Beta waves were discovered and named by the German psychiatrist Hans Berger, who invented electroencephalography in 1924, as a method of recording electrical brain activity from the human scalp. Berger termed the larger amplitude, slowerfrequency waves that appeared over the posterior scalp when the subject's eye were closedalpha waves. The smaller amplitude, faster frequency waves that replaced alpha waves when the subject opened his or her eyes were then termed beta waves.
Function
Low amplitude beta waves with multiple and varying frequencies are often associated with active, busy or anxious thinking and active concentration. Over the motor cortex beta waves are associated with the muscle contractions that happen in isotonic movements and are suppressed prior to and during movement changes. Bursts of beta activity are associated with a strengthening of sensory feedback in static motor control and reduced when there is movement change. Beta activity is increased when movement has to be resisted or voluntarily suppressed. The artificial induction of increased beta waves over the motor cortex by a form of electrical stimulation called Transcranial alternating-current stimulation consistent with its link to isotonic contraction produces a slowing of motor movements. Investigations of reward feedback have revealed two distinct beta components; a high beta component and low beta component. In association with unexpected gains, the high beta component is more profound when receiving an unexpected outcome, with a low probability. However the low beta component is said to be related to the omission of gains, when gains are expected.
Relationship with GABA
Beta waves are often considered indicative of inhibitory cortical transmission mediated by gamma aminobutyric acid, the principal inhibitory neurotransmitter of the mammalian nervous system. Benzodiazepines, drugs that modulate GABAA receptors, induce beta waves in EEG recordings from humans and rats. Spontaneous beta waves are also observed diffusely in scalp EEG recordings from children with duplication 15q11.2-q13.1 syndrome who have duplications of GABAA receptor subunit genes GABRA5, GABRB3, and GABRG3. Similarly, children with Angelman syndrome with deletions of the same GABAA receptor subunit genes feature diminished beta amplitude. Thus, beta waves are likely biomarkers of GABAergic dysfunction, especially in neurodevelopmental disorders caused by 15q deletions/duplications.
