What is Reduced Effect Display?

Introduction

Reduced affect display, sometimes referred to as emotional blunting, is a condition of reduced emotional reactivity in an individual.

It manifests as a failure to express feelings (affect display) either verbally or nonverbally, especially when talking about issues that would normally be expected to engage the emotions. Expressive gestures are rare and there is little animation in facial expression or vocal inflection. Reduced affect can be symptomatic of autism, schizophrenia, depression, posttraumatic stress disorder, depersonalisation disorder, schizoid personality disorder or brain damage. It may also be a side effect of certain medications (e.g. antipsychotics and antidepressants).

Reduced affect should be distinguished from apathy and anhedonia, which explicitly refer to a lack of emotion, whereas reduced affect is a lack of emotional expression (affect display) regardless of whether emotion (underlying affect) is actually reduced or not.

Types

Constricted Affect

A restricted or constricted affect is a reduction in an individual’s expressive range and the intensity of emotional responses.

Blunted and Flat Affect

Blunted affect is a lack of affect more severe than restricted or constricted affect, but less severe than flat or flattened affect. “The difference between flat and blunted affect is in degree. A person with flat affect has no or nearly no emotional expression. They may not react at all to circumstances that usually evoke strong emotions in others. A person with blunted affect, on the other hand, has a significantly reduced intensity in emotional expression”.

Shallow Affect

Shallow affect has equivalent meaning to blunted affect. Factor 1 of the Psychopathy Checklist identifies shallow affect as a common attribute of psychopathy.

Brain structures

Individuals with schizophrenia with blunted affect show different regional brain activity in fMRI scans when presented with emotional stimuli compared to individuals with schizophrenia without blunted affect. Individuals with schizophrenia without blunted affect show activation in the following brain areas when shown emotionally negative pictures: midbrain, pons, anterior cingulate cortex, insula, ventrolateral orbitofrontal cortex, anterior temporal pole, amygdala, medial prefrontal cortex, and extrastriate visual cortex. Individuals with schizophrenia with blunted affect show activation in the following brain regions when shown emotionally negative pictures: midbrain, pons, anterior temporal pole, and extrastriate visual cortex.

Limbic Structures

Individuals with schizophrenia with flat affect show decreased activation in the limbic system when viewing emotional stimuli. In individuals with schizophrenia with blunted affect neural processes begin in the occipitotemporal region of the brain and go through the ventral visual pathway and the limbic structures until they reach the inferior frontal areas. Damage to the amygdala of adult rhesus macaques early in life can permanently alter affective processing. Lesioning the amygdala causes blunted affect responses to both positive and negative stimuli. This effect is irreversible in the rhesus macaques; neonatal damage produces the same effect as damage that occurs later in life. The macaques’ brain cannot compensate for early amygdala damage even though significant neuronal growth may occur. There is some evidence that blunted affect symptoms in schizophrenia patients are not a result of just amygdala responsiveness, but a result of the amygdala not being integrated with other areas of the brain associated with emotional processing, particularly in amygdala-prefrontal cortex coupling. Damage in the limbic region prevents the amygdala from correctly interpreting emotional stimuli in individuals with schizophrenia by compromising the link between the amygdala and other brain regions associated with emotion.

Brainstem

Parts of the brainstem are responsible for passive emotional coping strategies that are characterised by disengagement or withdrawal from the external environment (quiescence, immobility, hyporeactivity), similar to what is seen in blunted affect. Individuals with schizophrenia with blunted affect show activation of the brainstem during fMRI scans, particularly the right medulla and the left pons, when shown “sad” film excerpts. The bilateral midbrain is also activated in individuals with schizophrenia diagnosed with blunted affect. Activation of the midbrain is thought to be related to autonomic responses associated with perceptual processing of emotional stimuli. This region usually becomes activated in diverse emotional states. When the connectivity between the midbrain and the medial prefrontal cortex is compromised in individuals with schizophrenia with blunted affect an absence of emotional reaction to external stimuli results.

Prefrontal Cortex

Individuals with schizophrenia, as well as patients being successfully reconditioned with quetiapine for blunted affect, show activation of the prefrontal cortex (PFC). Failure to activate the PFC is possibly involved in impaired emotional processing in individuals with schizophrenia with blunted affect. The mesial PFC is activated in aver individuals in response to external emotional stimuli. This structure possibly receives information from the limbic structures to regulate emotional experiences and behaviour. Individuals being reconditioned with quetiapine, who show reduced symptoms, show activation in other areas of the PFC as well, including the right medial prefrontal gyrus and the left orbitofrontal gyrus.

Anterior Cingulate Cortex

A positive correlation has been found between activation of the anterior cingulate cortex and the reported magnitude of sad feelings evoked by viewing sad film excerpts. The rostral subdivision of this region is possibly involved in detecting emotional signals. This region is different in individuals with schizophrenia with blunted affect.

Diagnoses

Schizophrenia

Flat and blunted affect is a defining characteristic in the presentation of schizophrenia. To reiterate, these individuals have a decrease in observed vocal and facial expression as well as the use of gestures. One study of flat affect in schizophrenia found that “flat affect was more common in men, and was associated with worse current quality of life” as well as having “an adverse effect on course of illness”.

The study also reported a “dissociation between reported experience of emotion and its display” – supporting the suggestion made elsewhere that “blunted affect, including flattened facial expressiveness and lack of vocal inflection … often disguises an individual’s true feelings.” Thus, feelings may merely be unexpressed, rather than totally lacking. On the other hand, “a lack of emotions which is due not to mere repression but to a real loss of contact with the objective world gives the observer a specific impression of ‘queerness’ … the remainders of emotions or the substitutes for emotions usually refer to rage and aggressiveness”. In the most extreme cases, there is a complete “dissociation from affective states”. To further support this idea, a study examining emotion dysregulation found that individuals with schizophrenia could not exaggerate their emotional expression as healthy controls could. Participants were asked to express whatever emotions they had during a clip of a film, and the participants with schizophrenia showed deficits in behavioural expression of their emotions.

There is still some debate regarding the source of flat affect in schizophrenia. However, some literature indicates abnormalities in the dorsal executive and ventral affective systems; it is argued that dorsal hypoactivation and ventral hyperactivation may be the source of flat affect. Further, the authors found deficits in the mirror neuron system may also contribute to flat affect in that the deficits may cause disruptions in the control of facial expression.

Another study found that when speaking, individuals with schizophrenia with flat affect demonstrate less inflection than normal controls and appear to be less fluent. Normal subjects appear to express themselves using more complex syntax, whereas flat affect subjects speak with fewer words, and fewer words per sentence. Flat affect individuals’ use of context-appropriate words in both sad and happy narratives are similar to that of controls. It is very likely that flat affect is a result of deficits in motor expression as opposed to emotional processing. The moods of display are compromised, but subjective, autonomic, and contextual aspects of emotion are left intact.

Post-Traumatic Stress Disorder

Post-traumatic stress disorder (PTSD) was previously known to cause negative feelings, such as depressed mood, re-experiencing and hyperarousal. However, recently, psychologists have started to focus their attention on the blunted affects and also the decrease in feeling and expressing positive emotions in PTSD patients. Blunted affect, or emotional numbness, is considered one of the consequences of PTSD because it causes a diminished interest in activities that produce pleasure (anhedonia) and produces feelings of detachment from others, restricted emotional expression and a reduced tendency to express emotions behaviourally. Blunted affect is often seen in veterans as a consequence of the psychological stressful experiences that caused PTSD. Blunted affect is a response to PTSD, it is considered one of the central symptoms in post-traumatic stress disorders and it is often seen in veterans who served in combat zones. In PTSD, blunted affect can be considered a psychological response to PTSD as a way to combat overwhelming anxiety that the patients feel. In blunted affect, there are abnormalities in circuits that also include the prefrontal cortex.

Assessment

In making assessments of mood and affect the clinician is cautioned that “it is important to keep in mind that demonstrative expression can be influenced by cultural differences, medication, or situational factors”; while the layperson is warned to beware of applying the criterion lightly to “friends, otherwise [he or she] is likely to make false judgments, in view of the prevalence of schizoid and cyclothymic personalities in our ‘normal’ population, and our [US] tendency to psychological hypochondriasis”.

R.D. Laing in particular stressed that “such ‘clinical’ categories as schizoid, autistic, ‘impoverished’ affect … all presuppose that there are reliable, valid impersonal criteria for making attributions about the other person’s relation to [his or her] actions. There are no such reliable or valid criteria”.

Differential Diagnosis

Blunted affect is very similar to anhedonia, which is the decrease or cessation of all feelings of pleasure (which thus affects enjoyment, happiness, fun, interest, and satisfaction). In the case of anhedonia, emotions relating to pleasure will not be expressed as much or at all because they are literally not experienced or are decreased. Both blunted affect and anhedonia are considered negative symptoms of schizophrenia, meaning that they are indicative of a lack of something. There are some other negative symptoms of schizophrenia which include avolition, alogia and catatonic behaviour.

Closely related is alexithymia – a condition describing people who “lack words for their feelings. They seem to lack feelings altogether, although this may actually be because of their inability to express emotion rather than from an absence of emotion altogether”. Alexithymic patients however can provide clues via assessment presentation which may be indicative of emotional arousal.

“If the amygdala is severed from the rest of the brain, the result is a striking inability to gauge the emotional significance of events; this condition is sometimes called ‘affective blindness'”. In some cases, blunted affect can fade, but there is no conclusive evidence of why this can occur.

What is Hyperthymic Temperament?

Introduction

Hyperthymic temperament, or hyperthymia, from Ancient Greek ὑπέρ (“over”, meaning here excessive) + θυμός (“spirited”), is a proposed personality type characterised by an exceptionally, or in some cases, abnormally positive mood and disposition.

Also known as Hyperthymic Personality-Type and Chronic Hypomania.

Refer to Bipolar Disorder.

Graph showing showing hyperthymia in comparison to other bipolar spectrum disorders.

Background

It is generally defined by increased energy, vividness and enthusiasm for life activities, as opposed to dysthymia. Hyperthymia is similar to but more stable than hypomania.

Characteristics of the hyperthymic temperament include:

  • Increased energy and productivity.
  • Short sleep patterns.
  • Vividness, activity extroversion.
  • Self-assurance, self-confidence.
  • Strong will.
  • Extreme talkativeness.
  • Tendency to repeat oneself.
  • Risk-taking/sensation seeking.
  • Breaking social norms.
  • Very strong libido.
  • Love of attention.
  • Low threshold for boredom.
  • Generosity and tendency to overspend.
  • Emotion sensitivity.
  • Cheerfulness and joviality.
  • Unusual warmth.
  • Expansiveness.
  • Tirelessness.
  • Irrepressibility, irresistible, and infectious quality.

The clinical, psychiatric understanding of hyperthymia is evolving. Studies have shown that hyperthymic temperament promotes efficient performance of complex tasks under time pressure or extreme conditions. Despite this positive characterisation, hyperthymia can be complicated with depressive episodes manifesting as a softer form of bipolar illness, such as cyclothymia. Research also suggests a familial genetic connection of the temperament to bipolar I.

Aside from references in historical and more recent writings on the spectrum of mood disorders, further literature on the temperament is lacking. There is a lack of agreement on its definition, implications or whether it is pathological. It is not known where to place hyperthymia on the affective spectrum.

Hyperthymia manifesting intermittently or in an unusual way may mask hypomania or another psychiatric disorder. Hyperthymia can be most accurately diagnosed by a psychologist or psychiatrist with the help of a patient’s family and/or close friends.

What is Cyclothymia?

Introduction

Cyclothymia, also known as cyclothymic disorder, is a mental and behavioural disorder that involves numerous periods of symptoms of depression and periods of symptoms of elevated mood.

These symptoms, however, are not sufficient to be a major depressive episode or a hypomanic episode. Symptoms must last for more than one year in children and two years in adults.

The cause of cyclothymia is unknown. Risk factors include a family history of bipolar disorder. Cyclothymia differs from bipolar in that major depression, mania, or hypomania have never occurred.

Treatment is generally with counselling and mood stabilisers such as lithium. It is estimated that 0.4-1% of people have cyclothymia at some point in their life. Onset is typically in late childhood to early adulthood. Males and females are affected equally often.

Brief History

In 1883, Karl Ludwig Kahlbaum identified a disorder characterised by recurring mood cycles. The disorder contained both melancholic and manic episodes that occurred in a milder form than in bipolar disorder. This condition was coined “cyclothymia” by Kahlbaum and his student Ewald Hecker. Kahlbaum developed his theory of cyclothymia through his work with people presenting with these symptoms at the Kahlbaum Sanitarium in Goerlitz, Silesia (Germany). He was recognised as a leading hypnotherapist and psychotherapist of his day. He was a progressive in the field of mental health, believing that mental illness should not carry a stigma and that people dealing with mental health issues should be treated humanely. Kalhbaum was the first to recognise that people with cyclothymia often do not seek help for the disorder due to its mild symptoms.

Cyclothymia has been conceptualised in a variety of ways, including as a subtype of bipolar disorder, a temperament, a personality trait, and a personality disorder. There is also an argument that cyclothymia should be considered a neurodevelopmental disorder. The two defining features of the disorder, according to DSM-5, are the presence of depressive and hypomanic symptoms, not meeting the threshold for a depressive or hypomanic episode. Cyclothymia is also classified as a subtype of bipolar disorder in DSM-5, but some researchers disagree with this classification and argue that it should be primarily defined as an exaggeration of mood and emotional instability. In the past, cyclothymia has been conceptualised to include other characteristics in addition to the flux between depression and hypomania, such as mood reactivity, impulsivity, and anxiety.

Symptoms

People with cyclothymia experience both depressive phases and hypomanic phases (which are less severe than a full hypomanic episode). The depressive and manic symptoms in cyclothymia last for variable amounts of time due to the unstable and reactive nature of the disorder. The depressive phases are similar to major depressive disorder and are characterised by dulled thoughts and sensations and the lack of motivation for intellectual or social activities. Most people with cyclothymia are generally fatigued and tend to sleep frequently and for long periods of time. However, other people experience insomnia.

Other symptoms of cyclothymic depression include indifference toward people or activities that used to be extremely important. Cyclothymic depression also leads to difficulty making decisions. In addition, people with this condition tend to be critical and complain easily. Suicidal thoughts are common, even in mild forms of cyclothymia. In the depressive state, people with cyclothymia also experience physical complaints including frequent headaches, tightness in the head and chest, an empty sensation in the head, weakness, weight loss, and hair loss.

The distinguishing factor between typical depression and cyclothymic depression is that in cyclothymic depression, there are instances of hypomania. People with cyclothymia can switch from the depressive state to the hypomanic state without warning to them or others. The duration and frequency of phases is unpredictable.

In the hypomanic state, people’s thoughts become faster and they become more sociable and talkative. They may engage in spending sprees, spontaneous actions, have heightened self-esteem, and greater vanity. In contrast to a regular manic state that would be associated with bipolar I, symptoms in the hypomanic phase generally occur in a less severe form.

Comorbidities

Cyclothymia commonly occurs in conjunction with other disorders. Between 20-50 percent of people with depression, anxiety, and related disorders also have cyclothymia. When people with cyclothymia seek mental health resources it tends to be for symptoms of their comorbid condition rather than for their symptoms of cyclothymia. In children and adolescents, the most common comorbidities with cyclothymia are anxiety disorders, impulse control issues, eating disorders, and ADHD. In adults, cyclothymia also tends to be comorbid with impulse control issues. Sensation-seeking behaviours occur in hypomanic states. These often include gambling and compulsive sexuality in men, or compulsive buying and binge eating in women.

In addition to sensation-related disorders, cyclothymia has also been associated with atypical depression. In one study, a connection was found between interpersonal sensitivity, mood reactivity (i.e. responding to actual or potential positive events with brighter mood), and cyclothymic mood swings, all of which are symptoms of atypical depression. Cyclothymia also tends to occur in conjunction with separation anxiety, where a person has anxiety as a result of separation from a caregiver, friend, or loved one. Other issues that tend to co-occur with cyclothymia include social anxiety, fear of rejection and a tendency toward hostility to those connected with past pain and rejection. People with cyclothymia tend to seek intense interpersonal relationships when in a hypomanic state and isolation when in a depressed state. This generally leads to short, tumultuous relationships.

Causes

The cause is unknown. Risk factors include a family history of bipolar disorder.

First-degree relatives of people with cyclothymia have major depressive disorder, bipolar I disorder, and bipolar II disorder more often than the general population. Substance-related disorders also may be at a higher risk within the family. First-degree relatives of a bipolar I individuals may have a higher risk of cyclothymic disorder than the general population.

Diagnosis

Cyclothymia is classified in DSM-5 as a subtype of bipolar disorder. The criteria are:

  • Periods of elevated mood and depressive symptoms for at least half the time during the last two years for adults and one year for children and teenagers.
  • Periods of stable moods last only two months at most.
  • Symptoms create significant problems in one or more areas of life.
  • Symptoms do not meet the criteria for bipolar disorder, major depression, or another mental disorder.
  • Symptoms are not caused by substance use or a medical condition.

The DSM-5 criteria for cyclothymia are restrictive according to some researchers. This affects the diagnosis of cyclothymia because fewer people get diagnosed than potentially could. This means that a person who has some symptoms of the disorder might not be able to get treatment because they do not meet all of the necessary criteria described in DSM-5. Furthermore, it also leads to more attention being placed on depression and other bipolar-spectrum disorders because if a person does not meet all the criteria for cyclothymia they are often given a depression or bipolar spectrum diagnosis. Improper diagnosis may lead some people with cyclothymia to be treated for a comorbid disorder rather than having their cyclothymic tendencies addressed.

Cyclothymia is often not recognised by the affected individual or medical professionals due to its ostensibly mild symptoms. In addition, it is difficult to identify and classify. Due to disagreement and misconceptions among health and mental health professionals, cyclothymia is often diagnosed as “bipolar not otherwise specified”. Cyclothymia is also often confused with borderline personality disorder due to their similar symptoms, especially in older adolescents and young adults.

Most people with the disorder present in a depressive state, not realising that their hypomanic states are abnormal. Mild manic episodes tend to be interpreted as part of the person’s personality or simply a heightened mood. In addition, the disorder often manifests during childhood or adolescence, making it even more difficult for the person to distinguish between symptoms of the disorder and their personality. For example, people may think that they just suffer from mood swings and not realise that these are a result of a psychiatric condition.

Management

Cognitive behavioural therapy (CBT) is considered potentially effective for people diagnosed with cyclothymia.

Medication can be used in addition to behavioural approaches. However, mood stabilisers should be used before antidepressants, and if antidepressants are used they should be used with caution. Antidepressants are a concern due to the possibility of inducing hypomanic switches or rapid cycling.

Epidemiology

Cyclothymia, known today as cyclothymic disorder, tends to be underdiagnosed due to its low intensity. The exact rates for cyclothymia have not been widely studied. Some studies estimate that between 5 and 8% are affected at some point in their life whereas other studies suggest a rate ranging from 0.4 to 2.5%.

Males appear to be affected equally often, though women are more likely to receive treatment. Cyclothymia is diagnosed in around fifty percent of people with depression who are evaluated in psychiatric outpatient settings.

Etymology

Cyclothymia is derived from the Greek word κυκλοθυμία (from κῦκλος kyklos, “circle” and θυμός thymos, “mood, emotion”). Therefore, it means “to cycle or circle between moods or emotions”.

Research

Whether subtypes of bipolar disorder, such as cyclothymia, truly represent separate disorders or are part of a unique bipolar spectrum is debated in research. Cyclothymia is typically not described in research studies or diagnosed in clinical settings, making it less recognisable and less understood by professionals. This absence of cyclothymia in research and clinical settings suggests that cyclothymia is either being diagnosed as another mood disorder or as a non-affective psychiatric disorder or not coming to scientific or clinical attention due to a lack of diagnostic clarity or because the nature of cyclothymia is still highly contested. Additionally, the current diagnostic criterion for cyclothymia emphasizes that symptoms are persistent, which suggests that they are enduring traits rather than a psychological state, thus, it has been argued that it should be diagnosed as a personality disorder. Since the symptoms tend to overlap with personality disorders, the validity and distinction between these two diagnostic categories has been debated.

Lastly, the tendency of cyclothymia to be comorbid with other mental disorders makes diagnosis difficult. These issues prevent consensus on the definition of cyclothymia and its relationship with other mental disorders among researchers and clinicians. This lack of consensus on an operational definition and symptom presentation is especially pronounced with children and adolescents because the diagnostic criteria have not been adequately adapted to take into account their developmental level.

Society and Culture

Actor Stephen Fry has spoken about his experience with cyclothymia, which was depicted in the documentary Stephen Fry: The Secret Life of the Manic Depressive.

Singer Charlene Soraia had cyclothymia and wrote a song about her experiences with the disorder.