Biofeedback in the treatment of epilepsy

Platform for a dual research approach

These two studies provided several interesting conclusions that directed our subsequent scientific efforts. First, in the cat study we observed a common prodrome in both SMR-trained and control animals even though the SMR-trained animals had acquired protection against seizures. This suggested a direct effect on the seizure process and not on MMH toxicity in general. Second, in our human epileptic patient, the seizures that were suppressed arose out of the unconscious state of sleep, a fact that eliminated the possibility of any voluntary countermeasure and again indicated a direct effect on the seizure mechanism. Accordingly, we undertook a dual approach to understanding the basis of this effect, involving both additional animal electrophysiologic and human clinical studies.

Animal studies evaluated motor behavior, motor reflexes, motor and thalamic unit firing, and somatosensory pathway correlates of the SMR response. Clinical studies, as reviewed in the following section, sought to further document the anticonvulsant effects of SMR operant conditioning and examine this effect on various seizure types. Possible alternative explanations, such as altered medication compliance and placebo effects, were also addressed in several comprehensive studies. Additionally, by this time other laboratories were beginning to add to the research literature in this new field.

Reproduced, with permission of the American Academy of Sleep Medicine, from Sleep (Sterman MB, et al. Sensorimotor electroencephalogram rhythmic activity: a functional gate mechanism. Sleep 1981; 4(4):408–422).

Neurophysiologic studies in cats revealed a convergent pattern of changes that were directly correlated with the SMR pattern in the EEG and clearly indicated reduced motor excitability. These included a specific attenuation of cellular activity and reflex excitability in the motor pathway, a reduction in muscle tone and associated motor unit firing, and cessation of behavioral movements. Further, unit studies in afferent nuclei of the somatosensory pathway revealed evidence of reduced somatic afferent firing and the onset of reciprocal burst oscillation between the thalamic reticular nucleus and the adjacent ventrobasal relay nucleus. This oscillation provides the thalamic source of the cortical SMR pattern. These findings are summarized in Figure 4.⁶ Details of the studies and resulting publications are provided in recent review articles.^7–9 They represent empirical evidence for significant reorganization of neuronal function when SMR activity appears in the sensorimotor EEG.

CLINICAL STUDIES

A series of human studies followed our initial clinical report, including group studies involving crossover and placebo-controlled designs. These studies consistently reported significant seizure reductions in epileptic patients in response to reward for increasing sensorimotor EEG rhythmic activity.

Two independent meta-analyses of the peer-reviewed papers in this literature have appeared in the last decade.^8,10 In a review of 24 studies involving 243 patients with predominantly partial complex seizures provided with central cortical SMR feedback training, Sterman determined that 82% of these subjects registered seizure reductions greater than 50%.⁸ More recently, Tan and colleagues evaluated data from 63 studies and selected for comprehensive analysis 10 studies that met stringent criteria for controls and population and seizure details.¹⁰ They reported that 79% of the patients treated with SMR feedback training experienced a statistically significant reduction in seizure frequency despite a collective history of failed medication therapy.

Data are from Lantz and Sterman.11

Data from one of the studies¹¹ evaluated in both of these systematic reviews are summarized in Figure 5. In this study, 24 subjects with complex partial seizures, many with seizure foci confirmed through depth recordings, were randomly assigned to three experimental treatment groups:

• One group simply tabulated their seizure experiences for 6 weeks using a comprehensive logging method.
• The second group received EEG feedback training for 1 hour three times a week for 6 weeks; however, the EEG signal responsible for reward was previously recorded from a different individual. This noncontingent feedback constituted a “yoked control” group.
• The third group received 6 weeks of contingent training for increasing SMR activity in somatosensory cortex while simultaneously suppressing slower 4- to 8-Hz activity.

After the initial 6 weeks, all 24 subjects were combined into one group that received 6 more weeks of contingent training only. This was followed by a 4-week period of gradual withdrawal from training and then by a final tabulation of seizure incidence during a 6-week period after training was terminated. As can be seen in Figure 5, the seizure tabulation control was associated with an increased seizure count and the “yoked control” noncontingent SMR training was associated with no significant change in seizure incidence, whereas contingent SMR training was associated with a statistically significant reduction in seizures. The statistical significance of this reduction increased progressively as subjects from the other two groups were added to a second 6-week period of contingent training, and after an additional 6 weeks following withdrawal from training. In addition to this exclusive seizure reduction after SMR contingent training, pre-/post-training neuropsychological testing showed that responding SMR-trained subjects also improved significantly in performance of tasks specific to the hemisphere contralateral to their frontotemporal lesion, indicating a reduced corrosive disturbance from the seizure focus.¹¹