Discovery of Neurofeedback and the underpinning neuroscience
Neurofeedback therapy was discovered serendipitously by Barry Sterman through possibly the ultimate placebo-controlled, fully-blinded experiment.
In 1968 Barry Sterman, who was studying localised EEG patterns in relation to specific behaviors in cats, demonstrated the use of operant conditioning to train cats to generate a distinctive brainwave rhythm over the motor cortex, the part of the brain associated with movement control, when rewarded with milk45:
Cats conditioned to generate brainwaves by reward
This pattern, in the frequency range 12-20Hz, was termed the ‘sensorimotor rhythm’ (SMR).
Months later, unrelated research46 funded by the space race into the effects of rocket fuel (hydrazine) involved injecting rocket fuel into a number of cats and observing the results as all the cats cried, vomited, salivated, and after an hour, most of them had a seizure.
Initially Sterman could not understand why a minority of the cats had not had a seizure after 1 hour, until it was realised that these seizure-resistant cats were the only ones that had taken part in the previous study to condition the cats to generate enhanced SMR47. The operational conditioning of the SMR had been transferred to immunity to seizures:
This experiment was repeated and then extended to primates and later humans, including an ‘double-crossover’ study design48 on epileptic patients where part of the experimental protocol was to reverse the direction of operant conditioning at 12-15Hz unknown (blinded) to the subjects, which increased the incidence of seizures.
Examining the underlying neuroscience, the ‘sensorimotor rhythms’ (SMR) are generated within the somatosensory nuclei of the thalamus, relayed to the somatosensory cortex (where they can be picked up via scalp electrodes) and to the nucleus reticularies thalami, which responds with a similar burst, at the same time releasing the neurotransmitter GABA, which causes the process to begin again49. This back-and-forth rhythm controls excitability and enables control over motor function.
Hydrazine interferes with the synthesis of GABA45, effectively abolishing these EEG rhythmic patterns, increasing cortical and thalamic excitability, and making the brain vulnerable to seizure when stimulated45.
Therefore it can be concluded that the strengthening of the SMR rhythms through conditioning either increased GABA synthesis, up-regulated GABA receptors, or facilitating another inhibitory process50.
45Wyrwicka, W, & Sterman, M. B. (1968). Instrumental conditioning of sensorimotor cortex EEG spindles in the waking cat. Physiology and Behavior, 3, 703-707.
46Sterman, M. B., LoPresti, R. W., & Fairchild, M. D. (1969). Electroencephalographic and behavioral studies of monomethylhydrazine toxicity in the cat. CALIFORNIA UNIV LOS ANGELES BRAIN RESEARCH INST.
47Sterman, M. B. (2000). Basic concepts and clinical findings in the treatment of seizure disorders with EEG operant conditioning. Clinical EEG and Neuroscience, 31(1), 45-55.
48Hagemann, D., Hewig, J., Seifert, J., Naumann, E., & Bartussek, D. (2005). The latent state trait structure of resting EEG asymmetry: Replication and extension. Psychophysiology, 42(6), 740-752.
49Wood, J. D., & Peesker, S. J. (1974). Development of an expression which relates the excitable state of the brain to the level of GAD activity and GABA content, with particular reference to the action of hydrazine and its derivatives. Journal of neurochemistry, 23(4), 703-712.
50Sterman, M. B. (1996). Physiological origins and functional correlates of EEG rhythmic activities: implications for self-regulation. Biofeedback and self-regulation, 21(1), 3-33.
LIKE TO KNOW MORE?
If you would like to learn more about the benefits of neurofeedback for treating trauma please call BrainTrain UK. We offer a free initial telephone consultation, will answer any questions you have and explain the treatment to you. There is no obligation to get treatment after the consultation if you decide it isn’t for you.