Sociology
Research Papers
EEG feedback training in the treatment of epilepsy: Some questions and some answers
A basic question in EEG feedback training of epileptic patients is whether the decrease in seizures is specifically due to the training or to other factors. Questions may also be raised as to what EEG changes are involved. Preliminary results in five patients suggest that seizure reductions can occur with training which are not due to placebo or nonspecific effects or to changes in medication compliance. These changes occurred rapidly during EEG-contingent feedback training but not when feedback was random in relation to the EEG. Reliable changes in the EEG were also observed, but the question of which mechanism accounts for these results has yet to be answered.
View Full Paper →Operant conditioning of the EEG in two patients with epilepsy: Methodologic and clinical considerations
Methodologic and clinical considerations are discussed in sensorimotor rhythm (SMR) biofeedback research on two dissimilar but severe epileptic males. The first case, an akinetic epileptic who prior to feedback training experienced 80–100 clinical seizures every 10 hours, showed considerable seizure reduction after 6 months of SMR and epileptiform training. A number of methodologic and instrumentation advances were pioneered with the akinetic patient: (1) development of and ultra-sharp band-pass filter; (2) use of epileptiform inhibit and feed-back circuitry; (3) use of monetary rewards as additional incentive; (4) use of correlational analysis for evaluation of acquisition in the major dependent variables and; (5) use of noncontingent feedback and rein-forcement as control techniques. The second case, a psychomotor epileptic, also showed therapeutic benefit from SMR training. Clinical information regarding the effect of anticonvulsant medications on the course and therapeutic outcome of SMR training are described. In conjunction with operant conditioning of 12 Hz activity, corresponding changes for other EEG parameters are examined.
View Full Paper →Sensorimotor EEG operant conditioning: Experimental and clinical effects
Neurophysiological studies in cats have established a functional relationship between waking 12–15 Hz sensorimotor cortex rhythmic EEG activity (the sensorimotor rhythm or SMR) and a similar pattern during sleep, the sleep spindle. Both result from oscillatory thalamocortical discharge involving ventrobasal thalamus and sensorimotor cortex, and both are associated with a state of suppressed motor excitability. Enhancement of the SMR with operant conditioning methods in the cat clearly led to reduced seizure susceptibility. The experimental application of this approach to seizure control in epileptics has resulted in (A) evidence that EEG patterns can be manipulated significantly in man with operant conditioning, (B) suggestive observations concerning a potential component of pathology in epilepsy, and (C) strong preliminary evidence that SMR operant conditioning in epileptics is specifically therapeutic. Current research has focused upon the EEG during sleep in epileptics with primary motor symptomatology. This measure often reveals several hard signs of pathology. These include the presence of abnormal activity in the 4–7 Hz frequency band and the absence or disturbance of activity in the 11–15 Hz frequency band. Power spectral analysis is being utilized to quantify these sleep EEG components in five groups of epileptic patients, studied with different frequency patterns rewarded in an A-B-A design which provides for counterbalancing of order effects. Initial laboratory training is followed by 9–12 months of training at home with portable feedback equipment. Reward contingencies are reversed within each group at approximately three month intervals. Clinical EEG data, blood anticonvulsant measures and patient seizure logs supplement sleep EEG data obtained before training and after each phase of the design. Early results have again indicated specific therapeutic benefits following training of high frequency rhythmic central cortical activity.
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