What is Emotional Conflict?

Introduction

Emotional conflict is the presence of different and opposing emotions relating to a situation that has recently taken place or is in the process of being unfolded.

They may be accompanied at times by a physical discomfort, especially when a functional disturbance has become associated with an emotional conflict in childhood, and in particular by tension headaches “expressing a state of inner tension…[or] caused by an unconscious conflict”.

For C.G. Jung, “emotional conflicts and the intervention of the unconscious are the classical features of…medical psychology”. Equally, “Freud’s concept of emotional conflict as amplified by Anna Freud…Erikson and others is central in contemporary theories of mental disorder in children, particularly with respect to the development of psychoneurosis”.

In Childhood Development

“The early stages of emotional development are full of potential conflict and disruption”. Infancy and childhood are a time when “everything is polarised into extremes of love and hate” and when “totally opposite, extreme feelings about them must be getting put together too. Which must be pretty confusing and painful. It’s very difficult to discover you hate someone you love”. Development involves integrating such primitive emotional conflicts, so that “in the process of integration, impulses to attack and destroy, and impulses to give and share are related, the one lessening the effect of the other”, until the point is reached at which “the child may have made a satisfactory fusion of the idea of destroying the object with the fact of loving the same object”.

Once such primitive relations to the mother or motherer have been at least partially resolved, “in the age period two to five or seven, each normal infant is experiencing the most intense conflicts” relating to wider relationships: “ideas of love are followed by ideas of hate, by jealousy and painful emotional conflict and by personal suffering; and where conflict is too great there follows loss of full capacity, inhibitions…symptom formation”.

Defences

Defences against emotional conflict include “splitting and projection. They deal with intrapsychic conflict not by addressing it, but by sidestepping it”. Displacement too can help resolve such conflicts: “If an individual no longer feels threatened by his father but by a horse, he can avoid hating his father; here the distortion way a way out of the conflict of ambivalence. The father, who had been hated and loved simultaneously, is loved only, and the hatred is displaced onto the bad horse”.

Physical Symptoms

Inner emotional conflicts can result in physical discomfort or pain, often in the form of tension headaches, which can be episodic or chronic, and may last from a few minutes or hours, to days – associated pain being mild, moderate, or severe.

“The physiology of nervous headaches still presents many unsolved problems”, as in general do all such “physical alterations…rooted in unconscious instinctual conflicts”. However physical discomfort or pain without apparent cause may be the way our body is telling us of an underlying emotional turmoil and anxiety, triggered by some recent event. Thus for example a woman “may be busy in her office, apparently in good health and spirits. A moment later she develops a blinding headache and shows other signs of distress. Without consciously noticing it, she has heard the foghorn of a distant ship, and this has unconsciously reminded her of an unhappy parting”.

While it is not easy, by relaxing, calming down, and trying to become aware of what recent experience or event could have been the cause of the inner conflict, and then rationally looking at and dealing with the conflicting desires and needs, a gradual dissipation and relief of the pain may be possible.

In the Workplace

With respect to the post-industrial age, “LaBier writes of ‘modern madness’, the hidden link between work and emotional conflict…feelings of self-betrayal, stress and burnout”. His “idea, which gains momentum in the post-yuppie late eighties…concludes that real professional success without regret of emotional conflict requires insanity of one kind or another”.

Cultural Examples

  • Advice on fiction writing emphasises the “necessity of creating powerful, emotional conflicts” in one’s characters: “characters create the emotional conflict and the action emerges from the characters”.
  • Shakespeare’s sonnets have been described as “implying an awareness of the possible range of human feelings, of the existence of complex and even contradictory attitudes to a single emotion”.
  • For Picasso “the presence of death is always coincident with the taste for life…the superb violence of these emotional transports have led some people to call his work expressionist”.

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 Alexithymia?

Introduction

Alexithymia is a personality trait characterised by the subclinical inability to identify and describe emotions experienced by one’s self.

The core characteristic of alexithymia is marked dysfunction in emotional awareness, social attachment, and interpersonal relation. Furthermore, people with high levels of alexithymia can have difficulty distinguishing and appreciating the emotions of others, which is thought to lead to non-empathic and ineffective emotional responses.

High levels of alexithymia occur in approximately 10% of the population and can occur with a number of psychiatric conditions as well as any neurodevelopmental disorder. Difficulty with recognising and talking about their emotions appears at subclinical levels in men who conform to western cultural notions of masculinity (such as thinking that sadness is a feminine emotion). This is called normative male alexithymia by some researchers. However, both alexithymia itself and its association with traditionally masculine norms are consistent across genders.

Lexicology

The term alexithymia was coined by psychotherapists John Case Nemiah and Peter Sifneos in 1973. The word comes from Greek: ἀ- (a-, ‘not’, privative prefix, alpha privative) + λέξις (léxis, ‘words’) + θῡμός (thȳmós, ‘heart’ or ’emotions’ or ‘seat of speech’) (cf. dyslexia), literally meaning “no words for emotions”.

Another etymology: Greek: Αλεξιθυμία ἀλέξω (to ward off) + θῡμός. Means to push away emotions, feelings

Nonmedical terms describing similar conditions include emotionless and impassive. People with the condition are called alexithymics or alexithymiacs.

Classification

Alexithymia is considered to be a personality trait that places affected individuals at risk for other medical and psychiatric disorders while reducing the likelihood that these individuals will respond to conventional treatments for the other conditions. Alexithymia is not classified as a mental disorder in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders. It is a dimensional personality trait that varies in intensity from person to person. A person’s alexithymia score can be measured with questionnaires such as the Toronto Alexithymia Scale (TAS-20), the Perth Alexithymia Questionnaire (PAQ), the Bermond-Vorst Alexithymia Questionnaire (BVAQ), the Levels of Emotional Awareness Scale (LEAS), the Online Alexithymia Questionnaire (OAQ-G2), the Toronto Structured Interview for Alexithymia (TSIA), or the Observer Alexithymia Scale (OAS). It is distinct from the psychiatric personality disorders, such as antisocial personality disorder.

Traditionally, alexithymia has been conceptually defined by four components:

  • Difficulty identifying feelings (DIF).
  • Difficulty describing feelings to other people (DDF).
  • A stimulus-bound, externally oriented thinking style (EOT).
  • Constricted imaginal processes (IMP),

However, there is some ongoing disagreement in the field about the definition of alexithymia. When measured in empirical studies, constricted imaginal processes are often found not to statistically cohere with the other components of alexithymia. Such findings have led to debate in the field about whether IMP is indeed a component of alexithymia. For example, in 2017, Preece and colleagues introduced the attention-appraisal model of alexithymia, where they suggested that IMP be removed from the definition and that alexithymia be conceptually composed only of DIF, DDF, and EOT, as each of these three are specific to deficits in emotion processing. In practice, since the constricted imaginal processes items were removed from earlier versions of the TAS-20 in the 1990s, the most used alexithymia assessment tools (and consequently most alexithymia research studies) have only assessed the construct in terms of DIF, DDF, and EOT.

Studies (using measures of alexithymia assessing DIF, DDF, and EOT) have reported that the prevalence rate of high alexithymia is less than 10% of the population. A less common finding suggests that there may be a higher prevalence of alexithymia amongst males than females, which may be accounted for by difficulties some males have with “describing feelings”, but not by difficulties in “identifying feelings” in which males and females show similar abilities.

Psychologist R. Michael Bagby and psychiatrist Graeme J. Taylor have argued that the alexithymia construct is inversely related to the concepts of psychological mindedness and emotional intelligence and there is “strong empirical support for alexithymia being a stable personality trait rather than just a consequence of psychological distress”.

Signs and Symptoms

Typical deficiencies may include problems identifying, processing, describing, and working with one’s own feelings, often marked by a lack of understanding of the feelings of others; difficulty distinguishing between feelings and the bodily sensations of emotional arousal; confusion of physical sensations often associated with emotions; few dreams or fantasies due to restricted imagination; and concrete, realistic, logical thinking, often to the exclusion of emotional responses to problems. Those who have alexithymia also report very logical and realistic dreams, such as going to the store or eating a meal. Clinical experience suggests it is the structural features of dreams more than the ability to recall them that best characterises alexithymia.

Some alexithymic individuals may appear to contradict the above-mentioned characteristics because they can experience chronic dysphoria or manifest outbursts of crying or rage. However, questioning usually reveals that they are quite incapable of describing their feelings or appear confused by questions inquiring about specifics of feelings.

According to Henry Krystal, individuals exhibiting alexithymia think in an operative way and may appear to be super-adjusted to reality. In psychotherapy, however, a cognitive disturbance becomes apparent as patients tend to recount trivial, chronologically ordered actions, reactions, and events of daily life with monotonous detail. In general, these individuals can, but not always, seem oriented toward things and even treat themselves as robots. These problems seriously limit their responsiveness to psychoanalytic psychotherapy; psychosomatic illness or substance abuse is frequently exacerbated should these individuals enter psychotherapy.

A common misconception about alexithymia is that affected individuals are totally unable to express emotions verbally and that they may even fail to acknowledge that they experience emotions. Even before coining the term, Sifneos (1967) noted patients often mentioned things like anxiety or depression. The distinguishing factor was their inability to elaborate beyond a few limited adjectives such as “happy” or “unhappy” when describing these feelings. The core issue is that people with alexithymia have poorly differentiated emotions limiting their ability to distinguish and describe them to others. This contributes to the sense of emotional detachment from themselves and difficulty connecting with others, making alexithymia negatively associated with life satisfaction even when depression and other confounding factors are controlled for.

Associated Conditions

Alexithymia frequently co-occurs with other disorders. Research indicates that alexithymia overlaps with autism spectrum disorders (ASD). In a 2004 study using the TAS-20, 85% of the adults with ASD fell into the “impaired” category and almost half fell into the “severely impaired” category; in contrast, among the adult control population only 17% were “impaired”, none “severely impaired”. Fitzgerald & Bellgrove pointed out that, “Like alexithymia, Asperger’s syndrome is also characterised by core disturbances in speech and language and social relationships”. Hill & Berthoz agreed with Fitzgerald & Bellgrove (2006) and in response stated that “there is some form of overlap between alexithymia and ASDs”. They also pointed to studies that revealed impaired theory of mind skill in alexithymia, neuroanatomical evidence pointing to a shared aetiology and similar social skills deficits. The exact nature of the overlap is uncertain. Alexithymic traits in ASD may be linked to clinical depression or anxiety; the mediating factors are unknown and it is possible that alexithymia predisposes to anxiety. On the other hand, while the total alexithymia score as well as the difficulty in identifying feelings and externally oriented thinking factors are found to be significantly associated with ADHD, and while the total alexithymia score, the difficulty in identifying feelings, and the difficulty in describing feelings factors are also significantly associated with symptoms of hyperactivity/impulsivity, there is no significant relationship between alexithymia and inattentiveness symptom.

There are many more psychiatric disorders that overlap with alexithymia. One study found that 41% of US veterans of the Vietnam War with post-traumatic stress disorder (PTSD) were alexithymic. Another study found higher levels of alexithymia among Holocaust survivors with PTSD compared to those without. Higher levels of alexithymia among mothers with interpersonal violence-related PTSD were found in one study to have proportionally less caregiving sensitivity. This latter study suggested that when treating adult PTSD patients who are parents, alexithymia should be assessed and addressed also with attention to the parent-child relationship and the child’s social-emotional development.

Single study prevalence findings for other disorders include 63% in anorexia nervosa, 56% in bulimia, 45% to 50% in major depressive disorder, 34% in panic disorder, 28% in social phobia, and 50% in substance abusers. Alexithymia is also exhibited by a large proportion of individuals with acquired brain injuries such as stroke or traumatic brain injury.

Alexithymia is correlated with certain personality disorders, particularly schizoid, avoidant, dependent and schizotypal, substance use disorders, some anxiety disorders and sexual disorders as well as certain physical illnesses, such as hypertension, inflammatory bowel disease and functional dyspepsia. Alexithymia is further linked with disorders such as migraine headaches, lower back pain, irritable bowel syndrome, asthma, nausea, allergies and fibromyalgia.

An inability to modulate emotions is a possibility in explaining why some people with alexithymia are prone to discharge tension arising from unpleasant emotional states through impulsive acts or compulsive behaviours such as binge eating, substance abuse, perverse sexual behaviour or anorexia nervosa. The failure to regulate emotions cognitively might result in prolonged elevations of the autonomic nervous system (ANS) and neuroendocrine systems, which can lead to somatic diseases. People with alexithymia also show a limited ability to experience positive emotions leading Krystal (1988) and Sifneos (1987) to describe many of these individuals as anhedonic.

Alexisomia is a clinical concept that refers to the difficulty in the awareness and expression of somatic, or bodily, sensations. The concept was first proposed in 1979 by Dr. Yujiro Ikemi when he observed characteristics of both alexithymia and alexisomia in patients with psychosomatic diseases.

Causes

It is unclear what causes alexithymia, though several theories have been proposed.

Early studies showed evidence that there may be an interhemispheric transfer deficit among people with alexithymia; that is, the emotional information from the right hemisphere of the brain is not being properly transferred to the language regions in the left hemisphere, as can be caused by a decreased corpus callosum, often present in psychiatric patients who have suffered severe childhood abuse. A neuropsychological study in 1997 indicated that alexithymia may be due to a disturbance to the right hemisphere of the brain, which is largely responsible for processing emotions. In addition, another neuropsychological model suggests that alexithymia may be related to a dysfunction of the anterior cingulate cortex. These studies have some shortcomings, however, and the empirical evidence about the neural mechanisms behind alexithymia remains inconclusive.

French psychoanalyst Joyce McDougall objected to the strong focus by clinicians on neurophysiological explanations at the expense of psychological ones for the genesis and operation of alexithymia, and introduced the alternative term “disaffectation” to stand for psychogenic alexithymia. For McDougall, the disaffected individual had at some point “experienced overwhelming emotion that threatened to attack their sense of integrity and identity”, to which they applied psychological defences to pulverise and eject all emotional representations from consciousness. A similar line of interpretation has been taken up using the methods of phenomenology. McDougall has also noted that all infants are born unable to identify, organize, and speak about their emotional experiences (the word infans is from the Latin “not speaking”), and are “by reason of their immaturity inevitably alexithymic”. Based on this fact McDougall proposed in 1985 that the alexithymic part of an adult personality could be “an extremely arrested and infantile psychic structure”. The first language of an infant is nonverbal facial expressions. The parent’s emotional state is important for determining how any child might develop. Neglect or indifference to varying changes in a child’s facial expressions without proper feedback can promote an invalidation of the facial expressions manifested by the child. The parent’s ability to reflect self-awareness to the child is another important factor. If the adult is incapable of recognising and distinguishing emotional expressions in the child, it can influence the child’s capacity to understand emotional expressions.

Molecular genetic research into alexithymia remains minimal, but promising candidates have been identified from studies examining connections between certain genes and alexithymia among those with psychiatric conditions as well as the general population. A study recruiting a test population of Japanese males found higher scores on the Toronto Alexithymia Scale among those with the 5-HTTLPR homozygous long (L) allele. The 5-HTTLPR region on the serotonin transporter gene influences the transcription of the serotonin transporter that removes serotonin from the synaptic cleft, and is well studied for its association with numerous psychiatric disorders. Another study examining the 5-HT1A receptor, a receptor that binds serotonin, found higher levels of alexithymia among those with the G allele of the Rs6295 polymorphism within the HTR1A gene. Also, a study examining alexithymia in subjects with obsessive-compulsive disorder found higher alexithymia levels associated with the Val/Val allele of the Rs4680 polymorphism in the gene that encodes Catechol-O-methyltransferase (COMT), an enzyme which degrades catecholamine neurotransmitters such as dopamine. These links are tentative, and further research will be needed to clarify how these genes relate to the neurological anomalies found in the brains of people with alexithymia.

Although there is evidence for the role of environmental and neurological factors, the role and influence of genetic factors for developing alexithymia is still unclear. A single large scale Danish study suggested that genetic factors contributed noticeably to the development of alexithymia. However, such twin studies are controversial, as they suffer from the “equal environments assumption” and the “heritability” estimates in no way correspond to actual DNA structures. Traumatic brain injury is also implicated in the development of alexithymia, and those with traumatic brain injury are six times more likely to exhibit alexithymia.

In Relationships

Alexithymia can create interpersonal problems because these individuals tend to avoid emotionally close relationships, or if they do form relationships with others they usually position themselves as either dependent, dominant, or impersonal, “such that the relationship remains superficial”. Inadequate “differentiation” between self and others by alexithymic individuals has also been observed. Their difficulty in processing interpersonal connections often develops where the person lacks a romantic partner.

In a study, a large group of alexithymic individuals completed the 64-item Inventory of Interpersonal Problems (IIP-64) which found that “two interpersonal problems are significantly and stably related to alexithymia: cold/distant and non-assertive social functioning. All other IIP-64 subscales were not significantly related to alexithymia.”

Chaotic interpersonal relations have also been observed by Sifneos. Due to the inherent difficulties identifying and describing emotional states in self and others, alexithymia also negatively affects relationship satisfaction between couples.

In a 2008 study alexithymia was found to be correlated with impaired understanding and demonstration of relational affection, and that this impairment contributes to poorer mental health, poorer relational well-being, and lowered relationship quality. Individuals high on the alexithymia spectrum also report less distress at seeing others in pain and behave less altruistically toward others.

Some individuals working for organisations in which control of emotions is the norm might show alexithymic-like behaviour but not be alexithymic. However, over time the lack of self-expressions can become routine and they may find it harder to identify with others.

Treatment

Generally speaking, approaches to treating alexithymia are still in their infancy, with not many proven treatment options available.

In 2002, Kennedy and Franklin found that a skills-based intervention is an effective method for treating alexithymia. Kennedy and Franklin’s treatment plan involved giving the participants a series of questionnaires, psychodynamic therapies, cognitive-behavioural and skills-based therapies, and experiential therapies. After treatment, they found that participants were generally less ambivalent about expressing their emotion feelings and more attentive to their emotional states.

In 2017, based on their attention-appraisal model of alexithymia, Preece and colleagues recommended that alexithymia treatment should target trying to improve the developmental level of people’s emotion schemas and reduce people’s use of experiential avoidance of emotions as an emotion regulation strategy (i.e. the mechanisms hypothesized to underlie alexithymia difficulties in the attention-appraisal model of alexithymia).

In 2018, Löf, Clinton, Kaldo, and Rydén found that mentalisation-based treatment is also an effective method for treating alexithymia. Mentalisation is the ability to understand the mental state of oneself or others that underlies overt behaviour, and mentalisation-based treatment helps patients separate their own thoughts and feelings from those around them. This treatment is relational, and it focuses on gaining a better understanding and use of mentalising skills. The researchers found that all of the patients’ symptoms including alexithymia significantly improved, and the treatment promoted affect tolerance and the ability to think flexibly while expressing intense affect rather than impulsive behaviour.

A significant issue impacting alexithymia treatment is that alexithymia has comorbidity with other disorders. Mendelson’s 1982 study showed that alexithymia frequently presented in people with undiagnosed chronic pain. Participants in Kennedy and Franklin’s study all had anxiety disorders in conjunction with alexithymia, while those in Löf et al. were diagnosed with both alexithymia and borderline personality disorder. All these comorbidity issues complicate treatment because it is difficult to examine people who exclusively have alexithymia.

What is Rigidity (Psychology)?

Introduction

In psychology, rigidity or mental rigidity refers to an obstinate inability to yield or a refusal to appreciate another person’s viewpoint or emotions characterised by a lack of empathy.

It can also refer to the tendency to perseverate, which is the inability to change habits and the inability to modify concepts and attitudes once developed. A specific example of rigidity is functional fixedness, which is a difficulty conceiving new uses for familiar objects.

Background

Rigidity is an ancient part of our human cognition. Systematic research on rigidity can be found tracing back to Gestalt psychologists, going as far back as the late 19th to early 20th century with Max Wertheimer, Wolfgang Köhler, and Kurt Koffka in Germany. With more than 100 years of research on the matter there is some established and clear data. Nonetheless, there is still much controversy surrounding several of the fundamental aspects of rigidity. In the early stages of approaching the idea of rigidity, it is treated as “a unidimensional continuum ranging from rigid at one end to flexible at the other”. This idea dates back to the 1800s and was later articulated by Charles Spearman who described it as mental inertia. Prior to 1960 many definitions for the term rigidity were afloat. One example includes Kurt Goldstein’s, which he stated, “adherence to a present performance in an inadequate way”, another being Milton Rokeach saying the definition was, “[the] inability to change one’s set when the objective conditions demand it”. Others have simplified rigidity down to stages for easy defining. Generally, it is agreed upon that it is evidenced by the identification of mental or behavioural sets.

Lewin and Kounin also proposed a theory of cognitive rigidity (also called Lewin-Kounin formulation) based on a Gestalt perspective and they used it to explain a behaviour in mentally retarded persons that is inflexible, repetitive, and unchanging. The theory proposed that it is caused by a greater “stiffness” or impermeability between inner-personal regions of individuals, which influence behaviour. Rigidity was particularly explored in Lewin’s views regarding the degree of differentiation among children. He posited that a mentally retarded child can be distinguished from the normal child due to the smaller capacity for dynamic rearrangement in terms of his psychical systems.

Mental Set

Mental sets represent a form of rigidity in which an individual behaves or believes in a certain way due to prior experience. The reverse of this is termed cognitive flexibility. These mental sets may not always be consciously recognised by the bearer. In the field of psychology, mental sets are typically examined in the process of problem solving, with an emphasis on the process of breaking away from particular mental sets into formulation of insight. Breaking mental sets in order to successfully resolve problems fall under three typical stages:

  1. Tendency to solve a problem in a fixed way;
  2. Unsuccessfully solving a problem using methods suggested by prior experience; and
  3. Realising that the solution requires different methods.

Components of high executive functioning, such as the interplay between working memory and inhibition, are essential to effective switching between mental sets for different situations. Individual differences in mental sets vary, with one study producing a variety of cautious and risky strategies in individual responses to a reaction time test.

Causes

Rigidity can be a learned behavioural trait for example the subject has a Parent, Boss or Teacher who demonstrated the same form of behaviour towards them

Stages

Rigidity has three different main “stages” of severity, although it never has to move to further stages.

  • The first stage is a strict perception that causes one to persist in their ways and be close-minded to other things.
  • The second involves a motive to defend the ego.
  • The third stage is that it is a part of one’s personality and you can see it in their perception, cognition, and social interactions.

Accompanying Externalising Behaviours

They could be external behaviours, such as the following:

  • Insistently repetitious behaviour.
  • Difficulty with unmet expectations.
  • Perfectionism.
  • Compulsions (as in OCD).
  • Perseveration.

Accompanying Internalising Behaviours

Internalizing behaviours also are shown:

  • Perfectionism.
  • Obsessions (as in OCD).

Associated Conditions

Cognitive Closure

Mental rigidity often features a high need for cognitive closure, meaning that they assign explanations prematurely to things with a determination that this is truth, finding that resolution of the dissonance as reassuring as finding the truth. Then, there is little reason to correct their unconscious misattributions if it would bring uncertainty back.

Autism Spectrum Disorder

Cognitive rigidity is one feature of autism and its spectrum (ASD), but is even included in what’s called the Broader Autism Phenotype, where a collection of autistic traits still fail to reach the level of ASD. This is one example of how rigidity does not show up as a single trait, but comes with a number of related traits.

Effects

Ethnocentrism

M. Rokeach tested for ethnocentrism’s relatedness to mental rigidity by using the California Ethnocentrism Scale (when measuring American college students’ views) and the California Attitude Scale (when measuring children’s views) before they were given what is called by cognitive scientists “the water jar problem.” This problem teaches students a set pattern for how to solve each one. Those that scored higher in ethnocentrism also showed attributes of rigidity such as persistence of mental sets and more complicated thought processes.

Strategies for Overcoming Rigidity

Consequences of Unfulfillment

If a person with cognitive rigidity does not fulfil their rigidly held expectations, the following could occur:

  • Agitation.
  • Aggression.
  • Self-injurious behaviour.
  • Depression.
  • Anxiety.
  • Suicidality.

These are clearly maladaptive, and so there must be other ways to overcome it.

What is Role Suction?

Introduction

Role suction is a term introduced in the United States by Fritz Redl in the mid-20th century to describe the power of a social group to allocate roles to its members.

W.R. Bion’s group dynamics further explored the ways whereby the group (unconsciously) allocates particular functions to particular individuals in order to have its covert emotional needs met; and the process has recently been highlighted anew within the systems-centred therapy of Yvonne Agazarian.

Among regularly occurring group roles are those of the scapegoat for the group’s troubles; the joker; the peacemaker; the critic/spokesperson for group standards; the idol, or upholder of the group ideal; and the identified patient. In mixed gender groups, women may be disproportionately pressured by role suction into playing a nurturing/peacemaker role.

Refer to Karpman Drama Triangle.

Driving Forces

The ease whereby people pick out those who play complementary games, and the psychological splitting of good and bad help fuel such role differentiation.

Behind role suction, such forces as projective identification and countertransference have been singled out as operating at an unconscious level in the group.

Role lock – confirming mutual suction into complementary roles, such as victim and abuser – is ensured by the intermeshing of projective identifications.

Wider Systems

The British anti-psychiatrists explored the theme of group suction in connection with role attribution in the family nexus, as well as with the allocations of roles in the wider social system, David Cooper suggesting that ‘there are always good or bad, loved or hated ‘mothers’ and ‘fathers’, older or younger ‘brothers’ and ‘sisters’…in any institutional structure”.

A wider variety of roles can however be found in organisational life, the person-in-role acting as a container for the (unconscious) group forces.

Role of the Therapist

Bion has described his experience as a group therapist when he “feels he is being manipulated so as to be playing a part, no matter how difficult to recognise, in somebody else’s phantasy…a temporary loss of insight, a sense of experiencing strong feelings, and at the same time a belief that their existence is quite adequately justified by the objective situation”. Bion’s work has also been used to illustrate the part played by role suction in the selection of group leaders – dependent groups favouring narcissistic leaders, the fight/flight group paranoids.

R.D. Laing considered that a central part of the therapist’s job was “not to allow himself to collude with the patients in adopting a position in their phantasy-system: and, alternatively, not to use the patients to embody any phantasy of their own” – to resist role suction. Later therapists however have explored how a measure of adaptation to patients’ role suction – a degree of role responsiveness – can be a useful element in the therapeutic use of the countertransference.

Criticism

From the point of view of systems-centred therapy, the debate relates to the interface between a personal system and the psycho-dynamics of social systems themselves.

Debate has arisen about how far the group imposes roles, and how far the individual’s own personality goes to meet the group halfway. Earl Hopper has used the term personification to challenge Redl’s concept, suggesting instead that group roles reflect the underlying personality of the individual involved. However, Kibel objects that in many cases the roles imposed are in fact ego-dystonic; with others pointing to how personal tendencies combine with group expectations with varying degrees of fit.

What is Emotional Detachment?

Introduction

In psychology, emotional detachment, also known as emotional blunting, has two meanings:

  • One is the inability to connect to others on an emotional level; and
  • The other is as a positive means of coping with anxiety.

This coping strategy, also known as emotion focused-coping, is used by avoiding certain situations that might trigger anxiety. It refers to the evasion of emotional connections. Emotional detachment may be a temporary reaction to a stressful situation, or a chronic condition such as depersonalisation-derealisation disorder. It may also be caused by certain antidepressants. Emotional blunting as reduced affect display is one of the negative symptoms of schizophrenia.

Signs and Symptoms

Emotional detachment may not be as outwardly obvious as other psychiatric symptoms. Patients diagnosed with emotional detachment have reduced ability to express emotion, to empathise with others or to form powerful emotional connections. Patients are also at an increased risk for many anxiety and stress disorders. This can lead to difficulties in creating and maintaining personal relationships. The person may move elsewhere in their mind and appear preoccupied or “not entirely present”, or they may seem fully present but exhibit purely intellectual behaviour when emotional behaviour would be appropriate. They may have a hard time being a loving family member, or they may avoid activities, places, and people associated with past traumas. Their dissociation can lead to lack of attention and, hence, to memory problems and in extreme cases, amnesia. In some cases, they present an extreme difficulty in giving or receiving empathy which can be related to the spectrum of narcissistic personality disorder.

In children (ages 4-12 were studied), traits of aggression and antisocial behaviours were found to be correlated with emotional detachment. Researchers determined that these could be early signs of emotional detachment, suggesting parents and clinicians to evaluate children with these traits for a higher behavioural problem in order to avoid bigger problems (such as emotional detachment) in the future.

Causes

Emotional detachment and/or emotional blunting have multiple causes, as the cause can vary from person to person. Emotional detachment or emotional blunting often arises due to adverse childhood experiences, or to psychological trauma in adulthood.

Emotional blunting is often caused by antidepressants in particular selective serotonin reuptake inhibitors (SSRIs) used in major depressive disorder, and often as an add-on treatment in other psychiatric disorders.

Behavioural Mechanism

Emotional detachment is a behaviour which allows a person to react calmly to highly emotional circumstances. Emotional detachment in this sense is a decision to avoid engaging emotional connections, rather than an inability or difficulty in doing so, typically for personal, social, or other reasons. In this sense it can allow people to maintain boundaries, psychic integrity and avoid undesired impact by or upon others, related to emotional demands. As such it is a deliberate mental attitude which avoids engaging the emotions of others.

This detachment does not necessarily mean avoiding empathy; rather, it allows the person to rationally choose whether or not to be overwhelmed or manipulated by such feelings. Examples where this is used in a positive sense might include emotional boundary management, where a person avoids emotional levels of engagement related to people who are in some way emotionally overly demanding, such as difficult co-workers or relatives, or is adopted to aid the person in helping others.

Emotional detachment can also be “emotional numbing”, “emotional blunting”, i.e., dissociation, depersonalisation or in its chronic form depersonalisation disorder. This type of emotional numbing or blunting is a disconnection from emotion, it is frequently used as a coping survival skill during traumatic childhood events such as abuse or severe neglect. Over time and with much use, this can become second nature when dealing with day to day stressors.

Emotional detachment may allow acts of extreme cruelty and abuse, supported by the decision to not connect empathically with the person concerned. Social ostracism, such as shunning and parental alienation, are other examples where decisions to shut out a person creates a psychological trauma for the shunned party.

What is Reduced Affect 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. He or she 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 characterized 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

Patients with schizophrenia have long been recognized as showing “flat or inappropriate affect, with splitting of feelings from events … feelings seem flat instead of being in contact with what is going on”. 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”.

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 Emotionality?

Introduction

Emotionality is the observable behavioural and physiological component of emotion. It is a measure of a person’s emotional reactivity to a stimulus.

Most of these responses can be observed by other people, while some emotional responses can only be observed by the person experiencing them. Observable responses to emotion (i.e. smiling) do not have a single meaning. A smile can be used to express happiness or anxiety, while a frown can communicate sadness or anger. Emotionality is often used by experimental psychology researchers to operationalise emotion in research studies.

Early Theories

By the late 1800s, many high-quality contributions became interested in analysing emotion because of the works of psychologists and scientists such as Wilhelm Wundt, George Stout, William McDougall, William James, and George Herbert Mead. William James preferred to focus on the physiological aspects of emotional response, although he did not disregard the perceptual or cognitive components. William McDougall thought of emotion as the articulation of a natural response built on instinct. Other psychologists reasoned that although gestures express emotion, this is not the entirety of their function. Wundt analysed that emotion portrays both expression and communication.

As Irrational

One of the oldest views of emotion is that emotion indicates inferiority. In early psychology, it was believed that passion (emotion) was a part of the soul inherited from the animals and that it must be controlled. Solomon identified that in the Romantic movement of the eighteenth and nineteenth centuries, reason and emotion were discovered to be opposites.

As Physiological

Physiological responses to emotion originate in the central nervous system, the autonomic nervous system, and the endocrine system. Some of the responses include: heart rate, sweating, rate and depth of respiration, and electrical activity in the brain. Many researchers have attempted to find a connection between specific emotions and a corresponding pattern of physiological responses, but the results have been inconclusive.

Later Theories

The significant theories of emotion can be divided into three primary categories: physiological, neurological, and cognitive. Physiological theories imply that activity within the body can be accountable for emotions. Neurological theories suggest that activity within the brain leads to emotional responses. Lastly, cognitive theories reason that thoughts and other mental activity have a vital role in the stimulation of emotions. Common sense suggests that people first become consciously aware of their emotions and that the physiological responses follow shortly after. Theories by James-Lange, Cannon-Bard, and Schachter-Singer contradict the common-sense theory.

James-Lange

The James-Lange theory of emotion was proposed by psychologist William James and physiologist Carl Lange. This theory suggests that emotions occur as a result of physiological responses to outside stimuli or events. For example, this theory suggests that if someone is driving down the road and sees the headlights of another car heading toward them in their lane, their heart begins to race (a physiological response) and then they become afraid (fear being the emotion).

Cannon-Bard

The Cannon-Bard theory, which was conceptualized by Walter Cannon and Phillip Bard, suggests that emotions and their corresponding physiological responses are experienced simultaneously. Using the previous example, when someone sees the car coming toward them in their lane, their heart starts to race and they feel afraid at the same time.

Schachter-Singer

Stanley Schachter and Jerome Singer proposed a theory also known as the two-factor theory of emotion, which implies emotion have two factors: physical arousal and cognitive label. This suggests that if the physiological activity occurs first, then it must cognitively be distinguished as the cause of the arousal and labelled as an emotion. Using the example of someone seeing a car coming towards them in their lane, their heart would start to race and they would identify that they must be afraid if their heart is racing, and from there they would begin to feel fear.

Gender Differences

The opposition of rational thought and emotion is believed to be paralleled by the similar opposition between male and female. A traditional view is that “men are seen as rational and women as emotional, lacking rationality.” However, in spite of these ideas, and in spite of gender differences in the prevalence of mood disorders, the empirical evidence on gender differences in emotional responding is mixed.

When engaging in social interaction, studies show that women smile significantly more than men do. It is difficult to determine the exact difference between males and females to explain this disparity. It is possible that this difference in expression of emotions is due to societal influences and conformity to gender roles. However, this may not fully explain why men smile less than women do.

The male gender role involves characteristics such as strength, expert knowledge, and a competitive nature. Smiling may be stereotypically associated with weakness. Men may feel that if they engage in this perceived weakness, it may contradict their attempts to show strength and other traits of the male gender role. Another broad explanation for the contrast in male and female gender expression is that women have reported to experience greater levels of emotional intensity than men, in both positive and negative aspects, which could naturally lead to greater emotional response. It has also been reported that men are more likely to confide in female companions, revealing their emotions and intimacy, while females are typically comfortable confiding in both genders. This suggests that men are more particular about how they express the emotions they feel, potentially relating back to gender roles.

Across Cultures

There are six universal emotions which expand across all cultures. These emotions are happiness, sadness, anger, fear, surprise, and disgust. Debate exists about whether contempt should be combined with disgust. According to Ekman (1992), each of these emotions have universally corresponding facial expressions as well.

In addition to the facial expressions that are said to accompany each emotion, there is also evidence to suggest that certain autonomic nervous system (ANS) activity is associated with the three emotions of fear, anger, and disgust. Ekman theorizes that these specific emotions are associated with the universal physiological responses due to evolution. It would not be expected to observe the same physiological responses for emotions not specifically linked to survival, such as happiness or sadness.

Ekman’s theories were early challenged by James A. Russell, and have since been tested by a variety of researchers, with ambiguous results. This seems to reflect methodological problems relating to both display rules and to the components of emotion. Current thinking favours a mix of underlying universality combined with significant cultural differences in the articulation and expression of emotion. Emotions serve different functions in different cultures.

Positive

Positive emotionality is the ability to control positive mood and emotions, people with positive emotions seek for social reward. Positive emotionality can be a preventive factor in blocking out certain types of mental illness. In a study of a sample of 1,655 youth (54% girls; 7-16 years), it found that the higher their positive emotionality was, the lower their depression would be. Depression was considered by its definition of the inability to receive positive emotions or pleasure. The youth’s temperament, adaptive emotion regulation (ER) strategies, and depressive symptoms were determined through a questionnaire. The study also reported that depressive symptoms could be reduced through emotion regulation of positive mood. A study by Charles T. Taylor et al. linked being exposed to positive emotions before a surgery to less anxiety and a decrease in having symptoms after treatment.

Negative

Negative emotionality is the opposite of positive emotionality. People are unable to control their positive mood and emotions. Everyone experiences negative emotionality in different levels, there are different factors that effect each individual in a different way. Negative emotionality effects many aspects of our lives in terms of coping and the relationship that people share with one another. Neuroticism is one of the biggest factors found in negative emotionality. Someone on the higher spectrum of neuroticism is often more anxious and enjoy the feelings of their negative emotion. Some research suggests that obese children compared to children who are not obese have higher levels of negative emotionality and the ability to control emotions.

What is the Differential Susceptibility Hypothesis?

Introduction

The differential susceptibility hypothesis proposed by Jay Belsky is another interpretation of psychological findings that are usually discussed according to the diathesis-stress model.

Both models suggest that people’s development and emotional affect are differentially susceptible to experiences or qualities of the environment. Where the Diathesis-stress model suggests a distinct and mostly negativity-sensitive group, Belsky describes a group that is sensitive to negative experiences but also to positive experiences. These models may be complementary, if some individuals are dually or uniquely positivity-sensitive, while other people are uniquely negativity-sensitive.

Differential Susceptibility versus Diathesis-Stress

The idea that individuals vary in their responsivity to negative qualities of the environment is generally framed in diathesis-stress or dual-risk terms. That is, some individuals, due to their biological, temperamental and/or behavioural characteristics (i.e. “diathesis” or “risk 1”), are more vulnerable to the adverse effects of negative experiences (i.e., “stress” or “risk 2”), whereas others are relatively resilient with respect to them (see Figure 1, an adaptation of Bakermans-Kranenburg and van IJzendoorn’s (2007) Figure 1). A fundamentally different, even if not competing view, of the very same phenomenon is central to Belsky’s differential susceptibility hypothesis and Boyce and Ellis’ (2005) related notion of biological sensitivity to context: Individuals do not simply vary in the degree to which they are vulnerable to the negative effects of adverse experience but, more generally, in their developmental plasticity.

On this hypothesis, more “plastic” or malleable individuals are more susceptible than others to environmental influences in a for-better-and-for-worse manner. That is, susceptible to both the adverse developmental sequelae associated with negative environments and the positive developmental consequences of supportive ones. Less susceptible individuals, in contrast, are less affected by rearing conditions, be they presumptively supportive or undermining of well being (see Figure 2, an adaptation of Bakermans-Kranenburg and Van IJzendoorn’s (2007) Figure 1).

Figure 1. The diathesis-stress/dual-risk model. Developmental outcome as it relates to environmental quality. A “vulnerable” group experiences negative outcome when exposed to a negative environment, although this group is identical to the other, “resilient” group in a positive environment.
Figure 2. The differential susceptibility model. The lines depict two categorical groups that differ in their responsiveness to the environment: the “plastic” group is disproportionately more affected by both negative and positive environments compared to the “fixed” group.

Theoretical Background

Belsky suggests that evolution might select for some children who are more plastic, and others who are more fixed in the face of, for example, parenting styles.

Belsky offers that ancestral parents, just like parents today, could not have known (consciously or unconsciously) which childrearing practices would prove most successful in promoting the reproductive fitness of offspring – and thus their own inclusive fitness. As a result, and as a fitness optimising strategy involving bet hedging, natural selection might have shaped parents to bear children varying in plasticity. This way, if an effect of parenting had proven counterproductive in fitness terms, those children not affected by parenting would not have incurred the cost of developing in ways that ultimately proved “misguided”.

Importantly, natural selection might favour genetic lines with both plastic and fixed developmental and affective patterns. In other words, there is value to having both kinds at once. In light of inclusive-fitness considerations, children who were less malleable (and more fixed) would have “resistance” to parental influence. This could be adaptable some times, and maladaptive other times. Their fixedness would not only have benefited themselves directly, but even their more malleable siblings indirectly. This is because siblings, like parents and children, have 50% of their genes in common. By the same token, had parenting influenced children in ways that enhanced fitness, then not only would more plastic offspring have benefited directly by following parental leads, but so, too, would their parents and even their less malleable siblings who did not benefit from the parenting they received, again for inclusive-fitness reasons. The overall effect may be to temper some of the variability in parenting. That is, to make more conservative bets.

This line of evolutionary argument leads to the prediction that children should vary in their susceptibility to parental rearing and perhaps to environmental influences more generally. As it turns out, a long line of developmental inquiry, informed by a “transactional” perspective, has more or less been based on this unstated assumption.

Criteria for the Testing of Differential Susceptibility

Belsky, Bakermans-Kranenburg, & Van IJzendoorn, (2007) delineated a series of empirical requirements – or steps – for evidencing the differential susceptibility hypothesis. Particularly they identify tests that distinguish differential susceptibility from other interaction effects including diathesis-stress/dual-risk.

While diathesis-stress/dual-risk arises when the most vulnerable are disproportionately affected in an adverse manner by a negative environment but do not also benefit disproportionately from positive environmental conditions, differential susceptibility is characterised by a cross-over interaction: the susceptible individuals are disproportionately affected by both negative and positive experiences. A further criterion that needs to be fulfilled to distinguish differential susceptibility from diathesis-stress/dual-risk is the independence of the outcome measure from the susceptibility factor: if the susceptibility factor and the outcome are related, diathesis-stress/dual-risk is suggested rather than differential susceptibility. Further, environment and susceptibility factor must also be unrelated to exclude the alternative explanation that susceptibility merely represents a function of the environment. The specificity of the differential-susceptibility effect is demonstrated if the model is not replicated when other susceptibility factors (i.e. moderators) and outcomes are used. Finally, the slope for the susceptible subgroup should be significantly different from zero and at the same time significantly steeper than the slope for the non- (or less-) susceptible subgroup.

Susceptibility Markers and Empirical Evidence

Characteristics of individuals that have been shown to moderate environmental effects in a manner consistent with the differential susceptibility hypothesis can be subdivided into three categories:

  • Genetic factors;
  • Endophenotypic factors; and
  • Phenotypic factors.

Bakermans-Kranenburg and Van IJzendoorn (2006) were the first to test the differential susceptibility hypothesis as a function of Genetic Factors regarding the moderating effect of the dopamine receptor D4 7-repeat polymorphism (DRD4-7R) on the association between maternal sensitivity and externalising behaviour problems in 47 families. Children with the DRD4-7R allele and insensitive mothers displayed significantly more externalising behaviours than children with the same allele but with sensitive mothers. Children with the DRD4-7R allele and sensitive mothers had the least externalising behaviours of all whereas maternal sensitivity had no effect on children without the DRD4-7R allele.

Endophenotypic Factors have been examined by Obradovic, Bush, Stamperdahl, Adler and Boyce’s (2010). They investigated associations between childhood adversity and child adjustment in 338 5-year-olds. Children with high cortisol reactivity were rated by teachers as least prosocial when living under adverse conditions, but most prosocial when living under more benign conditions (and in comparison to children scoring low on cortisol reactivity).

Regarding characteristics of the category of Phenotypic Factors, Pluess and Belsky (2009) reported that the effect of child care quality on teacher-rated socioemotional adjustment varied as a function of infant temperament in the case of 761 4.5-year-olds participating in the NICHD Study of Early Child Care and Youth Development (NICHD Early Child Care Research Network, 2005). Children with difficult temperaments as infants manifest the most and least behaviour problems depending on whether they experienced, respectively, poor or good quality care (and in comparison to children with easier temperaments).

Table 1: List of Proposed Susceptibility Factors that emerge across studies, according to Belsky and colleagues.

What is Emotional Dysregulation?

Introduction

Emotional dysregulation is a term used in the mental health community that refers to emotional responses that are poorly modulated and do not lie within the accepted range of emotive response.

Emotional dysregulation can be associated with an experience of early psychological trauma, brain injury, or chronic maltreatment (such as child abuse, child neglect, or institutional neglect/abuse), and associated disorders such as reactive attachment disorder. Emotional dysregulation may be present in people with psychiatric disorders such as attention deficit hyperactivity disorder, autism spectrum disorders, bipolar disorder, borderline personality disorder, complex post-traumatic stress disorder, and foetal alcohol spectrum disorders. In such cases as borderline personality disorder and complex post-traumatic stress disorder, hypersensitivity to emotional stimuli causes a slower return to a normal emotional state. This is manifested biologically by deficits in the frontal cortices of the brain.

Possible manifestations of emotional dysregulation include extreme tearfulness, angry outbursts or behavioural outbursts such as destroying or throwing objects, aggression towards self or others, and threats to kill oneself. Emotional dysregulation can lead to behavioural problems and can interfere with a person’s social interactions and relationships at home, in school, or at place of employment.

Etymology

The word “dysregulation” is a neologism created by combining the prefix “dys-” to “regulation”. According to Webster’s Dictionary, dys- has various roots and is of Greek origin. With Latin and Greek roots, it is akin to Old English tō-, te- “apart” and in Sanskrit dus- “bad, difficult.” It is frequently confused with the spelling “disregulation” with the prefix “dis” meaning “the opposite of” or “absence of”.

Child psychopathology

There are links between child emotional dysregulation and later psychopathology. For instance, ADHD symptoms are associated with problems with emotional regulation, motivation, and arousal. One study found a connection between emotional dysregulation at 5 and 10 months, and parent-reported problems with anger and distress at 18 months. Low levels of emotional regulation behaviours at 5 months were also related to non-compliant behaviours at 30 months. While links have been found between emotional dysregulation and child psychopathology, the mechanisms behind how early emotional dysregulation and later psychopathology are related are not yet clear.

Symptoms

Smoking, self-harm, eating disorders, and addiction have all been associated with emotional dysregulation. Somatoform disorders may be caused by a decreased ability to regulate and experience emotions or an inability to express emotions in a positive way. Individuals who have difficulty regulating emotions are at risk for eating disorders and substance abuse as they use food or substances as a way to regulate their emotions. Emotional dysregulation is also found in people who have an increased risk of developing a mental disorder, in particularly an affective disorder such as depression or bipolar disorder.

Early Childhood

Research has shown that failures in emotional regulation may be related to the display of acting out, externalizing disorders, or behaviour problems. When presented with challenging tasks, children who were found to have defects in emotional regulation (high-risk) spent less time attending to tasks and more time throwing tantrums or fretting than children without emotional regulation problems (low-risk). These high-risk children had difficulty with self-regulation and had difficulty complying with requests from caregivers and were more defiant. Emotional dysregulation has also been associated with childhood social withdrawal. Common signs of emotional dysregulation in early childhood include isolation, throwing things, screaming, lack of eye contact, refusing to speak, rocking, running away, crying, dissociating, high levels of anxiety, or inability to be flexible.

Internalising Behaviours

Emotional dysregulation in children can be associated with internalizing behaviours including:

  • Exhibiting emotions too intense for a situation.
  • Difficulty calming down when upset.
  • Difficulty decreasing negative emotions.
  • Being less able to calm themselves.
  • Difficulty understanding emotional experiences.
  • Becoming avoidant or aggressive when dealing with negative emotions.
  • Experiencing more negative emotions.

Externalising Behaviours

Emotional dysregulation in children can be associated with externalizing behaviours including:

  • Exhibiting more extreme emotions.
  • Difficulty identifying emotional cues.
  • Difficulty recognizing their own emotions.
  • Focusing on the negative.
  • Difficulty controlling their attention.
  • Being impulsive.
  • Difficulty decreasing their negative emotions.
  • Difficulty calming down when upset.

Protective Factors

Early experiences with caregivers can lead to differences in emotional regulation. The responsiveness of a caregiver to an infant’s signals can help an infant regulate their emotional systems. Caregiver interaction styles that overwhelm a child or that are unpredictable may undermine emotional regulation development. Effective strategies involve working with a child to support developing self-control such as modelling a desired behaviour rather than demanding it.

The richness of an environment that a child is exposed to helps the development of emotional regulation. An environment must provide appropriate levels of freedom and constraint. The environment must allow opportunities for a child to practice self-regulation. An environment with opportunities to practice social skills without over-stimulation or excessive frustration helps a child develop self-regulation skills.

Emotional Dysregulation and Substance Use

Several variables have been explored to explain the connection between emotional dysregulation and substance use in young adults, such as child maltreatment, cortisol levels, family environment, and symptoms of depression and anxiety. Vilhena-Churchill and Goldstein (2014) explored the association between childhood maltreatment and emotional dysregulation. More severe childhood maltreatment was found to be associated with an increase in difficulty regulating emotion, which in turn was associated with a greater likelihood of coping by using marijuana. Kliewer et al. (2016) performed a study on the relationship between negative family emotional climate, emotional dysregulation, blunted anticipatory cortisol, and substance use in adolescents. Increased negative family emotional climate was found to be associated with high levels of emotional dysregulation, which was then associated with increased substance use. Girls were seen to have blunted anticipatory cortisol levels, which was also associated with an increase in substance use. Childhood events and family climate with emotional dysregulation are both factors seemingly linked to substance use. Prosek, Giordano, Woehler, Price, and McCullough (2018) explored the relationship between mental health and emotional regulation in collegiate illicit substance users. Illicit drug users reported higher levels of depression and anxiety symptoms. Emotional dysregulation was more prominent in illicit drug users in the sense that they had less clarity and were less aware of their emotions when the emotions were occurring.

Treatment

While cognitive behavioural therapy is the most widely prescribed treatment for such psychiatric disorders, a commonly prescribed psychotherapeutic treatment for emotional dysregulation is dialectical behavioural therapy, a psychotherapy which promotes the use of mindfulness, a concept called dialectics, and emphasizes the importance of validation and maintaining healthy behavioural habits.

When diagnosed as being part of ADHD, norepinephrine and dopamine reuptake inhibitors such as methylphenidate (Ritalin) and atomoxetine are often used.

References

Kliewer, W., Riley, T., Zaharakis, N., Borre, A., Drazdowski, T.K. & Jäggi, L. (2016) Emotion Dysregulation, Anticipatory Cortisol, and Substance Use in Urban Adolescents. Personality and Individual Differences. 99, pp.200-205. doi:10.1016/j.paid.2016.05.011. PMC 5082236. PMID 27795602.

Prosek, E.A., Giordano, A.L., Woehler, E.S., Price, E. & McCullough, R. (2018) Differences in Emotion Dysregulation and Symptoms of Depression and Anxiety among Illicit Substance Users and Nonusers. Substance Use & Misuse. 53(11), pp.1915-1918. doi:10.1080/10826084.2018.1436563. PMID 29465278. S2CID 3411848.

Vilhena-Churchill, N. & Goldstein, A.L. (2014) Child Maltreatment and Marijuana Problems in Young Adults: Examining the Role of Motives and Emotion Dysregulation. Child Abuse & Neglect. 38(5), pp.962-972. doi:10.1016/j.chiabu.2013.10.009. PMID 24268374.