Motivation and emotion/Book/2022/Hypomania and emotion

Overview
This chapter discusses the emotional characteristics affecting hypomania. Hypomania is a state of mind where an individual experiences elevated or irritable mood for multiple days; in which emotions and vitality are elevated often with poor impulse control and risk-taking behaviours (Parker, 2012). Hypomania is considered a less severe version of mania and is commonly associated with mood disorders. Hypomania also has a co-morbid relationship with anxiety disorders and substance abuse (e.g., Angst, 1998).

Hypomania is important because the subset of emotional characteristics normally observed in an individual change during an episode and this can impact on meaningful day-to-day relationships through influence of extreme behaviour changes (Angst, 1998). Psychologically based emotional theories can help us understand the role emotions play in hypomania (Reeve, 2018, p. 41); this includes affected brain regions and functional specialisation (Heissler et al., 2013).

Hypomania is also a current focus area of research involving adolescent participants to improve understanding of the condition, and identify early warning signs and onset of both hypomania and other mood disorders (Gruber et al., 2021). Additional research on understanding the emotional characteristics of those likely to develop hypomania is paramount to improved patient outcomes by tailoring early intervention treatment plans and effective balances between pharmacological and psychotherapy treatment (Heissler et al., 2013).

Focus questions:
 * What is hypomania?
 * What are the emotional characteristics of hypomania?
 * How do emotion theories explain hypomania?
 * How can hypomania be managed?

What is hypomania?
Hypomania is a mood disorder symptom typically described as a less severe experience of mania (see Figure 1). During a hypomanic episode, an individual experiences an abnormally elevated positive or irritable mood that is constant or almost constant for at least four consecutive days (National Library of Medicine, n.d.). Hypomania is often a symptom of bipolar disorder II but can also develop as a symptom in other mood disorders (Stanton et al., 2019). A way to conceptualise a hypomanic episode for those who have never experienced one can be captured by comparing the extreme elevated emotions felt in adolescent romantic love during the initial and intense ‘honeymoon phase' (Brand et al., 2007). According to Brand et al. (2007), these early love stages elicit similarly comparable behaviours such as increased risk taking, reduced impulse control, reduced need for sleep, imbalanced highs and lows, and an elevated mood that is observably different to the baseline.

Definition
An emotion is defined as a neuro-chemical episode that expresses human emotional characteristics reacting to environmental, physiological and psychological stimuli (Izard, 2010). An emotion occurs to regulate behaviour and cognitively process an encountered life event. A mood is a prolonged emotional state where behaviour and attitudes form the foundations of an feeling experience. In a hypomanic state these moods are considered a disorder (Izard, 2010).

Prevalence and tendency to develop disorder
It is reported that the worldwide prevalence of hypomania is 5.5% for up to age 35 meeting the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) hypomania/mania criteria, and further cases involving brief episodes lasting 1-3 days (recurrent) is reported at 2.8% (Angst,1998). Jansen et al. (2011) also found a similar 5.3% statistical prevalence of lifetime hypomanic episodes for over eighteen-year-olds in a large research sample of participants, suggesting that this figure is consistent over time and likely an accurate current representation. There is also evidence that hypomania stigma and social awareness that hypomania is a condition have continued over time to contribute to underreporting statistics (Berjot & Gillet, 2011).

Predicting future hypomanic vulnerability is a growing field of research, often focusing on younger participants in the emerging adulthood generation with an age range around 18-25 (e.g., Devlin et al., 2015b; Kirkland et al., 2015). Participants often complete the standardised hypomania risk self-report scales (e.g., Angst, 2005; Eckblad & Chapman, 1986), while being subject to either personality assessments (e.g., Kirkland et al., 2015) and/or visual stimulation exercises involving pictures of people presenting positive or negative affect emotions (e.g., Devlin et al., 2015b). Based off these participant results, researchers use data analysis tools to determine the likelihood of hypomanic tendencies for specific emotional characteristic and orientation profiles (e.g., Devlin et al., 2015b; Kirkland et al., 2015). These profiles develop an understanding of the emotional characteristics of adolescents at risk of experiencing hypomania in the future, and may even add to early intervention treatment models such as pharmacology and psychotherapy (Heissler et al., 2013). Nevertheless, there are also early-diagnosis indicators in determining hypomanic risk assessments, as the condition is a key indicator for mood disorders pathogenesis, and in particular bipolar disorder (Heissler et al., 2013). Individuals at high risk of developing hypomanic symptoms on self-report scales (e.g., Eckblad & Chapman, 1986), have been found to display higher emotional characteristic levels of emotional reactivity in baseline states through higher amygdala activation and typically incur barriers in regulating emotions downwards from elevated mood states (Heissler et al., 2013).



Hypomanic risk factors and associated neurology
Risk-taking behaviour is often associated with hypomania because of emotional elevation in individuals experiencing an episode, such as excessive gambling as seen on the gaming machine in figure 2. Building on this, Devlin et al. (2015a) collected self-reported evidence from participants that scored high on hypomanic risk factor scales (Eckblad & Chapman, 1986) and that these individuals also predicted further risk-taking behaviour was expected to occur in the proceeding six-month period (Devlin et al., 2015a; Devlin et al., 2015b).

A neurological explanation of hypomania risk factors is found in the nucleus accumbens, the reward centre of the brain that is often considered the heart of our addiction drivers (Berridge et al., 2008). In the nucleus accumbens, the brain is normally able to differentiate between our wants (basic needs/impulses) and likes (rewarded preferences) using dopamine stimulation, that balances out opioid levels in the brain (Berridge et al., 2008). Overstimulation of dopamine levels in the nucleus accumbens can lead to poor impulse control and elevated mood with extraversion factors such as those experienced during a hypomania episode (Berridge et al., 2008; Kirkland et al., 2015). Hence, during such an episode, it is likely emotional regulation around the ability to determine the difference between a want and a like contributing to the risk-taking behaviour (Berridge et al., 2008; Kirkland et al., 2015).

{Hypomania is described as a less severe version of mania? + True - False
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{In the fictional case study; Jackie has a close relationship with her immediate family due to her hypomanic presentations? - True + False
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What are the emotional characteristics of hypomania?


Hypomania is associated with heightened mood and elevated emotions including euphoria, excitement, happiness, grandiosity, increased sexual energy, irritability and a lack of attention span (Stanton et al., 2019), see figure 3. Additionally, research suggests a positive bias and a sensitivity towards reading positive emotions in others, and an overly positive interpretation of those experiencing negative emotions; this suggests that hypomania may impact empathy because of the heightened mood experienced by the individual (Devlin et al., 2015b).

Gruber et al. (2021) studied a younger sample of participants (Μage = 18.68) with hypomania (and mania) with the findings suggesting that proneness likely experience a visual bias towards positive facial features, and not fearful or angry facial features; this reinforces earlier research by Devlin et al. (2015b) in acknowledging that the heightened positive emotions experienced in a hypomanic state likely make comprehension of others experiencing negative emotions difficult to perceive and therefore as a by-product become less empathetic in nature during an episode (Gruber et al., 2021). Nonetheless, limited evidence supports high risk individuals lacking sensitivity to negative emotion in others, as this has been observed neurologically by using functional Magnetic Resonance Imaging (fMRI). This highlighted a higher amygdala activation during day-to day tasks, which could also suggest a heightened sensitivity to negative emotion in others (Heissler et al., 2013).

On balance, both results are likely correct outcomes of participant behaviour and are explainable; a heightened amygdala reactivity to baseline day-to-day tasks (Heissler et al., 2013) would likely incur a greater sensitivity to fearful and angry faces and create a visual bias towards reassuring positive emotion facial features (Gruber et al., 2021). This suggests that high risk individuals may still have a reduced empathetic response to others in both baseline and hypomanic states, due to aversion to potential triggered fear-based reactions to those displaying negative emotions; however, further research would need to be conducted to verify this, and arguably such research would not be beneficial (Gruber et al., 2021; Heissler et al., 2013). Altered perceptual bias and sensitivity are only part of a hypomania emotional profile picture, as research by Kelly et al. (2012) has demonstrated that those experiencing hypomania can stay in the state longer when positively appraised and drop down suddenly into depressive emotional characteristics when negatively appraised in the same state; particularly in bipolar II where internal states may incur mood swing symptoms.

How do emotion theories explain hypomania?
Modern day psychology has a broad range of theories to explain emotion (Reeve, 2018, p. 314); emotion theory then offers us a unique lens to examine hypomania through. Please note the following elaboration of three such theories:

James-Lange theory
Early interpretations of emotion started with the James–Lange theory (Dashiell, 1922) and indicates a three-step process that presents an environmental stimulus (life event), then a bodily reaction (e.g., a release of adrenaline to increase the heart rate), and finally an emotional characteristic (Reeve, 2018, p. 314). The James–Lange process matches a hypomania experience in aspects of exacerbation, where environmental triggers prolong, depress, heighten and respond to the condition; hence, this exacerbation then creates a bodily reaction flow-on-effect to maladjusted emotional responses (Kelly et al., 2012). Also following the James–Lange theory, it is environmental stimuli that create an anticipation of reward, that instigates (or exacerbates) the hypomania risk-taking behaviour, for example, excessive gambling when at a poker game (Reeve, 2018, p. 314). Hence, the James–Lange theory supports the value of Cognitive Behaviour Therapy (CBT) as a psychotherapy treatment model to intercept the emotional symptoms mid process to assist regulation and minimise intensity (Reeve, 2018, p. 314). Today, with technology such as fMRI and other scanning equipment, it is possible to intimately observe this neuro-chemical action taking place to create a bodily reaction referenced in the James–Lange theory (Brand et al., 2007). Nonetheless, there are limits to this theory, namely the steps in the James–Lange process do not account for hypomania risk profiling that is the standard of today’s research testing (Eckblad & Chapman, 1986); in summary, a specific life event is not required for an individual to be susceptible (and later develop) hypomania (Brand et al., 2007). The James–Lange Theory identifies the parts of an emotional process, but does not explain the emotional characteristics observed in a mood disorder comprehensively, and does not explain the interaction of how neurology, environment and emotional characteristics all appear to interact with each other in hypomanic affect (Brand et al., 2007).

Lazarus theory
Lazarus' theory of emotion brings a new perspective to consider with hypomania, that of the relationship between cognitions, emotions and a prior appraisal of an encountered environmental emotional trigger (Lazarus, 1991; Lazarus & Folkman, 1984). The environment can influence hypomania, and so too can individual perception and orientation (Kelly et al., 2012); what remains unclear with the theory is how the act of appraising the environment itself before an emotion occurs (according to the theory) influences the outcome of the condition (Reeve, 2018, p. 327). Basically, these pre-emotional appraisals may potentially prolong, delay or even stop an episode.

It can also be established from Lazarus theory that beneficial coping mechanisms exist in a person prone to hypomania through CBT strategies after a life trigger occurs, for example, to calm someone immediately after a car accident (Smith et al., 1993); in this way, the individual’s appraisal of the situation should be less intense and likely to experience a less severe post emotional reaction that requires affect regulation (Smith et al., 1993).

Hypomania brain regions and functional specialisation
An emotional characteristic requires a life event to initiate presentation and in the case of brain specialisation theory; physiological and neurochemical changes would instead explain the underpinning of hypomanic emotion (Heissler et al., 2013). Supporting this underpinning, hypomania can occur days after deep brain stimulation, dopamine medication changes or even surgical microlesions; suggesting that the hypomania emotional characteristics can be entirely artificially and biologically sourced; if the correct area of the brain is stimulated (Costa, 2019). fMRI studies have also shown in high-risk individuals, increased activity in the left inferior parietal and right amygdala brain regions; this is suggestive of a clear dopamine neurotransmitter regulation link (also see hypomanic risk factor and associated neurology above) to both emotional regulation and the later development of hypomanic affect (Heissler et al., 2013). Other findings suggest a more general increased limbic area glucose metabolisation, possibly indicating elevated emotional responses; and a decreased metabolism in the prefrontal and orbital frontal cortex, likely impacting decision making and increasing risk taking behaviour (Parker, 2012, p. 90). In contrast to this, not all hypomania patients display abnormal brain changes (Parker, 2012, p. 91) and alternative theories argue the environment is the predominate factor of an emotion propose a minimal or lack of a direct emotion relationship to a physiological change (Newman et al., 1930), and that brain activation under fMRI merely measures blood flow usually associated with small sample sizes, hence allocating functionality is premature (Wang et al., 2021).

How can hypomania be managed?
Education and awareness are key to reducing the isolation and stigma associated with hypomania and related mood disorders (Berjot & Gillet, 2011), as diagnosing between different mood disorders can often be tricky; people often receive multiple mental health diagnoses after symptom presentation before enough evidence is available for a diagnosis that is accurate, permanent and comprehensive (Stanton et al., 2019). A number of medications can assist with managing hypomania and associated disorders, and this will depend on a case by case assessment from a treating general practitioner of psychiatrist (Stanton et al., 2019). Common medications that assists with hypomania symptoms include antipsychotics haloperidol, olanzapine (Zyprexa), quetiapine (Seroquel), risperidone (Risperdal); and mood stabilisers such as lithium, valproate and carbamazepine (Cleveland clinic, 2022). Additionally, psychotherapy options include a range of CBT strategies. Strategies include (but not limited to):


 * Analysing and deducting out negative or automatic thought patterns into positive or grounded thoughts, e.g., ‘I am in danger from that strange car’ is challenged with ‘I jumped to a conclusion, I am actually safe and will talk out my surroundings’.
 * Rating emotional characteristic, strength and reflecting.
 * Identifying risky behaviours and creating management plans.
 * Reducing alcohol, caffeine and drugs.
 * Setting a two-factor rule, meaning I need to ask two trusted family or friend members before acting.
 * Waiting 48 hours before acting on a desired behaviour such as shopping or gambling.

These strategies can be supervised by a trained psychologist or practiced in a non-clinically setting, for best results a large degree of self-management is required (Roberts, 2014, pp. 117-130).

Key take-away: Non-clinical support measures include education combined with omega-3 fatty acids supplementation, sleep routine strategies, and regular exercise (Parker, 2012, p. 26).

Conclusion
Hypomania is a mood disorder symptom that can be used as a key diagnostic determinant in differentiating between unipolar and bipolar depression diagnoses, because unipolar is associated with low levels of positive elevated mood and bipolar is indicative of difficulties regulating downward from hyper states (Stanton et al., 2019). The emotional characteristics of hypomania are best described as an individual wearing rose-coloured glasses with elevated mood highs and lows (Parker, 2012). These moods are neuro-chemical in nature and an environment inspired view of the world can lead to risk taking behaviours, irregular sleep patterns, irritability, relationship stress, hyper-sexuality and potentially even a lack of empathy (Gruber et al., 2021; Roberts, 2014, p. 117-130).

Emotion theories add value by explaining aspects of hypomania in unique and versatile ways (Reeve, 2018, p. 313). There is benefit in exploring these theories further to understand the relationship between environments, physiognomy (bodily reaction and brain function), and psychological perception to understand the adaptive way emotions can influence each other and their impact to hypomanic affect (Izard, 2010). Hypomania is managed through general practice, psychologist, psychiatrist management, and important CBT self-work. More investigation is required in neurobiological theory as it was established that a hypomanic episode can be artificially induced; hence, it stands to reason it may be reversed with alternative neurological actions (Costa, 2019).

Research remains observing hypomania through imaging and self report scales; these focus on the emotional characteristic profiles of adolescents in predicting hypomania tendencies for future treatment intervention (e.g., Costa, 2019; Devlin et al., 2015b). Arguably, the most important relationship between hypomania and emotional characteristics are about the human relationship interactions and quality of life to all involved; hence, perhaps some areas of research could re-visit case studies of affected individuals and their immediate relationships (Reeve, 2018, p. 20).