The learning mechanism underlying neurofeedback training for ADHD, as opposed to pharmacotherapy
Dr. Daniel Ben Eliezer Chief psychologist, Excellent Brain
Currently, the most common treatment for attention deficit disorder (ADHD) is pharmacological. As I mentioned in a previous article, the most common medications for ADHD are stimulants that delay the reabsorption of dopamine and norepinephrine at certain synapses in the brain, thus causing a stronger effect on attentional cycles. The most common drugs are methylphenidate (Ritalin, Concerta), and amphetamine (Vivans, Adderall, Attent). These drugs have a stimulant effect, that is, they cause overactivity of systems in the body, including stress-related systems and in some cases can cause side effects.
Delayed reabsorption in the synapse causes a longer effect remains in attention-related circuits, reinforcements and rewards and movement planning, so that these circuits operate in a longer and more efficient manner, reducing the gap between a person without ADHD and a person with ADHD. However, as drugs, their effect is for a limited number of hours, and do not solve the problem.
In contrast, neurofeedback focuses on strengthening areas of the brain related to attention, planning and initiating behavior, by providing the trainee with feedback on brain activity in these areas. These people are usually characterized by a slightly higher amount of low-frequency waves (theta), as well as a slightly lower amount of medium-frequency waves -High (beta), compared to situations of normal attention.
Brain imaging studies (MRI) have shown that after a long neurofeedback training process (about 30 sessions) in which an increase in beta frequencies was found, there was an increase in the amount of gray matter (neurons in the cortex) in different areas of the cerebral cortex. As well as an increase in the white matter that links between nerve cells – that is, the axons of nerve cells that carry information from the cell body to other cells) in attention-related circuits. (Ghaziri et al., 2013)
How exactly does this process occur? Although there is difficulty examining it today, it seems that using neurofeedback, the trainee continually activates areas of the brain involved in the attentional cycle, thus strengthening the connections between neurons by creating new synapses in the synaptogenesis process. This is a neurological explanation for Hebb’s hypothesis that activating areas of the brain at the same time will strengthen the connection between them.
Simultaneous neural activity in both the preceding “pre-synaptic” cells, which send axons to the synapses – the connecting regions – to the subsequent, the post-synaptic cells, causes long-term learning to occur. This process, called long term potentiation (LTP), involves the neurotransmitter glutamate, and AMPA and NMDA receptors, leading to the construction of new synapses parallel to the existing ones, so that in practice the connections between the regions in the attentional circles are strengthened and become durable over time.
The above description is well established in the literature of the neuroscience about the learning process. As for neurofeedback, since it cannot be reliably tested (most studies are conducted on rodents’ brain testing after learning processes, and neurofeedback is done in living humans). However, this is also the hypothesis suggested by Gaziri and colleagues (Ghaziri et al., 2013) as well as by Perry in her review ( Perry, 2015). Further hypothesizes that learning processes also improve neural conductivity (i.e. transport of electrically charged ions) along the axon by increasing the amount of fatty substance myelin, hence improving the conductivity of the axon (which also explains the thickening in the “white matter” in the brain).
reference:
Ghaziri, J. et al. (2013) Neurofeedback Training Induces Changes in White and Gray Matter. Clinical EEG and Neuroscience, 44: 1-7.
Perry, S. (2015). “How the Electrical Activity and Synaptogenesis of Neurons Contribute to the Efficacy of Neurofeedback Therapy.” Discussions, 11(1). Retrieved from http://www.inquiriesjournal.com/a?id=984
