Epidemiological studies of serotonin syndrome are difficult as many physicians are unaware of the diagnosis or they may miss the syndrome due to its variable manifestations. In 1998 a survey conducted in England found that 85% of the general practitioners that had prescribed the antidepressant nefazodone were unaware of serotonin syndrome. The incidence may be increasing as a larger number of pro-serotonergic drugs (drugs which increase serotonin levels) are now being used in clinical practice. One postmarketing surveillance study identified an incidence of 0.4 cases per 1000 patient-months for patients who were taking nefazodone. Additionally, around 14 to 16 percent of persons who overdose on SSRIs are thought to develop serotonin syndrome.

In some cases, children who enjoy learning may develop a sense of fear when faced with structured or planned work, especially long or group-based assignments that require extended focus, even if they thoroughly understand the topic. Children with ADHD may be at greater risk of academic failures and early withdrawal from school. Teachers and parents may make incorrect assumptions about the behaviours and attitudes of a child with ADHD-PI, and may provide them with frequent and erroneous negative feedback (e.g. "careless", "you're irresponsible", "you're immature", "you're lazy", "you don't care/show any effort", "you just aren't trying", etc.).

The inattentive children may realize on some level that they are somehow different internally from their peers. However, they are also likely to accept and internalize the continuous negative feedback, creating a negative self-image that becomes self-reinforcing. If these children progress into adulthood undiagnosed or untreated, their inattentiveness, ongoing frustrations, and poor self-image frequently create numerous and severe problems maintaining healthy relationships, succeeding in postsecondary schooling, or succeeding in the workplace. These problems can compound frustrations and low self-esteem, and will often lead to the development of secondary pathologies including anxiety disorders, mood disorders, and substance abuse.

Neuroleptic induced deficit syndrome is principally characterized by the same symptoms that constitute the negative symptoms of schizophrenia: emotional blunting, apathy, hypobulia, anhedonia, indifference, difficulty in thinking, difficulty or total inability in concentrating, lack of initiative, attention deficits, and desocialization. This can easily lead to misdiagnosis and mistreatment. Instead of decreasing the antipsychotic, the doctor may increase their dose to try to "improve" what they perceive to be negative symptoms of schizophrenia, rather than antipsychotic side effects. The concept of neuroleptic induced deficit syndrome was initially presented for schizophrenia, and it has rarely been associated in other mental disorders. In recent years, atypical neuroleptics are being more often managed to patients with bipolar disorder, so some studies about neuroleptic-induced deficit syndrome in bipolar disorder patients now available.

There are significant difficulties in the differential diagnosis of primary negative symptoms and neuroleptic deficiency syndrome (secondary negative symptoms), as well as depression.

It is difficult to say exactly how many children or adults worldwide have ADHD because different countries have used different ways of diagnosing it, while some do not diagnose it at all. In the UK, diagnosis is based on quite a narrow set of symptoms, and about 0.5–1% of children are thought to have attention or hyperactivity problems. In comparison, professionals in the U.S. used a much broader definition of the term ADHD until recently. This meant up to 10% of children in the U.S. were described as having ADHD. Current estimates suggest that ADHD is present internationally in about 7.2% of children. About five times more boys than girls are diagnosed with ADHD. Boys are seen as the prototypical ADHD child, therefore they are more often diagnosed with ADHD than girls. This may be partly because of the particular ways they express their difficulties. Boys and girls both have attention problems, but boys are more likely to be overactive and difficult to manage. Children from all cultures and social groups are diagnosed with ADHD. However, children from certain backgrounds may be particularly likely to be diagnosed with ADHD, because of different expectations about how they should behave. It is, therefore, important to ensure that a child's cultural background is understood and taken into account as part of the assessment.

A large number of medications and street drugs can cause serotonin syndrome when taken alone at high doses or in combination with other serotonergic drugs. The table below lists some of these drugs.

Many cases of serotonin toxicity occur in patients who have ingested drug combinations that synergistically increase synaptic serotonin. It may also occur as a symptom of overdose of a single serotonergic agent. The combination of MAOIs with precursors such as L-tryptophan or 5-HTP pose a particularly acute risk of life-threatening serotonin syndrome. The case of combination of MAOIs with tryptamine agonists (commonly known as ayahuasca) can present similar dangers as their combination with precursors, but this phenomenon has been described in general terms as the "cheese effect". Many MAOIs irreversibly inhibit monoamine oxidase. It can take at least four weeks for this enzyme to be replaced by the body in the instance of irreversible inhibitors.

Many medications may have been incorrectly thought to cause serotonin syndrome. For example, some case reports have implicated atypical antipsychotics in serotonin syndrome, but it appears based on their pharmacology that they are unlikely to cause the syndrome. It has also been suggested that mirtazapine has no significant serotonergic effects, and is therefore not a dual action drug. Bupropion has also been suggested to cause serotonin syndrome, although as there is no evidence that it has any significant serotonergic activity, it is thought unlikely to produce the syndrome. In 2006 the United States Food and Drug Administration issued an alert suggesting that the combined use of SSRIs or SNRIs and triptan medications or sibutramine could potentially lead to severe cases of serotonin syndrome. This has been disputed by other researchers as none of the cases reported by the FDA met the Hunter criteria for serotonin syndrome. The condition has however occurred in surprising clinical situations, and because of phenotypic variations among individuals, it has been associated with unexpected drugs, including mirtazapine.

The relative risk and severity of serotonergic side effects and serotonin toxicity, with individual drugs and combinations, is complex. Serotonin syndrome has been reported in patients of all ages, including the elderly, children, and even newborn infants due to in utero exposure. The serotonergic toxicity of SSRIs increases with dose, but even in over-dose it is insufficient to cause fatalities from serotonin syndrome in healthy adults. Elevations of central nervous system serotonin will typically only reach potentially fatal levels when drugs with different mechanisms of action are mixed together. Various drugs, other than SSRIs, also have clinically significant potency as serotonin reuptake inhibitors, (e.g. tramadol, amphetamine, and MDMA) and are associated with severe cases of the syndrome.

Neuroleptic-induced deficit syndrome (NIDS) is a psychopathological syndrome that develops in some patients who take high doses of an antipsychotic for an extended time. It is most often caused by high-potency typical antipsychotics, but can also be caused by high doses of many atypicals, especially those closer in profile to typical ones (that have higher D dopamine receptor affinity and relatively low 5-HT serotonin receptor binding affinity), like risperidone and amisulpride.

The mechanisms of antidepressant withdrawal syndrome have not yet been conclusively identified. The leading hypothesis is that after the antidepressant is discontinued, there is a temporary deficiency in the brain of one or more essential neurotransmitters that regulate mood, such as serotonin, dopamine, norepinephrine, and gamma-aminobutyric acid, and since neurotransmitters are an interrelated system, dysregulation of one affects the others.

Antidepressants, including SSRIs, can cross the placenta and have the potential to affect the fetus and newborns, presenting a dilemma whether pregnant women should take antidepressants at all, and if they do, whether tapering them near the end of pregnancy could have a protective effect for the newborn.

Postnatal adaptation syndrome (PNAS) (originally called “neonatal behavioral syndrome”, “poor neonatal adaptation syndrome”, or "neonatal withdrawal syndrome") was first noticed in 1973 in newborns of mothers taking antidepressants; symptoms in the infant include irritability, rapid breathing, hypothermia, and blood sugar problems. The symptoms usually develop from birth to days after delivery and usually resolve within days or weeks of delivery.

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.

Apathy is a lack of feeling, emotion, interest, and concern. Apathy is a state of indifference, or the suppression of emotions such as concern, excitement, motivation, or passion. An apathetic individual has an absence of interest in or concern about emotional, social, spiritual, philosophical, or physical life and the world.

The apathetic may lack a sense of purpose, worth, or meaning in their life. An apathetic person may also exhibit insensibility or sluggishness. In positive psychology, apathy is described as a result of the individuals feeling they do not possess the level of skill required to confront a challenge (i.e. "flow"). It may also be a result of perceiving no challenge at all (e.g. the challenge is irrelevant to them, or conversely, they have learned helplessness). Apathy may be a sign of more specific mental problems such as schizophrenia or dementia. However, apathy is something that all people face in some capacity. It is a natural response to disappointment, dejection, and stress. As a response, apathy is a way to forget about these negative feelings. This type of common apathy is usually only felt in the short-term and when it becomes a long-term or even lifelong state is when deeper social and psychological issues are most likely present.

Apathy should be distinguished from reduced affect, which refers to reduced emotional expression but not necessarily reduced emotion.

As with most mental disorders, BDD's causation is likely intricate, altogether biopsychosocial, through an interaction of multiple factors, including genetic, developmental, psychological, social, and cultural. BDD usually develops during early adolescence, although many patients note earlier trauma, abuse, neglect, teasing, or bullying. Though twin studies on BDD are few, one estimated its heritability at 43%. Yet BDD's causation may also involve introversion, negative body image, perfectionism, heightened aesthetic sensitivity, and childhood abuse and neglect. Media influence has also been identified as a factor causing poor body image.

Often, apathy is felt after witnessing horrific acts, such as the killing or maiming of people during a war, e.g. posttraumatic stress disorder. It is also known to be a distinct psychiatric syndrome that is associated with many conditions, some of which are: CADASIL syndrome, depression, Alzheimer's disease, Chagas disease, Creutzfeldt–Jakob disease, dementia (and dementias such as Alzheimer's disease, vascular dementia, and frontotemporal dementia), Korsakoff's syndrome, excessive vitamin D, hypothyroidism, hyperthyroidism, general fatigue, Huntington's disease, Pick's disease, progressive supranuclear palsy (PSP), brain damage, schizophrenia, schizoid personality disorder, bipolar disorder, autism, ADHD, Asperger's syndrome, and others. Some medications and the heavy use of drugs such as opiates or GABA-ergic drugs may bring apathy as a side effect.

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.

Some individuals experience only a few outbreaks of the disorder. However, in most cases, factitious disorder is a chronic and long-term condition that is difficult to treat. There are relatively few positive outcomes for this disorder; in fact, treatment provided a lower percentage of positive outcomes than did treatment of individuals with obvious psychotic symptoms such as people with schizophrenia. In addition, many individuals with factitious disorder do not present for treatment, often insisting their symptoms are genuine. Some degree of recovery, however, is possible. The passage of time seems to help the disorder greatly. There are many possible explanations for this occurrence, although none are currently considered definitive. It may be that an FD individual has mastered the art of feigning sickness over so many years of practice that the disorder can no longer be discerned. Another hypothesis is that many times an FD individual is placed in a home, or experiences health issues that are not self-induced or feigned. In this way, the problem with obtaining the 'patient' status is resolved because symptoms arise without any effort on the part of the individual.

Winter depression is a common slump in the mood of some inhabitants of most of the Nordic countries. It was first described by the 6th century Goth scholar Jordanes in his "Getica" wherein he described the inhabitants of Scandza (Scandinavia). Iceland, however, seems to be an exception. A study of more than 2000 people there found the prevalence of seasonal affective disorder and seasonal changes in anxiety and depression to be unexpectedly "low" in both sexes. The study's authors suggested that propensity for SAD may differ due to some genetic factor within the Icelandic population. A study of Canadians of wholly Icelandic descent also showed low levels of SAD. It has more recently been suggested that this may be attributed to the large amount of fish traditionally eaten by Icelandic people, in 2007 about 90 kilograms per person per year as opposed to about 24 kg in the US and Canada, rather than to genetic predisposition; a similar anomaly is noted in Japan, where annual fish consumption in recent years averages about 60 kg per capita. Fish are high in vitamin D. Fish also contain docosahexaenoic acid (DHA), which help with a variety of neurological dysfunctions.

Published epidemiological data for akathisia are mostly limited to treatment periods preceding the arrival of second-generation antipsychotics. Sachdev (1995) reported an incidence rate of acute akathisia of 31% for 100 patients treated for 2 weeks with antipsychotic medications. Sachdev (1995) reported a prevalence range from 0.1% to 41%. In all likelihood, rates of prevalence are lower for current treatment as second-generation antipsychotics carry a lower risk of akathisia.

There are many possible causes for this disorder. One such possibility is an underlying personality disorder. Individuals with FD may be trying to repeat a satisfying childhood relationship with a doctor. Perhaps also an individual has a desire to deceive or test authority figures. The underlying desire to resume the role of a patient and be cared for can also be considered an underlying personality disorder. Abuse, neglect, or abandonment during childhood are also probable causes.

These individuals may be trying to reenact unresolved issues with their parents. A history of frequent illnesses may also contribute to the development of this disorder. In some cases, individuals afflicted with FD are accustomed to actually being sick, and thus return to their previous state to recapture what they once considered the 'norm.' Another cause is a history of close contact with someone (a friend or family member) who had a severe or chronic condition. The patients found themselves subconsciously envious of the attention said relation received, and felt that they themselves faded into the background. Thus medical attention makes them feel glamorous and special.

In many species, activity is diminished during the winter months in response to the reduction in available food, the reduction of sunlight (especially for diurnal animals) and the difficulties of surviving in cold weather. Hibernation is an extreme example, but even species that do not hibernate often exhibit changes in behavior during the winter. Presumably, food was scarce during most of human prehistory, and a tendency toward low mood during the winter months would have been adaptive by reducing the need for calorie intake. The preponderance of women with SAD suggests that the response may also somehow regulate reproduction.

Various proximate causes have been proposed. One possibility is that SAD is related to a lack of serotonin, and serotonin polymorphisms could play a role in SAD, although this has been disputed. Mice incapable of turning serotonin into N-acetylserotonin (by serotonin N-acetyltransferase) appear to express "depression-like" behavior, and antidepressants such as fluoxetine increase the amount of the enzyme serotonin N-acetyltransferase, resulting in an antidepressant-like effect. Another theory is that the cause may be related to melatonin which is produced in dim light and darkness by the pineal gland, since there are direct connections, via the retinohypothalamic tract and the suprachiasmatic nucleus, between the retina and the pineal gland. Melatonin secretion is controlled by the endogenous circadian clock, but can also be suppressed by bright light.

One study looked at whether some people could be predisposed to SAD based on personality traits. Correlations between certain personality traits, higher levels of neuroticism, agreeableness, openness, and an avoidance-oriented coping style, appeared to be common in those with SAD.

Estimates of the numbers of people suffering from major depressive episodes and Major Depressive Disorder (MDD) vary significantly. In their lifetime, 10% to 25% of women, and 5% to 12% of men will suffer a major depressive episode. Fewer people, between 5% and 9% of women and between 2% and 3% of men, will have MDD, or full-blown depression. The greatest differences in numbers of men and women diagnosed are found in the United States and Europe. The peak period of development is between the ages of 25 and 44 years. Onset of major depressive episodes or MDD often occurs to people in their mid-20s, and less often to those over 65. Prepubescent girls and boys are affected equally. The symptoms of depression are the same in both children and adolescents though there is evidence that their expression within an individual may change as he or she ages.

In a National Institute of Mental Health study, researchers found that more than 40 percent of people with post-traumatic stress disorder suffered from depression 4 months after the traumatic event they experienced.

Cultural factors can influence the symptoms displayed by a person experiencing a major depressive episode. The values of a specific culture may also influence which symptoms are more concerning to the person or and their friends and family. It is essential that a trained professional knows not to dismiss specific symptoms as merely being the "norm" of a culture.

Women who have recently given birth may be at increased risk for having a major depressive episode. This is referred to as postpartum depression and is a different health condition than the baby blues, a low mood that resolves within 10 days after delivery.

Body dysmorphic disorder (BDD) is a mental disorder characterized by the obsessive idea that some aspect of one's own appearance is severely flawed and warrants exceptional measures to hide or fix it. In BDD's delusional variant, the flaw is imagined. If the flaw is actual, its importance is severely exaggerated. Either way, thoughts about it are pervasive and intrusive, occupying up to several hours a day. The "DSM-5" categorizes BDD in the obsessive–compulsive spectrum, and distinguishes it from anorexia nervosa.

BDD is estimated to affect up to 2.4% of the population. It usually starts during adolescence, and affects men and women roughly equally. The BDD subtype muscle dysmorphia, perceiving the body as too small, affects mostly males. Besides thinking about it, one repetitively checks and compares the perceived flaw, and can adopt unusual routines to avoid social contact that exposes it. Fearing the stigma of vanity, one usually hides the preoccupation. Commonly unsuspected even by psychiatrists, BDD has been underdiagnosed. Severely impairing quality of life via educational and occupational dysfunction and social isolation, BDD has high rates of suicidal thoughts and suicide attempts.

A study on comorbidity of GAD and other depressive disorders has shown that treatment is not more or less effective when there is some sort of comorbidity of another disorder. The severity of symptoms did not affect the outcome of the treatment process in these cases.

Posttraumatic embitterment disorder (PTED) is a proposed disorder modeled after posttraumatic stress disorder. Some psychiatrists are proposing this as a mental disorder because they believe that there are people who have become so bitter, they can barely function. PTED patients do not fit the formal criteria for PTSD and can be clinically distinguished from it, prompting the description of a new and separate disorder.

German psychiatrist Michael Linden, who has conducted research on the proposed disorder, describes its effect on people: "They feel the world has treated them unfairly. It's one step more complex than anger. They're angry plus helpless." He says that people with the disorder are almost treatment resistant and that; "These people usually don't come to treatment because 'the world has to change, not me. He believes that 1 to 2 percent of people are affected at any given time, and explains that, although sufferers of the disorder tend to have a desire for vengeance, "...Revenge is not a treatment."

PTED so far has no official status and is not listed in the DSM-IV-TR or ICD-10-CM.

There are no published or suggested studies on drug treatments for PTED. Selective serotonin reuptake inhibitors (SSRI's) are antidepressants like: Prozac, Paxil, Lexapro, Zoloft, Celexa, and Luvox. They have some benefit in PTED due to their antiobsessional properties. Anafranil, a TCA, is also used extensively.

Major depressive episodes may show comorbidity (association) with other physical and mental health problems. About 20-25% of individuals with a chronic general medical condition will develop major depression. Common comorbid disorders include: eating disorders, substance-related disorders, panic disorder, and obsessive-compulsive disorder. Up to 25% of people who experience a major depressive episode have a pre-existing dysthymic disorder.

Some persons who have a fatal illness or are at the end of their life may experience depression, although this is not universal.

Compulsive buying disorder (CBD), or oniomania (from Greek ὤνιος "ṓnios" "for sale" and μανία "manía" "insanity"), is characterized by an obsession with shopping and buying behavior that causes adverse consequences. According to Kellett and Bolton, compulsive buying "is experienced as an irresistible–uncontrollable urge, resulting in excessive, expensive and time-consuming retail activity [that is] typically prompted by negative affectivity" and results in "gross social, personal and/or financial difficulties". Most people with CBD meet the criteria for a personality disorder. Compulsive shopping is classified by ICD-10 (F63.8) as an "impulse control disorder, not otherwise classified". Several authors consider compulsive shopping rather as a variety of dependence disorder.