Among the many questions I fielded at the BFE Meeting in Venice, a large number came from individuals looking to know more about slow cortical potentials. Much of this was due to Dr. Ute Strehl's 2-day workshop on slow cortical potentials. If anyone ever has the chance to sit in on a talk by Dr. Strehl, I would highly recommend them to do so.
Slow cortical potentials (SCPs) are not particularly a topic for novice clinicians. Making sense of the underlying source of SCPs can be a little difficult. In terms of their functional measurement, it's an additional hurdle to overcome for collecting a clean signal and timing the training with the client correctly. We at the BFE have had several clinicians new to neurofeedback embark on the journey of SCPs for research at their university or clinical application in their private practice. I'm happy to report that each group that has reached out to us for guidance through our online class has attained their goals for using SCPs.
We thought it might be useful to review the basic concepts related to the nature of SCPs, for anyone that might be considering adding this EEG technique to their clinic. For those that are looking for more in-debt explanations, feel free to look up articles by Dr. Ute Strehl and Dr. Niels Birbaumer. Recommended articles have been added to the end of this post.
What are slow cortical potentials?
Slow cortical potentials are slow event-related, direct-current shifts in the EEG, originating from the large cell assemblies in the upper cortical layer. Let's break that previous, information-dense sentence down. SCPS are:
- Slow. In terms of speed, they can occur from 300 milliseconds to over several seconds. Compared to most EEG activity that is monitored for neurofeedback, that is a very long time. Equipment for measurement of SCPs must be specialized to collect these longer changes, and needs to average the activity from many trials to gain an overall trend of the EEG activity.
|Example of SCP average of activation and inhibition. Note - this image is generated by a subject that is not yet used to SCP training.
- Event-related potentials. This means there are changes in EEG activity based on responses to events. If an image or sound is presented to an individual, the presentation of the stimulus will cause a change in the brain's potential, as a reaction to the stimuli. Interestingly, this change in potential can be of exogenous origins (reaction to a presented external stimulus) or endogenous origins (reaction to expectation of stimuli). The brain reacting to the expectation of a stimulus, without actually being presented the stimulus, means the change in event related potential can be consciously generated at will. If it can be generated at will, it can be trained.
- Direct current shifts in EEG. SCPS are general measures of electrical activity. The vast majority of neurofeedback is based on measuring subsets of the EEG activity, divided into bandwidth frequencies (such as Theta, Alpha, Beta). The SCP signal however is general electrical activity in amplitude. These changes are weak shifts so it is necessary to run many trials to get an overall trend in activity.
- Originate from large cell assemblies in the upper cortical layers. The thalamo-cortical system acting as a "neuronal pacemaker" triggers the general activation of these cell assemblies, which then expands outward via cortico-cortical connections of inhibition and excitation. The degree of activation/depolarization of these cell assemblies is the focus of SCP training.
Studies show that changes in SCPs leading to increased negativity reflect greater depolarization of the large cell assemblies, which in turn lowers the threshold of excitement of neurons in the brain, leading to increased neuronal activity.
Inversely, changes in SCPs leading to increased positivity reflect less depolarization of the cell assemblies, which in turn increases the threshold of excitement of neurons in the brain (greater inhibition making it more difficult for neurons to activate), leading to less neuronal activity.
The clinical implications of slow cortical potentials and their training are reflected in epileptics, individuals with ADD and those suffering from migraines.
- Increased SCP negativity is observed in epileptics a few seconds before a seizure. Increased SCP positivity occur immediately after a seizure is finished. Training for increased positivity (less activity/greater inhibition) with SCPs has shown to decrease the frequency of seizures.
- Training for increased negativity with SCPs, reflecting greater activation of the cortical networks, has been shown to improve attention in individuals with ADHD.
- Migraine sufferers that pursue similar training as epileptics have shown decreases in the frequency of episodes and other headache parameters.
Slow Cortical Potentials Software Suite
Following Dr. Strehl and Dr. Birbaurmer's protocol, initial training starts with the subject taking turns practicing both to activate/excite and deactivate/inhibit their brain activity. Whether the subject is correctly activating or inhibiting their brain activity, the BFE's SCP Suite displays feedback to either show success in terms of each 0.5-second period of the 8-second trial or as a continuous single feedback output for the trial, depending on what the clinician and subject prefer. After training progresses past the first transfer trial session (training without feedback to see if the subject can generalize the training), the protocol then increases the focus on activating/exciting or deactivating/inhibiting brain activity, depending on the client's circumstance. For example, an ADHD child would now train to activate/excite their brain, such that they would focus on an activation to inhibition trial ratio of 2-to-1 (twice as many attempts to activate the brain than to inhibit the brain).
|Example of activation trial with feedback from 0.5-second periods. Subject had initial difficulty activating, but then persevered through the trial.
Self-regulation of Slow Cortical Potentials: Strehl, U., Birbaumer, N. A New Treatment for Children With Attention-Deficit/Hyperactivity Disorder Pediatrics November 1, 2006 118: e1530-e1540.