Alpha wave enhancement and theta wave suppression in the control of epileptic seizures

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Alpha wave enhancement and theta wave suppression in the control of epileptic seizures
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Theta wave suppression in the control of epileptic seizures, Alpha wave enhancement and
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Gercken, George Edward, 1945-
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Epileptics -- Care   ( lcsh )
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Biofeedback training   ( lcsh )
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Thesis--University of Florida.
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Includes bibliographical references (leaves 103-109).
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by George Edward Gercken.
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Typescript.
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Vita.

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ALPHA WAVE ENHANCEMENT AND THETA WAVE SUPPRESSION IN THE
CONTROL OF EPILEPTIC SEIZURES







By

GEORGE EDWARD GERCKEN


A DISSERTATION PRESENTED TO THE GRADUATE COUNCIL OF
THE UNIVERSITY OF FLORIDA
IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE
DEGREE OF DOCTOR OF PHILOSOPHY







UNIVERSITY OF FLORIDA


1978














ACKNOWLEDGEMENTS


In the romantic imagination of the public, scientific progress

is pictured as a single individual stumbling into some discovery

while toiling late and alone in a makeshift laboratory. In reality,

scientific progress is the sum total of the tiny and painstaking

contributions of generations of researchers. It seems fitting, there-

fore, that before beginning this report of my own small contribution

to the therapeutics of epilepsy, I should acknowledge the encouragement,

assistance, and cooperation of the many colleagues without whom this

work would not have been possible.

I am particularly grateful to the members of my committee:

Drs. Hugh C. Davis, Cynthia Belar, Robert Isaacson, Warren J. Rice,

and B. Joe Wilder. Dr. Davis, the chairman, stepped in unselfishly

to fill the void left by the sudden death of Sidney Jourard. Dr. Belar

loaned us the seemingly unloanable 5400 computer at a time when ours

had given up the ghost. Dr. Wilder's talk at the Michigan Epilepsy

Center in 1973 convinced me to come to the University of Florida.

Dr. Isaacson kindly shared his profound professional expertise and his

unerring eye for precision and detail. A special thanks to Dr. Warren

Rice, my cochairman, who contributed time, effort, and understanding

for which I can never fully express my gratitude.

I should also like to express my deep appreciation and gratitude

to the Veterans Administration for its excellent support, and

especially to the staff at the Jacksonville outpatient clinic.

ii







My sincerest thanks to Dr. Jack Smith and Jose Principe who

provided valuable computer access and programming efforts in the

analysis of my data.

Finally, to Dr. L. Jim Willmore, whose function as friend,

counselor, and colleague helped me flush out the real from the

fantastic in moments when I wasn't sure, a special thanks.

This project has been simultaneously frustrating, fascinating,

exhausting and stimulating. I hope as well that it will serve as a

stepping stone for other researchers exploring the new and intriguing

field of physiological feedback.














TABLE OF CONTENTS


Page


CHAPTER


ACKNOWLEDGEMENTS . . .

ABSTRACT . . .

I A REVIEW OF THE LITERATURE . .


Definition of Epilepsy . .
Medical Treatment of Epilepsy .
Learning-Theoretic Models of Epilepsy .
Learning Theory Models . .
Inhibitory Synchronous Activity and Seizure


Production .
Physiological Feedback .
The Initial Use of Physiological
Treatment of Epilepsy .
Recent Experimentation .
Summary and Hypotheses .


Feedback in


the


II METHOD . .


Subject Selection .
Individual Subject Profiles. .
Procedure . .
Experimental Design .
Apparatus . .
Data Analysis .


III RESULTS . . .

Data with Respect to Hypothesis 1 .
Data with Respect to Hypothesis 2 .
Data with Respect to Hypotheses 3 and 4 .
Data with Respect to Hypothesis 4 .
Between Slope and Mean Differences .

IV DISCUSSION . . .

Discrepancies Between Hypotheses and Results .
Design Critique and Suggestions for Improvement.
Suggestions for Future Research .










APPENDICES

A TRAINING TAPE SCRIPT . .

B CHI SQUARE PLOT OF OBSERVED VS. EXPECTED SEIZURE
FREQUENCIES BY CONDITION . .

C SUMMARY TABLE OF SIGNIFICANT SLOPES. .

D SELECTED PAIR-WISE CONTRASTS BETWEEN BASELINE AND
TREATMENT CONDITIONS FOR SLOPES AND LEVELS .

REFERENCES . . .

BIOGRAPHICAL SKETCH . .


Page


. 82


. 85

. 91


. 97

. 103

S. 110








Abstract of Dissertation Presented to the Graduate Council
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Doctor of Philosophy

ALPHA WAVE ENHANCEMENT AND THETA WAVE SUPPRESSION IN THE
CONTROL OF EPILEPTIC SEIZURES

By
George Edward Gercken

December 1978

Chairman: Hugh C. Davis
Major Department: Psychology

The present research was concerned with investigating the EEG

physiological feedback technique of combined alpha wave enhancement,

theta wave suppression, and its effect upon the attenuation of epilep-

tic seizures. A review of the literature indicated a possible link

between midrange synchronous EEG activity, chiefly in the alpha range,

and inhibition of seizures. In addition, the review demonstrated a

possible connection between slow wave hypersynchony, chiefly in the

theta range, and seizure propagation in focal seizure patients.

Five subjects, four male and one female, were employed in the

study. All subjects were classified as having uncontrolled focal

seizures of at least five years' duration. Each subject was required

to maintain a seizure diary one month prior to and throughout the

course of the experiment. All subjects were administered EEGs using

the training referents T3-T4, C3-C4 before training was begun and

immediately after completion.

Following an A-B1-C-B2-(D) research design (A=baseline, Bl

contingent feedback 1, C=noncontingent feedback, B2=contingent

feedback 2, D=theta suppression), subjects were trained to enhance EEG

alpha wave and suppress theta wave production.

vi








The results indicated support for the hypothesis that enhancement

of synchronous midfrequency activity had a significant effect upon

seizure rate. Discrepancies between these results and those of

Sterman were discussed in terms of homogeneity of seizure type. The

greater variability of seizure classification of Sterman's subjects

made his results difficult to interpret from an etiological standpoint.

The present study's concentration only on focal seizure patients

increases the specificity of results for this subgroup.

Methodological problems were discussed in terms of extending

baseline data or interjecting a multiple baseline approach to more

accurately gauge the effectiveness of training procedures. The

extension of the noncontingent condition was recommended to permit a

more direct assessment of treatment effects.















CHAPTER I
A REVIEW OF THE LITERATURE


The sky spun like a mighty wheel;
I saw the trees like drunkards reel
And a light flash sprang o'er my eyes,
Which saw no farther. He who dies
Can die no more than I died.

I felt the blackness come and go,
And strove to wake, but could not make
My sense climb up from below.

Lord Byron
Mazeppa


Do not believe that the gods cause illness and madness
and do not hope to bring healing and help the sufferer
by means of magic spells or false sorceries.

Hippocrates
The Sacred Disease


The great contribution of Hippocratic medicine was its introduction

of an objective, naturalistic and empirical attitude to the biological--

and hence the behavioral--sciences. As early as 400 B.C., Hippocrates

had recognized the existence of epilepsy as a specific ailment (Esper,

1964, p. 119). Yet, even in Lord Byron's time--he himself was reputedly

an epileptic--seizures were still being attributed to mystical causes

rather than to any specific organic or functional disturbance. The

word seizure was originally used to describe epileptic convulsions

because the person was believed to have been seized by the devil.

Today these symptoms are known to be associated with abnormal

electrical activity in the brain. In some cases, this abnormal








activity can be shown to have its origin in a specific lesion in the

cortex. These cases are known as focal seizures. In many other cases,

no specific lesion or focus can be illustrated. These are nonfocal

epilepsies. The epileptic disorders have proven themselves to be stub-

born adversaries of modern medical science, and as yet there are no

generally reliable treatment modalities for the disabling and disturbing

handicaps epilepsy creates.

Recently, there has been interest in research which applies the

techniques of physiological feedback to the control of epileptic

seizures. While the results of this research are inconclusive, and the

entire effort has been fraught with controversy, the success that other

workers have had using physiological feedback techniques to treat

other clinical disturbances implies that this line of investigation

ought to be examined carefully. This review of the literature is

devoted to that end.


Definition of Epilepsy


It is important to note at the outset that epilepsy is not a

specific disease entity, but is rather the name given to certain signs

of central nervous system dysfunction. Penfield and Jasper (1954) have

described these clinical indications as a "state produced by an ab-

normal excessive discharge within the central nervous system" (p. 22).

Jasper, Ward and Pope (1969) define epilepsy as a "sudden paroxysmal

discharge" (p. 10) and add to it the concept of paroxysmal dysrhythmia

of the EEG and hypersynchrony to indicate not only excessive firing of

individual cells, but also massive discharge of many neurons in unison,

"abolishing the finely-organized tempero-spatial patterning character-

istics of the normal integrative activity of the brain" (p. 11).








Inherent in this definition is the diagnosis of a seizure disorder via

the abnormality of an individual's interictal EEG.

Epilepsy is often given as a diagnosis when clinical convulsions

and EEG manifestations are present, and the observed disturbances are

not secondary to an existing condition such as hypoglycemia, tumor, or

infection. Essential to this definition is a chronic recurrence of

symptoms.

Such a restriction is not entirely without reason, for although

the seizure is merely a sign of central nervous system dysfunction,

and thus has no one etiology or mechanism, the seizure in all cases does

utilize common neurophysiological mechanisms during its evolution. The usu-

al sequence of a seizure is characterized by aura, spread, generaliza-

tion, and cessation. The major motor seizure begins with an abnormal

electrical discharge in one part of the brain, spreads to other areas,

generalizing to a complete disruption of normal sensory and motor

activity, and then terminates (Jasper, 1969).


Medical Treatment of Epilepsy


While seizure activity may be the sign of some underlying neuro-

pathogic or neurochemical dysfunction of the brain, control of the

symptom alone is of immense benefit to the person with epilepsy and

indeed is the current goal of medical therapy. It is estimated that

approximately one-half of one percent of the population, or about

twenty million people worldwide, suffer from such seizures.

No single treatment procedure is effective in the treatment of

many epileptics. The condition is treated today principally through

medication with anticonvulsant drugs. These drugs, however, fail to








reduce seizure activity in 20 to 30 percent of all patients (Coatsworth,

1971). Even the patients who are helped by the medications risk side

effects that may be serious and debilitating. For example, phenytoin

sodium (Dilantin), perhaps the most widely prescribed antiepileptic

agent, is known to elicit some fifteen definite and eighteen possible

side effects (Bray, 1959), and to provoke a possible permanent degenera-

tion of cerebellar neurons (Selhourst, Kaufman and Horowitz, 1972;

Julien and Halperin, 1971). Phenacemide (Phenurone), a drug used in

particularly intractable cases, is highly toxic and can lead to such

bizarre psychic manifestations as suicidal ideation, paranoia, and

acute psychotic states (Livingston and Pauli, 1954).

Prior to the introduction of appropriate medication there was much

interest in dietary cures for epilepsy, but these treatments were not

effective. One dietary method was a dehydration regime pioneered by

Dr. Fay in Philadelphia in the 1930's. The ketogenic diet was developed

after investigators noted that seizures stopped shortly after the onset

of a fast, but the results did not extend beyond the starvation period.

One method involves starving and dehydrating the patient for a period

of several days, then prescribing a diet that contains four times as

much fat as carbohydrates and protein combined. The procedure works

best with children. This treatment can adversely affect the blood

vessels of adults and is extremely complicated to administer

(Livingston, 1960).

Surgical intervention is indicated when medical treatment has

proven ineffective and the results of the operation on the patient's

brain will not alter functioning or cause debilitating symptoms more

severe than the seizures themselves. Surgical treatment is only








possible if the lesion is accessible and its removal will not severely

impair the functioning of the brain.

The forms of surgical intervention most commonly used are:

1. the excision of localized cortical areas exhibiting

constant abnormal electrical discharge;

2. temporal lobectomy for patients with clinical psycho-

motor seizures associated with focal, temporal lobe

electroencephalographic abnormalities; and

3. partial hemispherectomy in certain cases of epilepsy

associated with unilateral cerebral atrophy (Livingston,

1960).

Surgery clearly is indicated for only a small number of epileptics,

and the probability of application to the general population of

epileptics is limited. Rasmussen (1975) reported that of 129 patients

treated surgically for the removal of nontumoral lesions, 48 percent

has a moderate to no reduction of seizure frequency. Thus, none of the

conventional techniques for the treatment of epileptic disorders are

completely satisfactory. Additionally some 30 percent of the total

epileptic population is left without an effective therapy.


Learning-Theoretic Models of Epilepsy


The two main types of medical intervention described in the pre-

ceding section are all based on the assumption that the epilepsy is a

sign of some physiopathology of the central nervous system. And,

indeed, it is often the case that seizure activity is related to some

specific lesion. But the origin of nonfocal seizures, where no lesion

is known to exist, is a matter of controversy. While many tentative








hypotheses for nonfocal seizure activity postulate some form of neuro-

physiological abnormality, other investigators believe that en-

vironmental conditions external to the epileptogenic tissue may be a

major source of potentiating or attenuating the seizure disorder "

(Mostofsky and Balaschak, 1977, p. 723). The above authors provide an

extensive review of the behavioral studies dealing with the treatment

of epilepsy. They organize the review into several paradigms consist-

ing of: 1) reward management, 2) self management, and 3) phycho-

physiological procedures. Since physiological mechanisms provide a

more fundamental intervention procedure related to the possible central

mechanism to explain seizures, the remainder of this literature review

will concentrate on phychophysiological procedures. It is this type of

etiological thinking that provides a theoretical underpinning for the

use of physiological feedback as a therapy in cases of uncontrolled

epilepsy. The following section will examine theories of both types,

beginning with the physiological approach.


Learning Theory Models


Since physiological explanations are usually employed in the

explanation of epilepsy, several weaknesses occur when it is employed

as a unitary explanation:

1. how does the patient's condition differ on the one day

which he has a seizure as opposed to the five on which

he has none; and

2. what accounts for spread--can it be explained adequately

in physiological terms? (Rodin, 1968)







The origin of learning theory explanation of epilepsy was the

discovery in 1960 that a normal brain could "learn" to develop an

epileptogenic focus without any physical trauma to the cells (Mostofsky

and Balaschak, 1977).1 Morrell's work (1960) demonstrated the forma-

tion of a "mirror focus," or secondary epileptogenic lesion (SEL),in

the hemisphere opposite the existing lesion. By Morrell's definition,

a SEL is "an electrophysiologically defined area of paroxsymal discharge,

at least one synapse removed from the primary zone, but connected with

massive neural pathways" (pp. 538).

The mirror focus type of SEL that Morrell studied developed in two

phases appearing in the hemisphere opposite the primary lesion in the

homologous brain area. In the first stage, the mirror focus develops

spikes only in response to spiking in the primary focus. In the later

stage, the secondary focus becomes entirely independent, no longer

requiring the primary focus to act as a trigger.

The SEL can be viewed in relation to the "kindling phenomenon"

first reported by Goddard, McIntyre, and Leech (1969). Goddard under-

took his research to study the possible epileptogenic outcome of a

"chronic irritant" on cortical tissue. His theory arose from the

observation that "some patients who seem to have made good recovery

from known head injuries become epileptic at a later date" (p. 297).

Goddard's experiment involved the use of low level stimulation of

the brain of his experimental rats with implanted electrodes. He

found that subthreshold stimulation, inadequate to trigger a seizure

on its own, would eventually produce a seizure after repeated


1"Learning" is used loosely here to refer to changes in the
electrical characteristics of brain tissue in the absence of known
physical or chemical events preceding the change.








stimulation of the area. Subsequent stimulation would produce a

seizure after repeated stimulation of the area, even months later.

This phenomenon has also been observed by Racine, Gartner, and Burnham

(1972), Tress and Herberg (1972) and Wada (1976).

Why is a learning-theoretic model invoked to explain these re-

sults? Goddard observed in his experiment that the optimum frequency

at which the stimulation should be applied to produce an eventual

seizure in the rat was one a day. Stimulating the brain more often

deterred the development of eventual epileptic activity. It is hard to

understand this in terms of direct tissue damage; moreover, the magni-

tude of the potential applied to the brain as a stimulus does not

effect the time interval before the area becomes an epileptic focus.

The neurons appear to exhibit a type of learning curve, reaching

100 percent accuracy when the area becomes an autonomous epileptic

focus. The kindling phenomenon has also been observed to occur when

subthreshold doses of seizure-inducing drugs such as pentylenetetrazol

(Metrazol) are administered.

The learning-theoretic model offers an explanation for the develop-

ment and spread of seizure activity. The immediate question, then, is

whether the process can be made to work in reverse, that is, can the

brain learn regulatory or pacemaker activity? To answer this question

a discussion of normal brain wave patterns and their controlling

mechanisms will be presented. Based upon these concepts, the possi-

bility of applying EEG physiological feedback as a means of attenuat-

ing the evolution of paroxysmal activity will be explored.

One way of analyzing EEG activity is to divide it between

synchronous and asynchronous patterns. Synchronous patterns consist







of steady, periodic activity which ultimately relate to the extent to

which neuronal activity is simultaneously active. In EEGs it has been

characterized by the coincidence of waves of similar shape. Though

there have been no exact quantitative measurements of synchrony and

its identification is usually based upon experience, it has been

estimated that normal synchronous activity requires between 0.1 to

1.0 percent of a cell population firing to produce a lOOuV wave on the

surface (Diver and MacGillivary, 1977). This activity has been described

by Chase and Harper (1971) as essentially cortical idling--the absence

of any specific information processing activity. Normal synchrony has

been most notably associated with alpha and slow-wave sleep.

Probably the best studied of human synchronous rhythms is the

alpha rhythm (8-12Hz), whose role in relaxation processes has been

lately popularized. The alpha frequency was discovered in 1929 by the

German neurologist Hans Berger (Berger, 1929). He learned of the

inhibitory nature of the alpha rhythm by observing that its production

was blocked by directing attention toward a stimulus or event. Adrian

and Matthews (1934) found that alpha is not always blocked by any form

of attention; what is required is the perception of attempted per-

ception of a pattern. They also found the difficulty of the task to

which attention was directed was a factor in the degree of alpha

blocking that occurred. Modern research on human occipital alpha has

shown that this pattern is likely to be dominant when the oculomotor

and visual systems are not activity tracking a target or attending to

visual information.

Asynchronous patterns appear as low voltage fast waves, similar

to random electrical activity and are associated with active attention








and the processing of information. These patterns in the frequency

range above 13 Hz are identified as beta activity (Kiloh and Osselton,

1966).


Inhibitory Synchronous Activity and Seizure Production


Andersen and Andersson (1968) postulate that the cortex is almost

totally dependent on the thalamus for its synchronous activity. Ac-

cording to their Facilitative Pacemaker Theory, all major thalamic

nuclei have the capacity to generate rhythmic activity. Each nucleus

functions as a small pacemaker, projecting to a specific cortical

area. There may be as many as thirty to forty thousand of these

pacemakers. Diver and MacGillivary (1977) describe the general principle

underlying pacemaker activity in the generation of synchronous rhythms,

particularly the alpha rhythm. They state that inhibitory activity

is promoted by a series of feedback mechanisms that cause a synchronous

inhibition through the action of a class of neurons, which they term

recurrent inhibition. Eccles (1969) has characterized inhibition as

"that action by a class of synapses that opposes excitation and tends

to prevent the generation of impulses by excitatory synapses" (p. 235).

Thatcher and John (1977), in speaking about inhibitory synchronous

activity, posit an interactive loop process which keeps excitatory/

inhibitory activity in bounds, and which functions to "prevent epilepsy

and regulate the levels of excitation such as sleep and wakefulness"

(p. 117). Thatcher and Purpura (1972) further argue that thalamocorti-

cal synchronization, particularly as it applies to the alpha rhythm,

may be characterized as a "scanning mechanism" which alternately excites

and inhibits cortical activity. According to Thatcher and John (1977)







a subcortical scanning pulse exists that monitors the state of neural

excitability. They cite evoked potential research which demonstrated

a phasic alteration in excitability corresponding to the frequency and

phase of the alpha rhythm. During faster, desynchronous activity,

usually coincident with active focusing of attention, the loop systems

are broken down into a large number of smaller loops or independent

oscillators parsing activity according to the specific system involved.

Hypersynchrony, considered by most the hallmark of seizure pro-

duction, has been characterized by Jasper (1969) and Penfield and

Jasper (1954) as having two main functional components: 1) existence

of an excessive firing of individual cells and 2) the excessive

synchronization of unit discharge activity which does away with the

organized patterned electrical activity that is characteristic of

normal brain function.

In discussing the mechanism of synchronization, Diver and

MacGillivary (1977) state that the production of normal alpha activity is

far different from the hypersynchronous patterns associated with

seizures. The general lack of inhibitory mechanisms in the recruit-

ment of adjacent neuronal areas is considered the prime mechanism of

the genesis of hypersynchrony. If the interactive loop hypothesis of

Thatcher and John is invoked, the excitatory/recruitment phase is not

counterbalanced by the normal inhibitory one. In such a case,greater

and greater portions of neuronal activity begin to respond without

control.

Given the consensus that seizure activity is characterized by a

lack of inhibitory synchronous activity, and in view of the concepts

derived from the SEL and the kindling phenomenon, the technique of








physiological feedback may be an efficacious method of establishing an

inhibitory augmentation mechanism. The remainder of this review will

be aimed at further development of this concept, beginning with an

overview of the topic area.


Physiological Feedback


Physiological feedback is a technique wherein the subject is given

continuous information about the state of some physiological variable of

which he is not normally aware, such as blood pressure or EEG activity.

As currently used, the technique involves the amplification of

minute biological electrical potentials into signals large enough to

record on a polygraph. The signals are then filtered to detect a cer-

tain frequency and voltage band to distinguish changes of a predeter-

mined sort. The information is then fed back to the subject using

devices such as tone generators, slide projectors, or indicator lamps.

In this manner, the individual is given information about his physio-

logical state in a useful form. Individuals have been taught with this

method to exhibit a heightened degree of control over heart rate, blood

pressure, galvanic skin response, muscle tension, skin temperature, and

EEG alpha activity (Barber, DiCara, Kamiya, Miller, Shapiro and Stoyva,

1970-77; Miller, 1978).

Researchers have investigated the applicability of physiological

feedback as a therapeutic intervention into a great variety of patho-

logical states. Some conditions for which physiological feedback

therapy seemed to yield promising results were muscle retraining after

atrophy or paralysis (Andrews, 1964), chronic anxiety (Raskin, Johnson,

and Rondestvedt, 1973), tension headache (Epstein, Hersen, and Hemphill,







1974; Budzinski, Stoyva, and Adler, 1970), heart rate control in

patients with heart disease (Troyer, Twentyman, Gatchel and Lang, 1973;

Weiss and Engle, 1971), and control of essential hypertension (Benson,

Shapiro, Tursky and Schwartz, 1971).

In these studies various physiological measurements were used as
the variables that the subjects were taught to control. In the studies

on muscle retraining, anxiety, and tension headache, the variable was
muscle tension as recorded on an electromyograph. For the insomnia
study, persons were taught to augment the theta wave of the EEG. In
heart rate and blood pressure studies, the subjects were taught to

control those variables directly.

While a variety of work has been done in the treatment of clinical

disorders through physiological feedback techniques, only recently has

EEG physiological feedback been used to investigate pathological

states (Mulholland and Benson, 1971). Prior to this time, most

physiological work using EEG rhythms as feedback variables was devoted

to studying normal processes, such as sleep, meditation, and relaxation

(Jonas, 1973). There is a growing body of literature reporting attempts

to treat epilepsy through physiological feedback techniques.

The Initial Use of Physiological Feedback in the
Treatment of Epilepsy

Early experiments in conditioning approaches to the treatment of

epilepsy differed from the methods of physiological feedback. In one

early sample, Stevens (1962) and her colleagues (Stevens, Milstein, and

Dodds, 1967) attempted to extinguish spiking and other abnormal

epileptiform EEG patterns. A tone and mild electric shock were

administered to the subject at the moment the abnormal wave form

occurred. When the tone was discontinued, discrimination disappeared







in all but one subject. That person was still able to respond in the

absence of the tone when there was a paroxysmal discharge.

Another model for learning-theoretic intervention was

explored by Efron (1956, 1957) who utilized the model of classical

conditioning. His work was dependent upon the existence of an uncon-

ditioned stimulus, an odor, in the case he studied, which could arrest

the seizure activity of the patient. He was then able to condition a

visual stimulus, a bracelet, to the dissolution of the aura.

In a series of studies, Forster and Booker (1964) and Foster

(1967 and 1972) developed a method for treating epilepsy where the
seizures are induced by sensory stimuli. A stimulus which usually

evokes a seizure was used via an extinction or habituation procedure

which is designed to weaken the ability of the stimulus to provoke a

seizure. Mostofsky and Balaschak (1977) have suggested that rather

than an extinction or habituation paradigm for the attenuation of

sensory specific induced seizures, Forster's method tends more to

shift attention away from the seizure stimuli and, therefore, act as

a competing stimuli that does not evoke the paroxysmal response.

The groundwork for efforts using the principles of operant con-

ditioning in the treatment of seizures was laid by Sterman, LoPresti,

and Fairchild (1969) who reported that cats who had been taught to

produce sensory-motor rhythm (SMR), which ranges in frequency between

12-16 Hz measured over the coronal gyrus, were unusually resistant to

seizure-producing drugs. In cats trained to increase SMR activity,

there was a significant delay between the administration of the drug

pentylenetetrazol (Metrazol) and the onset of preseizure symptoms. In

untrained cats, no such delay was noted; the administration of the drug








was followed by a much shortened interval between preseizure symptoms

and the seizure itself.

A few years later, Sterman and a colleague produced the first

report of a treatment of a human epileptic through this technique

(Sterman and Friar, 1972). In this case they reinforced an 11-13 Hz

rhythm, which they maintained was the analog of feline SMR. This

represented a break with earlier research that considered the mu, or

en arceau rhythm (7-11 Hz) to be the human correlate of the sensorimotor

rhythm.

Sterman and Friar (1972) now claim that human SMR is a rhythm

distinct from both the alpha and mu rhythms. The frequency that Sterman

and his colleagues have been identifying as SMR is extremely difficult

to detect, due to its low amplitude. While most cortical synchronous

rhythms are in the range of 50 PV or larger, human SMR is approximately

5-15 PV. It has thus been difficult to verify the existence and

properties of this rhythm in the human EEG.

Kaplan (1974) reported that the low amplitude SMR was discernable

in human EEG's through the use of a dual filtering system. The signal

was prefiltered through a conventional analog filter and then digitally

filtered on a PDP-12 computer.

Kaplan (1974) pointed out that the system used by Sterman and

associates was unable to distinguish SMR accurately and, therefore,

there was no proof that it was indeed SMR that was being reinforced.

She was especially critical of the fact that in none of Sterman's

experiments was there any documentation that the levels of SMR were

increased by the feedback training sessions. In her experiment there

could be no doubt about which rhythms were being reinforced.








Three dependent variables were measured in the Kaplan (1974)

study. They were evaluations of clinical EEG's, seizure incidence,

and power spectra (fast Fourier transforms of EEG epochs). The experi-

ment involved the training of two epileptic patients with 12-14 Hz

biofeedback for three months. No decrease in seizure activity re-

sulted, and one of the patients dropped out of the study. The

remaining patient and two others were then trained in the production

of the alpha frequency.

Necessary changes in the medication that the one patient in both

stages of the experiment received made it impossible to compare that

subject's results directly. It is believed that the observed changes

in both seizure incidence and power spectra for this subject are due to

the medication changes.

Kaplan's other two patients, trained only in the theta-alpha

production (6-12 Hz), showed a significant reduction in seizure

incidence. However, no changes in the power spectra of the EEG's were

evident. Thus, the clinical changes were not ascribed to learning of

EEG synchrony. Rather, Kaplan attributed the changes in the subjects'

learning to function on a lowered level of arousal. That two of the

subjects later reported an increase of seizure incidence under stress

was taken as a further indication of this interpretation.

In a later paper, Kaplan (1975) reiterated her criticisms of the

methodology employed by Sterman. She emphasized in particular the

impossibility of ascribing the observed clinical changes to changes in

the synchronous rhythm production if the fact that these rhythms were

indeed being produced was not demonstrable.








Gastaut (1975), the discoverer of the mu rhythm, agreed with

Kaplan's criticisms and maintained that there was in fact no rigorous

evidence that biofeedback training was ever effective in treating

clinical disorders.


Recent Experimentation


In the last few years, several researchers have attempted to

answer some of the questions and controversies surrounding this

earlier research. Table 1 presents a summary of selected EEGphysiological

feedback studies in epilepsy. This more recent research has tested

the effectiveness of alpha and theta rhythm training as well as the

human SMR and has experimented as well with the reinforcement of

combinations of synchronous activities of different frequencies. The

results of this research are also equivocal and leave the issue far

from settled.

Cabral and Scott (1976) contrasted the effects of alpha training

with a Jacobsonian relaxation technique on seizure reduction. Their

conclusion was that alpha training had a more consistent effect on

seizure reduction.

Kuhlman and Allison (1977) designed a study in which EEG train-

ing was used to effect significant seizure reduction in three out of

five patients. The study was designed to permit the determination of

the actual changes in the EEG produced. Prior to the initiation of

training to reduce seizures, three normal subjects were successfully

trained to enhance the central mu rhythm in the 9-11 Hz band using

50 20-minute sessions. Similarly, three normal subjects given the

same amount of training were unable to increase 12-14 Hz activity with









Table 1. Summary of EEG Feedback Studies in Epilepsy.


Study Frequency Subjects Design and Duration
Parameters Training


Sterman & Friar
(1972)

Sterman,
Macdonald, &
Stone (1974)

Finley, Smith,&
Etherton (1975)
and Finley
(1977)

Seifert & Lubar
(1975) and
Lubar & Bahler
(1976)

Kaplan (1975)


Kuhlman &
Allison (1976)

Wyler, Lockard,
& Inch (1976)

Sterman and
Macdonald
(1977)

Sterman and
Macdonald
(1978)


11-13 Hz (+)


12-14 Hz (+)


11-13 Hz (+)


Single case


Group
Pre-Post


Two single
cases


<10 (-)


12-14 Hz (+)

4- 7 Hz (-)


12-14 Hz (+)
6-12 Hz (+)

9-14 Hz (+)


9-14 Hz (+)


12-15 Hz
18-23 Hz
6- 9 Hz

12-15 Hz
18-23 Hz
6- 9 Hz


Group


Pre-Post


Group
Pre-Post

A-B


A-B-A


A-B-A-B



A-B-A-B


3 mo.


6-18 mo


10-22 mo.


6-9 mo.


3-4 mo.
5-6 Mo.

1-2 mo.


1.5-6 mo.


12 mo.



12 mo.







feedback training. When training to attenuate seizures was instituted,

none of the successful patients increased activity in the 12-14 Hz

range but did enhance significantly production in the 9-11 Hz range.

This same study observed that occipital alpha increased in the

successful cases. They state that "in fact, the increase in the

occipital alpha frequency is a virtual mirror image of the seizure

frequency" (p. 122).

One further implication of these results is that seizure reduction

is not dependent on alteration of a specific EEG pattern, or the increase

of any specific inhibitory cortical rhythms. Research byQuy (1977)on

three chronic seizure patients led him to the conclusion that indeed the

most effective form of biofeedback training for these patients was one

which reinforced all synchronous activity in a broad, midrange spectrum.

A number of investigations have borne out this role of the mid-

range spectrum in seizure reduction. In particular, the suppression

of the slow theta frequencies as well as the enhancement of the midrange

spectrum seems to bolster the effectiveness of the treatment. This

result has been reported by Finley, Smith and Etherton (1975), Lubar

and Bahler (1976), Wyler, Lockard, and Inch (1976), and Sterman and

Macdonald (1978).

Budzinski and Stoyva (1969) reported that when frontal EMG levels

became particularly low, the subjects tended to display an increase in

EEG theta waves. Sittenfeld, Budzinski, and Stoyva (1976) demon-

strated that profound muscular relaxation was associated with the

appearance of theta in the EEG. Budzinski, in "Clinical Implications of

Electromyographic Training" (1977, p. 438), reported that at the lower

levels of frontalis muscle tension there arose an an inverse relationship

with EEG theta.








Beatty, Greenberg, Deibler, and O'Hanlon (1974) reported that the

absence of theta (which they defined as 3-7 Hz) was particularly as-

sociated with the ability to maintain vigilance. O'Hanlon and Beatty

(1975) showed that theta suppression may prevent or lessen the perform-

ance decrements typically associated with long, exacting vigilance

tasks.

The link between theta rhythm and epileptic seizures has been

firmly established. Gibbs, Gibbs, and Lennox (1937), in a study of

400 epileptic patients, noted the tendency of seizures to occur when

the patient is awakening or falling asleep. Theybelieve pre- and post-

sleep stages modify the rate of normal cortical rhythm, placing a

strain on the self-regulatory mechanism of epileptics with which they

are unable to cope.

Gibbs, Fuster, and Gibbs (1948) and Jasper, Pertuiset, and

Flanigin (1951) have confirmed the focal cortical origin of theta

rhythms in a majority of epileptic patients.

In 1974, Johnson and Meyer devised a phased biofeedback treatment

procedure for an eighteen-year-old female epileptic who was allergic

to Dilantin. The treatment was administered in a phased sequence

beginning with alpha feedback, followed by alpha and theta feedback,

and concluding with theta feedback alone, in an attempt to establish

a low arousal antistress response. The patient, though unable to stop

a seizure once begun, was able to prevent the onset of seizures by

going into an alpha state when she felt an aura developing. At the

end of one year she had experienced a 46 percent decrease in seizures.

Sterman's most recent study (1978) was designed specifically to

investigate the importance of specific training frequencies in the








interpretation of EEG data. In his double blind study,patients were

alternately trained to produce EEG activity in one of three frequency

ranges. One was always the 6-9 Hz theta frequency, and the other was

either 12-15 Hz or 18-23 Hz. Patients were rewarded for producing one

in the absence of the other. After three months the contingencies were

reversed without the patient's knowledge. For six of the eight sub-

jects, significant seizure reduction occurred when the higher frequency

was trained and the lower suppressed. When the higher frequency was

within the 12-18 Hz band, the beneficial effects survived the reversal.

For the six patients with seizure reduction, the average reduction in

rate of seizures was 74 percent. Sterman interprets this as illustrat-

ing the specific role of training for various frequencies and rejects

the claims by some detractors that the beneficial effects are an

artifact of the design, produced by the patient sitting motionless and

functioning at a lower level of arousal.


Summary and Hypotheses


Epilepsy is the term applied to a complex set of central nervous

system dysfunctions with electrical and most often behavioral con-

sequences. A further delineation of this syndrome would characterize

it as an excessive firing of many neurons in unison, hypersynchrony,

and slow wave activity, particularly in the theta range. This has

been considered the hallmark of seizure initiation and propagation.

Complex partial seizure activity is associated with abnormal EEG ac-

tivity which generally begins in a localized area and generalizes as

the seizure develops.







As conventional therapies for seizures of this sort are unable

to effect significant improvement in 20-30 percent of epileptics,

interest in the possibility of alternative treatment modes by elicit-

ing learned changes in the brain's electrical activity became more

important.

This interest was spurred by observations, which seemed to

indicate that learning processes might,in some cases, be involved in

the development of seizure activity. Morrell's discovery of the mirror

focus phenomenon and Goddard's observation of the kindling phenomenon

are the two principal pieces of research in this area.

The techniques of biofeedback, which have been used with success

in the treatment of a great variety of other clinical entities, were

used to train patients in the production of these cortical rhythms.

Initially a great deal of interest was focused on those frequen-

cies believed to be the human analog of the SMR in cats. Feline SMR

was known to be associated with the suppression of motion and was also

observed to be correlated with resistance to seizures.

Further research has cast doubts on the specificity of the SMR

as a factor in seizure reduction. Criticisms of some of these early

studies, especially by Sterman et al. (1974), pointed out the importance

of illustrating changes in the EEG as well as proving seizure reduction

if any notion of cause and effect is to be developed.

It is the learning theory of seizure propagation that leads to

the physiological feedback method of therapy. There is considerable

evidence to suggest that brain cells can learn to be epileptogenic,

either through mirror focus mechanisms, Morrell's secondary epilepto-

genic lesion, or through the Goddard kindling phenomenon. If the







brain can learn to be more easily excitable, can it conversely be

made to learn inhibitory or pacemaker activity? This is what physiological

feedback techniques attempt to accomplish.

In order to be effective, however, considerably more information

on the precise mechanisms involved must be developed through research.

Even if one accepts the learning theory, what waveforms should be

reinforced? Sterman and his colleagues use a waveform assumed to be

the human counterpart of the cat SMR and have claimed success with a

small patient population. Additional study, however, has convinced

the same researchers that SMR in humans exists as a rhythm distinct

from either alpha or mu. Kaplan assumed that previous experiments were

using a filter system which could not discriminate signals in the ap-

propriate range adequately. Using more sophisticated electronic equip-

ment, she established that the Sterman rhythm, when used in biofeed-

back training, did not work. Using low frequency synchrony was also

inconclusive.

The literature,therefore,appears to indicate that biofeedback

techniques are promising avenues to explore in the treatment of

epilepsy, yet considerable fundamental research is needed before

understanding and effective therapy can be accomplished. The litera-

ture dealing with seizure initiation and propagation points to

inhibitory synchronous rhythms, especially the alpha rhythm, as a

means of attenuating this activity. Enhancing the percentage of time

the patient produces alpha while simultaneously diminishing the effects

of hypersynchrony via learned suppression of slow wave theta may well

provide a direct and parsimonious means of controlling seizure

activity.








The hypotheses to be tested are as follows:

1. There will be a significant difference between pre- and post-

EEG measurements. This difference will be manifested by a diminution

of slow wave activity, chiefly in the theta (3-8 Hz) and delta (1-3 Hz)

range, and an increase in the percentage of time in the faster range,

particularly the alpha (9-13 Hz) range.

2. Seizure incidence will diminish over time, as a function of

training, being significantly less at the completion of the study.

3. The time series measuring the rate of alpha production during

and following intervention can be represented by a significant (positive)

change in both level and slope as compared with baseline measures.

4. The time series measuring the rate of theta suppression

during and following intervention can be represented by a significant

negative change in level and slope as compared with baseline measures.















CHAPTER II
METHOD

The basic operations required to investigate these hypotheses

require:

1) measures of concurrent dependent variables of alpha percent,

average frequency, and average amplitude, theta percent and theta

count for each subject over a sufficiently long time course to permit

an evaluation of baseline, treatment, noncontingent treatment;

2) a measure of seizure activity via a diary begun before treat-

ment and kept throughout; and

3) an independent measure of EEG frequency changes pre- and post-

feedback training.


Subject Selection

Six subjects were selected using the following three main

criteria: seizure history, frequency of seizures, and subject's being

refractory to anticonvulsant medication. First, it was required that

each subject have a positive history of essentially uncontrolled

seizures for at least five years prior to the initiation of training.

They were identified via patient records at the Veterans Medical

Center, Gainesville, Florida, and through referrals from the Jacksonville

Epilepsy Foundation and subsequently through medical records of the

patient's neurologist. The second requirement was that following

long-term anticonvulsant therapy with good compliance, the seizure








condition was not under adequate control. Finally, the requirement

was established that the subject must be experiencing at least five

seizures per month that were verified by family members, friends, or

medical personnel.

Beginning approximately one month prior to the initiation of

training and continuing throughout training, each subject was sup-

plied with a seizure diary on which he indicated by day and time the

occurrence of seizures. In each case family members or close friends

were asked to monitor this record to ensure its accuracy. Subjects

were frequently reminded of the importance of this diary and asked to

bring it in weekly to assure understanding and compliance.

The following section presents Individual Subject Profiles

indicating summaries of each subject's background medications, EEG

data and pertinent medical and behavioral information.


Individual Subject Profiles


Subject #1 was a fifty-four-year-old divorced white male with a

history of seizures from age thirty-one. He has been diagnosed as

having complex-partial seizures with a right temporal parietal focus.

The patient has been operated on with right parietal lobe surgery as

a result of an old trauma. Medication prior to and throughout train-

ing consisted of Dilantin 300 mg.a day.

A review of EEG records revealed an asymmetry of fast activity

because of high amplitude over the right parietal and temporal regions.

Also, continuously low voltage and irregular slow waves in the theta

and delta range were seen over the right parietal and temporal regions.

This was considered an abnormal EEG because of the above. These







alterations were considered compatible with a structural lesion. The

asymmetry and lateralized fast activity were thought to be due to the

skull defect.

The patient's typical seizure pattern consisted of tactile

sensory loss accompanying partial hand and facial paralysis on left

side and an expressive aphasia ranging frommarkedly slurred speech to

no speech at all. There was no loss of consciousness during these

episodes.

Seizure frequency at the beginning of the study: 59 per month.

Subject #2 was a twenty-three-year-old single white male with

history of seizures from age ten. He has been diagnosed as having

psychomotor seizures with an unknown etiology. Medications prior to

and throughout the course of training consisted of: Tegretol, 600 mg.

a day; Tranxene, 7.5 mg.,five times a day.

A review of the patient's history indicated some behavioral

problems as a child, angry episodes, acting-out. These behaviors

have not been noted in the patient's record since 1971.

Review of EEG records revealed an initial abnormal EEG with left-

sided predominance; sharp activity was seen over both midtemporal and

posterior temporal areas. Later records indicated diffuse bitemporal

slowing with background rhythms almost continuously irregular in the

2-1/2 to 5 Hz range over the temporal, parietal, and occipital

regions. The latest clinical interpretation commented that little if

any trace of alpha rhythm was evident. The patient's diagnosis has

uniformly been psychomotor seizure presently with a bitemporal focus.

The patient experiences an aura with a "scary" feeling beginning

in his stomach and feeling of pressure in his head. A typical seizure








includes lip smacking and finger movements. There is a post-

ictal stupor and tiredness that lasts from several minutes to

several hours.

Seizure frequency at beginning of study: 27 per month.

Subject #3 was a thirty-two-year-old white married male with a

history of seizures, post traumatic in etiology, since 1975. Medica-

tions at the outset of training consisted of Dilantin 400 mg. a day

and Tegretol 1000 mg. a day. During the course of training Celontin

500 mg. was added.

Review of EEG records revealed an abnormal EEG with focus of

epileptiform discharge in the right anterior temporal regions.

Throughout the tracing a focus of epileptiform sharp waves and spikes

and slow waves were identified emanating from the right anterior

temporal regions.

Behaviorally the patient has been described by his neurologist as

having a decreased libido, a seemingly growing disinterest in sexual

relations with his wife though no reported inability to achieve and

maintain an erection, and a significant weight loss. The patient has

been described as being depressed due to his inability to maintain

his former lifestyle as worker and provider.

A typical seizure for this patient manifested itself with amnesia

and automatic auras of short and mild duration as to be not useful in

self-control. He also manifested various kinds of situational automa-

tisms. This subject attended the study for three baseline days and five

days of treatment trials but decided to drop out of the experiment.

Seizure frequency at beginning of study: 20 per month.

Subject #4 was a twenty-four-year-old white divorced female

with a history of seizures since age nineteen. She has been described








as having psychomotor seizures of traumatic origin. The patient

suffered a closed head injury in an auto accident two years prior to

the onset of seizures. Medication at the outset and during the course

of training consisted of Dilantin 100 mg.,five times a day.

Review of EEG records revealed an abnormal EEG with epileptiform

discharges in the right posterior temporal region. There was signifi-

cant slowing into the theta and delta range over these areas and the

fronto-temporal area.

Behaviorally the subject presented herself as the one patient

most positive and interested in maintaining a normal lifestyle which

included work and family. Even when the frequency of her seizures

made it impossible to work, she continued to plan for the time when

she would again be able to work. Despite large difficulties in her

personal life, the patient was able to complete training with few

disruptions.

A typical seizure for this subject consisted ofa feeling of

paralysis, a severe memory disruption, and often a feeling of dis-

orientation and anger postictally.

Seizure frequency at beginning of study: 207 per month.

Subject #5 was a twenty-six-year-old white married male who was

injured and sustained a subdural hematoma in 1969. The onset of

seizures was in 1971 with frequent major convulsions and brief

complex partial automatisms. Medication prior to and throughout the

course of training were Mysoline 1000 mg.a day and Dilantin 300 mg.

a day.

A review of EEG records revealed an initial abnormal EEG with

the primary focus over the right temporal area. Subsequent recordings








indicated a markedly abnormal tracing with the occurrence of bi-

synchronous generalized epileptiform activity maximal over the right

hemisphere. The patient's present diagnosis is a complex partial

seizure disorder with a right temporal focus with a secondary bi-

lateral synchrony. There is some generalization of seizures to the

grand mal type.

Seizure frequency at beginning of study: 19 per month.

Subject #6 was a twenty-four-year-old white single male with a

history of seizures from age twelve. He has been diagnosed as having

psychomotor seizures with a left-temporal focus secondary to two

surgical procedures in the left fronto-temporal area for obliteration

of an AV malformation in the middle cerebral circuit. Medications

prior to and throughout the course of training consisted of Dilantin

500 mg.a day and Celonten 1200 mg.a day.

A review of the patient's history indicated a psychiatric hospi-

talization for an acute psychotic episode. Presently he is attending

a day hospital program and is well motivated to seek employment.

A review of EEG records revealed an abnormal EEG with a dis-

organized rhythm with voltage in the range of 6-8 Hz. There was

considerable slowing in the delta range with a discrete spike focus in

the left midtemporal area (seen over the T3 electrode) and considerable

theta activity also. The diagnosis was a psychomotor seizure condi-

tion with a primary left-temporal focus.

The patient experienced an aura, a peculiar feeling in his chest,

and a salty taste in his mouth. His typical seizure was like a dream

of falling, temporary expressive aphasia and loss of train of thought.

Seizure frequency at beginning of study: 147 per month.







Procedure

Prior to the initiation of training each patient was administered
an EEG using bipolar referents T3-T4, C3-C4 with an ear ground (using

the 10-20 electrode placement system). The C3-C4 placement was collected
on channel 1 and T3-T4 was collected on channel 2. Twenty to fifty
minutes of recording was obtained for each subject. They were in-
structed to stay awake throughout the recording sessions but asked to
keep eyes closed. Though every attempt was made to instruct subjects
to remain awake, one subject, #1, did fall asleep during the post

session. The light sleep portion of his record was omitted from the
analysis. The record was obtained on paper and FM tape. This pro-

cedure was again followed immediately upon the completion of training.

During the preparatory phase each patient was individually inter-
viewed using Mostofsky and Balaschak's (1977) seizure questionnaire and
given a copy of a short article entitled An Introduction to Biofeedback

(Fuller, G. and Sempell, P., 1977), a layman's guide to physiological

feedback. This article was the basis for subsequent discussions of
the nature of physiological feedback. A tape recording instructing the
patient in proper procedure and providing samples of the kind of feed-

back sounds they might expect was played four times (see Appendix A for
script)--once during the initial interview and prior to sessions 4-5
and 6--so as to familiarize them with this feedback mode. It was

constructed to duplicate auditory feedback of 20 percent, 50 percent,
and 100 percent success in producing alpha. They also were provided

feedback for theta (alarm) and that of artifact from too much movement.
Subjects were instructed to increase the occurrence of one tone and

suppress the alarm. All subjects were instructed to keep their eyes
closed. On a chalkboard in the feedback room a diagram showing the
various frequencies and their respective feedback was provided to enable







the patient to grasp more concretely the nature and rationale behind

the desired response.

Training took place from three to four times per week with a ses-
sion, including electrode placement and posttraining feedback, lasting
one and one-half hours. Standard Grass Disc Electrodes were used for

recording. Placement was bipolar, using T3-T4 and C3-C4 for alpha en-
hancement and theta suppression, respectively, and an ear ground.

Hewlett-Packard Redux electrolyte paste was employed and the electrodes
were cemented to the scalp with collodion and dried with a compressed
air stream. The criterion for acceptable electrode contact was less

than 10,000 ohms resistance as measured on a digital volt-ohm meter.

Patients were seated in a comfortable, reclining chair, in a
quiet room 15 x 13 feet. The room was further subdivided and darkened
via the use of two cushioned standing partitions that served to
militate against any extraneous light and sound and give the feedback
space an isolated smaller appearance. To the rear and approximately
three feet away sat the experimenter who monitored all patient
behaviors and all feedback through a common headphone setup.

Feedback consisted of an auditory tone that varied in pitch (sig-
nifying frequency changes in the pass band) and loudness (indicating

EEG amplitude within the pass band) whenever the subject produced six
successive zero crossings in the alpha range (9-13 Hz). Also there

was an alarm that sounded whenever his EEG frequency exhibited six
successive zero crossings in the theta range (3-8 Hz) and remained on
until such time that he ceased to produce waves in this range.


Experimental Design

Using an A-B1-C-B2(D) design, each patient was run through

between 32 and 36 fifty-minute trials. Figure 1 indicates













PostTraining
PreTraining PreTreatment Treatment 1 NonContingent Treatment2 Theta EEG
EEG Baseline Phase Suppression Clinical
Record












SDiary



Measurement
of dependent
variables
alpha/
aver. freq.& SD

aver. amp.& SD
theta %
theta count






3 sessions 18 sessions 4 sessions 6 sessions 3-4 sessions


CONDITIONS:


Figure 1.


B1


B2 (D)


Schematic representing sequential operations of treatment
conditions.








the various operations and measurements over the entire study for

each subject. Each trial was divided into ten five-minute segments

(see Figure 2) with a 45-second lag time when no data were collected.

This lag time enabled the alpha-numeric component of the 5400 system

to print out the previous segments data. At the beginning of this

intermission the patient was required to respond to a light touch on

the arm by lifting the index finger on the right hand. The patient

was provided with the digital feedback obtained consisting of alpha

wave percentage and theta wave percentage. Supplemental encouragement

was given to enhance the alpha level and suppress the theta by keeping

the sound on and the alarm off.

The initial three trials (Condition A) were baseline sessions

when no feedback was provided. From trial four through twenty-two

(Condition Bl),contingent feedback was provided for segments two

through nine. Segments one and ten were again baseline where the

subject was not provided with auditory feedback. Sessions 23-26

(Condition C) consisted of the identical ten-segment procedure but

utilized noncontingent feedback for the eight feedback segments.

Tape recordings of each subject's sessions 21 and 22 were interfaced

with the feedback apparatus. Sessions 23 and 25 utilized the tape

recording from session 21 and sessions 24 and 26 were based upon

session 22. All procedures were identical to contingent trials

including the usage of the digital feedback from these previous

sessions. Upon debriefing at the conclusion of the study,it was

clear that none of the patients were aware of this manipulation as the

tape recorder had been used various times in the past during sessions

to accustom the patients to its presence.

























- Treatment phase -
8 5 minute segments
auditory feedback

tone for alpha
alarm for theta


Wiri"-Ir v I -i


SEGMENTS#


1


PostTreatment
(no feedback)
5 minutes


10


10 5-MINUTE SEGMENTS


Schematic representing typical treatment trial with ten
five-minute segments.


PreTreatment
(no feedback)
5 minutes


Figure 2.


I ---L9(~ __ _c_-~ .1 __


I _01


Ii








Sessions 27-32 (Condition B2) were again contingent trials when

feedback was provided depending upon the subject's alpha wave produc-

tion and theta suppression.

For three of the subjects (#2, #5, and #6) C3-C4 location was

employed as the active locus for feedback (Condition D), and the

subjects began receiving the analogue tone indicating only theta's

presence. They were told that the presence of the tone signaled theta

and were instructed to keep the sound off. Subjects #2 and #5

received four such trials while #6 received three theta suppression

trials.


Apparatus

The apparatus consisted of several major components: two EEG

waveform analyzers (an Autogen 120a and Autogen 70a), an Autogen 5400

data acquisition unit, and a tape recorder. Both the 120a and 70a

operate as variable bandpass filters for the EEG within the range

from 2-20 Hz. The Autogen 120a permits feedback for EEG frequency and

voltage levels continuous within its range of 2-20 Hz and 10-150 uV.

The 120a was set at 100 PV so as not to reinforce epileptiform EEG

activity. The output of the Autogen 120a consists of frequency,

amplitude, percent time in a pass band, and the output of the 70a of

discrete occurrences of a selected frequency within a pass band from

which both a percent time and a count measure was obtained. The 120a

was used to measure alpha (9-13 Hz) along the three parameters

specified above and provide an auditory feedback, varying in pitch

and loudness when the patient was producing EEG frequencies within







this range. Pitch varied with EEG within the pass band while loudness

varied with EEG amplitude shifts. A distinctive alarm sounded when

the subject's EEG frequency fell 1 Hz or more below the lowest fre-

quency in the pass band and came on at 8 Hz. This alarm served two

purposes: 1) to warn the subject of potential drowsiness and 2) to

serve as a theta indicator. The Autogen 70a was used to record the

percent time of theta and the number of discrete occurrences in the

five-minute period. The Autogen 120a monitored from T3-T4 leads

while the 70a monitored from C3-C4 leads. This was reversed only in

the last condition (D).

The Autogen 5400 and the attached Alpha-Numeric Printer were

employed to tabulate the data from the 120a and 70a and produce a

paper tape recording that was timed to print out a data summary every

five minutes. In addition to the means of each of the variables it

provided standard deviations of alpha amplitude and average frequency

standard deviations between 2-20 Hz.

The Akai tape recorder was interfaced with the feedback units to

allow for tape recording and playback capabilities during the

noncontingent trials.


Data Analysis

The two channels of EEG data collected were obtained, before and

after physiological feedback training, both on chart paper and FM

tape, C3-C4, channel 1, and T3-T4, channel 2, (International 10-20

electrode system). They were analyzed via the method of frequency

analysis. The program, run on a PDP-8E computer, was designed to

analyze results between the frequencies 1-20 Hz in 0.5 Hz increments.







The input from the FM tape was prefiltered with a Krohn-Hite filter set

between 1-20 Hz to exclude frequency artifact. The program sampled the

input 1000 times/second and timed each zero crossing, storing each in

a register. At the end of a ten-minute epoch, input was terminated,

and the contents of each register were printed. It then measured the

time elapsed since the last data input and formed a histogram indicat-

ing the number of counts in each of the 0.5 Hz period bins. In addi-

tion, the average frequency within each of seven bands (1-3 Hz,

3.01-5.99....18.1-20 Hz) together with the percentage of total

time within each of the pass bands, was tabulated and printed. The

values of these bands were selected to approximate the ranges of

delta, theta, and alpha frequencies in three Hertz increments. To

produce a meaningful frequency axis, the data were collected in time

intervals such that their inverse was close to the integer frequencies

and their midpoints (i.e., 1, 1.5, 2, 2.5, etc.).

A Chi-square test was performed to examine the two histograms

to test the hypothesis that the EEG data were drawn from different

populations. Further, the individual Chi-squares were obtained in

approximately 3 Hz bands to determine where significant effects took

place within the 1-20 Hz population.

Seizure diary data were examined as a function of treatment

conditions to determine the possible correlation of seizure rate with

the acquisition of the dependent variables. In addition, a correlation

between seizure rate and all dependent variables was performed.

The statistical analysis was directed to determining the sig-

nificance of changes between the separate conditions of the experiment,

A-B -C-B2-(D), in the sequence of treatment shifts. The output from

the Autogen 5400 was punched onto cards and subjected to a time-series







analysis using an autocorrelation function and curve-fitting procedure.
The data in the study represented a 7 x 1761 matrix (each of the depen-

end variables times each of ten five-minute epochs foreach of the thirty-six

trials). An autocorrelation function is a correlation of a time-series
with itself. It is obtained by pairing observations of x units apart
(Gottman, McFall and Barnett, 1969). This then provided the serial

correlation of these data as a function of lag. For the baseline period
lags of one through ten were employed, while for the pre- and post-

periods lags of one were employed. The curvefitting procedure involved

fitting the data to the least squares straight lines. The difference

between slopes and between means was then calculated using as a test

of significance a series of all possible t-tests.

Changes affected by the treatment procedures were analyzed by three

procedures: 1) slopes within treatment conditions were assessed with

respect to whether each slope was negative, zero, or positive; 2) dif-
ferences between slopes within each period for each variable and,

finally, 3) the differences between the means of all baseline-

treatment combinations within each subject were calculated.

The presence of a slope significantly different from zero within a
condition indicted that a relationship existed between the treatment

conditions and the EEG variable under consideration. For example, a sig-

nificant positive slope demonstrated that a direct relationship existed

between application of the treatment and an increase in the EEG variable.
Likewise, a negative slope demonstrated that the EEG variable decreased
in magnitude over the course of the treatment condition.

The significance of the slopes was evaluated following the removal
of the autocorrelation effects. This removal of the autocorrelation
was made necessary since EEG data collected on a subject was predictive

of data produced over successive periods. Once accomplished, the data
assured the independence of repeated observations over time. Following




* L


this, a least squares line was determined for the EEG data within each

subject, for each variable during each condition.

The autocorrelation and least squares analysis was accomplished by an

evaluation of the data with a commercially available autoregression program

(Barr, Goodnight, Soll, andHelwig, 1976). The program's output provided

ordinary least squares analysis, autocorrelation statistics and estimates

of the least squares statistics after removal of autocorrelation, to-
gether with the calculation of the significance levels of the tests.

Next, selected contrasts between slopes were calculated using a modi-

fied "t" statistic. The difference was calculated by the following equation:

X1 X2
t= (1)
2 2
"1 1 2 2 1s 1
n1 + n2 2 n1 n2

where x1 = baseline slope estimate

x2 = treatment slope estimate
n1 = number of observations in baseline condition

n2 = number of observations in treatment condition

S2 = baseline slope variance
1
S2 = treatment slope variance

The significance was evaluated to allow for adjustment of alpha
error as a function of multiple pairwise contrasts using t-statistics

(Games, 1977).

Finally, selected contrasts between the means within each condition
were accomplished. The equation was the same as (1) above but employed

the estimated mean condition value for Xl & i2, and s & 2 terms were

replaced by the error sum of squares obtained from the autoregression

program. Again, the table provided by Games (1977) was employed to

evaluate significance levels.














CHAPTER III
RESULTS


The results are detailed in three major sections: 1) hypothesis 1,

frequency analysis data of pre-/post-EEG measures; 2) hypotheses 3 and

4, time-series analysis of day-by-day training data comprised of

alpha and theta changes; 3) hypothesis 2, seizure diary data and its

relation to treatment conditions.


Data with Respect to Hypothesis 1


Changes in the Frequency of EEG Occurrence <8 Hz and in the
9.02-12.05 Hz Range


This hypothesis predicted that subjects will display a frequency

shift from slow frequency ranges <8 Hz toward predominantly alpha

activity in the 9-13 Hz range. This result was predicted from the

contingencies presented in the experiments, namely, a) physiological

feedback and instructions to suppress low frequency activity in the

<8 Hz range, and b) instructions to increase the occurrence of

frequencies between 9-13 Hz (exclusive). (See Tables 2-11 for chi-

squares, number of counts and mean frequency data for all subjects.)

Subjects #4, #5, and #6 displayed a frequency shift from low

frequency activity toward faster as measured by the mean frequencies

of the pre-/post-EEGs.

Subject #1, because of a skull defect which allows high frequency

activity to be observed without normally occurring attenuation, showed



















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a significant reduction in average frequency. For this subject this

shift was considered a normalizing one. He, unlike the other subjects

on the initial EEG, had not manifested overall slowing but instead

produced an increased amount of faster activity in the 7-13 Hz range.

Subject #2 displayed a slowing of activity with pre-/post-

measurement, and this result does not appear to support the hypothesis.

Dividing the overall frequency pattern into approximately three Hertz

bands allowed a finer discrimination to see where shifts did or did

not take place.

Subjects #4, #5, and #6 displayed a significant diminution of low

frequency responses in the frequency bands 1.0-3.01 Hz and 3.01-6.02 Hz

Subjects #1 and #2 did not exhibit the predicted change in these bands,

instead their post measures showed an augmentation of slow frequency

responses. Both subjects #1 and #2 did, however, evidence a signifi-

cant diminution of response in the 6.02-9.10 Hz range.

Subject #4 was the only person who displayed a significant in-

crease in the number of counts in the 9.10-12.20 Hz range. Subjects

#5 and #6 produced a positive but nonsignificant count increase in

this band. Subjects #1 and #2 exhibited a significant decrease in

the number of counts, contrary to hypothesis 1.


Other Associated Changes in EEG Pattern Suggested by Frequency
Analysis


Though not reinforced, a significant augmentation in the number

of counts was demonstrated within the 12.2-15.2 Hz and 18.2-20 Hz range

for subject #5 on both channels. Subjects #4 and #6 demonstrated a

significant increase in the 12.20-15.15Hz range in channel 1. Though

nonsignificant, subjects #4, #5, and #6 produced a consistent trend







toward the faster frequencies from 9.10 Hz on. Subjects #1 and #2

demonstrated the opposite effect; subject #1 evidenced a significant

diminution on channel 2 in the ranges of 9.10-18.18 Hzand on channel 1

in the 12.20-20.0 Hz range. Subject #2 displayed a significant slowing

in the 9.10-12.20 Hz range and a nonsignificant slowing trend in the

12.20-18.18 Hz range.

Since the Chi-square changes represented both distributional and

level changes, the mean frequency shift was more instructive in

describing those changes. It did, however, reflect the combined

effects of all frequency bands and, in the specific case of alpha

diminution, may have distorted the picture.

Unfortunately, in dealing with dependent data, percentages were

employed and a shift in one frequency band was expressed as a change

in another. If the EEG is perceived on a continuum from hyper-

synchrony (many synaptic potentials occurring together) to synchrony

(with synaptic potentials largely out of phase), attempts to shift

toward a midfrequency range may result in diminished desynchronization.


Data with Respect to Hypothesis 2

Hypothesis 2 made the following predictions: 1) overall, seizure

incidence will diminish over time and be significantly less at the

completion of the study, and 2) this decrease will be a function of

the training condition (see Table 12 and Appendix B) and the abundance

of alpha and theta activity throughout all conditions (see Table 13).


Overall Seizure Incidence

Table 12 illustrates the test of the hypothesis that no shift
in the seizure rate occurs throughout the study. That is, the null


























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hypothesis that the treatment administered in a condition had no

effect upon seizure rate. The expected value reported for each condi-

tion in the table then is the product of the total number of seizures

each subject had throughout the study multiplied by the percentage

of total time occupied by each condition. This test appears con-

servative since the influence of the experimental conditions was of

interest rather than a pre-post test of seizure rate. Appendix B

presents a graphic summary of the observed and expected Chi-square

values from Table 12 for each subject.

Subject #1 produced a nonsignificant Chi-square indicating no

change in seizure incidence over the course of treatment. Subjects

#2, #4, #5, and #6 all displayed significant Chi-square values indicat-

ing a change in the frequency of seizures over the time course of

training. Taking into account the average seizures per day, subjects

#2, #4, #5, and #6 displayed an overall decrease. Subject #1, in

effect, displayed no change in the average seizures per day.

Seizure Incidence as a Function of Training Conditions

During baseline condition A, subjects #4, #5, and #6 produced a

significant departure from expectation by exhibiting a greater number

of reported seizures as measured by the average seizure per day figures.

This result was in keeping with the predictions of hypothesis 2 since

the baseline period (A) was assumed to measure the frequency of seizures

prior to intervention. Subjects #1 and #2 evidenced nonsignificant

results during this condition, which indicated no elevation in seizure

activity during the baseline period.

During the first treatment condition (B1), subject #4 demonstrated

a highly significant departure from expectation in seizure frequency.







This result was consistent with the predictions of hypothesis 2. Sub-

jects #2, #5, and #6 produced a nonsignificant diminution in seizure

incidence during treatment B1. Subject #1 displayed an increase in

seizure production during this condition, a result which was con-

tradictory to the expectations of hypothesis 2.

During condition C, the noncontingent feedback phase, subjects #2,

#4, and #6 displayed significant decreases in seizure rate--a result

not predicted during this condition. Subjects #1 and #5 displayed

nonsignificant decreases in seizure frequency--a result that was also

not predicted by the noncontingent feedback of condition C. This

matter will be explored further in the next chapter.

During the second feedback condition (B2) only subjects #4 and

#6 evidenced a significant negative correlation. For these subjects

these results indicate a decrease in seizure frequency.

Of the three subjects taking part in condition D, the direct sup-

pression of theta activity without concurrent alpha enhancement, subject

#6 was the only one to display a significant diminution in seizure

incidence. Subject #1 produced a significant increase in seizure

frequency. From the standpoint of hypothesis 2, only subject #6's

result was predicted.

Table 13 presents the correlations of EEG variables with seizure

frequency over all subjects and each individual subject. For all sub-

jects there was a significant negative correlation between alpha per-

centage and seizure incidence. As alpha percent diminished, the

seizure rate increased. On an individual basis, subjects #4 and #6

evidenced significant negative correlations while subjects #1, #2, and

#5 produced negative but not significant ones.




;)


For all subjects there was a significant positive correlation be-

tween average frequency and seizure incidence. In effect, as the aver-

age frequency increased, the rate of seizures also increased. On an

individual basis this result was particularly displayed by subject #4.

Though the overall correlation between average amplitude and

seizure frequency was not significant, subjects #2, #4, and #6 all

displayed significant positive correlations. This indicated that as

the average amplitude in their EEG waves increased there was a

similar increase in seizure frequency.

In reference to theta percentage and theta count subject #2

displayed a significant positive correlation indicating that there

was an increase in seizure rate as theta production increased. This

was the only subject for which this was true.


Data with Respect to Hypotheses 3 and 4


Hypotheses 3 and 4 were evaluated in two ways: one, the

significance of the slopes within each condition was determined.

These data allowed statements to be made as to the rate of change

within each condition testing it against the null hypothesis that

slope = 0. Second, the significance of the difference in slopes

between conditions and the difference in means was determined. These

data, too, allowed statements to be made as to the possible differences

in treatment versus baseline conditions testing against the null

hypothesis that the differences between slopes and mean = 0 (Kazdin,

1976). The slope data obtained within treatment conditions was

presented first, followed by the combined presentation of the contrasts

between the slopes and means for baseline versus all treatment

conditions.







Data with Respect to Baseline Condition A


Condition A stated that during the initial three-trial baseline,

subjects will display a zero slope (see Appendix C within condition

for data). Subjects #1 and #5 produced the predicted nonsignificant

slopes indicating no change in alpha percent during the baseline

period. Subjects #2, #4, and #6 displayed significant slopes with

subject #2 producing a positive one, which indicated an increase in

alpha and subjects #4 and #6 producing negative slopes which indicated

a diminution in alpha percent.


Data with Respect to Condition B1

During the eighteen-trial treatment condition, subjects will

display a positive slope and an increase in level change from baseline

condition A. In this context, level and mean represented the same

concept--namely, that a change occurs in the mean or average level of

a given dependent variable between one condition and other. It should

be noted that this definition differs from the one usually applied in

the classical time-series literature, which refers to a level change

as occurring when a discontinuity exists between the data at the

point when a treatment is introduced (Hersen and Barlow, 1976).

This condition consisted of a five-minute segment pre-/post-

alpha feedback where no feedback was forthcoming. These segments

were termed pretreatment B1 and posttreatment Bl, respectively.

Between these no-feedback segments there was a forty-minute alpha

enhancement condition to be called treatment B1.

During the pretreatment B1 period for within condition slopes,
subject #5 displayed no change in the rate of alpha production, a








result that was not coincident with a combined feedback/no-feedback

condition as one might have expected, as one might have expected a

gradual increase in alpha acquisition over time. Subjects #1, #2,

#4, and #6 all displayed a significant increase of alpha percent, a

positive slope. This result was coincident with the hypothesis.

During the treatment B1 condition, subjects #1, #4, #5, and #6

displayed the predicted enhancement of alpha percent during this

feedback phase. Subject #2 yielded a nonsignificant slope indicating

no change in alpha percent during this phase.

During the posttreatment B1 condition, subjects #1, #2, and #6

displayed nonsignificant slopes indicating no change in alpha produc-

tion. As with the expectations of pretreatment B1, this result was

not in keeping with the hypothesis. Subjects #4 and #5 produced a

significant positive slope indicating an increase in alpha percent.

Because these subjects also produced a significant treatment B1 effect,

this carryover to an immediate posttreatment no-feedback phase may

well have been a function of learning and, therefore, consistent with

the predictions of hypothesis 3.


Data with Respect to Condition C


During the four-trial noncontingent condition, subjects will

produce a negative slope as compared with Condition B. As with the

treatment B1 condition, the noncontingent phase was divided into

three parts: 1) pre-noncontingent phase of five minutes with no

feedback; 2) forty-minute noncontingent phase, when sham feedback was

given; and 3) post-noncontingent phase of five minutes when no

feedback was forthcoming.








Subject #1 yielded a significant negative slope, indicating a

diminution in alpha percentage during this phase. Given this sub-

ject's prior history of a skull defect and inability to filter out

faster waves, this result might have been expected. During this time

this subject began again to produce fast activity very similar to that

produced during condition A. Subjects #2, #4, #5, and #6 yielded

nonsignificant slopes.

During the noncontingent feedback phase, subjects #1 and #5 pro-

duced significant negative slopes indicating a diminution in alpha

production as a result of this false feedback stage. This result was

in keeping with the tenets of hypothesis 3. Subjects #2 and #4 yielded

nonsignificant slopes, indicating no change in alpha production as

compared with baseline measures. Subject #6 displayed a significant

positive slope which indicated an increase in alpha percent.

During the post-noncontingent phase, subjects #1, #2, #5, and #6

all produced nonsignificant slopes indicating no change in alpha wave

percentage. These results were predicted especially in the case of

subject #5, who produced a significant diminution in alpha in the

prior phase and a nonsignificant slope in the pre-noncontingent phase.

These results, taken together, indicated that for this subject the use

of noncontingent feedback had a direct effect upon his response. When

he was released from this feedback, he reverted to a no change status.

Subject #4 produced a significant negative slope indicating a

continued diminution of alpha percent during this latter phase.







Data with Respect to Condition B2


During the six-trial contingent alpha enhancement condition

subjects will display a positive slope and a significant increase in

level from baseline condition A.

During the pretreatment phase subjects #1, #2, #4, #5, and #6 all

yielded nonsignificant slopes indicating no change in alpha production.

During the contingent feedback phase, subjects #1, #2, and #4

yielded nonsignificant slopes indicating no change in alpha production

as a result of feedback. Subjects #5 and #6 produced significant

negative slopes demonstrating a decrease in alpha wave production.

These results are contrary to the direction predicted by the contingent

phase of hypothesis 3.

During the posttreatment phase all subjects yielded nonsignificant

slopes, indicating no change in alpha production during this phase.


Data with Respect to Hypothesis 4

Data with Respect to Condition A


During the initial three-trial baseline, subjects' data level will

be stable and a least-squares line fitted to the data will have a

zero slope.

Subjects #2, #4, and #6 displayed the predicted nonsignificant

slopes indicating no change in theta percent during the baseline

period. Subject #1 produced a significant positive slope indicating

an increasing amount of theta production in the absence of feedback.

Subject #5 exhibited a significant negative slope indicating a

decreased theta production during the baseline period.







Data with Respect to Condition B1


During the eighteen-trial treatment condition, subjects will

display a negative slope and a decrease in level from baseline

condition A.

This was a tripartate condition consisting of a five-minute

segment pre-/posttheta suppression where no feedback was forthcoming.

These segments will be termed pretreatment B1 and posttreatment B1,

respectively. Between these no-feedback segments there was a forty-

minute theta suppression condition to be called treatment B1.

During the pretreatment B1 phase subjects #1, #2, #4, #5, and #6

all displayed nonsignificant slopes. This result was not in keeping

with hypothesis 4. Because of the contiguity in time of treatment Bl,

a gradual increase in slope indicating a learned generalization was to

have been expected.

During the treatment B phase, subjects #1 and #4 displayed a sig-

nificant diminution in theta production, a result which is coincident

with hypothesis 4. Subjects #2, #5, and #6 evidenced nonsignificant

slopes indicating no change in the amount of theta produced.

During posttreatment B1, all subjects displayed nonsignificant

slopes indicating no change in theta production during this no-feedback

phase, again inconsistent with the hypothesis.


Data with Respect to Condition C


During this four-trial noncontingent phase, subjects will produce

a positive slope and a decrease in level from baseline condition A.

Like the treatment B1 condition, the noncontingent phase was

divided into three parts: 1) pre-noncontingent phase of five minutes







with no feedback; 2) forty-minute noncontingent phase where feedback

was supplied; and 3) post-noncontingent phase of five minutes with no

feedback.

During the pre-noncontingent phase all subjects produced non-

significant slopes indicating no change in theta production, a result

coincident with hypothesis 4.

During the noncontingent feedback phase, subject #5 displayed a

significant negative slope indicating a diminution in the amount of

theta produced. Subjects #1, #2, #4, and #6 evidenced nonsignificant

slopes indicating no change due to noncontingent feedback.

During the post-noncontingent phase, all subjects displayed

nonsignificant slopes indicating no change in the production of theta.


Data with Respect to Condition B2


During the six-trial contingent phase, subjects will display a

negative slope and a significant decrease in level from baseline

condition A.

As in the B1 condition, B2 was contingent and divided into three

phases: 1) a five-minute pretreatment phase with no feedback;

2) forty-minute treatment phase with theta suppression; and 3) a

five-minute posttreatment phase with no feedback.

During the pretreatment B2 phase, subject #1 produced a significant

diminution in theta percent, and subject #5 displayed a positive slope

which indicated an increase in theta production. Subjects #2, #5,

and #6 produced nonsignificant slopes which indicated no change in the

production of theta.







During the treatment phase of B2, subjects #1 and #5 displayed

significant negative slopes indicating a diminution in theta production

during this phase. This result was consistent with the tenets of

hypothesis 4. Subjects #2, #4, and #6 displayed nonsignificant slopes

indicating no change in theta production due to the combined alpha

augmentation and theta suppression.

During the posttreatment phase of condition B2, subjects #2 and

#5 produced negative slopes indicating a decrease in theta production

in this phase. Subjects #1, #4, and #6 displayed nonsignificant slopes

showing no change in theta production.


Data with Respect to Condition D


During the three- to four-trial theta suppression condition,

subjects will display a negative slope and a significant decrease in

level from condition A.

During the pretreatment phase of condition D, subjects #1, #2,

and #6, the only ones taking part in this condition, all displayed

nonsignificant slopes indicating no change during this phase.

During the treatment phase of condition D, subjects #1 and #6

both evidenced a significant negative slope indicating a diminution

in the production of theta. This result was consistent with

hypothesis 4. Subject #2 produced a nonsignificant slope showing

no suppression in theta production.

During the posttreatment phase of condition D, all subjects

displayed nonsignificant slopes indicating no change in theta during

this phase.








Between Slope and Mean Differences


Though all pair-wise comparisons were determined, only the dif-

ferences between conditions A-B1, A-C, A-B2 and A-D, that is, the

differences in baseline and treatment conditions, were reported for

alpha percent and theta percent. Appendix D presented the selected

pair-wise contrasts between these conditions for slopes and levels.


Data with Respect to A-B1 Alpha/Theta Comparisons


The pretreatment phase condition B1 yielded a significant ac-

celerated alpha slope for subjects #1, #4, and #6. Subject #2 dis-

played a deceleration in alpha production in this comparison.

During the treatment phase subjects #1, #4, #5, and #6 evidenced

a significant accelerated alpha response slope as compared to baseline.

Subject #2 yielded a significant deceleration in slope in this

comparison.

During the posttreatment B1 phase subjects #1, #4, and #5

yielded slopes that were accelerating significantly when compared to

baseline recordings.

In reference to the slope of theta production during the pre-

treatment B1 phase, subject #1 produced a significant decelerated slope

which indicated that this phase had an effect on changing responding

in a negative direction. Subjects #2 and #5 displayed an A-B1 slope

comparison which indicated a greater acceleration of theta as compared

to baseline.

During the treatment phase the slope of theta production was

significantly decelerated for subjects #1, #4, and #6. Subjects #2








and #5 displayed significantly accelerating slopes which indicated

an increase in theta production as compared to baseline.

The posttreatment A-B1 comparison yielded a significant decelera-

tion in slope for subject #6. Subject #5 produced an acceler-

ated slope which indicated an increase in theta responding.


Data with Respect to A-C Alpha/Theta Comparisons


The pre-noncontingent phase yielded a significant deceleration in

slope for alpha percent for subjects #1 and #2. Subjects #4 and #6

displayed an acceleration in alpha production as compared to baseline.

The noncontingent phase of condition C yielded a significant

deceleration in the slope of alpha percent for subjects #1 and #2 as

compared to baseline. Subject #6 displayed significantly

accelerating slopes which indicated a continued increase in alpha

production.

The post-noncontingent phase yielded a significant deceleration

in the slope of alpha for subject #2. Subject #6 displayed an

accelerated slope as compared to baseline.

The A-C slope comparisons of theta production during pre-

noncontingent phase of condition C yielded a significant deceleration

for subject #1 as compared to baseline. Subject #6 displayed an

accelerated slope which indicated greater theta responding as compared

to baseline. Subject #5 displayed no significance difference in

slopes but did evidence a significant level difference, indicating

greater theta responding though no change in direction of response.

During the noncontingent feedback phase subject #1 displayed a

significant deceleration in slope which indicated a decrease in theta








productivity as compared to baseline. Subject #5 displayed a lessened

deceleration as compared to baseline. Subject #2 produced an acceler-

ated comparison which indicated an increase in theta responding.

During the post-noncontingent phase subject #1 displayed a

difference in slopes that indicated a deceleration of theta produc-

tion. Subjects #5 and #6 produced a significant acceleration in

theta production as compared to baseline.


Data with Respect to A-B2 Alpha/Theta Comparisons


The pretreatment phase of condition B2 yielded a significant

acceleration in the slope of alpha production for subjects #4, #5,

and #6. Subject #2 yielded a slope comparison which indicated a

deceleration in alpha responding as compared to baseline.

During the treatment phase of condition B2 subjects #4, #5, and

#6 yielded significant accelerating slopes as compared to baseline.

Subject #2 displayed a deceleration which indicated a lessening of

alpha production in this comparison.

The posttreatment B2 comparison yielded a significant accelera-

tion in slope for subjects #4 and #6. Subjects #2 and #5 displayed a

comparative deceleration in alpha production.

In reference to the A-B2 slope comparisons of theta production

during the pretreatment phase, subject #1 displayed a significant

deceleration in slope as compared to baseline. Subjects #2, #4,

and #5 produced A-B2 slope comparisons that indicated an acceleration

in theta production in the B2 pretreatment phase.








During the treatment phase subjects #1, #4, #5, and #6 displayed

significant decelerations in slope indicating a lessened production of

theta. Subject #2 displayed a significant slope difference

which indicated an acceleration in theta percent in the comparison.

The posttreatment A-B2 comparison yielded a significant decelera-

tion in responding for subjects #1 and #6. Subject #5 displayed

a difference in slopes that indicated an acceleration in responding

during the posttreatment B2 condition.


Data with Respect to A-D Alpha/Theta Comparisons


Since only three subjects (#1, #2, and #6) took part in the D theta

suppression condition, A-D comparisons were confined to them.

Subjects #1 and #2 displayed a significant deceleration in the

slope of alpha percent during the pretreatment phase. Subject #6

yielded a slope comparison which indicated a significant acceleration

in this phase as compared to baseline.

During the treatment phase subjects #1 and #2 again yielded a

significant deceleration in alpha production as compared to baseline.

Subject #6 again yielded a significant acceleration in alpha

production.

The posttreatment phase yielded a significant deceleration in

the slope of alpha percent for subjects #1 and #2. Subject #6 displayed

an acceleration of slope which indicated an increase in alpha responding

as compared to baseline.

During the pretreatment phase of condition D the A-D comparison

in slopes for theta production yielded a significant deceleration in

slope for D condition as compared to baseline for subject #1.








Subject #2 yielded a t-ratio of slope comparisons that indicated that

there was an acceleration of theta production.

During the treatment phase the A-D slope comparison yielded

significant deceleration in responding for subjects #1, #2, and #6

which indicated a lessened production of theta during this phase.

The posttreatment phase of the A-D slope comparisons yielded a

significant t-ratio which indicated a significant deceleration in the

slope of theta for subject #1. The remaining two subjects yielded

insignificant differences.

Of the fifty-four individual pair-wise contrasts for alpha

percent, none of the mean differences between slopes were significant.

This lack of difference, combined with the fact that the vast majority

of the differences between slopes were significant, harkened to a

change in direction of the individual slopes but not to level. This

result may well have been due to a baseline period that did not allow

differences in baseline versus treatment conditions to be discerned.

Of the fifty-four individual pair-wise contrasts for theta per-

cent,only three (subject #5 A-C, significant increase in slope and

level; subject #5 A-B2, significant increase in slope and level; and

subject #2 A-B2 significant increase in theta percent) proved to be

significant. As with measurement of alpha percent, the inadequacy

of baseline data may well have accounted for this result.

If physiological feedback can be considered a slowly learned

discrimination task, the results of significant slopes and nonsignifi-

can level might have been expected. A skill that required time to

develop would have produced stable maximal levels before the cumulative

effect of training produced significant differences in the means of




I L




Conditions. The fact that there were many significant within condi-

tion slope changes was seen as supporting this contention.














CHAPTER IV
DISCUSSION

The present study provides additional evidence for the efficacy

of EEG physiological feedback training in the midfrequency range as a

means of controlling seizures. To explore this matter further, this

chapter will be divided into three sections: first, a discussion of

individual hypotheses and the basis for their support or rejection;

second, critique of the experimental design and suggestions for

improvement; lastly, suggestions for future research.


Discrepancies Between Hypotheses and Results


Hypothesis #1 predicted an increase in EEG frequency during

feedback training. The overall results support this contention in

three of five subjects (#4, #5, #6). These subjects increased their

average frequencies in this pre-/postmeasurement condition.

Subject #1 displayed a decrease in average EEG frequency across

both bipolar electrode sites (T3-T4, C3-C4) in the pre-/postfrequency

analysis. As stated before, this subject's skull defect caused him

not to attenuate higher frequency activity, and, hence, the pretraining

EEG displayed this overabundance of fast-wave activity. The alpha

band (8-13 Hz) is essentially the middle range of the typical frequen-

cies recorded in the human EEG; an individual with predominantly

desynchronized beta activity when presented with the contingencies

of alpha feedback is likely to decrease his frequency to maximize







feedback in accordance with established set. The question that

is of course left unanswered in this subject's case is whether

diminishing the frequency reduces the subject's seizure rate. Since

no significant decrease in seizure rate occurred, it appears his

response to the task requirements was not beneficial.

Subject #2 was unable to increase mean frequency pre/post.

The conclusion one draws from this and the fact that he was also

virtually unable to control alpha and theta training contingencies is

that the procedure, as it is presently constructed, does not work for

him. This subject had a successful diminution of seizure rate only in

the C or noncontingent condition. Heightened arousal level resulting

from stimulus novelty (orienting reflex) cannot account for this

result in the subject's response because his average frequency

decreased during noncontingent periods.


Seizure Incidence and Treatment Condition Analysis


The finding that seizure rate was positively correlated with

average frequency is a potentially important result. This is in

contrast to Sterman's most recent statement (1978) where he indicates

an increase in average frequency is negatively correlated with seizure

rate. In discussing this discrepancy it is most important to note

the differences in the subject's seizure types chosen for the two

studies. Sterman chose subjects heterogeneous in seizure type ranging

from the centrencephalic to focal type. The present study chose

subjects only with focal seizures because it was thought best to

test the role of physiology feedback on a homogeneous population. It

is clear that the mechanism of seizure propagation is quite different







in centrencephalic versus focal seizures (Jasper, 1969). To attempt

to make any generalizations as to the efficacy of any one approach,

a distinctly homogeneous population is a prerequisite.

From the standpoint of focal seizure patients, the results indi-

cated an increase in seizure rate with an increase in average frequency.

As the variability of alpha production decreased, the seizure rate also

increased. From the standpoint of the malleability of the control

mechanisms of the brain, this result supports the notion that a

lessening of synchronous activity reduces the ability to inhibit

seizures for these subjects (Jasper, 1969). In effect, as the

thalamocortical synchronization reflected in alpha percentage decreases

during the production of faster, essentially desynchronous activity,

seizure rate increases. This result argues for a midrange hypothesis,

in effect a normalization, for individuals with focal motor seizures.


Alpha Acquisition


Alpha percentage was significantly and positively correlated with

feedback in the B1 treatment condition for four out of five subjects.

These results indicated an ability to acquire the alpha response as a

function of the treatment condition. When noncontingent reinforcement

was instituted, there was a significant within condition shift and a

between condition slope difference for three of these four subjects.

This same overall result was not forthcoming for the second contingent

condition (B2) and argues to the brevity of this condition as a cause

for its failure. This matter will be explored further in the section

on design critique.






Subject #2 displayed no effect from alpha acquisition training

during any of the treatment conditions. There were no readily explain-

able reasons for this result; this subject assiduously maintained

appointments, understood the task requirements and very much wanted

improvement. As will be stated later, the anomalous nature of this

subject's results argues toward the institution of an individually

designed treatment program using a prolonged baseline as a means of

discerning the appropriate contingencies for reinforcement.


Theta Suppression


Two of the five subjects were able to suppress theta occurrence

during the treatment B1 condition. The instability of this suppression

is mirrored by the fact that neither of them had any transfer to

either the pretreatment B1 phase or the posttreatment B1 phase. It is

well to view the general lack of success in the suppression of theta in

view of the pre-/posttraining EEGs. Three of the four subjects who

were successful in seizure abatement produced significant decreases in

the 1.0-3.01 and 3.01-6.02 Hz band (#4, #5, #6). None of these subjects

produced a significant change in the 6.02-9.10 Hz range. It is sug-

gested that the abnormally large number of counts in the 1.0-6.02 Hz

range to begin with as compared to posttraining constitutes an important

normalizing of these subjects' EEG patterns. In effect, these subjects

began with slower average frequencies than was anticipated by the

fourth hypothesis. Their training lessened the occurrence of delta

activity. It is likely that more extensive training would have had

an eventual effect upon the higher theta range (6-9 Hz).







Design Critique and Suggestions for Improvement


In discussing the strengths and weaknesses of the design we must

begin by realizing that the results taken as whole indicate an

acquisition of alpha without a similar diminution of theta.

From the standpoint of design the major weakness of this study

lies in an insufficient extended baseline period of EEG recording. If

these periods were sufficiently extended, one would expect a non-

significant slope indicating a consistent response mode from the

subject. Two of the five subjects displayed significantly negative

slopes in alpha percent and had this trend been allowed to continue

may well have enabled the significance of the mean difference between

baseline and contingent feedback (Bl) to be greater.

This statement is particularly important in regards to the mean

differences between conditions. Given that the vast majority of the

t-ratios for the differences between baseline and treatment conditions

were significant, a stable baseline period may well have enhanced

the possibility of significant differences in level,too.

One method of evaluating these changes from the baseline would be

to employ a multiple baseline procedure. Essentially this entails a

number of responses identified and measured over time to provide

baselines against which changes can be evaluated. When the baselines

are established, the experimenter then applies a treatment condition

to one of the behaviors and observes little or no change in the other

variable (Baer, Wolf and Risley, 1968). In this way significant

results would be more readily determined through the contrast of

concurrent baseline and treatment conditions.







Next, there appeared to be significant carryover effects with

measures of the dependent variables. In some cases, seizure rate

continued to remain depressed during the noncontingent conditions as

it had during the contingent ones. There are two aspects of the

carryover effect that must be explored: one, its relationship to

learning, a positive aspect and, second, its duration indicating the

need for a longer noncontingent period.

First, if the subject is being trained to respond under stimulus

control, one would expect some form of generalization outside of the

training situation. If the subject can only inhibit seizure production

during training trials, this procedure would be of little utility in

his everyday life. This carryover then can be considered a partially

positive result because of the presumed learned nature of feedback

contingencies.

Second, in attempting to demonstrate an effect one would assume

that by preventing the connection between EEG production and the

physiological feedback signal responding would return to baseline

levels. This did not take place presumably because tne noncontingent

condition was of insufficient duration to reestablish the baseline

levels. Yet, the only method of determining the permanence of the

changed level would be to utilize a prolonged noncontingent feedback

phase.

Lastly, in dealing with noncontingent manipulations in seizure

reduction, the ethical dilemma arises of reintroducing seizure activity

where it may have attenuated. In dealing with human subjects who

experience the debilitating effects of seizures, one sees a clash

between the very real necessities of scientific inquiry and the best

interests of the subject.







Why was alpha activity significantly controlled and not theta?

From the standpoint of task complexity both alpha acquisition and

theta suppression can be confidently considered fairly simple dis-

crimination tasks involving markedly different stimuli. It would seem

that it is easier to enhance an ongoing response set than to inhibit

it. In this dual task we are looking at the acquisition and recogni-

tion of a stimulus and the subject's response. These are two very

different tasks; the recognition of a stimulus may be far easier than

actually responding appropriately. Response differentiation could

have been facilitated by reinforcing each response individually over

time and then combining feedback signals.


Suggestions for Future Research


The aim of the present study was two-fold: one, to evaluate the

proposition that feedback of midrange EEG frequencies of the EEG via

synchronous alpha wave enhancement and theta wave suppression was an

efficacious means of seizure control; two, to attempt to develop a

procedure that was clinically viable in the sense of being able to

diminish the time needed to train an individual to attenuate seizure

rate.

In any suggestions for future research the aforementioned

methodological considerations are prominent and provide many of the

suggestions for part one of this section.

In devising future studies, one method of deciding upon the most

efficacious dependent variables is by correlating seizure diary

information rate with EEG parameters over a prolonged baseline. When

this is done, one would select only those EEG variables for reinforce-

ment which are positively related with seizure rate. This might well







permit the optimal choice of EEG variables for an individual subject

which, when reinforced or suppressed, would lead to seizure diminution.

This procedure would lend itself to an empirical evaluation of EEG

parameters, which when modified would lead to normalizing the EEG

of epileptics.

Certainly an important covariant in a study of this nature is the

subject's present and prior history of adherence to an anticonvulsant

regimen. In this regard, it is suggested that along with a prolonged

baseline of EEG and seizure diary data anticonvulsant blood levels be

included prior to and throughout the course of training. Richens

(1976) has indicated that the very fact of telling subjects that you

are able to monitor the level of medication changes their rate of

compliance in a positive direction. If, during the course of physio-

logical feedback training, it is seen that seizures are beginning to

attenuate, it would be well to monitor these levels closely to see if

there has been any change due to increased compliance. In effect,

what is argued for is a multidisciplinary approach that combines the

medical approach of diagnosis and anticonvulsant therapy with that of

the behavioral, which seeks to modify the ability of the individual

to become aware of and control pertinent physiological states that

are antithetical to seizure production.

In developing a consistent, long lasting program for seizure

control, the role of home feedback equipment is an important adjunct.

Sterman (1978) utilized such devices and 4-channel strip chart

recorders which kept track of the time of each session, its duration,

and the number of rewards obtained. As the advances of technology

make this a more cost effective approach, the benefit to the subject








and investigator is great. The subject has a means of training

available to him that increases the ease and possibility of compliance.

For the investigator data are collected in the subject's natural en-

vironment, and the problem of generalization from laboratory to home

is considerably lessened.

Another important subject covariant is that of expectancy of

success. Each of the subjects had experienced a prolonged and chronic

illness which modified their life in significant ways. Stroebel and

Glueck (1973), in discussing the expectancy or placebo effects common

to all therapies, contends that individuals who acquire and maintain

a realistic set of expectancies (basically, one that views the

procedure as possibly beneficial within the constraints of what is

possible) will have a greater chance of success than those who either

over- or undervalue the possible outcome of the procedure. Stroebel

and Glueck (1973) consider simple, well presented information as the

backbone of a realistic set of expectancies. It is incumbent upon

any research in this area to devise a means of gauging the subject's

initial knowledge and attitudes about the disorder and the training

procedure and, then, to attempt to increase realistic expectancy by

a systematic program to educate and inform him in a step-by-step

fashion. During this procedure it is important to have an ongoing

method to measure expectancy so as to gauge the effectiveness of the

training.













APPENDIX A
TRAINING TAPE SCRIPT


As examples of what you may expect to hear, short excerpts, previ-

ously recorded, will be played for you.

First, a tone stays on 20 percent of the time. You will notice

the tone varies both in loudness and pitch and goes on and off

frequently.

(tape here)

Next, a tone with 50 percent success. Notice also that the tone

varies in loudness and pitch and stays on about 50 percent of the

time.

(tape here)

Now, a tone that stays on 100 percent of the time. Here the

tone stays on nearly all of the time but slightly varies in terms of

pitch and loudness.

(tape here)

If you become sleepy or produce slow waves associated with

seizures, an alarm will sound.

(tape here)

This alarm will remain on as long as you are producing these slow

waves. Your job is to keep the alarm off and the sound on.




83


If you move around very much, a crackling sound called artifact

will be heard.

(tape here)

Try to remain as still as. possible so as not to produce this dound.

Again, try not to become sleepy and work at keeping the sound

on and the alarm off. This session will begin now.



























APPENDIX B
CHI SQUARE PLOT OF OBSERVED VS. EXPECTED SEIZURE FREQUENCIES
BY CONDITION








number of
seizures


2C-0













130


125-


11--

100-



















CONTONS: A


Chi Square Plot of Observed
by Condition


vs. Expected Seizure Frequencies
for Subject #1


observed
expected


B2


I__ _




86



number of
seizures


observed
195 expected -


150-
175-
17C0
165-
160.



15c0












2 5-




5"-














CoNoToS: A B1 C B2 D


Chi Square Plot of Observed vs. Expected Seizure Frequencies
by Condition for Subject #2
C-v




















by Condition for Subject #2







number of
seizures

20C -

10-







160







125
4A -












100-














20-
12-
0-
-U






















CON EDITIONS:


Chi Square
LP-

CONIIOS



ChiSqar


B1


B2


Plot of Observed vs. Expected Seizure Frequencies
by Condition for Subject #4


observed I
expected ,-- I








number of
seizures

205-
23D- observe m
tI expected --
19C

16-
175-

1--
I

















C.
16C-






i5c-
126-
10-




c,.
15-







Ac-




















..CONDITIONS,. A B1 C B2 D


Chi Square Plot of Observed vs. Expected Seizure Frequencies
by Condition for Subject #5
4--















by Condition for Subject #5




89


number of
seizures

205
20C- observed
expected -



179
7
1655
160



j .







10
i-S




CONDITIONS: \

























Chi Square Plot of Observed vs. Expected Seizure Frequencies
by Condition for Subject #6
I,,






.4-



1 -.




CNoDII.ONSo A B1 C B2 D


Chi Square Plot of Observed vs. Expected Seizure Frequencies
by Condition for Subject #6

























APPENDIX C
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