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Self Regulation


Self regulation refers to the processes that enable a person to guide their goal directed activities or behaviours over time and across changing contexts. There is no universally agreed upon definition of self regulation. Many terms are used interchangeably with self regulation including freedom, autonomy, agency, willpower, voluntary action, self discipline, self control and intrinsic motivation. [1]

Components of Self Regulation

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In self regulation there are deliberate alterations to thought, affect, behaviour and attention through the use of specific mechanisms and metacognition.[1]

Self regulation can be thought of as a series of phases:

1. Goal Selection: First, one must select a goal from the available alternatives. When choosing a goal one must consider two things. First are self relevant factors, which refer to one’s own needs and motivations. Second are contextual factors, for instance time constraints or level of ability.[1]

2. Goal Cognition: One must also further consider a goal until it is more clearly specified, evaluated, organized and stored.[1] Setting clear goals is important because once one deviates too much from the original plan it is increasingly hard to get back on track again.[2]

3. Goal Striving/Self Monitoring: Once the goal has been set you must start performing behaviours that will lead to goal attainment. These could include initiating action, putting in effort, trying different strategies and persisting in the face of obstacles.[3] Self monitoring will be used to try to attain greater self awareness of both internal and external cues that could lead to behaviours that compromise the goal. This will lead to faster and more appropriate control over one’s mental state and faster implementation of intervention strategies so that goals are not compromised. The degree of conscious and automatic control for a given cue will vary from person to person; some people will just be better self monitors than others. [2]

4. Goal Evaluation/Termination: In this stage one evaluates whether their goal is still feasible or desirable. They may make changes to their goal or select a new goal. If the goal has been reached or if it is no longer desired it will be terminated.[3]

Neural Substrates

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In day to day life an organism values many goals at a given time; this makes it necessary to select which goals to pursue. In order to represent goals mentally, assign a value to them, and select actions on how to go about pursuing them we rely on the prefrontal cortex and related brain areas. Completion of a goal requires a complex sequence of actions that require motivation in order to ignore distractions and overcome obstacles. This requires cognitive control that depends on the active maintenance and reassessment of goal representations in the prefrontal cortex. [4]

Orbitofrontal Cortex (OFC)

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The OFC is implicated in playing a key role in processing reward. Information from various sources regarding the outcomes of reward are integrated by the OFC to determine which reward is most beneficial in satisfying our needs, or in other words, determining how rewarding a reward is. This is a preliminary step in self-regulation as it helps to guide a person toward behaviour actions that will lead to the most desirable outcome. It is related to the 'Goal Selection' phase mentioned above.

Working memory then store the information, which is later accessed by the lateral prefrontal cortex to plan and organize behaviour toward obtaining the outcome. The medial prefrontal cortex then evaluates the overall action in terms of its success and the effort that was required, thus implicating learning either for improvement in achieving a future goal or for changing or redefining a goal. [5]

Dorsolateral Prefrontal Cortex (DL-PFC)

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The DLPFC plays a role in working memory. It is involved in situations when it is necessary to mentally plan and prepare for a predictable sequence of actions, based on the information in short term memory.[6] The DLPFC is also involved in multi-tasking, as well as in representing and maintaining the attention required for the demands of the task.[7] It is related to the ‘Goal Striving/Self Monitoring’ phase mentioned above. In order to regulate your actions appropriately, one must continually be aware of internal mental states and external stimuli available to you that may affect the completion of a goal. [2]

Anterior Cingulate Cortex (ACC)

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The ACC may be involved in evaluative processes, such as monitoring the occurrence of errors or the presence of response conflict, which occurs when two different responses are both appealing. This function in monitoring errors and response conflicts is necessary in order to provide feedback so that better strategic processes can be used to customize behaviour accordingly. [7] This is related to the ‘Goal Evaluation/Termination’ phase mentioned above. In order to self regulate effectively, one must look back and evaluate if the goal that was originally set was met, if it has yet to be achieved, if it needs to be reevaluated, or if it is any longer relevant.[3]

Neuroimaging Tools

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The neuroimaging tools commonly used in cognitive neuroscience are used to determine possible correlations between changes in neuronal activity, blood flow and/or glucose metabolism in specific regions of the brain, and the corresponding behaviours and psychological processes which may offer insight into causal relationships and treatments for diagnosable psychological disorders. These neuroimaging tools are commonly used when measuring changes in brain activation during tasks involving self-regulation, such as goal seeking, decision making, and error evaluation.

Single-Photon Emission Computed Tomography (SPECT): A radioactive tracer is injected into the bloodstream and directly emits gamma rays in regions of neuronal activity or increased blood flow.[8]

Positron Emission Tomography (PET): A radioactive tracer is injected into the bloodstream. As it decays it releases a positron, which travels in the tissue a few millimeters before colliding with an electron. This results in the emission of two gamma rays travelling in oposite directions which are then registered by detectors placed near the head. The tracer will emit a greater signal in areas of the brain with high regional cerebral blood flow, indicating increased glucose metabolism and subsequently, increased neuronal activity in that region. [9]

Functional Magnetic Resonance Imaging (fMRI): Uses standard MRI equipment, and the MR signal is sensitive to the amount of deoxyhaemoglobin in the blood. Neurons consuming oxygen convert oxyhaemolglobin to deoxyhaemoglobin, which produces distortions in the magnetic field, and indicates the concentration of deoxyhaemoglobin in the blood. BOLD (blood-oxygen-level-dependent contrast) evolves in response to an increase in neuronal activity, and is termed the haemodynamic response function (HRF).[10]

Brain Reward Circuit

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An integral part of self-regulation is knowing and evaluating which goals or goal directed behaviours are worth pursuit. The reward circuit provides vital feedback to self-regulation as it provides cues as to which actions to initiate or inhibit in order to reach a goal. The reward circuit will also be affected in disorders of self regulation.

In order for an organism to survive it must obtain resources despite the risks involved. To make this challenge more appealing, ‘natural goals’ (i.e. food, shelter, consummation) act as rewards. That is, an organism anticipates that obtaining food will lead to a positive desired outcome (it will ease their hunger, it will make them feel better). Internal motivational states (hunger, thirst, sexual arousal) increase the incentive for an organism to achieve its goal. Additionally, external cues, such as the sight or smell of food, can initiate motivational states. The stronger the incentive, the stronger the pleasure involved with goal obtainment will be (food always tastes better when you are hungry). Additionally, an organism finds the action itself (eating) rewarding, as well as the actual reward. Thus, behaviours are automatically positively reinforcing, this means that the behaviours will not be easily given up and will increase over time.[4]

The following brain areas are implicated in the reward circuit:

Medial Forebrain Bundle (MFB): Is a loosely strung together fiber system that runs adjacent to the lateral hypothalamus. This is where the nerve fibers that make up the reward circuit are located. [11]

Ventral Tegmental Area (VTA): Axons of dopaminergic neurons run through the MFB to the VTA. Neurons from here project the neurotransmitter dopamine to the nucleus accumbens, as well as to other areas such as the prefrontal cortex and the amygdala. [4] Dopamine is released from the VTA in response to a motivationally relevant event. The release of dopamine signals the reward circuit to initiate behavioral responses to the event and by doing so creates neuronal changes. By this process the organism learns associations between the event and relevant behaviours. This will be adaptive if the organism ever encounters the event again.[12]

Nucleus Accumbens: Eighty percent of dopaminergic neurons from the VTA project to the nucleus accumbens. [13] The VTA uses dopamine to regulate the activity of nucleus accumbens. [4] Research proposes that the nucleus accumbens is involved in generating conditioned responses and in consolidating memory related to conditioned responses based on an association between stimulus and outcome. [14]

Dopamine: Dopamine is involved in learning the conditioned response. Evidence for this comes from studies where the learning ability of rats is severely disabled if they are injected with a dopamine antagonist (a drug that block dopamine receptors) before a learning session begins. [14]

Disorders of Self Regulation

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Drug Addiction

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Addiction can be seen as the pathological narrowing of goal selection to those that are only related to a maladaptive behaviour. [4]It is a chronically relapsing disorder. It is defined by a compulsion to take drugs until the behaviours engaged in narrow to those only involved with drug taking, as well as a loss of control in limiting the amount of drugs taken. Addicts feel controlled by overwhelming emotional states and compulsions to use drugs, and they are not dissuaded by memories of the negative effects of their drug taking in the past.

A failure to self regulate drug use on one occasion can lead to emotional distress, this distress leads to further failure in self regulation, which makes the person feel worse or more distressed. This is sometimes called ‘spiraling distress cycle’ and can lead to the progressive deregulation of the reward circuit. The spiraling distress cycle has three components:

Binge Intoxication: Positive reinforcement effects are the rewarding and pleasurable effects the drugs have on a person. There is incentive to perform behaviours in order to obtain something desirable. Positive reinforcement is said to occur when the presentation of a drug increases the probability of behaviour to obtain the drug. This leads to binge intoxication and abuse of a substance. This component of the cycle is shown by activation of dopaminergic and opioid peptide systems.

Withdrawal Negative Affect: Negative reinforcement effects are the rewarding effects that drugs have in alleviating an aversive state caused by drugs (withdrawal). There is motivation to perform behaviours in order to discard something undesirable. This leads to further abuse of a drug. This component of the cycle is shown by decrease in dopamine and opioid peptide function and increased activity in brain stress systems.

Preoccupation-Anticipation: Both the positive and negative reinforcement condition a person until they get to a stage where their only motivation is to obtain and use the substance. This stage is also characterized by craving, which is an intense desire or need for the substance. [15]

Dopamine Hypothesis

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The current explanation of why self regulation of drug use is such a struggle is that the rewarding properties of addictive drugs largely depend on their ability to increase dopamine in the midbrain. This effects the reward circuit as dopamine is integral to the correct functioning of the ventral tegmental area (VTA) and the nucleus accumbens.[4] PET imaging studies have shown that the positive reinforcing effects of drugs are associated with large increases in dopamine.[16] Generally, addictive drugs in a sense mimic natural rewards by releasing dopamine into the nucleus accumbens and thus promote reward learning, and shape behaviour, despite the fact that drugs have no intrinsic ability to benefit a person’s biological needs.[4]

The dopamine hypothesis also explains the phenomenon of drug tolerance. Dopamine cells only fire in response to salient stimuli, and drug use is considered highly salient, but with long-term drug use the threshold required for dopamine release is raised and so more cell activation is required in order to increase dopamine levels. PET studies have shown that long-term drug users show decreased activation in dopamine release in the orbitofrontal cortex (which is involved in attributing saliency), the cingulate gyrus (involved in inhibitory control) and the dorsolateral prefrontal cortex (involved in executive function).[16] This could explain lack of regulation over drug intake. Additionally, dopamine is also said to affect the activation of memory circuits including the amygdala, hippocampus, and dorsal striatum, all of which are implicated in habit learning. [17]

It is important to note that addictive substances do not have to use dopamine channels in order to be effective. For instance, opioids especially, through the neurotransmitter norepinephrine may act directly on the nucleus accumebms to produce reward learning.[4]

Eating Disorders and OCD

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Many people suffer from disorders that involve abnormalities in the normal functioning of self-regulation. Eating disorders and anxiety disorders are characterized by problems in normal thought processing, often involving brain regions typically associated with self-regulation.

Individuals with anorexia nervosa and bulimia nervosa suffer from a distorted body image and harbour a strong fear of gaining weight or becoming fat, causing them to maintain a dangerously thin, unhealthy figure.[18] Studies have employed the use of single-photon emission computer tomography (SPECT), positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) to analyze which neural circuits and brain regions are active in patients with anorexia. Using SPECT, in comparison to control groups, decreased blood flow to regions such as the frontal cortex, parietal cortex and anterior cingulate cortex was seen in anorexics. [19] This decreased regional cerebral blood flow (rCBF) is also evident in recovered anorexics after weight gain. [18] Decreases in perfusion, or the flow of blood to regions of the brain, were observed in frontal regions, such as the dorsolateral prefrontal cortex before weight gain, and in the orbitofrontal cortex and right dorsolateral prefrontal cortex after weight gain.[18] Functional neuroimaging studies have found an association with the orbitofrontal cortex in the evaluation of punishment and whether changing behaviour is desirable. Their goals are distorted as they are driven towards maintaining an unhealthy bodyweight and avoidance of gaining any body fat.

Anxiety disorders such as obsessive-compulsive disorder (OCD) are often associated with patients who suffer from eating disorders. Individuals with OCD have unwanted, recurrent thoughts and engage in repetitive behaviours, and the worry they experience is far greater than the actual threat.[19] Studies involving PET found that similar neurological abnormalities were exhibited in OCD in comparison to anorexia, including increased glucose metabolism in the orbitofrontal cortex and anterior cingulate cortex. It has been hypothesized that the abnormal processing observed in anxiety disorders such as OCD stems from dysfunction of the corpus striatum, which disrupts normal processing of sensory information in the thalamus, leading to an increased activity level in the orbitofrontal cortex. This hyperactivity in the orbitofrontal cortex is thought to be responsible for the unwanted thoughts that patients with OCD suffer from, and the accompanying anxiety is thought to be a result of the hyperactivity of the anterior cingulate cortex.[19]

In addition, the prefrontal cortex is tightly regulated with other brain regions that are involved in motivation and emotion, which may account for the associated psychological disorders that may arise from or co-occur with these conditions, such as depression. Since the prefrontal cortex is implicated in decision making and error evaluation, individuals with anorexia and/or obsessive compulsive disorder exhibit altered decision making behaviour, as they are able to suppress or unable to control normal decision making abilities, respectively.

See Also

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Working Memory

Metacognition

Self Control

Issues In fMRI

Social Neuroscience

Reinforcement

References

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  1. ^ a b c d Karoly, P. (1993). Mechanisms of self regulation: a systems review. Annual Review of Psychology, 44, 23-52.
  2. ^ a b c Behncke, L. (2002). Self-Regulation: A Brief Review. Athletic Insight. The Online Journal of Sport Psychology, 4 (1). http://www.athleticinsight.com/Vol4Iss1/SelfRegulation.htm.
  3. ^ a b c Kanfer R., Chen, G., & Pritchard, R.D (Eds). (2008). Work motivation, past, present and future. Taylor and Francis Group, New York: NY.
  4. ^ a b c d e f g h Hyman, S.E. (2005). Addiction: a disease of learning and memory. American Journal of Psychiatry 162, 1414-1422.
  5. ^ Wallis, J.D. (2007). Orbitofrontal Cortex and Its Contribution to Decision-Making. Annual Review of Neuroscience, 30, 31-56.
  6. ^ Pochon, J.B., Levy, R., Poline, J.B., Crozier, S., Lehéricy, S., Pillon, B., Deweer, B., Le Bihan, D. & Dubois, B. (2001). The Role of Dorsolateral Prefrontal Cortex in the Preparation ofForthcoming Actions: an fMRI Study. Cerebral Cortex, 11, 260-266.
  7. ^ a b MacDonald, A., Cohen, J.D., Stenger, A. & Carter, C. (2000). Dissociating the Role of the Dorsolateral Prefrontal and Anterior Cingulate Cortex in Cognitive Control. Science, 288,1835-1838.
  8. ^ Knoll, G.F. (1983). Single-photon emission computed tomography. Proc. of the IEEE, 71 (3), 320-329.
  9. ^ Lammertsma,A, A. (1992). Positron emission tomography. Brain Topography, 5 (2), 113-117.
  10. ^ Logothetis. N.K., Pauls, J., Augath, M., Trinath, T., & Oeltermann A. (2001). Neurophysiological investigation of the basis of the fMRI signal. Nature 412, 150–157.
  11. ^ Veening, J.G., Swanson, L.W., Maxwell Cowan, W., Nieuwenhuys, R., & Geeraedts, L.M.G. (1982). The Medial Forebrain Bundle of the Rat. 11. An Autoradiographic Study of the Topography of the Major Descending and Ascending Components. The Journal of Comparative Psychology. 206, 82-108.
  12. ^ Nestler, E.J., & Chao, J. (2004). Molecular Neurobiology of Drug Addiction. Annual Review of Medicine, 55, 113-132.
  13. ^ Swanson, L.W. (1982). The projections of the ventral tegmental area and adjacent regions: a combined fluorescent retrograde tracer and immunofluorescence study in the rat. Brain Research Bulletin, 9 (1-6), 321-53.
  14. ^ a b Ikemoto, S. (2007). Dopamine reward circuitry: Two projection systems from the ventral midbrain to the nucleus accumbens–olfactory tubercle complex. Brain Research Review, 56, 27-78.
  15. ^ Koob, G.F., Moal, M.L. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 21 (2), 97-129.
  16. ^ a b Volkow, N.D., Fowler, J.S., Wang, G.J., Baler, R., & Telang, F. (2009). Imaging dopamine’s role in drug abuse and addiction. Neuropharmacology, 56 (1), 3-8.
  17. ^ Volkow, N.D., Fowler, J.S, Wang, G.J., Goldstein, R.Z. (2002). Role of dopamine, the frontal cortex and memory circuits in drug addiction: insight from imaging studies. Neurobiology of Learning and Memory, 78 (3). 610-624.
  18. ^ a b c Kuyck, K., Gérard, N., Laere G.V., Casteels, C., Pieters, G., Gabriëls, L. & Nuttin, B. (2009). Towards a neurocircuitry in anorexia nervosa: Evidence from functional neuroimaging studies. Journal of Psychiatric Research, 43, 1133–1145.
  19. ^ a b c Kraly, F.S. (2009). The Unwell Brain. New York (NY): W.W. Norton & Company.
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