As described by Eysenck et al. (2007), Attentional Control Theory involves two systems of attentional control; one that is a top-down, goal directed system, and another that is a bottom-up stimulus-driven system. These two systems are supposed to interact and function together; however, under conditions of stress or worry in people with high trait anxiety, the balance is disrupted such that there is an increased influence of the stimulus-driven system and a decrease in the goal-directed system.
The goal-directed system of attentional control is a component of the central executive which is housed within the prefrontal cortex and includes three attentional functions; inhibition, shifting and working memory updating. As the influence of the stimulus-driven system disproportionately increases, it interferes with or impairs the ability of the central executive to ignore irrelevant stimuli, disengage from a primary stimulus to engage with something else, and to adaptively shift attentional control based on goal-relevant task demands (Eysenck et al., 2007).
Attentional control can also be impaired through chronic or repeated exposure to stress (Lupien et al., 2009). As these authors explain, when a threatening internal or external stimulus is detected, the amygdala, (responsible for processing fear), activates the hypothalamus-pituitary-adrenal axis which results in the production and release of stress hormones; glucocorticoids and catecholamines. While these hormones are designed to address and re-regulate the body’s physiological arousal state once the perceived stressor has subsided; there is an inverted U relationship between arousal and stress hormones such that too little or too many can impair pre-frontal cortex functioning (Lupien et al., 2009).
Long term exposure to adverse or traumatic environments; particularly during sensitive periods (prenatal, infancy, childhood, adolescence) can cause an over-firing of the amygdala in response to both real and conditioned threat associations (Lupien et al., 2009). As a result, functional and structural changes to various brain regions can occur. These include a decrease in the size, volume and activity of the prefrontal cortex and an increase in the size of the amygdala. Other changes include an altering of neural pathways and feedback loops between the pre-frontal cortex, the amygdala and other parts of the brain circuitry. ADHD symptoms such as inattentiveness, hyperactivity and impulsiveness are all associated with impaired attention control originating in the pre-frontal cortex (Gamo & Arnsten, 2011).
An example of a situation in which stress affected my attention was right at the start of a national or international ice or ball hockey game. Fear or worry about making a mistake and letting my teammates down sometimes caused me to have difficulty focussing on the game and really “seeing” what was happening while I was on the bench waiting to go on. Interestingly, I was usually fine once I was directly involved in the play although sometimes these feelings and accompanying distractibility resurface near the end of a close scoring game. This would be an example of state anxiety in which the internally perceived threat caused either a maladaptive narrowing of focus or an equally maladaptive diffusion of attention.
Stress on cognitive functioning can be mitigated through a variety of strategies depending on the specific area of functioning (attention, memory, learning etc.) and on the source of the stress. In the case of ADHD, a drug known as guanfacine has been shown to restore alpha-2A and D1 receptor stimulation leading to the strengthening working memory and impulse control while also reducing distraction (Gamo & Arnsten, 2011).
In my hockey example, a Sports Psychologist who worked with one of the teams I was on taught us to use visualization techniques in the dressing room right before we went out onto the ice.
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Gamo, N. J., & Arnsten, A. F. T. (2011). Molecular modulation of prefrontal cortex:
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Lupien, S. J., McEwen, B. S., Gunnar, M. R., & Heim, C. (2009). Effects of stress
throughout the lifespan on the brain, behaviour, and cognition. Nature Reviews
Neuroscience, 10(6), 434–445.