Categories: Generelt

ADHD: WTF is Emotional Dysregulation?

Emotional Dysregulation has become the talk of the town, but what is it, and why should we with ADHD even care about it? Well, it’s a pretty essential part of our symptomatology, so we’ve better get a handle on it.

Emotional Dysregulation has become the talk of the town, but what is it, and why should we with ADHD even care about it? Well, it’s a pretty essential part of our symptomatology, so we’ve better get a handle on it.

It is used both for salutation and valediction. Namaste is usually spoken with a slight bow and hands pressed together, palms touching and fingers pointing upwards, thumbs close to the chest. This gesture is called Añjali Mudrā or Pranamasana. In Hinduism, it means “I bow to the divine in you”.

Here’s a few random quotes from Google:

Emotional dysregulation (ED) is a term used in the mental health community to refer to an emotional response that is poorly modulated, and does not fall within the conventionally accepted range of emotive response.”

Emotional dysregulation refers to the inability of a person to control or regulate their emotional responses to provocative stimuli. It can also be termed “emotional hyperreactivity.”

Emotional dysregulation is characterized by difficulty in the regulation of emotional responses and behavior.”

Emotional dysregulation (ED), also called ‘emotional hyperactivity’, means that you are more emotionally responsive than an average person. Your emotions will be triggered more quickly, and will tend to be on a bigger scale. You also have more difficulty controlling your emotions than others do. Your might often feel taken over and lost in your emotional states.”

So what to so then …?

As you can see, everyone is talking about Emotional Dysregulation, but few agree on what it actually is, right? The above quotes are littered with subjective definitions that are created to fit subjective agendas.

So I thought that I’d might have to ‘go down the rabbit hole’ and see if I could provide an ADHD-friendly definition, since ED is becoming more and more – reintroduced – as a core symptom of ADHD.


Defining Emotional Dysregulation in ADHD

Dr. Russell A. Barkley, Ph.D., who wrote the unifying theory of ADHD back in 1997, which is today the foundation of our collective knowledge of ADHD, have since then tried to get Emotional Dysregulation (back) into the symptomatology of ADHD, but to no prevail in DSM-5, in ICD-11 though, it seems to have been adopted, but time will tell in 2022.

On the historical background of ED, Dr. Barkley writes: […] ADHD is currently understood to be a disorder of inattention, impulsivity, and usually hyperactivity that arises in childhood or early adolescence and is highly persistent over time in most cases. However, since the first medical papers have been published on ADHD starting in 1798, emotion has always been included in the conceptualization of the disorder up through the 1970s. But beginning with DSM-II and progressing to the present, emotional dysregulation has been excluded from the clinical conceptualization of the disorder and the diagnostic criteria and relegated to an associated problem or the result of comorbid disorders. This presentation reviews the evidence from the history, neuropsychology, neuro-anatomy, and observational research that shows that emotional impulsiveness and deficient emotional self-regulation are an integral part of ADHD. Returning emotion to its rightful place as a core feature of the disorder also serves to better explain the development of comorbid disorders, such as oppositional defiant disorder, and well as various life course impairments. […] (Barkley, R. A. (Ed.). (2015). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed.). New York, NY, US: Guilford Press.)

Dr. Barkley comments on the focusing on symptoms of ADHD as being simply hyperactivity, impulsivity, and inattentiveness …

“Here I argue that this overemphasis on the most observable and objectively measurable features of the disorder has led to the exclusion or a deemphasis of another feature of the disorder that is just as central to its understanding yet considerably more difficult to quantify.”

Barkley, R. A. (Ed.). (2015). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed.). New York, NY, US: Guilford Press.

This [Emotional Dysregulation] largely neglected element is a deficiency in both the effortful (executive or cognitive) inhibition and the top-down self-control of emotions in general and particularly those pertaining to the self-regulation of frustration, impatience, and anger.

Barkley, R. A. (Ed.). (2015). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed.). New York, NY, US: Guilford Press.

“The most noticeable and initial consequence of this deficiency in people with ADHD is a striking propensity for failure to inhibit emotions, or emotional impulsivity (EI). EI refers to the quickness or speed with which, and the greater likelihood that an individual will react with primary (particularly negative) emotions in response to events compared to others of the same developmental level or age.

Barkley, R. A. (Ed.). (2015). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed.). New York, NY, US: Guilford Press.

“It is not the same as emotional intensity, which itself can vary across individuals and is not thought to be a problem in those with ADHD. The primary emotional reactions of those with ADHD are not so much more intense initially as they are less moderated by conscious, effortful executive self-regulation of those emotions.”

Barkley, R. A. (Ed.). (2015). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed.). New York, NY, US: Guilford Press.

The scientific evidence

Shaw et al., 2014: […] It has long been recognized that many individuals with ADHD also have difficulties with Emotional Dysregulation but lack of consensus on how to conceptualize this clinically challenging domain renders a review timely. We examined the current literature using both quantitative and qualitative methods. Three key findings emerge: First, Emotional Dysregulation is prevalent in ADHD throughout the lifespan and is a major contributor to impairment. Second, Emotional Dysregulation in ADHD may arise from deficits in orienting towards, recognizing and/or allocating attention to emotional stimuli; these deficits that implicate dysfunction within a striato-amygdalo-medial prefrontal cortical network. Third, while current treatments for ADHD often also ameliorate Emotional Dysregulation, a focus on this combination of symptoms reframes clinical questions and could stimulate novel therapeutic approaches. […] (Shaw et al., 2014)

Shaw et al., 2014 continues with […] Three models to explain the overlap between Emotional Dysregulation and ADHD are considered: Emotional Dysregulation and ADHD are correlated but distinct dimensions; Emotional Dysregulation is a core, diagnostic feature of ADHD; and the combination constitutes a nosological entity, distinct from both ADHD and Emotional Dysregulation alone. […] (Shaw et al., 2014)

Summary of Emotional Dysregulation

Emotional Dysregulation have been a part of the symptomatology since at least 1798, but have been disregarded during the earlier editions of the DSM. The focus on the results (hyperactivity, impulsivity, and inattentiveness) instead of the underlying root cause, delayed maturation of the Inhibitory Control, which causes an dysfunction in […] the sensory predictions [which] arise from motor predictions; simulations [which] arise as a function of visceromotor predictions (to control your autonomic nervous system, your neuroendocrine system, and your immune system) and voluntary motor predictions, which together anticipate and prepare for the actions that will be required in a moment from now […] (Barrett, 2017).

What this means, it that Emotional Dysregulation is symptom which is a result of the the underlying dysfunction in sensory predictions, which is made by your Amygdala, by stitching sensory predictions from your body, to the rest of the system, including the prefrontal cortex, where our Executive Functions (EF) live. Since EF is majorly impaired in ADHD, the term ‘garbage in – garbage out’ may be appropriate to describe why ADHD causes Emotional Dysregulation.

ADHD is a specific developmental disorder, meaning that it primarily affect specific areas of functioning (e.g. Executive Functions). But still, the brain is dependent on the ‘garbage in’ to try to make sense of the world outside, and since any process needs a good input to work optimally, so does our brain, and when it gets ‘garbage in’ it will almost certainly be more prone toward sending ‘garbage out’ – Emotional Dysregulation is the result of this.

The key point to take home is, that Emotional Dysregulation is just as involuntary as the rest of the core symptoms of ADHD, since the underlying causes relates to deficits in the anatomical and physiological systems, which then affects the psychological and behavioral symptoms, out of cognitive, voluntary control.

Let’s call it ‘an emotional tic’, since involuntary motor movements and involuntary emotional self-control must be recognized as comparative deficits.

/ADDspeaker


Additional information on emotions

The ‘theory of constructed emotion’ (Barrett, 2017) proposes that emotions should be modeled holistically, as whole brain-body phenomena in context.

In other words, allostasis (predictively regulating the internal milieu) and interoception (representing the internal milieu) are at the anatomical and functional core of the nervous system. 

Barrett (2017)

[…] My key hypothesis is that the dynamics of the default mode, salience and frontoparietal control networks form the computational core of a brain’s dynamic internal working model of the body in the world, entraining sensory and motor systems to create multi-sensory representations of the world at various time scales from the perspective of someone who has a body, all in the service of allostasis. […]

[…] These insights offer a range of new hypotheses—e.g. that reappraisal and other regulation processes are accomplished with predictions that categorize sensory inputs and control action with concepts. […]

The theory of constructed emotion also views the distinction between the central and peripheral nervous systems as historical rather than as scientifically accurate.

Barrett (2017)

[…] For example, ascending interoceptive signals bring sensory prediction errors from the internal milieu to the brain via lamina I and vagal afferent pathways, and they are anatomically positioned to be modulated by descending visceromotor predictions that control the internal milieu. […]

[…] This suggests the hypothesis that concepts (i.e. prediction signals) act like a volume dial to influence the processing of prediction errors before they even reach the brain. […]

[…] This provides new hypotheses about the chronification of pain that considers pain and emotion as two sides of the same coin, rather than separate phenomena that influence one another. […]

Barrett (2017)

Emotions are constructions of the world, not reactions to it

Barrett (2017)

This insight is a game changer for the science of emotion. It dissolves many of the debates that remained mired in philosophical confusion

Barrett (2017)

[…] It provides a common framework for understanding mental, physical, and neurodegenerative disorders, and collapses the artificial boundaries between cognitive, affective, and social neurosciences. […]

[…] Ultimately, the theory of constructed emotion equips scientists with new conceptual tools to solve the age-old mysteries of how a human nervous system creates a human mind. […]


Understanding how emotion works …

In 2017, Barrett, LF., published a hypothesis called “The theory of constructed emotion: an active inference account of interoception and categorization” which is a fascinating read, so I’ve selected some references from the article on PMC, to give some intriguing insights into our emotional experiences.

What is a brain?

A brain is a network of billions of communicating neurons, bathed in chemicals called neurotransmitters, which permit neurons to pass information to one another. The firing of a single neuron (or a small population of neurons) represents the presence or absence of some feature at a moment in time.

However, a given neuron (or group of neurons) represents different features from moment to moment because many neurons synapse onto one (many-to-one connectivity), and a neuron’s receptive field depends on the information it receives (i.e. depends on its neural context in the moment.

Conversely, one neuron also synapses on many other neurons (one-to-many connectivity) to help implement instances of different psychological categories. As a consequence, neurons are multipurpose, even in subcortical regions like the amygdala.

How does a brain perform allostasis?

For a brain to effectively regulate its body in the world, it runs an internal model of that body in the world.

In psychology, we refer to this modeling as ‘embodied simulation’. An internal model is metabolic investment, implemented by intrinsic activity that, in humans, occupies 20% of our total energy consumed.

Given these considerations, modeling the world ‘accurately’ in some detached, disembodied manner would be metabolically reckless. Instead, the brain models the world from the perspective of its body’s physiological needs.

As a consequence, a brain’s internal model includes not only the relevant statistical regularities in the extrapersonal world, but also the statistical regularities of the internal milieu.

Collectively, the representation and utilization of these internal sensations is called ‘interoception’. Recent research suggests that interoception is at the core of the brain’s internal model and arises from the process of allostasis.

Interoceptive sensations are usually experienced as lower dimensional feelings of affect. As such, the properties of affect — valence and arousal —are basic features of consciousness that, importantly, are not unique to instances of emotion.

All animals run an internal model of their world for the purpose of allostasis (i.e. the notion of an internal model is species-general). Even single-celled organisms that lack a brain learn, remember, make predictions, and forage in service to allostasis.

The content of any internal model is species-specific, however, including only the parts of the animal’s physical surroundings that its brain has judged relevant for growth, survival and reproduction (i.e. a brain creates its affective niche in the present based on what has been relevant for allostasis in the past).

Everything else is an extravagance that puts energy regulation at risk

Barrett (2017)

As an animal’s integrated physiological state changes constantly throughout the day, its immediate past determines the aspects of the sensory world that concern the animal in the present, which in turn influences what its niche will contain in the immediate future. This observation prompts an important insight: neurons do not lie dormant until stimulated by the outside world, denoted as stimulus→response.

Ample evidence shows that ongoing brain activity influences how the brain processes incoming sensory information (e.g. and that neurons fire intrinsically within large networks without any need for external stimuli.

The implications of these insights are profound: namely, it is very unlikely that perception, cognition, and emotion are localized in dedicated brain systems, with perception triggering emotions that battle with cognition to control behavior. 

This means classical accounts of emotion, which rely on this S→R narrative, are highly doubtful.

(Barrett 2017)

What is a brain for?

A brain did not evolve for rationality, happiness or accurate perception

Barrett (2017)

All brains accomplish the same core task: to efficiently ensure resources for physiological systems within an animal’s body (i.e. its internal milieu) so that an animal can grow, survive and reproduce. This balancing act is called ‘allostasis’. Growth, survival and reproduction (and therefore gene transmission) require a continual intake of metabolic and other biological resources. Metabolic and other expenditures are required to plan and execute the physical movements necessary to acquire those resources in the first place (and to protect against threats and dangers).

Allostasis is not a condition of the body, but a process for how the brain regulates the body according to costs and benefits; ‘efficiency’ requires the ability to anticipate the body’s needs and satisfy them before they arise.

An animal thrives when it has sufficient resources to explore the world, and to consolidate the details of experience within the brain’s synaptic connections, making those experiences available to guide later decisions about future expenditures and deposits.

Too much of a resource (e.g. obesity in mammals) or not enough (e.g. fatigue) is suboptimal. Prolonged imbalances can lead to illness that remodels the brain and the sympathetic nervous system, with corresponding behavior changes.

Whatever else your brain is doing — thinking, feeling, perceiving, emoting — it is also regulating your autonomic nervous system, your immune system and your endocrine system as resources are spent in seeking and securing more resources.

Barrett (2017)

All animal brains operate in the same manner (i.e. even insect brains coordinate visceral, immune and motor changes.

This regulation helps explain why, in mammals, the regions that are responsible for implementing allostasis (the amygdala, ventral striatum, insula, orbitofrontal cortex, anterior cingulate cortex, medial prefrontal cortex (mPFC), collectively called ‘visceromotor regions’) are usually assumed to contain the circuits for emotion.

In fact, many of these visceromotor regions are some of the most highly connected regions in the brain, and they exchange information with midbrain, brainstem, and spinal cord nuclei that coordinate autonomic, immune, and endocrine systems with one another, as well as with the systems that control skeletomotor movements and that process sensory inputs.

Therefore these regions are clearly multipurpose when it comes to constructing the mental events that we group into mental categories.

An internal model is predictive, not reactive

An increasingly popular hypothesis is that the brain’s simulations function as Bayesian filters for incoming sensory input, driving action and constructing perception and other psychological phenomena, including emotion.

Simulations are thought to function as prediction signals (also known as ‘top-down’ or ‘feedback’ signals, and more recently as ‘forward’ models) that continuously anticipate events in the sensory environment. This hypothesis is variously called predictive coding, active inference, or belief propagation.

Without an internal model, the brain cannot transform flashes of light into sights, chemicals into smells and variable air pressure into music. You’d be experientially blind. Thus, simulations are a vital ingredient to guide action and construct perceptions in the present.

They are embodied, whole brain representations that anticipate (i) upcoming sensory events both inside the body and out as well as (ii) the best action to deal with the impending sensory events. Their consequence for allostasis is made available in consciousness as affect.

I hypothesize that, using past experience as a guide, the brain prepares multiple competing simulations that answer the question, ‘what is this new sensory input most similar to?’.

Similarity is computed with reference to the current sensory array and the associated energy costs and potential rewards for the body.

That is, simulation is a partially completed pattern that can classify (categorize) sensory signals to guide action in the service of allostasis.

Each simulation has an associated action plan 

Barrett (2017)

Using Bayesian logic, a brain uses pattern completion to decide among simulations and implement one of them, based on predicted maintenance of physiological efficiency across multiple body systems (e.g. need for glucose, oxygen, salt etc.).

From this perspective, unanticipated information from the world (prediction error) functions as feedback for embodied simulations (also known as ‘bottom-up’ or, confusingly, ‘feedforward’ signals).

Error signals track the difference between the predicted sensations and those that are incoming from the sensory world (including the body’s internal milieu). Once these errors are minimized, simulations also serve as inferences about the causes of sensory events and plans for how to move the body (or not) to deal with them.

By modulating ongoing motor and visceromotor actions to deal with upcoming sensory events, a brain infers their likely causes. Their consequence for allostasis is made available in consciousness as affect.

Barrett (2017)

In predictive coding, as we will see, sensory predictions arise from motor predictions; simulations arise as a function of visceromotor predictions (to control your autonomic nervous system, your neuroendocrine system, and your immune system) and voluntary motor predictions, which together anticipate and prepare for the actions that will be required in a moment from now.

These observations reinforce the idea that the stimulus→response model of the mind is incorrect.

For a given event, perception follows (and is dependent on) action, not the other way around.

Therefore, all classical theories of emotion are called into question, even those that explain emotion as iterative stimulus →response sequences.


I can highly recommend this article for in-depth understanding.

References

Barrett LF., (2017), The theory of constructed emotion: an active inference account of interoception and categorization., Soc Cogn Affect Neurosci. 2017 Jan 1;12(1):1-23. doi: https://dx.doi.org/10.1093/scan/nsw154, Erratum in: Soc Cogn Affect Neurosci. 2017 Nov 1;12(11):1833. PMID: 27798257, PMC: 5390700

Shaw, P., Stringaris, A., Nigg, J., & Leibenluft, E. (2014). Emotion dysregulation in attention deficit hyperactivity disorder. The American journal of psychiatry, 171(3), 276–293. doi: 10.1176/appi.ajp.2013.13070966

Barkley, R. A. (Ed.). (2015). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (4th ed.). New York, NY, US: Guilford Press.

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