Siegfried Othmer, Susan F. Othmer, & Clifford S. Marks
September 1991
INTRODUCTION
A number of studies evaluating EEG biofeedback for hyperactivity, attention deficit disorder (ADD), and learning disabilities have already yielded evidence of improvement in cognitive skills and academic performance. (Shouse, 1979; Lubar, 1984; Tansey, 1990). The focus initially was on remediation of hyperactivity in cases which were responsive to stimulant medication, and hence were thought to be most obviously traceable to cortical underarousal (Lubar, 1976). This work was grounded on earlier success of EEG augmentation training in the 12-15 Hz region with epileptic seizures of predominantly motor symptomatology (Sterman, 1972). Such augmentation training was then combined with inhibition of excessive activity in the 4-7 Hz region (Sterman, 1974). Viewing hyperactivity as motor disinhibition motivated use of the same protocol.
The 12-15 Hz region was identified by Sterman as associated with specific rhythmic activity (referred to as sensorimotor rhythm, or SMR) which governs the setpoint, or the poise, of the motor system (Sterman, 1982a). Subsequently, it was found that cases of attention deficit disorder without hyperactivity (as defined in the DSM III) were also responsive to the training, and that cognitive deficits associated with attentional deficits could be effectively remediated with both 15-18 Hz training (Lubar, 1984) and with 12-15 Hz training (Tansey, 1990). The more universal applicability of the technique meant that a more generalized model was needed, and the efficacy of both 15-18 Hz and 12-15 Hz training also called into question any simple identification of the mechanism with the SMR rhythm. No comparable rhythm has been identified in the 15-18 Hz regime, which is referred to as "beta" in the following.
The present work is motivated by the need to confirm the previous studies, and to quantify and particularize the benefits in terms of cognitive function and short-term memory which may be attributable to the training. There were differences in protocol, in electrode placement, in instrumentation, and in the role of the biofeedback therapist in the prior studies. This variety in approach also calls for additional studies which may allow discernment of the preferred protocol. Finally, there has been sufficient anecdotal evidence of a more generalized efficacy of the present EEG training protocol, e.g. for behavioral problems, that a more inclusive model may be required to explain all of the findings.
The previous work supports the hypothesis that deficits in cortical activation and control are observable in the statistics of cortical neuronal activity, as reflected in EEG spectral density distributions and in time domain phenomena such as spikes, other characteristic waveforms, and paroxysmal activity. It is therefore proposed that EEG biofeedback training in general, and beta and SMR training in particular, may effect cortical regulation in a very broad sense when it is used to train the EEG toward more state- appropriate frequency distributions. This is accomplished by impacting on those mechanisms, originating in the reticular formation of the brain stem and mediated by the thalamus and the hypothalamus, which govern states of arousal and level of consciousness, including cortical activation. The mode of generating SMR or other rhythmic brain wave activity via the stimulation of a thalamic gating mechanism was first described by Sterman (1982).
Specifically, the presence of high-amplitude, low-frequency activity is inappropriate for a state of attentive arousal under which the training takes place. Similarly, low amplitude in the beta region appears to be associated with cortical underarousal (Lubar, 1989). Obversely, excessive high frequency activity may be observed in children showing anxiety symptoms (our own observation). Such waveforms yield high amplitude in the upper beta band of 22-30 Hz. The training protocol, in terms of reward and inhibit bands, follows directly from these observations. Extraneous factors impinge as well: head and neck muscle activity intrudes into the beta band, allowing clients to obtain rewards inappropriately, unless such activity is specifically inhibited.