out the diagnosis. As imaging studies of the brain do not give consistent results between individuals, they are only used for research purposes and not diagnosis.

In North America, DSM-5 criteria are used for diagnosis, while European countries usually use the ICD-10. With the DSM-IV criteria a diagnosis of ADHD is more likely than with the ICD-10 criteria. It is classified as neurodevelopmental psychiatric disorder. Additionally, it is classified as a disruptive behavior disorder along with oppositional defiant disorder, conduct disorder, and antisocial personality disorder. A diagnosis does not imply a neurological disorder.

Associated conditions that should be screened for include anxiety, depression, oppositional defiant disorder, conduct disorder, and learning and language disorders. Other conditions that should be considered are other neurodevelopmental disorders, tics, and sleep apnea.

Diagnosis of ADHD using quantitative electroencephalography (QEEG) is an ongoing area of investigation, although the value of QEEG in ADHD is currently unclear. In the United States, the Food and Drug Administration has approved the use of QEEG to evaluate the morbidity of ADHD.

Self-rating scales, such as the ADHD rating scale and the Vanderbilt ADHD diagnostic rating scale are used in the screening and evaluation of ADHD.

As with many other psychiatric disorders, formal diagnosis should be made by a qualified professional based on a set number of criteria. In the United States, these criteria are defined by the American Psychiatric Association in the DSM. Based on the DSM criteria, there are three sub-types of ADHD:

1. ADHD predominantly inattentive type (ADHD-PI) presents with symptoms including being easily distracted, forgetful, daydreaming, disorganization, poor concentration, and difficulty completing tasks.

2. ADHD, predominantly hyperactive-impulsive type presents with excessive fidgetiness and restlessness, hyperactivity, difficulty waiting and remaining seated, immature behavior; destructive behaviors may also be present.

3. ADHD, combined type is a combination of the first two subtypes.

This subdivision is based on presence of at least six out of nine long-term (lasting at least six months) symptoms of inattention, hyperactivity–impulsivity, or both. To be considered, the symptoms must have appeared by the age of six to twelve and occur in more than one environment (e.g. at home and at school or work). The symptoms must be not appropriate for a child of that age and there must be evidence that it is causing social, school or work related problems.

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).

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.

Clinically induced RA has been achieved using different forms of electrical induction.

- Electroconvulsive therapy (ECT), used as a depression therapy, can cause impairments in memory. Tests show that information of days and weeks before the ECT can be permanently lost. The results of this study also show that severity of RA is more extreme in cases of bilateral ECT rather than unilateral ECT. Impairments can also be more intense if ECT is administered repetitively (sine wave simulation) as opposed to a single pulse (brief-pulse stimulation).

- Electroconvulsive shock (ECS): The research in this field has been advanced by using animals as subjects. Researchers induce RA in rats, for example, by giving daily ECS treatments. This is done to further understand RA.

As previously mentioned, RA can affect people's memories in different degrees, but testing is required to help determine if someone is experiencing RA. Several tests exist, for example, testing for factual knowledge such as known public events. A problem with this form of testing is that people generally differ in their knowledge of such subjects. Other ways to test someone is via autobiographical knowledge using the Autobiographical Memory Interview (AMI), comprising names of relatives, personal information, and job history. This information could help determine if someone is experiencing RA and the degree of memory affected. However, due to the nature of the information being tested, it is often difficult to verify the accuracy of the memories being recalled, especially if they are from a distant past. Some researchers have found that the time interval after the head injury occurred did not seem to matter. The effect of the memory loss was the same no matter how long it had been after from the injury.

Brain abnormalities can be measured using magnetic resonance imaging (MRI), computed tomography scan (CT) and electroencephalography (EEG), which can provide detailed information about specific brain structures. In many cases, an autopsy helps identify the exact brain region affected and the extent of the damage that caused RA once the patient has died.

There are some aspects essential to the patient that remain unaffected by RA. In many patients, their personality remains the same. Also, semantic memory, that is general knowledge about the world, is usually unaffected. However, episodic memory, which refers to one's life experiences, is impaired.

Another real life problem with RA is malingering, which is conceived as the rational output of a neurologically normal brain aiming at the surreptitious achievement of a well identified gain. Since it is common for people who have committed a crime to report having RA for that specific event in order to avoid their punishment, the legal system has pushed for the creation of a standardized test of amnesia. However, since most cases differ in onset, duration, and content forgotten, this task has shown to be a rather complex one.

At least one study suggests that gluten neuropathy can be effectively treated with a gluten-free diet. In the study, 35 patients with gluten neuropathy adhered to a gluten-free diet, where adherence was monitored serologically. After one year, the treatment group had improved significantly compared to the control group. The indicators of improvements were improvements of sural sensory action potential and subjective improvement of neuropathic symptoms. Subgroup analysis suggested that severe neuropathy might imply reduced capacity for recovery of the peripheral nerves or longer recovery.

Diagnosis of gluten-sensitive neuropathies without a clear cause is on the rise. These "idiopathic" neuropathies were first identified by screening for anti-gliadin IgG (AGA). The criteria have been critiqued because of the large misdiagnosis rate of coeliac disease (CD), and because AGA exists in the normal population at over 12%, far more abundant than cases of neuropathy. The problem in diagnosis arises because there are precursor states prior to coeliac disease. These are called coeliac disease and early gluten-sensitive enteropathy and are defined as Marsh grade 1 and 2 coeliac disease. Coeliac disease was diagnosed by duodenal biopsy, often misinterpreted as negative as high as grade 3 on the Marsh scale. Anti-gliadin antibodies may precede or lag the appearance of coeliac disease. Studies in Scandinavia found an increase of pathologies as much as 10 years before coeliac disease. These included gastrointestinal symptoms, anemia or other autoimmune disease. In addition IgG and IgA responses sometimes accompany allergic responses to proteins. Gliadin is exceptional in that it has several proteins which remain peptides of considerable length after digestion, and migrate into systemic circulation.

A subset of people with idiopathic neuropathies have only anti-gliadin antibodies but none of the other enteropathic criteria. About 1/3 have no DQ2 or DQ8 and an apparent abundance of HLA-DQ1. One percent of coeliacs in Europe have no DQ2 and DQ8 but have DQ1. The DQ1 serotype is very common in the normal population, over 65% of Americans have one copy, therefore the linkage is speculative.

Treatment of tics present in conditions such as Tourette’s syndrome begins with patient, relative, teacher and peer education about the presentation of the tics. Sometimes, pharmacological treatment is unnecessary and tics can be reduced by behavioral therapy such as habit-reversal therapy and/or counseling. Often this route of treatment is difficult because it depends most heavily on patient compliance. Once pharmacological treatment is deemed most appropriate, lowest effective doses should be given first with gradual increases. The most effective drugs belong to the neuroleptic variety such as monoamine-depleting drugs and dopamine receptor-blocking drugs. Of the monoamine-depleting drugs, tetrabenazine is most powerful against tics and results in fewest side effects. A non-neuroleptic drug found to be safe and effective in treating tics is topiramate. Botulinum toxin injection in affected muscles can successfully treat tics; involuntary movements and vocalizations can be reduced, as well as life-threatening tics that have the potential of causing compressive myelopathy or radiculopathy. Surgical treatment for disabling Tourette’s syndrome has been proven effective in cases presenting with self-injury. Deep Brain Stimulation surgery targeting the globus pallidus, thalamus and other areas of the brain may be effective in treating involuntary and possibly life-threatening tics.

An electroencephalogram (EEG) can assist in showing brain activity suggestive of an increased risk of seizures. It is only recommended for those who are likely to have had an epileptic seizure on the basis of symptoms. In the diagnosis of epilepsy, electroencephalography may help distinguish the type of seizure or syndrome present. In children it is typically only needed after a second seizure. It cannot be used to rule out the diagnosis and may be falsely positive in those without the disease. In certain situations it may be useful to perform the EEG while the affected individual is sleeping or sleep deprived.

Diagnostic imaging by CT scan and MRI is recommended after a first non-febrile seizure to detect structural problems in and around the brain. MRI is generally a better imaging test except when bleeding is suspected, for which CT is more sensitive and more easily available. If someone attends the emergency room with a seizure but returns to normal quickly, imaging tests may be done at a later point. If a person has a previous diagnosis of epilepsy with previous imaging, repeating the imaging is usually not needed even if there are subsequent seizures.

For adults, the testing of electrolyte, blood glucose and calcium levels is important to rule out problems with these as causes. An electrocardiogram can rule out problems with the rhythm of the heart. A lumbar puncture may be useful to diagnose a central nervous system infection but is not routinely needed. In children additional tests may be required such as urine biochemistry and blood testing looking for metabolic disorders.

A high blood prolactin level within the first 20 minutes following a seizure may be useful to help confirm an epileptic seizure as opposed to psychogenic non-epileptic seizure. Serum prolactin level is less useful for detecting focal seizures. If it is normal an epileptic seizure is still possible and a serum prolactin does not separate epileptic seizures from syncope. It is not recommended as a routine part of the diagnosis of epilepsy.

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.