What is Dispositional Affect?

Introduction

Dispositional affect, similar to mood, is a personality trait or overall tendency to respond to situations in stable, predictable ways.

This trait is expressed by the tendency to see things in a positive or negative way. People with high positive affectivity tend to perceive things through “pink lens” while people with high negative affectivity tend to perceive things through “black lens”. The level of dispositional affect affects the sensations and behaviour immediately and most of the time in unconscious ways, and its effect can be prolonged (between a few weeks to a few months).

Research shows that there is a correlation between dispositional affect (both positive and negative) and important aspects in psychology and social science, such as personality, culture, decision making, negotiation, psychological resilience, perception of career barriers, and coping with stressful life events. That is why this topic is important both in social psychology research and organiaational psychology research.

Characteristics

Conceptual Distinctions from Emotion and Mood

Besides dispositional affect, there are other concepts for expressions of emotion such as mood or discrete emotions. These concepts are different from dispositional affect though there is a connection among them.

Dispositional affect is different from emotion or affect, by being a personality trait while emotion is a general concept for subjective responses of people to certain situations.Emotion includes both general responses (positive or negative emotion) and specific responses (love, anger, hate, fear, jealousy, sadness etc. The strength of emotions a person feels can stem from his level of dispositional affect.
Dispositional affect is also different from moods since mood relates to general feeling that usually tends to be diffusing and not focused on a specific cause or object.Though mood is specific, it is not a personality trait. Still, positive affectivity can explain why a person has good mood in general, since positive affectivity means viewing the world in a good light. The same thing is true for negative affectivity, which can explain why a person has bad mood in general, since negative affectivity means viewing the world in a dark light.

Dimensions

In general, though emotion researchers disagree about the way that emotions and dispositional affect should be classified, a common classification of emotions assumes that each emotion is a combination of pleasantness (pleasant or unpleasant) and activation (high or low). For example, excitement is a combination of pleasantness and high activation, while calmness is a combination of pleasantness and low activation. Dispositional Affect is also a combination of pleasantness and activation. According to this classification, the different combinations of high or low pleasantness and high or low activation create four Quarters. In line with the classification mentioned above, there is a well-known and common model that is being used in organisational psychology research to analyse and classify dispositional affect, which was developed by Watson and Tellegen. The researchers claim that there are two dimensions of dispositional affect: positive affectivity and negative affectivity and that each person has a certain level of both positive affectivity and negative affectivity. Hence, according to the model and contrary to intuition, positive affectivity does not represent the opposite of negative affectivity, but a different aspect from it. According to Watson & Tellegen one must regard these quarters as two pivots which determine the positive affectivity and negative affectivity of a person. These two dimensions of dispositional affect are bipolar, distinct and independent, relating to different emotion groups, so that each person can be classified with a positive affectivity and negative affectivity grade.

Positive AffectivityDescribes a person’s tendency to be cheerful and energetic, and who experience positive moods, (such as pleasure or well-being), across a variety of situations, perceiving things through a “pink lens”. Individuals who have low levels of positive affectivity tend to be low energy and sluggish or melancholy. High level of positive affectivity represents the extent to which an individual feels energetic and excited, while low level of positive affectivity represents the extent to which an individual feels sadness, sluggishness or weariness”.
Negative AffectivityDescribes a person’s tendency to be distressed and upset, and have a negative view of self over time and across situations, perceiving things through a “black lens”. It is important to explain that low levels of negative affectivity are perceived as positive traits since they represent individuals who are more calm, serene and relaxed. High levels of negative affectivity represents the extent to which an individual feels anger, irritability, fear or nervousness, while low level of negative affectivity represents the extent to which an individual feels calm and serene”.

Relation to Personality Traits

There has been some debate over how closely related affect and some of the Big Five Model of personality traits are related. Some maintain that negative affect and positive affect are should be viewed as the same concept as Neuroticism and Extraversion from the Big Five Model, respectively. However, other researchers maintain that these concepts are related but should remain distinctly separate as they have traditionally had weak to moderate correlations, around.

Measurement

Operationalisations for dispositional affect can be measured by questionnaires. In English researchers use the Positive Affect Negative Affect Scale (PANAS). According to the instructions of this questionnaire, the individual is asked to indicate to what extent he or she feels a certain feeling or emotion such as happy, sad, excited, enthusiastic, guilty, distressed, afraid, etc. An individual has to indicate the most appropriate answer to each item (feeling or emotion) on a scale ranging from 1-5 (1- Very slightly or not at all, 5- Extremely). Early mapping of these emotions by the researchers, helps determine the positive affectivity and negative affectivity of the individual. Another advantage that was discovered while developing this questionnaire is that though it is intended for personality analysis, people can respond to the questions according to specific time frames, for example people can indicate the emotions or sensations they feel at this moment, in the past week, or in general. This way we can learn about dispositional affect to a certain situation and not only about dispositional affect as a general personality trait. By responding to the questions about feelings “in general” we can learn about positive and negative affectivity as a personality trait. By responding to the questions about feelings “at this moment” we can learn about situational dispositional affect as a response to a certain situation. For example, Rafaeli et al. showed in their research that waiting in line cause an increase in negative affectivity levels.

Physical and Mental Aspects

AspectOutline
Physical healthWhen it comes to people with different illness, it is interesting to see that there are differences in the physical health according to the levels of dispositional affect. Individuals who have high levels of positive affectivity, had longer life span, reported fewer pains and illness symptoms (such as blood pressure), and were less likely to develop a cold when exposed to a virus compared with individuals who have high levels of negative affectivity, while both had the same illness. It was also discovered that when it comes to people with chronic diseases that has decent prospects for long-term survival, (such as coronary heart disease), people may benefit from high levels of positive affectivity. However, when it comes to people with chronic diseases that has short-term prognoses (e.g. metastatic breast cancer) and poor survival chances, high levels of positive affectivity may be detrimental to the health of these individuals, possibly as a consequence of underreporting of symptoms resulting in inadequate care, or of a lack of adherence to treatment.
LifestyleEven when it comes to healthy individuals, it seems that there are differences between people’s life style, due to their dispositional affect trait. Individuals who have high levels of positive affectivity tend to attend healthier activities such as improved sleep quality, more physical exercise, and more intake of dietary vitamins, and tend to socialise more often and maintain more and higher-quality social ties. It was also found that high levels of positive affectivity may result in more and closer social contacts because it facilitates approach behaviour, and because others are drawn to form attachments with pleasant individuals.
Psychological ResilienceIndividuals who have high levels of positive affectivity have lower levels of the stress hormones (such as epinephrine, norepinephrine, and cortisol), thus physiology gives one explanation in favour of psychological resilience that provides positive resources to confront stressful life events. On the other hand, the broaden-and-build theory provides a different explanation from the physiological one, and claim that individuals who have high levels of positive affectivity and experience positive events in the present, create a spiral or “snow ball” effect, that may lead to higher probability to experience positive events in the future as well. This means that happiness and well-being sensations in the present, are the ones which creates the likelihood to feel the same in the future, which helps us in building a strong and improved system of coping with stressful life events.
Dispositional Affect and the WorkplaceSome studies have suggested that worker’s perceived career barriers might be due to their dispositional affect.
Positive/Negative AffectNegative affect (NA) is said to have some relation with positive affect (PA), however the actual answer to that is still up in the air. Research of negative affect noted that the contents related to specific-situation in a negative way.
CopingSome studies have found a relationship between Dispositional affect and the coping mechanisms used in attaining ones goals. Those with a positive dispositional affect were more successful in using task-oriented coping methods ( which involve directly addressing the issue at hand), while those with a negative dispositional affect were more successful in using avoidant coping strategies (which involve managing stressful situations in an indirect way).

Culture

Though it is agreed that there are differences between one culture and another, most of the differences that were addressed in researches are related to the comparison between individualism and collectivism. In individualistic cultures, it was found that there is a strong relationship between dispositional affect (either positive or negative) and general life satisfaction (though the relationship was stronger for positive affectivity compared to negative affectivity). On the other hand, in many collectivistic cultures, it was found that there is a no relationship between negative affectivity and general life satisfaction, and it may result from the great variance in the ways that different cultures regulate their positive affectivity compared to negative affectivity.

Decision Making and Negotiation

Decision-MakingIn dealing with interesting and important situations, it was found that individuals who have high levels of positive affectivity make a thorough and efficient cognitive processing, and therefore their decision making process is more efficient, flexible, creative and innovative. It was also found that positive affectivity facilitate creativity, cognitive flexibility, novel responses, openness to new information and dealing with mental problems. This stems from the fact that positive affectivity encourages problem solving approach and searching for variety, in order to achieve a suitable result. At last, it was found that high levels of positive affectivity does not encourage risk taking, though it does facilitates negotiation processes, and improves the results of face to face negotiation processes, in order to reach to agreement.
NegotiationWhen individuals negotiate, it was found that high levels of positive affectivity was related to optimistic view of the upcoming results, planning and using cooperation strategies, and better results regarding the agreements that were made, both in personal (and not formal) negotiation, and group (formal) negotiation. It was also found that positive affectivity increases the likelihood to use cooperation strategies (but not other strategies such as “an eye for an eye”) and improves the results of the negotiation, even if just one of the negotiators has the desired trait of positive affectivity, and increases the likelihood and willingness to agree with counter–arguments, and behaviour changes as a result. Another support for the findings presented above, showed that high levels of positive affectivity was related to willingness to compromise and give up, finding creative solutions, using cooperative strategies, less cheating and better results in negotiation processes. On the contrary to the findings about positive affectivity, it was found that high levels of negative affectivity was related to usage of competitive strategies, and much worse results regarding the agreements that were made. Another support for these finding showed that high levels of negative affectivity was related to competition, lower offers, rejecting ultimatums and lower combined gains, as a result of the negotiation process, and minimum willingness to continue the cooperation strategy in the future.

What is Group Emotion?

Introduction

Group emotion refers to the moods, emotions and dispositional affects of a group of people. It can be seen as either an emotional entity influencing individual members’ emotional states (top down) or the sum of the individuals’ emotional states (bottom up).

Top Down Approach

This view sees the group’s dynamic processes as responsible for an elusive feeling state which influences the members’ feelings and behaviour. This view, that groups have an existence as entities beyond the characters that comprise them, has several angles.

Effects on Individuals

One angle of this approach was depicted in early works such as Le Bon’s and Freud’s who reasoned that there is a general influence of a crowd or group which makes the members of the group “feel, think and act” differently than they would have as isolated individuals. The reassurance of belonging to a crowd makes people act more extremely. Also, the intense uniformity of feelings is overwhelming and causes people to be emotionally swept to join the group’s atmosphere. Thus, the effect of the group causes emotions to be exaggerated.

Norms

Another aspect of the group as a whole perspective sees the normative forces a group has on its members’ emotional behaviour such as norms for the amount of feelings’ expression and even which emotions it is best to feel. The group’s norms control which emotions would (or at least should) be displayed at a specific situation according to the group’s best interest and goals. The norms help differentiate felt emotions, what the individuals actually feel, from expressed emotions, what they display in the current situation. This perspective has practical implications as shown by researchers. Thus, according to this angle the group causes the emotions to be moderated and controlled.

Binding Force

Another perspective emphasizes the importance of emotional attraction in group settings. It defines group emotion as members’ desire to be together, and finds that emotional ties are a type of glue which holds groups together and influences the group’s cohesiveness and the commitment to the task. This perspective focuses on the positive emotions of liking the other group members and the task at hand.

Indicator

This perspective of the group as a whole approach studies the dynamic development of the group, from its establishment to its disassembly. Along the course the group changes in its interrelationships and interdependence amongst its members. These changes are accompanied by emotional processes which shape the outcome of the group. For instance, the midpoint in a group’s development is characterised by anxiety and anticipation about the capacity of the team to complete its goals, which drives teams to restructure their interaction patterns following the midpoint. Should the group harness these feelings and overcome the crisis stronger, its chances of completing the group’s goals are higher. In other cases, negative emotions towards members of the group or towards the task might jeopardise the group’s existence. This perspective sees the temporal changes of the emotions that govern the group.

Bottom Up

Contrary to the former approach, this approach views group-level emotion as the sum of its individuals’ affective compositions. These affective compositions are actually the emotional features each member brings with them to the group, such as: dispositional affect, mood, acute emotions, emotional intelligence, and sentiments (affective evaluations of the group). The team affective composition approach helps to understand the group emotion and its origins, and how these individual members’ affective predisposition combine to become one common entity. For the purpose of combining these individual characteristics, one can embrace several viewpoints:

Average Mood

Research has shown that by averaging the members’ dispositional affective tone it is possible to predict group-level behaviour such as absenteeism and prosocial behaviour. Also, when the average mood of employees was positive, it was positively related to the team’s performance.

Emotional Variance

Affective-homogenous groups are expected to behave differently from heterogeneous ones. The verdict is yet to be decided as to whether homogeneity is better than heterogeneity. In favour of affective homogeneity stand the notion that familiarity and similarity bring feelings of liking, comfort and positive emotions, and thus presumably better group outcomes and performances. It has long been found that people prefer to be in a group similar to them in many perspectives. A support for the positive effects of homogeneity can be found in a study that examined homogeneity in managers’ positive affectivity (PA) and its influence on several aspects of performance such as satisfaction, cooperation and financial outcome of the organisation. On the other hand, according to the view of opposites being beneficial, affective heterogeneity may lead to more emotional checks and balances which could then lead to better team performance. This was found to be true especially in groups where creativity is needed to complete the task appropriately. Homogeneity might lead to groupthink and hamper performance. It is necessary though for group members in heterogeneous groups to accept and allow one another to enact their different emotional roles.

Emotionally Extreme Members

Even if there is only one member in an otherwise averaged group which is extremely negative (or positive) in effect, that person might influence the affective state of the other members and cause the group to be much more negative (or positive) than would be expected from its mean-level dispositional affect. This mood shift might happen through emotional contagion, in which members are “infected” by others’ emotions, as well as through other processes. Emotional contagion has been observed even in absence of non-verbal cues, for example on online social networks like Facebook and Twitter.

Combining Approaches

The above approaches can be combined in a way that they maintain reciprocal relations. For instance, members bring dispositional affective states and norms for expressing them to the team. These components are then factors determining the creation of group norms, which may in turn alter the moods, feelings and their expression by the members. Thus, the top-down and bottom-up approaches coalesce along the dynamic formation and lifespan of teams.

Empirical Definition

One study compared the reports of team members to reports of outside-observers. It showed that team affect and emotions were observable by and agreed upon by outsiders as well as by members of the team interacting face to face. So, it is possible to identify the group’s affective tone by aggregating self-reports of members of the group, as well as by viewing the group from the outside and looking for emotional gestures, both verbal and nonverbal.

Affecting Group Emotion

Studies show that the leader of the team has an important part in determining the moods of their team’s members. Such that members of a team with a leader in a negative affective state tend to be more negative themselves than members of teams with a leader in a positive mood. However, any member of the group might influence the other members’ emotions. The leader may do so either by way of implicit, automatic, emotional contagion or by explicit, deliberate, emotional influence in order to promote his interests. Other factors that affect the forming of the group’s emotional state are its emotional history, its norms for expressing feelings and the broader organisational norms regarding emotions.

Influence on Performance

The emotional state of the group influences team processes and outcomes. For example, a group in a positive mood displays more coordination between members, yet sometimes the effort they apply is not as high as groups in a negative mood. Another role emotions play in group dynamics and performance is the relation between intra-group task-conflicts and relationship-conflicts. It is assumed that conflicts related to the task can be beneficial for achieving the goal, unless these task-conflicts lead to relationship-conflicts among the team members, in which case the performance is hindered. The traits that decouple task from relationship conflicts are emotional attributes such as emotional intelligence, intragroup relational ties, and norms for reducing or preventing negative emotionality. Hence aspects of group emotion affect the outcome. Other findings are that an increase in positive mood will lead to greater cooperativeness and less group conflict. Also, positive mood results in elevated perceptions of task performance.

Evolutionary-Psychological Perspective

According to the evolutionary psychology approach, group affect has a function of helping communication between members of the group. The emotional state of the group informs its members about factors in the environment. For instance, if everyone is in a bad mood it is necessary to change the conditions, or perhaps work harder to achieve the goal and improve the conditions. Also, shared affect in groups coordinates group activity through fostering group bonds and group loyalty.

Emotional Aperture

Emotional aperture has been defined as the ability or skill to perceive features of group emotions. Examples of features of group emotions include the level of variability of emotions among members (i.e. affective diversity), the proportion of positive or negative emotions, and the modal (i.e. most common) emotion present in a group. The term “emotional aperture” was first defined by the social psychologist, Jeffrey Sanchez-Burks and organisational theorist, Quy Huy. Analogous to adjusting a camera’s aperture setting to increase depth of field, emotional aperture involves adjusting one’s depth of field to bring into focus not solely the emotions of one person but also others scattered across a visual landscape. The difference between perceiving individual-level emotions versus group-level emotions is builds upon the distinction between analytic versus holistic perception.

What is Kleine-Levin Syndrome?

Introduction

Kleine-Levin syndrome (KLS) is a rare disorder characterised by persistent episodic hypersomnia and cognitive or mood changes. Sometimes known as the Sleeping Beauty Syndrome.

Many patients also experience hyperphagia, hypersexuality and other symptoms. Patients generally experience recurrent episodes of the condition for more than a decade and may return at a later age. Individual episodes generally last more than a week, sometimes lasting for months. The condition greatly affects the personal, professional, and social lives of sufferers. The severity of symptoms and the course of the syndrome vary between sufferers. Patients commonly have about 20 episodes over about a decade. Several months generally elapse between episodes.

The onset of the condition usually follows a viral infection; several different viruses have been observed to trigger KLS. It is generally only diagnosed after similar conditions have been excluded; magnetic resonance imaging (MRI), computed tomography (CT) scans, lumbar puncture, and toxicology tests are used to rule out other possibilities. The syndrome’s mechanism is not known, but the thalamus is thought to possibly play a role. Single-photon emission computed tomography (SPECT) has shown thalamic hypoperfusion of patients during episodes.

KLS is very rare, occurring at a rate of 1 in 1 million, which limits research into genetic factors. The condition primarily affects adolescent males, though females can also be affected and the age of onset varies. There is no known cure, and there is little evidence supporting drug treatment. Lithium has been reported to have limited effects in case reports, decreasing the length of episodes and duration between them in some patients. Stimulants have been shown to promote wakefulness during episodes, but they do not counteract cognitive symptoms or decrease the duration of episodes. The condition is named after Willi Kleine and Max Levin, who described cases of the disease in the early 20th century. It was added to the International Classification of Sleep Disorders in 1990.

Brief History

In 1815, there was a report of a young man who showed excessive appetite and prolonged sleep after experiencing a fever; this may have been an early description of the condition. Another case with similar symptoms was described by Brierre de Boismont in 1862.

Five patients with symptoms of persistent sleepiness were described in detail in 1925 by Willi Kleine, a neurologist from Frankfurt. This report was followed four years later by details of a similar case by New York-based psychiatrist Max Levin. In 1935, Levin published information about several more cases, including one described by Kleine. Levin noted that some patients displayed an intense appetite in addition to their persistent tiredness. MacDonald Critchley, who first wrote about the condition in 1942, described 11 cases he had examined and reviewed 15 other published cases in a 1962 publication. In the report, which included patients he had examined in the Royal Navy during World War II, he observed that irritability and depersonalisation often occurred while patients were awake. He named the condition Kleine-Levin syndrome and noted four common traits: hypersexuality, adolescent onset, spontaneous resolution, and compulsive eating. He believed that the condition only affected males, but later studies showed some female patients. In the 1970s, several psychoanalytic and psychodynamic explanations for the condition were proposed. In 1980, a Hawaiian-Caucasian family was found in which nine family members suffered from the condition.

Diagnostic criteria for KLS was established by Schmidt in 1990, and the International Classification of Sleep Disorders further refined them. KLS is classified as a sleep disorder, specifically one of recurrent hypersomnia. Before 2005, hyperphagia and hypersexuality were thought to occur in all cases. That was changed with the guidelines published that year, which noted that they did not always occur.

Epidemiology

Population-based studies of KLS have not been performed. Its prevalence is about 1 case per million people. In France, KLS has a prevalence of 1.5 per million people. It occurs most frequently among Jews in the US and Israel. First-degree relatives of people who have suffered from the syndrome are much more likely than the general population to suffer from it, although only in about one percent of cases do family members contract it. About 70% to 90% of patients are male. Patients with the syndrome are more likely than the general population to have genetic disorders, and about a third of people with the syndrome encountered some form of birth difficulty. In a study of 186 older patients, about ten percent had pre-existing psychiatric issues. One study found that about ten percent of patients had a neurological condition before KLS developed. The condition does not appear to occur most frequently in one season.

Symptoms

Patients with KLS experience recurring episodes of prolonged sleep (hypersomnia). In most cases, patients sleep 15 to 21 hours a day during episodes. Excessive appetite (hyperphagia) and unusual cravings are present in half to two thirds of cases. About half of patients, mainly male patients, experience dramatically increased sexual urges (hypersexuality). Several other symptoms usually accompany the syndrome, including marked changes in mood and cognitive ability. Derealisation and severe apathy are present in at least 80% of cases. About one third of patients experience hallucinations or delusions. Depression and anxiety occur less commonly; one study found them in about 25% of patients. Individuals usually cannot remember what happened during episodes. Repetitive behaviours and headaches are commonly reported. Some patients act very childlike during episodes, and communication skills and coordination sometimes suffer.

Sleep studies of KLS show varying results based on the amount of time the patient is observed. Slow wave sleep is often reduced at the beginning of episodes, and rapid eye movement (REM) sleep is reduced near the end. Conversely, REM sleep is often normal at the beginning, and slow wave sleep is often normal by the conclusion. Stage two non-rapid eye movement sleep is often interrupted during KLS. Studies also show that stage one and three non-rapid eye movement sleep become more efficient when the episodes end. The Multiple Sleep Latency Test has yielded inconsistent results when given to KLS patients. In many cases, hours are spent in a withdrawn sleep-like state while awake during episodes. Most sleep studies have been performed while subject is near the end of their episodes. Some patients experience brief insomnia and become very happy and talkative after the episode ends.

The first time a patient experiences KLS, it usually occurs along with symptoms that are similar to those of the flu or encephalitis. In at least 75% of cases, symptoms occur after an airway infection or a fever. Viruses observed before the development of the condition include Epstein-Barr virus, varicella zoster virus, herpes zoster virus, influenza A virus subtypes, and adenovirus. Several days after symptoms first occur, patients become very tired. In cases that occur after an infection, KLS usually starts within three to five days for teenagers and fewer for children. In other cases, alcohol consumption, head injury, or international travel precede symptoms. Lifestyle habits, such as stress, alcohol abuse and lack of sleep and stress, have also been proposed as possible triggers. First episodes of KLS are preceded by a clear event in about 90% of cases. Recurrences generally do not have clear triggers; only about 15% have a precipitating event.

The condition generally disrupts the social lives and academic or professional obligations of sufferers. Some patients also gain weight during episodes. The most severe cases cause a long-term impact on mood and cognitive attention. In rare cases, patients experience long-term memory problems.

In patients with KLS, MRI and CT scans show normal brain morphology. When SPECT is performed, hypoperfusion can often be observed in the brain, particularly in the thalamic and frontotemporal areas. The hypoperfusion is significantly diminished between episodes. Serum biology, c-reactive proteins and leptins, the hormonal pituitary axis, and protein in the cerebral spinal fluid (CSF) are normal in KLS patients.

Cause

It is not known what causes KLS, but several mechanisms have been proposed. One possible explanation is hypothalamic or circadian dysfunction. The thalamus probably plays a role in the out-of-control sleeping, and patients with diencephalic-hypothalamic dysfunction caused by tumours experience symptoms similar to those of KLS patients. Specifically, the medial temporal regions of the thalamus may be involved, although examinations of KLS patients have not consistently found abnormalities in this area. The temporal lobe also appears to play a role in the condition, possibly causing cognitive difficulties. The apathy and disinhibition found in some KLS sufferers suggest that the condition may include frontal lobe dysfunction as well. The involvement of the thalamus, temporal lobe, and frontal lobe of the brain suggests that there is a multifocal, localised encephalopathy. There are also persistent subclinical abnormalities in KLS sufferers.

Another possible explanation concerns the metabolism of serotonin and dopamine. An imbalance in the neurotransmitter pathways of these chemicals could play a role. Viral infections have also been suggested as a possible cause. Evidence for their role includes lesions found in autopsies. Cerebral spinal fluid (CSF) samples from KLS patients indicate that the condition has a different cause than influenza-associated encephalopathy. Triggers of KLS may also affect the blood-brain barrier, which could play a role in the condition. There is limited evidence of what role hypocretin may play, although it often influences hypersomnia.

Androgen might (indirectly) block melatonin receptors, possibly by means of vasodilation, and cause cholinergic abnormalities in some cases of KLS.

Because KLS occurs at a much higher rate in Jews and in some families, it is likely that there is some genetic component in addition to environmental factors. Genetic studies hold promise for understanding the disease, but they have yielded inconsistent results and few patients are available for testing.

Epilepsy and depression do not appear to cause KLS. The condition’s rapid onset after infections indicates that the immune system is not to blame.

One study has suggested a link to the gene LMOD3 on chromosome 3.

Diagnosis

KLS can be diagnosed when there is confusion, apathy, or derealisation in addition to frequent bouts of extreme tiredness and prolonged sleep. The earliest it can be diagnosed is the second episode, this is not common. The condition is generally treated as a diagnosis of exclusion. Because KLS is rare, other conditions with similar symptoms are usually considered first.

MRIs can determine if the symptoms are caused by certain brain disorders, stroke, and multiple sclerosis. Lumbar puncture can determine if encephalitis is the cause. KLS must be differentiated from substance abuse by toxicology tests. The use of electroencephalography (EEG) can exclude temporal status epilepticus from consideration. EEGs are normal in about 70% of KLS patients, but background slowing may sometimes be detected. In addition, low-frequency high-amplitude waves can be observed during waking hours.

Initially, KLS appears similar to bipolar depression. Patients with frontal-lobe syndromes and Klüver-Bucy syndrome also display similar symptoms, but these conditions can be differentiated by the presence of brain lesions. KLS should also be distinguished from very rare cases of menstruation-caused hypersomnia.

Prevention

Lithium is the only drug that appears to have a preventive effect. In two studies of more than 100 patients, lithium helped prevent recurrence of symptoms in 20% to 40% of cases. The recommended blood level of lithium for KLS patients is 0.8-1.2 mEq/ml. It is not known if other mood stabilisers have an effect on the condition. Anti-depressants do not prevent recurrence.

Treatment

Several drug therapies have been used on patients with KLS, but none of them have been subject to randomized controlled trials. A 2016 Cochrane Review concluded that “No evidence indicates that pharmacological treatment for Kleine-Levin syndrome is effective and safe”.

In several cases, stimulants, including modafinil, have been reported to have a limited effect on patients, often alleviating sleepiness. They can cause behavioural problems, but they may pose fewer issues if used in older patients with mild symptoms. In some case reports, lithium has been reported to decrease the length of episodes and the severity of their symptoms and to increase the time between episodes. It has been reported to be effective in about 25 to 60% of cases. Its use carries the risk of side effects in the thyroid or kidneys. Antipsychotics and benzodiazepines can help alleviate psychotic and anxiety related symptoms, respectively. Carbamazepine has been reported to be less effective than lithium but more effective than some drugs in its class. Electroconvulsive therapy is not effective and worsens symptoms.

KLS patients generally do not need to be admitted to hospitals. It is recommended that caregivers reassure them and encourage them to maintain sleep hygiene. It may also be necessary for patients to be prevented from putting themselves in dangerous situations, such as driving.

Prognosis

The frequency of KLS episodes can vary from attacks one week in length occurring twice a year to dozens of episodes that follow each other in close succession. The median duration of KLS episodes is about ten days, but some last several weeks or months. A study of 108 patients found an average of 19 episodes over the duration of the disease. Another study found a median of 3.5 months between episodes. Outside of episodes, there is no disturbance in patients’ sleep patterns and they are generally asymptomatic. Patients do not experience the same symptoms in each episode.

About 80% of patients are adolescents when they first experience KLS. On some occasions though, its first occurrence comes in childhood or adulthood. In most adolescent-onset patients, symptoms cease by the time they are 30 years old. A French study of 108 patients found a median duration of 13 years, but a review of 186 cases found a median duration of 8 years. Unusually young or old patients and those who experience hypersexuality tend to have a more severe course. Patients who initially have frequent attacks generally see the disease cease earlier than others. The condition spontaneously resolves, and the patient is considered to be cured if there have been no symptoms for six years.

What is Mania?

Introduction

Mania, also known as manic syndrome, is a mental and behavioural disorder defined as a state of abnormally elevated arousal, affect, and energy level, or “a state of heightened overall activation with enhanced affective expression together with lability of affect.”

During a manic episode, an individual will experience rapidly changing emotions and moods, highly influenced by surrounding stimuli. Although mania is often conceived as a “mirror image” to depression, the heightened mood can be either euphoric or dysphoric. As the mania intensifies, irritability can be more pronounced and result in anxiety or anger.

The symptoms of mania include elevated mood (either euphoric or irritable), flight of ideas and pressure of speech, increased energy, decreased need and desire for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states. However, in full-blown mania, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behaviour.

Refer to Bipolar I Disorder, Bipolar II Disorder, and Mixed Affective State.

Etymology

The nosology of the various stages of a manic episode has changed over the decades. The word derives from the Ancient Greek μανία (manía), “madness, frenzy” and the verb μαίνομαι (maínomai), “to be mad, to rage, to be furious”.

Causes and Diagnosis

Mania is a syndrome with multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (such as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, such as multiple sclerosis; certain medications may perpetuate a manic state, for example prednisone; or substances prone to abuse, especially stimulants, such as caffeine and cocaine. In the current DSM-5, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterised as either mild, moderate, or severe, with certain diagnostic criteria (e.g. catatonia, psychosis). Mania is divided into three stages:

  • Hypomania, or stage I;
  • Acute mania, or stage II; and
  • Delirious mania (delirium), or stage III.

This “staging” of a manic episode is useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardised tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic/hypomanic bipolar patient needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have “gone manic” severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

Classification

Mixed States

Refer to Mixed Affective State.

In a mixed affective state, the individual, though meeting the general criteria for a hypomanic (discussed below) or manic episode, experiences three or more concurrent depressive symptoms. This has caused some speculation, among clinicians, that mania and depression, rather than constituting “true” polar opposites, are, rather, two independent axes in a unipolar – bipolar spectrum.

A mixed affective state, especially with prominent manic symptoms, places the patient at a greater risk for suicide. Depression on its own is a risk factor but, when coupled with an increase in energy and goal-directed activity, the patient is far more likely to act with violence on suicidal impulses.

Hypomania

Refer to Hypomania.

Hypomania, which means “less than mania”, is a lowered state of mania that does little to impair function or decrease quality of life. It may, in fact, increase productivity and creativity. In hypomania, there is less need for sleep and both goal-motivated behaviour and metabolism increase. Some studies exploring brain metabolism in subjects with hypomania, however, did not find any conclusive link; while there are studies that reported abnormalities, some failed to detect differences. Though the elevated mood and energy level typical of hypomania could be seen as a benefit, true mania itself generally has many undesirable consequences including suicidal tendencies, and hypomania can, if the prominent mood is irritable as opposed to euphoric, be a rather unpleasant experience. In addition, the exaggerated case of hypomania can lead to problems. For instance, trait-based positivity for a person could make them more engaging and outgoing, and cause them to have a positive outlook in life. When exaggerated in hypomania, however, such a person can display excessive optimism, grandiosity, and poor decision making, often with little regard to the consequences.

Associated Disorders

A single manic episode, in the absence of secondary causes, (i.e. substance use disorders, pharmacologics, or general medical conditions) is often sufficient to diagnose bipolar I disorder. Hypomania may be indicative of bipolar II disorder. Manic episodes are often complicated by delusions and/or hallucinations; and if the psychotic features persist for a duration significantly longer than the episode of typical mania (two weeks or more), a diagnosis of schizoaffective disorder is more appropriate. Certain obsessive-compulsive spectrum disorders as well as impulse control disorders share the suffix “-mania,” namely, kleptomania, pyromania, and trichotillomania. Despite the unfortunate association implied by the name, however, no connection exists between mania or bipolar disorder and these disorders. Furthermore, evidence indicates a B12 deficiency can also cause symptoms characteristic of mania and psychosis.

Hyperthyroidism can produce similar symptoms to those of mania, such as agitation, elevated mood, increased energy, hyperactivity, sleep disturbances and sometimes, especially in severe cases, psychosis.

Signs and Symptoms

A manic episode is defined in the American Psychiatric Association’s diagnostic manual as a “distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration, if hospitalisation is necessary),” where the mood is not caused by drugs/medication or a non-mental medical illness (e.g. hyperthyroidism), and: (a) is causing obvious difficulties at work or in social relationships and activities, or (b) requires admission to hospital to protect the person or others, or (c) the person is suffering psychosis.

To be classified as a manic episode, while the disturbed mood and an increase in goal-directed activity or energy is present, at least three (or four, if only irritability is present) of the following must have been consistently present:

  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep (e.g. feels rested after 3 hours of sleep).
  • More talkative than usual, or acts pressured to keep talking.
  • Flights of ideas or subjective experience that thoughts are racing.
  • Increase in goal-directed activity, or psychomotor acceleration.
  • Distractibility (too easily drawn to unimportant or irrelevant external stimuli).
  • Excessive involvement in activities with a high likelihood of painful consequences.(e.g. extravagant shopping, improbable commercial schemes, hypersexuality).

Though the activities one participates in while in a manic state are not always negative, those with the potential to have negative outcomes are far more likely.

If the person is concurrently depressed, they are said to be having a mixed episode.

The World Health Organisation’s classification system defines a manic episode as one where mood is higher than the person’s situation warrants and may vary from relaxed high spirits to barely controllable exuberance, is accompanied by hyperactivity, a compulsion to speak, a reduced sleep requirement, difficulty sustaining attention, and/or often increased distractibility. Frequently, confidence and self-esteem are excessively enlarged, and grand, extravagant ideas are expressed. Behaviour that is out-of-character and risky, foolish or inappropriate may result from a loss of normal social restraint.

Some people also have physical symptoms, such as sweating, pacing, and weight loss. In full-blown mania, often the manic person will feel as though their goal(s) are of paramount importance, that there are no consequences, or that negative consequences would be minimal, and that they need not exercise restraint in the pursuit of what they are after. Hypomania is different, as it may cause little or no impairment in function. The hypomanic person’s connection with the external world, and its standards of interaction, remain intact, although intensity of moods is heightened. But those who suffer from prolonged unresolved hypomania do run the risk of developing full mania, and may cross that “line” without even realising they have done so.

One of the signature symptoms of mania (and to a lesser extent, hypomania) is what many have described as racing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli. This experience creates an absent-mindedness where the manic individual’s thoughts totally preoccupy them, making them unable to keep track of time, or be aware of anything besides the flow of thoughts. Racing thoughts also interfere with the ability to fall asleep.

Manic states are always relative to the normal state of intensity of the afflicted individual; thus, already irritable patients may find themselves losing their tempers even more quickly, and an academically gifted person may, during the hypomanic stage, adopt seemingly “genius” characteristics and an ability to perform and articulate at a level far beyond that which they would be capable of during euthymia. A very simple indicator of a manic state would be if a heretofore clinically depressed patient suddenly becomes inordinately energetic, enthusiastic, cheerful, aggressive, or “over-happy”. Other, often less obvious, elements of mania include delusions (generally of either grandeur or persecution, according to whether the predominant mood is euphoric or irritable), hypersensitivity, hypervigilance, hypersexuality, hyper-religiosity, hyperactivity and impulsivity, a compulsion to over explain (typically accompanied by pressure of speech), grandiose schemes and ideas, and a decreased need for sleep (for example, feeling rested after only 3 or 4 hours of sleep). In the case of the latter, the eyes of such patients may both look and seem abnormally “wide open”, rarely blinking, and may contribute to some clinicians’ erroneous belief that these patients are under the influence of a stimulant drug, when the patient, in fact, is either not on any mind-altering substances or is actually on a depressant drug. Individuals may also engage in out-of-character behaviour during the episode, such as questionable business transactions, wasteful expenditures of money (e.g. spending sprees), risky sexual activity, abuse of recreational substances, excessive gambling, reckless behaviour (such as extreme speeding or other daredevil activity), abnormal social interaction (e.g. over-familiarity and conversing with strangers), or highly vocal arguments. These behaviours may increase stress in personal relationships, lead to problems at work, and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to the self and others.

Although “severely elevated mood” sounds somewhat desirable and enjoyable, the experience of mania is ultimately often quite unpleasant and sometimes disturbing, if not frightening, for the person involved and for those close to them, and it may lead to impulsive behaviour that may later be regretted. It can also often be complicated by the sufferer’s lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients are frequently grandiose, obsessive, impulsive, irritable, belligerent, and frequently deny anything is wrong with them. Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly. Racing thoughts and misperceptions lead to frustration and decreased ability to communicate with others.

Mania may also, as earlier mentioned, be divided into three “stages”. Stage I corresponds with hypomania and may feature typical hypomanic characteristics, such as gregariousness and euphoria. In stages II and III mania, however, the patient may be extraordinarily irritable, psychotic or even delirious. These latter two stages are referred to as acute and delirious (or Bell’s), respectively.

Cause

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69%. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the hypothalamic-pituitary-adrenal (HPA) axis. Lifestyle triggers include irregular sleep-wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioural changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behaviour. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behaviour in preclinical models.

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.

Deep brain stimulation of the subthalamic nucleus in Parkinson’s disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.

Mania can also be caused by physical trauma or illness. When the causes are physical, it is called secondary mania.

Mechanism

Refer to Biology of Bipolar Disorder.

The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the right prefrontal cortex, a common finding in neuroimaging studies. Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities in GSK-3, dopamine, Protein kinase C and Inositol monophosphatase.

Meta analysis of neuroimaging studies demonstrate increased thalamic activity, and bilaterally reduced inferior frontal gyrus activation. Activity in the amygdala and other subcortical structures such as the ventral striatum tend to be increased, although results are inconsistent and likely dependent upon task characteristics such as valence. Reduced functional connectivity between the ventral prefrontal cortex and amygdala along with variable findings supports a hypothesis of general dysregulation of subcortical structures by the prefrontal cortex. A bias towards positively valenced stimuli, and increased responsiveness in reward circuitry may predispose towards mania. Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.

Post-mortem examinations of bipolar disorder demonstrate increased expression of Protein Kinase C (PKC). While limited, some studies demonstrate manipulation of PKC in animals produces behavioural changes mirroring mania, and treatment with PKC inhibitor tamoxifen (also an anti-oestrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.

Manic episodes may be triggered by dopamine receptor agonists, and this combined with tentative reports of increased VMAT2 activity, measured via PET scans of radioligand binding, suggests a role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite 5-HIAA have been found in manic patients too, which may be explained by a failure of serotonergic regulation and dopaminergic hyperactivity.

Limited evidence suggests that mania is associated with behavioural reward hypersensitivity, as well as with neural reward hypersensitivity. Electrophysiological evidence supporting this comes from studies associating left frontal EEG activity with mania. As left frontal EEG activity is generally thought to be a reflection of behavioural activation system activity, this is thought to support a role for reward hypersensitivity in mania. Tentative evidence also comes from one study that reported an association between manic traits and feedback negativity during receipt of monetary reward or loss. Neuroimaging evidence during acute mania is sparse, but one study reported elevated orbitofrontal cortex activity to monetary reward, and another study reported elevated striatal activity to reward omission. The latter finding was interpreted in the context of either elevated baseline activity (resulting in a null finding of reward hypersensitivity), or reduced ability to discriminate between reward and punishment, still supporting reward hyperactivity in mania. Punishment hyposensitivity, as reflected in a number of neuroimaging studies as reduced lateral orbitofrontal response to punishment, has been proposed as a mechanism of reward hypersensitivity in mania.

Diagnosis

In the ICD-10 there are several disorders with the manic syndrome:

  • Organic manic disorder (F06.30).
  • Mania without psychotic symptoms (F30.1).
  • Mania with psychotic symptoms (F30.2).
  • Other manic episodes (F30.8).
  • Unspecified manic episode (F30.9).
  • Manic type of schizoaffective disorder (F25.0).
  • Bipolar affective disorder, current episode manic without psychotic symptoms (F31.1).
  • Bipolar affective disorder, current episode manic with psychotic symptoms (F31.2).

Treatment

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilisation of either a mood stabiliser (Carbamazepine, valproate, lithium, or lamotrigine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). The use of antipsychotic agents in the treatment of acute mania was reviewed by Tohen and Vieta in 2009.

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilise the patient’s mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabiliser to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine and topiramate, both anticonvulsants as well.

In some cases, long-acting benzodiazepines, particularly clonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms, lorazepam, combined with haloperidol, is used to promptly alleviate symptoms of agitation, aggression, and psychosis.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilisers in these patients. Some atypical antidepressants, however, such as mirtazepine and trazodone have been occasionally used after other options have failed.

Society and Culture

In Electroboy: A Memoir of Mania by Andy Behrman, he describes his experience of mania as “the most perfect prescription glasses with which to see the world… life appears in front of you like an oversized movie screen”. Behrman indicates early in his memoir that he sees himself not as a person suffering from an uncontrollable disabling illness, but as a director of the movie that is his vivid and emotionally alive life. There is some evidence that people in the creative industries suffer from bipolar disorder more often than those in other occupations. Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.

English actor Stephen Fry, who suffers from bipolar disorder, recounts manic behaviour during his adolescence: “When I was about 17 … going around London on two stolen credit cards, it was a sort of fantastic reinvention of myself, an attempt to. I bought ridiculous suits with stiff collars and silk ties from the 1920s, and would go to the Savoy and Ritz and drink cocktails.” While he has experienced suicidal thoughts, he says the manic side of his condition has had positive contributions on his life.

What is Hypomania?

Introduction

Hypomania (literally “under mania” or “less than mania”) is a mental and behavioural disorder, characterised essentially by an apparently non-contextual elevation of mood (euphoria) which contributes to persistently disinhibited behaviour.

The individual afflicted may suffer with irritability, not necessarily less severe than full mania; in fact, the presence of marked irritability is a documented feature of hypomanic and mixed episodes in Bipolar type II. According to DSM-5 criteria, hypomania is distinct from mania in that there is no significant functional impairment; mania, by DSM-5 definition, does include significant functional impairment and may have psychotic features.

Characteristic behaviours of persons experiencing hypomania are a notable decrease in the need for sleep, an overall increase in energy, unusual behaviours and actions, and a markedly distinctive increase in talkativeness and confidence, commonly exhibited with a flight of creative ideas. Other symptoms related to this may include feelings of grandiosity, distractibility, and hypersexuality. While hypomanic behaviour often generates productivity and excitement, it can become troublesome if the subject engages in risky or otherwise inadvisable behaviours, and/or the symptoms manifest themselves in trouble with everyday life events. When manic episodes are separated into stages of a progression according to symptomatic severity and associated features, hypomania constitutes the first stage of the syndrome, wherein the cardinal features (euphoria or heightened irritability, pressure of speech and activity, increased energy, decreased need for sleep, and flight of ideas) are most plainly evident.

Refer to Bipolar I Disorder, Bipolar II Disorder, and Mixed Affective State.

Etymology

The Ancient Greek physician Hippocrates called one personality type ‘hypomanic’ (Greek: ὑπομαινόμενοι, hypomainómenoi). In 19th century psychiatry, when mania had a broad meaning of insanity, hypomania was equated by some to concepts of ‘partial insanity’ or monomania. A more specific usage was advanced by the German neuro-psychiatrist Emanuel Ernst Mendel in 1881, who wrote, “I recommend, taking into consideration the word used by Hippocrates, to name those types of mania that show a less severe phenomenological picture, ‘hypomania'”. Narrower operational definitions of hypomania were developed in the 1960s and 1970s.

Signs and Symptoms

Individuals in a hypomanic state have a decreased need for sleep, are extremely gregarious and competitive, and have a great deal of energy. They are, otherwise, often fully functioning (unlike individuals suffering from a full manic episode).

Distinctive Markers

Specifically, hypomania is distinguished from mania by the absence of psychotic symptoms, and by its lesser degree of impact on functioning.

Hypomania is a feature of bipolar II disorder and cyclothymia, but can also occur in schizoaffective disorder. Hypomania is also a feature of bipolar I disorder; it arises in sequential procession as the mood disorder fluctuates between normal mood (euthymia) and mania. Some individuals with bipolar I disorder have hypomanic as well as manic episodes. Hypomania can also occur when moods progress downwards from a manic mood state to a normal mood. Hypomania is sometimes credited with increasing creativity and productive energy. Numerous people with bipolar disorder have credited hypomania with giving them an edge in their theatre of work.

People who experience hyperthymia, or “chronic hypomania”, encounter the same symptoms as hypomania but on a longer-term basis.

Associated Disorders

Cyclothymia, a condition of continuous mood fluctuations, is characterised by oscillating experiences of hypomania and depression that fail to meet the diagnostic criteria for either manic or major depressive episodes. These periods are often interspersed with periods of relatively normal (euthymic) functioning.

When a patient presents with a history of at least one episode of both hypomania and major depression, each of which meet the diagnostic criteria, bipolar II disorder is diagnosed. In some cases, depressive episodes routinely occur during the fall or winter and hypomanic ones in the spring or summer. In such cases, one speaks of a “seasonal pattern”.

If left untreated, and in those so predisposed, hypomania may transition into mania, which may be psychotic, in which case bipolar I disorder is the correct diagnosis.

Causes

Often in those who have experienced their first episode of hypomania – generally without psychotic features – there may be a long or recent history of depression or a mix of hypomania combined with depression (known as mixed-state) prior to the emergence of manic symptoms. This commonly surfaces in the mid to late teens. Because the teenage years are typically an emotionally charged time of life, it is not unusual for mood swings to be passed off as normal hormonal teen behaviour and for a diagnosis of bipolar disorder to be missed until there is evidence of an obvious manic or hypomanic phase.

In cases of drug-induced hypomanic episodes in unipolar depressives, the hypomania can almost invariably be eliminated by lowering medication dosage, withdrawing the drug entirely, or changing to a different medication if discontinuation of treatment is not possible.

Hypomania can be associated with narcissistic personality disorder.

Psychopathology

Mania and hypomania are usually studied together as components of bipolar disorders, and the pathophysiology is usually assumed to be the same. Given that norepinephrine and dopaminergic drugs are capable of triggering hypomania, theories relating to monoamine hyperactivity have been proposed. A theory unifying depression and mania in bipolar individuals proposes that decreased serotonergic regulation of other monoamines can result in either depressive or manic symptoms. Lesions on the right side frontal and temporal lobes have further been associated with mania.

Diagnosis

The DSM-IV-TR defines a hypomanic episode as including, over the course of at least four days, elevated mood plus three of the following symptoms OR irritable mood plus four of the following symptoms, when the behaviours are clearly different from how the person typically acts when not depressed:

  • Pressured speech.
  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep.
  • Flight of ideas or the subjective experience that thoughts are racing.
  • Easily distracted.
  • Increase in goal-directed activity (e.g. social activity, at work, or hypersexuality), or psychomotor agitation.
  • Involvement in pleasurable activities that may have a high potential for negative psycho-social or physical consequences (e.g. the person engages in unrestrained buying sprees, sexual indiscretions, reckless driving, physical and verbal conflicts, foolish business investments, quitting a job to pursue some grandiose goal, etc.).

Treatment

Medications

Antimanic drugs are used to control acute attacks and prevent recurring episodes of hypomania combined with a range of psychological therapies. The recommended length of treatment ranges from 2 years to 5 years. Anti-depressants may also be required for existing treatments but are avoided in patients who have had a recent history with hypomania. Sertraline has often been debated to have side effects that can trigger hypomania.

What is Euthymia?

Introduction

In psychiatry and psychology, euthymia is a normal, tranquil mental state or mood.

In those with bipolar disorder, euthymia is a stable mental state or mood that is neither manic nor depressive, yet distinguishable from the state of healthy people. Euthymia is also the “baseline” of other cyclical mood disorders like major depressive disorder (MDD), borderline personality disorder (BPD) and narcissistic personality disorder (NPD). This state is the goal of psychiatric and psychological interventions.

Background

The term euthymia is derived from the Greek words “eu”, well, and “thymo”, soul or emotion. The word “thymos” also had four additional meanings: life energy; feelings and passions; desires and inclinations; and thought or intelligence. Euthymia is also derived from a verb, “euthymeo”, that means both “I am happy, in good spirits” and “I make others happy, I reassure and encourage”. This is the basis on which the first formal definition of euthymia was built.

Democritus, who coined the philosophical concept of euthymia, said that euthymia is achieved when “one is satisfied with what is present and available, taking little heed of people who are envied and admired and observing the lives of those who suffer and yet endure”. This was later amended in the translation given by the Roman philosopher Seneca the Younger in which euthymia means a state of internal calm and contentment. Seneca was also the first to link the state of euthymia to a learning process; in order to achieve it, one must be aware of psychological well-being. Seneca’s definition included a cache about detachment from current events. Later, the Greek biographer Plutarch removed this cache with his definition which focused more on learning from adverse events.

In 1958, Marie Jahoda gave a modern clinical definition of mental health in the terms of positive symptoms by outlining the criteria for mental health: “autonomy (regulation of behaviour from within), environmental mastery, satisfactory interactions with other people and the milieu, the individual’s style and degree of growth, development or self-actualization, the attitudes of an individual toward his/her own self”. In her definition she acknowledged the absence of disease as being necessary, but not enough, to constitute positive mental health, or euthymia.

Carol Ryff (1989) was the first to develop a comprehensive scale that could assess euthymia: the six-factor model of psychological well-being. The 84-item scale includes facets of self-acceptance, positive relations with others, autonomy, environmental mastery, purpose in life, and personal growth. It did not include a notion of resilience, which people in the field started working to add in the 2000s.

Parathymia, on the other hand, is related to pathological laughter (called “Witzelsucht”).

What is Emotional Lability?

Introduction

In medicine and psychology, emotional lability is a sign or symptom typified by exaggerated changes in mood or affect in quick succession.

Background

Sometimes the emotions expressed outwardly are very different from how the person feels on the inside. These strong emotions can be a disproportionate response to something that happened, but other times there might be no trigger at all. The person experiencing emotional lability usually feels like they do not have control over their emotions. For example, someone might cry uncontrollably in response to any strong emotion even if they do not feel sad or unhappy.

Emotional lability is seen or reported in various conditions including borderline personality disorder, histrionic personality disorder, hypomanic or manic episodes of bipolar disorder, and neurological disorders or brain injury (where it is termed pseudobulbar affect), such as after a stroke. It has sometimes been found to have been a harbinger, or early warning, of certain forms of thyroid disease. Emotional lability also results from intoxication with certain substances, such as alcohol and benzodiazepines. It can also be an associated feature of ADHD.

Children who display a high degree of emotional lability generally have low frustration tolerance and frequent crying spells or tantrums. During preschool, ADHD with emotional lability is associated with increased impairment and may be a sign of internalising problems or multiple comorbid disorders. Children who are neglected are more likely to experience emotional dysregulation, including emotional lability.

Potential triggers of emotional lability may be: excessive tiredness, stress or anxiety, over-stimulated senses (too much noise, being in large crowds, etc.), being around others exhibiting strong emotions, very sad or funny situations (such as jokes, movies, certain stories or books), death of a loved one, or other situations that elicit stress or strong emotions.

What is Dysthymia?

Introduction

Dysthymia, also known as persistent depressive disorder (PDD), is a mental and behavioural disorder, specifically a disorder primarily of mood, consisting of the same cognitive and physical problems as depression, but with longer-lasting symptoms.

The concept was coined by Robert Spitzer as a replacement for the term “depressive personality” in the late 1970s.

In the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), dysthymia is a serious state of chronic depression, which persists for at least two years (one year for children and adolescents). Dysthymia is less acute than major depressive disorder, but not necessarily less severe.

As dysthymia is a chronic disorder, sufferers may experience symptoms for many years before it is diagnosed, if diagnosis occurs at all. As a result, they may believe that depression is a part of their character, so they may not even discuss their symptoms with doctors, family members or friends. In the DSM-5, dysthymia is replaced by persistent depressive disorder. This new condition includes both chronic major depressive disorder and the previous dysthymic disorder. The reason for this change is that there was no evidence for meaningful differences between these two conditions.

Epidemiology

Globally dysthymia occurs in about 105 million people a year (1.5% of the population). It is 38% more common in women (1.8% of women) than in men (1.3% of men). The lifetime prevalence rate of dysthymia in community settings appears to range from 3 to 6% in the United States. However, in primary care settings the rate is higher ranging from 5 to 15 percent. United States prevalence rates tend to be somewhat higher than rates in other countries.

Signs and Symptoms

Dysthymia characteristics include an extended period of depressed mood combined with at least two other symptoms which may include insomnia or hypersomnia, fatigue or low energy, eating changes (more or less), low self-esteem, or feelings of hopelessness. Poor concentration or difficulty making decisions are treated as another possible symptom. Irritability is one of the more common symptoms in children and adolescents.

Mild degrees of dysthymia may result in people withdrawing from stress and avoiding opportunities for failure. In more severe cases of dysthymia, people may withdraw from daily activities. They will usually find little pleasure in usual activities and pastimes.

Diagnosis of dysthymia can be difficult because of the subtle nature of the symptoms and patients can often hide them in social situations, making it challenging for others to detect symptoms. Additionally, dysthymia often occurs at the same time as other psychological disorders, which adds a level of complexity in determining the presence of dysthymia, particularly because there is often an overlap in the symptoms of disorders.

There is a high incidence of comorbid illness in those with dysthymia. Suicidal behaviour is also a particular problem with those with dysthymia. It is vital to look for signs of major depression, panic disorder, generalised anxiety disorder, alcohol and substance use disorders, and personality disorder.

Causes

There are no known biological causes that apply consistently to all cases of dysthymia, which suggests diverse origin of the disorder. However, there are some indications that there is a genetic predisposition to dysthymia: “The rate of depression in the families of people with dysthymia is as high as fifty percent for the early-onset form of the disorder”. Other factors linked with dysthymia include stress, social isolation, and lack of social support.

In a study using identical and fraternal twins, results indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is in part caused by heredity.

Co-Occurring Conditions

Dysthymia often co-occurs with other mental disorders. A “double depression” is the occurrence of episodes of major depression in addition to dysthymia. Switching between periods of dysthymic moods and periods of hypomanic moods is indicative of cyclothymia, which is a mild variant of bipolar disorder.

“At least three-quarters of patients with dysthymia also have a chronic physical illness or another psychiatric disorder such as one of the anxiety disorders, cyclothymia, drug addiction, or alcoholism”. Common co-occurring conditions include major depression (up to 75%), anxiety disorders (up to 50%), personality disorders (up to 40%), somatoform disorders (up to 45%) and substance use disorders (up to 50%). People with dysthymia have a higher-than-average chance of developing major depression. A 10-year follow-up study found that 95% of dysthymia patients had an episode of major depression. When an intense episode of depression occurs on top of dysthymia, the state is called “double depression.”

Double Depression

Double depression occurs when a person experiences a major depressive episode on top of the already-existing condition of dysthymia. It is difficult to treat, as sufferers accept these major depressive symptoms as a natural part of their personality or as a part of their life that is outside of their control. The fact that people with dysthymia may accept these worsening symptoms as inevitable can delay treatment. When and if such people seek out treatment, the treatment may not be very effective if only the symptoms of the major depression are addressed, but not the dysthymic symptoms. Patients with double depression tend to report significantly higher levels of hopelessness than is normal. This can be a useful symptom for mental health services providers to focus on when working with patients to treat the condition. Additionally, cognitive therapies can be effective for working with people with double depression in order to help change negative thinking patterns and give individuals a new way of seeing themselves and their environment.

It has been suggested that the best way to prevent double depression is by treating the dysthymia. A combination of antidepressants and cognitive therapies can be helpful in preventing major depressive symptoms from occurring. Additionally, exercise and good sleep hygiene (e.g. improving sleep patterns) are thought to have an additive effect on treating dysthymic symptoms and preventing them from worsening.

Pathophysiology

There is evidence that there may be neurological indicators of early onset dysthymia. There are several brain structures (corpus callosum and frontal lobe) that are different in women with dysthymia than in those without dysthymia. This may indicate that there is a developmental difference between these two groups.

Another study, which used fMRI techniques to assess the differences between individuals with dysthymia and other people, found additional support for neurological indicators of the disorder. This study found several areas of the brain that function differently. The amygdala (associated with processing emotions such as fear) was more activated in dysthymia patients. The study also observed increased activity in the insula (which is associated with sad emotions). Finally, there was increased activity in the cingulate gyrus (which serves as the bridge between attention and emotion).

A study comparing healthy individuals to people with dysthymia indicates there are other biological indicators of the disorder. An anticipated result appeared as healthy individuals expected fewer negative adjectives to apply to them, whereas people with dysthymia expected fewer positive adjectives to apply to them in the future. Biologically these groups are also differentiated in that healthy individuals showed greater neurological anticipation for all types of events (positive, neutral, or negative) than those with dysthymia. This provides neurological evidence of the dulling of emotion that individuals with dysthymia have learned to use to protect themselves from overly strong negative feelings, compared to healthy people.

There is some evidence of a genetic basis for all types of depression, including dysthymia. A study using identical and fraternal twins indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is caused in part by heredity.

A new model has recently surfaced in the literature regarding the HPA axis (structures in the brain that get activated in response to stress) and its involvement with dysthymia (e.g. phenotypic variations of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP), and down-regulation of adrenal functioning) as well as forebrain serotonergic mechanisms. Since this model is highly provisional, further research is still needed.

Diagnosis

The Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV), published by the American Psychiatric Association, characterises dysthymic disorder. The essential symptom involves the individual feeling depressed for the majority of days, and parts of the day, for at least two years. Low energy, disturbances in sleep or in appetite, and low self-esteem typically contribute to the clinical picture as well. Sufferers have often experienced dysthymia for many years before it is diagnosed. People around them often describe the sufferer in words similar to “just a moody person”. Note the following diagnostic criteria:

  1. During a majority of days for two years or more, the adult patient reports depressed mood, or appears depressed to others for most of the day.
  2. When depressed, the patient has two or more of:
    1. decreased or increased appetite
    2. decreased or increased sleep (insomnia or hypersomnia)
    3. Fatigue or low energy
    4. Reduced self-esteem
    5. Decreased concentration or problems making decisions
    6. Feelings of hopelessness or pessimism
  3. During this two-year period, the above symptoms are never absent longer than two consecutive months.
  4. During the duration of the two-year period, the patient may have had a perpetual major depressive episode.
  5. The patient has not had any manic, hypomanic, or mixed episodes.
  6. The patient has never fulfilled criteria for cyclothymic disorder.
  7. The depression does not exist only as part of a chronic psychosis (such as schizophrenia or delusional disorder).
  8. The symptoms are often not directly caused by a medical illness or by substances, including substance use or other medications.
  9. The symptoms may cause significant problems or distress in social, work, academic, or other major areas of life functioning.

In children and adolescents, mood can be irritable, and duration must be at least one year, in contrast to two years needed for diagnosis in adults.

Early onset (diagnosis before age 21) is associated with more frequent relapses, psychiatric hospitalisations, and more co-occurring conditions. For younger adults with dysthymia, there is a higher co-occurrence in personality abnormalities and the symptoms are likely chronic. However, in older adults suffering from dysthymia, the psychological symptoms are associated with medical conditions and/or stressful life events and losses.

Dysthymia can be contrasted with major depressive disorder by assessing the acute nature of the symptoms. Dysthymia is far more chronic (long lasting) than major depressive disorder, in which symptoms may be present for as little as 2 weeks. Also Dysthymia often presents itself at an earlier age than Major Depressive Disorder.

Prevention

Though there is no clear-cut way to prevent dysthymia from occurring, some suggestions have been made. Since dysthymia will often first occur in childhood, it is important to identify children who may be at risk. It may be beneficial to work with children in helping to control their stress, increase resilience, boost self-esteem, and provide strong networks of social support. These tactics may be helpful in warding off or delaying dysthymic symptoms.

Treatment

Persistent depressive disorder can be treated with psychotherapy and pharmacotherapy. The overall rate and degree of treatment success is somewhat lower than for non-chronic depression, and a combination of psychotherapy and pharmacotherapy shows best results.

Therapy

Psychotherapy can be effective in treating dysthymia. In a meta-analytic study from 2010, psychotherapy had a small but significant effect when compared to control groups. However, psychotherapy is significantly less effective than pharmacotherapy in direct comparisons.

There are many different types of therapy, and some are more effective than others.

  • The empirically most studied type of treatment is cognitive-behavioural therapy.
    • This type of therapy is very effective for non-chronic depression, and it appears to be also effective for chronic depression.
  • Cognitive behavioural analysis system of psychotherapy (CBASP) has been designed specifically to treat PDD.
    • Empirical results on this form of therapy are inconclusive: While one study showed remarkably high treatment success rates, a later, even larger study showed no significant benefit of adding CBASP to treatment with antidepressants.
  • Schema therapy and psychodynamic psychotherapy have been used for PDD, though good empirical results are lacking.
  • Interpersonal psychotherapy has also been said to be effective in treating the disorder, though it only shows marginal benefit when added to treatment with antidepressants.

Medications

In a 2010 meta-analysis, the benefit of pharmacotherapy was limited to selective serotonin reuptake inhibitors (SSRIs) rather than tricyclic antidepressants (TCA).

According to a 2014 meta-analysis, antidepressants are at least as effective for persistent depressive disorder as for major depressive disorder. The first line of pharmacotherapy is usually SSRIs due to their purported more tolerable nature and reduced side effects compared to the irreversible monoamine oxidase inhibitors or tricyclic antidepressants. Studies have found that the mean response to antidepressant medications for people with dysthymia is 55%, compared with a 31% response rate to a placebo. The most commonly prescribed antidepressants/SSRIs for dysthymia are escitalopram, citalopram, sertraline, fluoxetine, paroxetine, and fluvoxamine. It often takes an average of 6-8 weeks before the patient begins to feel these medications’ therapeutic effects. Additionally, STAR*D, a multi-clinic governmental study, found that people with overall depression will generally need to try different brands of medication before finding one that works specifically for them. Research shows that 1 in 4 of those who switch medications get better results regardless of whether the second medication is an SSRI or some other type of antidepressant.

In a meta-analytic study from 2005, it was found that SSRIs and TCAs are equally effective in treating dysthymia. They also found that MAOIs have a slight advantage over the use of other medication in treating this disorder. However, the author of this study cautions that MAOIs should not necessarily be the first line of defence in the treatment of dysthymia, as they are often less tolerable than their counterparts, such as SSRIs.

Tentative evidence supports the use of amisulpride to treat dysthymia but with increased side effects.

Combination Treatment

When pharmacotherapy alone is compared with combined treatment with pharmacotherapy plus psychotherapy, there is a strong trend in favour of combined treatment. Working with a psychotherapist to address the causes and effects of the disorder, in addition to taking antidepressants to help eliminate the symptoms, can be extremely beneficial. This combination is often the preferred method of treatment for those who have dysthymia. Looking at various studies involving treatment for dysthymia, 75% of people responded positively to a combination of cognitive behavioural therapy and pharmacotherapy, whereas only 48% of people responded positively to just CBT or medication alone.

A 2019 Cochrane review of 10 studies involving 840 participants could not conclude with certainty that continued pharmacotherapy with antidepressants (those used in the studies) was effective in preventing relapse or recurrence of persistent depressive disorder. The body of evidence was too small for any greater certainty although the study acknowledges that continued psychotherapy may be beneficial when compared to no treatment.

Resistance

Because of dysthymia’s chronic nature, treatment resistance is somewhat common. In such a case, augmentation is often recommended. Such treatment augmentations can include lithium pharmacology, thyroid hormone augmentation, amisulpride, buspirone, bupropion, stimulants, and mirtazapine. Additionally, if the person also suffers from seasonal affective disorder, light therapy can be useful in helping augment therapeutic effects.

What is Affect (Psychology)?

Introduction

Affect, in psychology, refers to the underlying experience of feeling, emotion or mood.

Dimensions of Affect

Affective states are psycho-physiological constructs – meaning, largely, concepts that connect mental and physical processes. According to most current views, they vary along three principal dimensions: valence, arousal, and motivational intensity.

  • Valence is the subjective spectrum of positive-to-negative evaluation of an experience an individual may have had.
    • Emotional valence refers to the emotion’s consequences, emotion-eliciting circumstances, or subjective feelings or attitudes.
  • Arousal is objectively measurable as activation of the sympathetic nervous system, but can also be assessed subjectively via self-report.
  • Motivational intensity refers to the impulsion to act; the strength of an urge to move toward or away from a stimulus and whether or not to interact with said stimulus.
    • Simply moving is not considered approach (or avoidance) motivation.

It is important to note that arousal is different from motivational intensity. While arousal is a construct that is closely related to motivational intensity, they differ in that motivation necessarily implies action while arousal does not.

Affect Display

Affect is sometimes used to mean affect display, which is a facial, vocal, or gestural behaviour that serves as an indicator of affect.

Effects

In psychology, affect brings about an organism’s interaction with stimuli.

Affect can influence cognitive scope (the breadth of cognitive processes). Initially, it was thought that positive affects broadened whereas negative affects narrowed cognitive scope. However, evidence now suggests that affects high in motivational intensity narrow cognitive scope whereas affects low in motivational intensity broaden it. The construct of cognitive scope has proven valuable in cognitive psychology.

Affect Tolerance

According to a research article about affect tolerance written by psychiatrist Jerome Sashin (1985), “Affect tolerance can be defined as the ability to respond to a stimulus which would ordinarily be expected to evoke affects by the subjective experiencing of feelings.” Essentially it refers to one’s ability to react to emotions and feelings. One who is low in affect tolerance would show little to no reaction to emotion and feeling of any kind. This is closely related to alexithymia.

“Alexithymia is a subclinical phenomenon involving a lack of emotional awareness or, more specifically, difficulty in identifying and describing feelings and in distinguishing feelings from the bodily sensations of emotional arousal” (Glimcher & Fehr, 2014). At its core, alexithymia is an inability for an individual to recognise what emotions they are feeling – as well as an inability to describe them. According to Dalya Samur and colleagues (2013) people with alexithymia have been shown to have correlations with increased suicide rates, mental discomfort, and deaths.

Affect tolerance factors, including anxiety sensitivity, intolerance of uncertainty, and emotional distress tolerance, may be helped by mindfulness. Mindfulness refers to the practice of being hyper aware of one’s own feelings, thoughts, sensations, and the stimulus of the environment around you – not in an anxiety-inducing way, but in a gentle and pleasant way. Mindfulness has been shown to produce increased subjective well-being, reduced psychological symptoms and emotional reactivity, and improved behavioural regulation.

Relationship to Behaviour and Cognition

The affective domain represents one of the three divisions described in modern psychology: the other two being the behavioural, and the cognitive. Classically, these divisions have also been referred to as the “ABC’s of psychology”. However, in certain views, the cognitive may be considered as a part of the affective, or the affective as a part of the cognitive; it is important to note that “cognitive and affective states … [are] merely analytic categories.”

Instinctive and Cognitive Factors in Causation of Affect

Affect can mean an instinctual reaction to stimulation that occurs before the typical cognitive processes considered necessary for the formation of a more complex emotion. Robert B. Zajonc (1980) asserts this reaction to stimuli is primary for human beings and that it is the dominant reaction for non-human organisms. Zajonc suggests that affective reactions can occur without extensive perceptual and cognitive encoding and be made sooner and with greater confidence than cognitive judgments.

Many theorists, such as Lazarus (1982) consider affect to be post-cognitive: elicited only after a certain amount of cognitive processing of information has been accomplished. In this view, such affective reactions as liking, disliking, evaluation, or the experience of pleasure or displeasure each result from a different prior cognitive process that makes a variety of content discriminations and identifies features, examines them to find value, and weighs them according to their contributions (Brewin, 1989). Some scholars, such as Lerner and Keltner (2000) argue that affect can be both pre- and post-cognitive: initial emotional responses produce thoughts, which produce affect. In a further iteration, some scholars argue that affect is necessary for enabling more rational modes of cognition (Damasio, 2006).

A divergence from a narrow reinforcement model of emotion allows other perspectives about how affect influences emotional development. Thus, temperament, cognitive development, socialisation patterns, and the idiosyncrasies of one’s family or subculture might interact in nonlinear ways. For example, the temperament of a highly reactive/low self-soothing infant may “disproportionately” affect the process of emotion regulation in the early months of life (Griffiths, 1997).

Some other social sciences, such as geography or anthropology, have adopted the concept of affect during the last decade. In French psychoanalysis a major contribution to the field of affect comes from André Green (1973). The focus on affect has largely derived from the work of Deleuze and brought emotional and visceral concerns into such conventional discourses as those on geopolitics, urban life and material culture. Affect has also challenged methodologies of the social sciences by emphasizing somatic power over the idea of a removed objectivity and therefore has strong ties with the contemporary non-representational theory.

Brief History

A number of experiments have been conducted in the study of social and psychological affective preferences (i.e., what people like or dislike). Specific research has been done on preferences, attitudes, impression formation, and decision making. This research contrasts findings with recognition memory (old-new judgements), allowing researchers to demonstrate reliable distinctions between the two. Affect-based judgements and cognitive processes have been examined with noted differences indicated, and some argue affect and cognition are under the control of separate and partially independent systems that can influence each other in a variety of ways (Zajonc, 1980). Both affect and cognition may constitute independent sources of effects within systems of information processing. Others suggest emotion is a result of an anticipated, experienced, or imagined outcome of an adaptational transaction between organism and environment, therefore cognitive appraisal processes are keys to the development and expression of an emotion (Lazarus, 1982).

Psychometric Measurement

Affect has been found across cultures to comprise both positive and negative dimensions. The most commonly used measure in scholarly research is the Positive and Negative Affect Schedule (PANAS) (Watson, Clark & Tellegen, 1988). The PANAS is a lexical measure developed in a North American setting and consisting of 20 single-word items, for instance excited, alert, determined for positive affect, and upset, guilty, and jittery for negative affect. However, some of the PANAS items have been found either to be redundant or to have ambiguous meanings to English speakers from non-North American cultures. As a result, an internationally reliable short-form, the I-PANAS-SF, has been developed and validated comprising two 5-item scales with internal reliability, cross-sample and cross-cultural factorial invariance, temporal stability, convergent and criterion-related validities.

Mroczek and Kolarz (1998) have also developed another set of scales to measure positive and negative affect. Each of the scales has 6 items. The scales have shown evidence of acceptable validity and reliability across cultures.

Non-Conscious Affect and Perception

In relation to perception, a type of non-conscious affect may be separate from the cognitive processing of environmental stimuli. A monohierarchy of perception, affect and cognition considers the roles of arousal, attention tendencies, affective primacy (Zajonc, 1980), evolutionary constraints (Shepard, 1984; 1994), and covert perception (Weiskrantz, 1997) within the sensing and processing of preferences and discriminations. Emotions are complex chains of events triggered by certain stimuli. There is no way to completely describe an emotion by knowing only some of its components. Verbal reports of feelings are often inaccurate because people may not know exactly what they feel, or they may feel several different emotions at the same time. There are also situations that arise in which individuals attempt to hide their feelings, and there are some who believe that public and private events seldom coincide exactly, and that words for feelings are generally more ambiguous than are words for objects or events. Therefore, non-conscious emotions need to be measured by measures circumventing self-report such as the Implicit Positive and Negative Affect Test (IPANAT; Quirin, Kazén & Kuhl, 2009).

Affective responses, on the other hand, are more basic and may be less problematic in terms of assessment. Brewin has proposed two experiential processes that frame non-cognitive relations between various affective experiences: those that are prewired dispositions (i.e. non-conscious processes), able to “select from the total stimulus array those stimuli that are causally relevant, using such criteria as perceptual salience, spatiotemporal cues, and predictive value in relation to data stored in memory” (Brewin, 1989, p.381), and those that are automatic (i.e. subconscious processes), characterised as “rapid, relatively inflexible and difficult to modify… (requiring) minimal attention to occur and… (capable of being) activated without intention or awareness” (Brewin1989 p.381). But a note should be considered on the differences between affect and emotion.

Arousal

Arousal is a basic physiological response to the presentation of stimuli. When this occurs, a non-conscious affective process takes the form of two control mechanisms: one mobilising and the other immobilising. Within the human brain, the amygdala regulates an instinctual reaction initiating this arousal process, either freezing the individual or accelerating mobilisation.

The arousal response is illustrated in studies focused on reward systems that control food-seeking behaviour (Balleine, 2005). Researchers have focused on learning processes and modulatory processes that are present while encoding and retrieving goal values. When an organism seeks food, the anticipation of reward based on environmental events becomes another influence on food seeking that is separate from the reward of food itself. Therefore, earning the reward and anticipating the reward are separate processes and both create an excitatory influence of reward-related cues. Both processes are dissociated at the level of the amygdala, and are functionally integrated within larger neural systems.

Motivational intensity and Cognitive Scope

Measuring Cognitive Scope

Cognitive scope can be measured by tasks involving attention, perception, categorisation and memory. Some studies use a flanker attention task to figure out whether cognitive scope is broadened or narrowed. For example:

  • Using the letters “H” and “N” participants need to identify as quickly as possible the middle letter of 5 when all the letters are the same (e.g. “HHHHH”); and
  • When the middle letter is different from the flanking letters (e.g. “HHNHH”).

Broadened cognitive scope would be indicated if reaction times differed greatly from when all the letters were the same compared to when the middle letter is different. Other studies use a Navon attention task to measure difference in cognitive scope. A large letter is composed of smaller letters, in most cases smaller “L”‘s or “F”‘s that make up the shape of the letter “T” or “H” or vice versa. Broadened cognitive scope would be suggested by a faster reaction to name the larger letter, whereas narrowed cognitive scope would be suggested by a faster reaction to name the smaller letters within the larger letter. A source-monitoring paradigm can also be used to measure how much contextual information is perceived: for instance, participants are tasked to watch a screen which serially displays words to be memorised for 3 seconds each, and also have to remember whether the word appeared on the left or the right half of the screen. The words were also encased in a coloured box, but the participants did not know that they would eventually be asked what colour box the word appeared in.

Main Research Findings

Motivation intensity refers to the strength of urge to move toward or away from a particular stimulus.

Anger and fear affective states, induced via film clips, conferred more selective attention on a flanker task compared to controls as indicated by reaction times that were not very different, even when the flanking letters were different from the middle target letter. Both anger and fear have high motivational intensity because propulsion to act would be high in the face of an angry or fearful stimulus, like a screaming person or coiled snake. Affects high in motivational intensity, thus, narrow cognitive scope making people able to focus more on target information. After seeing a sad picture, participants were faster to identify the larger letter in a Navon attention task, suggesting more global or broadened cognitive scope. The sad emotion is thought to sometimes have low motivational intensity. But, after seeing a disgusting picture, participants were faster to identify the component letters, indicative of a localised more narrow cognitive scope. Disgust has high motivational intensity. Affects high in motivational intensity, thus, narrow cognitive scope making people able to focus more on central information. whereas affects low in motivational intensity broadened cognitive scope allowing for faster global interpretation. The changes in cognitive scope associated with different affective states is evolutionarily adaptive because high motivational intensity affects elicited by stimuli that require movement and action should be focused on, in a phenomenon known as goal-directed behaviour. For example, in early times seeing a lion (fearful stimulus) probably elicited a negative but high motivational affective state (fear) in which the human being was propelled to run away. In this case the goal would be to avoid getting killed.

Moving beyond just negative affective states, researchers wanted to test whether or not the negative or positive affective states varied between high and low motivational intensity. To evaluate this theory, Harmon-Jones and Gable (2009) created an experiment using appetitive picture priming and the Navon task, which would allow them to measure the attentional scope with the detection of the Navon letters. The Navon task included a neutral affect comparison condition. Typically, neutral states cause broadened attention with a neutral stimulus. They predicted that a broad attentional scope could cause a faster detection of global (large) letters, whereas a narrow attentional scope could cause a faster detection of local (small) letters. The evidence proved that the appetitive stimuli produced a narrowed attentional scope. The experimenters further increased the narrowed attentional scope in appetitive stimuli by telling participants they would be allowed to consume the desserts shown in the pictures. The results revealed that their hypothesis was correct in that the broad attentional scope led to quicker detection of global letters and the narrowed attentional scope led to quicker detection of local letters.

Bradley and colleagues (2001) wanted to further examine the emotional reactions in picture priming. Instead of using an appetitive stimulus they used stimulus sets from the International Affective Picture System (IAPS). The image set includes various unpleasant pictures such as snakes, insects, attack scenes, accidents, illness, and loss. They predicted that the unpleasant picture would stimulate a defensive motivational intensity response, which would produce strong emotional arousal such as skin gland responses and cardiac deceleration. Participants rated the pictures based on valence, arousal and dominance on the Self-Assessment Manikin (SAM) rating scale. The findings were consistent with the hypothesis and proved that emotion is organised motivationally by the intensity of activation in appetitive or defensive systems.

Prior to research in 2013, Harmon-Jones and Gable (2009) performed an experiment to examine whether neural activation related with approach-motivation intensity (left frontal-central activity) would trigger the effect of appetitive stimuli on narrowed attention. They also tested whether individual dissimilarities in approach motivation are associated with attentional narrowing. In order to test the hypothesis, the researchers used the same Navon task with appetitive and neutral pictures in addition to having the participants indicate how long since they had last eaten in minutes. To examine the neural activation, the researchers used an electroencephalography and recorded eye movements in order to detect what regions of the brain were being used during approach motivation. The results supported the hypothesis suggesting that the left frontal-central hemisphere is relative for approach-motivational processes and narrowed attentional scope. Some psychologists were concerned that the individuals who were hungry had an increase in the left frontal-central due to frustration. This statement was proved false because the research shows that the dessert pictures increase positive affect even in the hungry individuals. The findings revealed that narrowed cognitive scope has the ability to assist us in goal accomplishment.

Clinical Applications

Later on, researchers connected motivational intensity to clinical applications and found that alcohol-related pictures caused narrowed attention for persons who had a strong motivation to consume alcohol. The researchers tested the participants by exposing them to alcohol and neutral pictures. After the picture was displayed on a screen, the participants finished a test evaluating attentional focus. The findings proved that exposure to alcohol-related pictures led to a narrowing of attentional focus to individuals who were motivated to use alcohol. However, exposure to neutral pictures did not correlate with alcohol-related motivation to manipulate attentional focus. The Alcohol Myopia Theory (AMT) states that alcohol consumption reduces the amount of information available in memory, which also narrows attention so only the most proximal items or striking sources are encompassed in attentional scope. This narrowed attention leads intoxicated persons to make more extreme decisions than they would when sober. Researchers provided evidence that substance-related stimuli capture the attention of individuals when they have high and intense motivation to consume the substance. Motivational intensity and cue-induced narrowing of attention has a unique role in shaping people’s initial decision to consume alcohol. In 2013, psychologists from the University of Missouri investigated the connection between sport achievement orientation and alcohol outcomes. They asked varsity athletes to complete a Sport Orientation Questionnaire which measured their sport-related achievement orientation on three scales – competitiveness, win orientation, and goal orientation (Weaver et al., 2013). The participants also completed assessments of alcohol use and alcohol-related problems. The results revealed that the goal orientation of the athletes were significantly associated with alcohol use but not alcohol-related problems.

In terms of psychopathological implications and applications, college students showing depressive symptoms were better at retrieving seemingly “nonrelevant” contextual information from a source monitoring paradigm task. Namely, the students with depressive symptoms were better at identifying the colour of the box the word was in compared to non-depressed students. Sadness (low motivational intensity) is usually associated with depression, so the more broad focus on contextual information of sadder students supports that affects high in motivational intensity narrow cognitive scope whereas affects low in motivational intensity broaden cognitive scope.

The motivational intensity theory states that the difficulty of a task combined with the importance of success determine the energy invested by an individual. The theory has three main layers.

  • The innermost layer says human behaviour is guided by the desire to conserve as much energy as possible. Individuals aim to avoid wasting energy so they invest only the energy that is required to complete the task.
  • The middle layer focuses on the difficulty of tasks combined with the importance of success and how this affects energy conservation. It focuses on energy investment in situations of clear and unclear task difficulty.
  • The last layer looks at predictions for energy invested by a person when they have several possible options to choose at different task difficulties.

The person is free to choose among several possible options of task difficulty. The motivational intensity theory offers a logical and consistent framework for research. Researchers can predict a person’s actions by assuming effort refers to the energy investment. The motivational intensity theory is used to show how changes in goal attractiveness and energy investment correlate.

Mood

Refer to Mood (Psychology).

Mood, like emotion, is an affective state. However, an emotion tends to have a clear focus (i.e. its cause is self-evident), while mood tends to be more unfocused and diffuse. Mood, according to Batson, Shaw and Oleson (1992), involves tone and intensity and a structured set of beliefs about general expectations of a future experience of pleasure or pain, or of positive or negative affect in the future. Unlike instant reactions that produce affect or emotion, and that change with expectations of future pleasure or pain, moods, being diffuse and unfocused and thus harder to cope with, can last for days, weeks, months or even years (Schucman & Thetford, 1975). Moods are hypothetical constructs depicting an individual’s emotional state. Researchers typically infer the existence of moods from a variety of behavioural referents (Blechman, 1990). Habitual negative affect and negative mood is characteristic of high neuroticism.

Positive affect and negative affect (PANAS) represent independent domains of emotion in the general population, and positive affect is strongly linked to social interaction. Positive and negative daily events show independent relationships to subjective well-being, and positive affect is strongly linked to social activity. Recent research suggests that high functional support is related to higher levels of positive affect. In his work on negative affect arousal and white noise, Seidner (1991) found support for the existence of a negative affect arousal mechanism regarding the devaluation of speakers from other ethnic origins. The exact process through which social support is linked to positive affect remains unclear. The process could derive from predictable, regularised social interaction, from leisure activities where the focus is on relaxation and positive mood, or from the enjoyment of shared activities. The techniques used to shift a negative mood to a positive one are called mood repair strategies.

Social Interaction

Affect display is a critical facet of interpersonal communication. Evolutionary psychologists have advanced the hypothesis that hominids have evolved with sophisticated capability of reading affect displays.

Emotions are portrayed as dynamic processes that mediate the individual’s relation to a continually changing social environment. In other words, emotions are considered to be processes of establishing, maintaining, or disrupting the relation between the organism and the environment on matters of significance to the person.

Most social and psychological phenomena occur as the result of repeated interactions between multiple individuals over time. These interactions should be seen as a multi-agent system – a system that contains multiple agents interacting with each other and/or with their environments over time. The outcomes of individual agents’ behaviours are interdependent: Each agent’s ability to achieve its goals depends on not only what it does but also what other agents do.

Emotions are one of the main sources for the interaction. Emotions of an individual influence the emotions, thoughts and behaviours of others; others’ reactions can then influence their future interactions with the individual expressing the original emotion, as well as that individual’s future emotions and behaviours. Emotion operates in cycles that can involve multiple people in a process of reciprocal influence.

Affect, emotion, or feeling is displayed to others through facial expressions, hand gestures, posture, voice characteristics, and other physical manifestation. These affect displays vary between and within cultures and are displayed in various forms ranging from the most discrete of facial expressions to the most dramatic and prolific gestures.

Observers are sensitive to agents’ emotions, and are capable of recognising the messages these emotions convey. They react to and draw inferences from an agent’s emotions. The emotion an agent displays may not be an authentic reflection of his or her actual state (refer to Emotional Labour).

Agents’ emotions can have effects on four broad sets of factors:

  • Emotions of other persons.
  • Inferences of other persons.
  • Behaviours of other persons.
  • Interactions and relationships between the agent and other persons.

Emotion may affect not only the person at whom it was directed, but also third parties who observe an agent’s emotion. Moreover, emotions can affect larger social entities such as a group or a team. Emotions are a kind of message and therefore can influence the emotions, attributions and ensuing behaviours of others, potentially evoking a feedback process to the original agent.

Agents’ feelings evoke feelings in others by two suggested distinct mechanisms:

  • Emotion contagion:
    • People tend to automatically and unconsciously mimic non-verbal expressions.
    • Mimicking occurs also in interactions involving textual exchanges alone.
  • Emotion interpretation:
    • An individual may perceive an agent as feeling a particular emotion and react with complementary or situationally appropriate emotions of their own.
    • The feelings of the others diverge from and in some way complement the feelings of the original agent.

People may not only react emotionally, but may also draw inferences about emotive agents such as the social status or power of an emotive agent, his competence and his credibility. For example, an agent presumed to be angry may also be presumed to have high power.

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Linking Depression & Internet Gaming Disorder

Research Paper Title

Depressive symptoms and depression in individuals with internet gaming disorder: A systematic review and meta-analysis.

Background

Although depression has frequently been associated with Internet Gaming Disorder (IGD), its epidemiological impact on this emerging condition has not been systematically assessed. In this study, the researchers aimed to synthesize the available evidence focusing on depression and depressive symptoms in individuals with IGD.

Methods

The researchers searched PubMed, Embase, PsycINFO, GreyLit, OpenGrey, and ProQuest up to March 2020 for observational studies focusing on depression-related outcomes in IGD. They conducted random-effects meta-analyses on 1) rate of comorbid depression in IGD; 2) severity of depressive symptoms in IGD participants without depression.

Results

The researchers identified 92 studies from 25 different countries including 15,148 participants. 21 studies (n = 5025 participants) provided data for the first analysis, resulting in a pooled event rate of depression of 0.32 (95% Confidence Interval 0.21-0.43). The pooled Beck Depression Inventory scores in individuals without depression were suggestive of mild severity (13 studies, n = 508; 10.3, 95% Confidence Interval 8.3-12.4).

Conclusions

The considerable inconsistency of methods employed across studies limits the transferability of these findings to clinical practice.

The prevalence of depression in individuals with IGD varied considerably across studies, affecting approximately one out of three participants overall. Furthermore, a globally major severity of depressive symptoms was found in those without a clinical diagnosis of depression, compared to the general population.

These findings confirm a relevant impact of mood disturbances in IGD.

Reference

Ostinelli, E.G., Zangani, C., Giordano, B., Maestri, D., Gambini, O., D’Agostino, A., Furukawa, T.A. & Purgato, M. (2021) Depressive symptoms and depression in individuals with internet gaming disorder: A systematic review and meta-analysis. Journal of Affective Disorders. doi: 10.1016/j.jad.2021.02.014. Online ahead of print.