Not all children who have ADD or ADHD diagnoses have a stressful home and family environment. But some do. And then there is school. From a personal, adult perspective, many classrooms are found for young children to be exceedingly overstimulating. And I'm referring just to visual stimuli. Add in some audio and noise and stimulation increases dramatically. After school, children often return home to, you guessed it, watch television or play video games that make me dizzy. If a child is predisposed to have attention-deficit problems and/or genetically inclined, as we discuss above, to be vigilant, in my opinion, such an overabundance of stimuli is the last thing the child needs. a constant overabundance of stimuli could easily produce unfocused behavior that could be misinterpreted as attention-deficit hyperactivity disorder (ADHD). It is my opinion that, especially for vulnerable children and adults, high levels of stimulation, over time, is a form of stress, even when everybody else is doing it.
In "Stress Signalling Pathways That Impair Prefrontal Cortex Structure and Function", Amy F.T. Arnstem writes: "The same neurochemical events that impair prefrontal working memory abilities actually strengthen the emotional operations of the amygdala. Thus, uncontrollable stress switches control of behaviour from the thoughtful PFC to the more primitive conditioned responses of the amygdala." (See The amygdala, stress, OCD, and PTSD in Part 1 of CorticalBrain.com.)
In Part 1 of CorticalBrain.com, we discuss the frontal lobes in a general way and, more specifically, the orbital-frontal cortex (see The brain's frontal lobes and The orbital-frontal cortex). Now we turn our attention to what is called the prefrontal cortex, which is nicely illustrated in the image to the right (links to NIH source). Bear in mind that the prefrontal cortex includes the orbital-frontal cortex.
Regarding what she calls the prefrontal cortex, in "Stress Impairs Prefrontal Cortical Function" (1988) Amy F.T. Arnsten writes:
Neurochemical changes in the prefrontal cortex (PFC) during periods of stress may take this brain region "off-line," making the child less able to govern his behavior. The PFC is situated anterior to the motor cortices in the frontal lobe. It is much larger in primates than in other mammals. It continues to develop throughout adolescence. This region of our brains is critical for using "working memory," a form of memory that is required to appropriately guide behavior. Working memory has been called "scratch-pad" memory, because this type of memory must be constantly updated. Memories can be called up from long-term storage or from more recent buffers. The PFC uses these representations to effectively guide behavior, freeing us from responding only to our immediate environment, inhibiting inappropriate responses or distractions, and allowing us to plan and organize. Animals or humans with lesions to the PFC exhibit poor attention regulation, disorganized and impulsive behavior, and hyperactivity.
Arnsten succinctly explains the role of catecholamines in prefrontal cortex processing. She writes:
During stress exposure, catecholamines are released in both the peripheral and central nervous systems. In the periphery, the catecholamines norepinephrine and epinephrine are released from the sympathetic nervous system and adrenal gland, respectively. These catecholamine actions serve to "turn on" our heart and muscles and "turn off" the stomach to prepare for fight-or-flight responses during stress. In the brain, high levels of the catecholamines dopamine and norepinephrine are released in the PFC during stress exposure, even during relatively mild psychological stress. As basal levels of dopamine and norepinephrine have essential beneficial influences on PFC function, it was originally presumed that high levels of catecholamine release during stress might facilitate PFC function. However, research in monkeys and rats demonstrated the contrary: exposure to stress impairs the working memory functions of the PFC. These findings in animals are consistent with older literature demonstrating that humans exposed to loud noise stress are less able to sustain attention or to inhibit inappropriate responses, functions now known to be carried out by the PFC.
Arnsten points out that "Electrophysiological recordings similarly indicate that high levels of D1 receptor stimulation can interfere with PFC neuronal function." She explains that "Active neurochemical mechanisms to take the PFC 'off-line' during stress may have had survival value in evolution, allowing faster, instinctual mechanisms regulated by subcortical and posterior cortical areas to regulate behavior during stress. However, these brain actions may often be maladaptive in human society when we are in need of PFC regulation to act appropriately, e.g., in the classroom when behavior must be highly controlled."
The image to the left—illustrating normal brain activity during a task that activates working memory—is from an MRI connected with a supercomputer to create a three-dimensional image and links to source. It is from a webpage Pittsburgh Supercomputing Center developed titled "Watching the Brain in Action." The project's researchers include Jonathan Cohen, University of Pittsburgh and Carnegie Mellon University; Nigel Goddard, Pittsburgh Supercomputing Center; Bill Eddy, Carnegie Mellon University; and Doug Noll, University of Pittsburgh.
Based on Zahrt et al., "Supranormal Stimulation of D1 Dopamine Receptors in the Rodent Cortex Impairs Spatial Working Memory Performance" (1997), Arnsten writes: "Dopamine acting at D1 receptors in the prefrontal cortex (PFC) produces an inverted U dose response whereby either too little or too much D1 receptor stimulation impairs neuronal or cognitive function." She explains that "With insufficient D1 receptor stimulation, all signals are conveyed to the soma [nerve cell body], resulting in diffuse, unfocused information." On the other hand, with optimal levels of D1 receptor stimulation, "signal transfer is focused such that only the largest, coordinated signals are conveyed to the cell." This results in "optimal working memory and attention regulation." Arnsten writes: "At very high levels of D1 receptor stimulation such as during stress, calcium currents are blocked and signal transfer is abolished." Thus, an excessively high level of dopamine results in "poor working memory and attention regulation."
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