Discovery of Neurofeedback and the underpinning neuroscience

Discovery

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.

→Continue reading about how Neurofeedback Therapy  has developed since discovery and how contemporary approaches follow the the developmental sequencing advocated by Dr Bruce Perry. 

References

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.