Effects of EMG-activated alarms on nocturnal bruxism

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Effects of EMG-activated alarms on nocturnal bruxism
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x, 146 leaves : ill. ; 29 cm.
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Cassisi, Jeffrey E., 1957-
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Bruxism -- therapy   ( mesh )
Biofeedback (Psychology) -- instrumentation   ( mesh )
Clinical and Health Psychology thesis Ph.D   ( mesh )
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Thesis:
Thesis (Ph.D.)--University of Florida, 1986.
Bibliography:
Bibliography: leaves 133-145.
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by Jeffrey E. Cassisi.
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Typescript.
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Vita.

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EFFECTS OF EMG-ACTIVATED ALARMS
ON NOCTURNAL BRUXISM



By

JEFFREY E. CASSISI


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

UNIVERSITY OF FLORIDA


1986













ACKNOWLEDGEMENTS

The author would like to thank his wife, mother, father

and entire family for their unwaivering support,

encouragement, and confidence. This work is dedicated to

Emil F. Ersay, M.D., who continues to inspire a long line of

health-care professionals.

This research could not have taken place without the

electrical-engineering expertise of James "Buddy" Lee. He

is one of the University of Florida's finest assets and

illustrates more than anyone that knowledge and

understanding are their own reward.

The author also expresses appreciation to his chairman,

F. D. McGlynn, Ph.D. This research could not have taken

place without him either. His knowledge and experience in

research design and methodology were indispensable. The

other members of the supervisory committee were extremely

helpful too. They contributed many suggestions which

enhanced the execution and interpretation of this

experiment.

The Dental Occlusion and Facial Pain Center under the

direction of Parker E. Mahan, D.D.S., Ph.D, has greatly

facilitated many aspects of this research. The staff in

that clinic are truly in the business because they want to

help people. Michael Henry, D.D.S., was always ready to












examine a new potential subject and he gave each one

individual attention.

Charles Gibbs, Ph.D. answered many questions about

muscle physiology early in the study. Scott Vrana and John

Steele helped with computer programming. Dale Belles and

Larry Kapel assisted with editing. Marc Wruble asked some

tough questions.

Many people are due thanks for being there when they

were needed: Robert and Connie Head, Michael Jamerson, Rade

Musulin, Carol Cornell, Laura Mee, Lynn Harllee, Charles

Bichajian, Alan and Elizabeth Dougherty, Lynn Cornell, and

Tom and Iris Spikes.


iii















TABLE OF CONTENTS

Page
ACKNOWLEDGEMENTS .................................... ii

LIST OF TABLES ................... ....... ......... vi

LIST OF FIGURES ...................................... viii

ABSTRACT .............................................. ix

INTRODUCTION .......................................... 1

ETIOLOGICAL THEORIES OF BRUXISM ....................... 3

Dental Theories ..................................... 5
Psychological Theories .............................. 6
Interactive Theories ............... .............. 7
Sleep Theories ...................................... 8

THE ASSESSMENT OF BRUXISM ............................ 10

Dental Signs ....................................... 10
Intraoral Telemetry ................................. 11
Audible Grinds .................................... 12
Bruxscore Monitor ................................... 13
Electromyography ................................... 14

AVAILABLE TREATMENTS FOR NOCTURNAL BRUXISM ............ 18

Dental Therapies .................................... 18
Psychological Therapies ............................. 20

EMG-ACTIVATED ALARM THERAPY ........................... 24

Early Research ..................................... 24
Contemporary Research ............................... 25

PURPOSES OF THE EXPERIMENT ........................... 43

METHODS ............................................... 47

Subjects ............................................ 47
Instrumentation ................................... 51
Measures .......................... ...... ......... 55
Procedure and Experimental Protocal ................ 60













RESULTS ................................. ............ .

Impact of Treatment .................................
Evidence Concerning Rebound Effects .................
Self-Monitored Versus Automated Alarm Count .........
Effects of Treatment on Vigor, Fatigue,
Sleepiness, and Pain ............................

DISCUSSION ...........................................

Impact of Treatment ................................
Evidence Concerning Rebound Effects .................
Self-Monitored Versus Automated Alarm Count .........
Effects of Treatment on Vigor, Fatigue, and
Sleepiness ....... .. ... ..... .......... ...........
Effects of Treatment on Facial Pain .................


Theoretical Explanations for Alarm Therapy
Effects ................................ ..

APPENDICES

A SUBJECT RECRUITMENT NOTICE .............

B STANDARDIZED DENTAL SCREENING EXAM .....

C SCREENING QUESTIONNAIRE ................

D INSTRUCTIONS FOR USING THE BRUX-MONITOR ..

E SCHEMATIC OF ALARM/MONITOR .............

F MORNING QUESTIONNAIRE ..................

G NIGHTLY ALARM RECORD .....................

H NIGHTTIME QUESTIONNAIRE ..................

I INSTRUCTIONS FOR USING THE BRUX-ALARM ....

J SUMMARY TABLES FOR ALL ANOVAs ............


K GRAPHS OF NIGHTLY BRUX RESPONSE FREQUENCY PER
HOUR FOR SUBJECTS 1 THROUGH 10 .................

REFERENCES ................................... ...

BIOGRAPHICAL SKETCH .................................


86

87

90

98

100

101

102

104

105

108


123

133

146


o o o







o....... o
....o..... .

.... .. .














LIST OF TABLES


Table Page

1 Subject Demographics ........................... 49

2 Means and Standard Deviations for the Nightly
Brux Responses per Hour by Group and Phase ... 67

3 Mean Self-Monitored Alarm-Count Versus
Automated Alarm-Count ...................... 71

4 Means and Standard Deviations for Daily
Ratings of Fatigue, Vigor, Sleepiness,
Tension, and Pain by Group ................... 72

J-1 Summary Table for the 2 x 3 ANOVA for Hourly
Bruxing Frequencies within the Screening ..... 108

J-2 Summary Table for the 2 x 2 x 14 ANOVA for
Hourly Bruxing Frequencies across 28 Nights .. 109

J-3 Summary Table for the 2 x 14 ANOVA for Hourly
Bruxing Frequencies within Phase 1 ........... 110

J-4 Summary Table for the 2 x 14 ANOVA for Hourly
Bruxing Frequencies within Phase 2 .......... 111

J-5 Summary Table for the 2 x 14 ANOVA for Hourly
Bruxing Frequencies for both Treatment
Phases ....................................... 112

J-6 Summary Table for the 2 x 14 ANOVA for Hourly
Bruxing Frequencies for Group 1 .............. 113

J-7 Summary Table for the 2 x 14 ANOVA for Hourly
Bruxing Frequencies for Group 2 .............. 114

J-8 Summary Table for the 2 x 14 ANOVA for Hourly
Bruxing Frequencies for both Baselines ....... 115

J-9 Summary Table for the 2 x 14 ANOVA for Method
of Alarm Count ............................... 116

J-10 Summary Table for the 2 x 2 x 14 ANOVA for
Vigor Ratings Across 28 Nights ............... 117

J-11 Summary Table for the 2 x 2 x 14 ANOVA for
Fatigue Ratings Across 28 Nights ............. 118












J-12 Summary Tables for the 2 x 2 x 14 ANOVA for
SSS Ratings for 28 Days ...................... 119

J-13 Summary Table for the 2 x 2 x 14 ANOVA for
Facial Pain/Discomfort Ratings for 28
Nights ..................................... 120

J-14 Summary Table for the 2 x 2 x 14 ANOVA for
Anxiety Ratings for 28 Nights ............... 121


vii














LIST OF FIGURES


Figure Page


1 Flow-chart of the Alarm/Monitor ................. 53

2 Overview of the Experimental Design ............. 62

3 Brux Frequency by Condition and Group ........... 68

K-1 Brux Episode Frequency Per Night
For Subject 1 ............................... 123

K-2 Brux Episode Frequency Per Night
For Subject 2 ................................ 124

K-3 Brux Episode Frequency Per Night
For Subject 3 ............................... 125

K-4 Brux Episode Frequency Per Night
For Subject 4 ......................... ..... 126

K-5 Brux Episode Frequency Per Night
For Subject 5 ......................... ........ 127

K-6 Brux Episode Frequency Per Night
For Subject 6 ....................................... 128

K-7 Brux Episode Frequency Per Night
For Subject 7 ................................. 129

K-8 Brux Episode Frequency Per Night
For Subject 8 ............................... 130

K-9 Brux Episode Frequency Per Night
For Subject 9 ............................... 131

K-10 Brux Episode Frequency Per Night
For Subject 10 .............................. 132


viii














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


EFFECTS OF EMG-ACTIVATED ALARMS
ON NOCTURNAL BRUXISM

By

JEFFREY E. CASSISI

December, 1986

Chairperson: F. Dudley McGlynn
Major Department: Clinical Psychology

Nocturnal bruxism is nonfunctional grinding and/or

clenching of the teeth during sleep. This behavior has been

directly implicated in various facial pain and

temporomandibular joint (TMJ) disorders. The present study

examines the effectiveness and contraindications of one

psychological treatment for bruxism, namely EMG-activated

feedback alarms.

Modification of bruxism is attempted ideally by a

dentist-psychologist team. Therefore, selected theories

related to dental and psychological practice are first

reviewed. Then alternative strategies for the assessment

and treatment for the problem are identified.

The overview of alarm treatment suggests that it might

be a relatively beneficial approach. The present study

tested the effectiveness of an alarm therapy protocol in

which alarm termination required wakeful operation of a











push-button switch. Ten heavy bruxers, as determined by a

dental screening and ambulatory monitoring, volunteered for

the 28 day study and were paid for participation. They were

divided into two groups that differed in sequencing of

baseline and treatment phases.

Comparisons both within and between groups revealed

that treatment significantly reduced bruxes per hour. Some

evidence suggested that treatment had an enduring effect.

Unobtrusive counts of alarm soundings during the night

were compared with subjects self-monitored tallies and they

were found to be significantly higher. This finding

suggests that self-monitoring is not an adequate method for

assessing nightly alarm sounding frequency.

Ratings of anxiety, fatigue, vigor, and sleepiness,

were made each evening. No evidence was found that alarm

therapy affected fatigue or sleepiness ratings. No evidence

was found that alarm therapy decreased rated vigor.

However, a significant increase in anxiety ratings was

detected during treatment phases.

The conclusion is offered that alarm therapy requiring

manual alarm termination is an effective treatment approach.

The conclusion is offered also that informed consent

requires information concerning the possible side-effect of

increased psychological tension. Future research avenues

are discussed.













INTRODUCTION

Recently there has been growth in the health-care

liaison between the professions of dentistry and psychology.

The dental community has encouraged the liaison by granting

support for behavioral science research in dentistry, by

publishing results from such research in dental journals,

and by hiring psychologists to participate in dental

education (Cohen, 1977; Sachs, Eigenbrode & Kruper, 1979).

Psychologists, in turn, have facilitated the liaison by

undertaking behavioral research related to dentistry, by

publishing findings in both dental and psychological

journals, and by adding content as well as methods to dental

curricula (Cohen, 1977; Page, 1978).

The continuing relationship between dentistry and

psychology has resulted in the emergence of "behavioral

dentistry," a special field of subject matter devoted to

areas such as promoting oral-hygiene self-care behaviors

(cf. Claerhout & Lutzker, 1981; Iwata & Becksfort, 1981;

McGlynn, Mings, Marks, & Goebel, 1985), and evaluating and

treating fear of dental settings (cf. Kleinknecht, McGlynn,

Thorndike, & Harkavy, 1984; Melamed, 1979). Substantial

research effort within behavioral dentistry also has been

devoted to evaluating and treating the various disorders of

craniomandibular articulation, e.g. the so-called

temporomandibular joint (TMJ) and myofascial pain











dysfunction (MPD) "syndromes" (Mealiea & McGlynn, 1986;

Moss, Garrett, & Chiodo, 1982; Rugh & Solberg, 1985; Scott,

1980). A closely related problem that has received renewed

research interest is nocturnal bruxism (Glaros & Rao, 1977;

McGlynn, Cassisi, & Diamond, 1985).

The experiment reported here is concerned with the

treatment of bruxism and facial pain. In the experiment an

attempt was made to reduce the frequency of nocturnal

bruxist behavior with the use of a portable biofeedback-like

device called a wake-up alarm. By way of introducing the

experiment, the following narrative overviews the various

theories concerning the etiology of nocturnal bruxism as

well as various assessment and treatment approaches for the

problem. Following this, the narrative reviews research

using EMG-activated wake-up alarms. The early sections of

the introduction are adapted from various sources to which

the author has contributed including Cassisi, McGlynn, and

Belles (1986) and McGlynn et al. (1985).













ETIOLOGICAL THEORIES OF BRUXIST BEHAVIOR

Bruxism is defined most frequently as a class of

oral-motor behaviors that includes nonfunctional or

parafunctional clenching, grinding, and gnashing of the

teeth (cf. Dubner, Sessle, & Storey, 1978; Scharer, 1974).

Bruxism is significant to health-care professionals because

it is widespread (cf. Scharer, 1974) and because its

symptomatic correlates frequently prompt help seeking.

Common among these symptomatic correlates are abnormal tooth

wear, damage to the temporomandibular joint (TMJ), various

facial pains, referred pains, and headache (Alling & Mahan,

1977; Ramfjord & Ash, 1983).

Frohman (1931) first used the English word bruxism. It

was derived from the French "la bruxomanie" used by Marie

and Pietkiewicz (1907). Bruxism has subsumed several

nonfunctional behaviors of the masticatory system and

uniform standards for defining and detecting bruxism have

not been used. Hence, there is extreme variability in

existing estimates of the incidence of the behavior (Glaros

& Rao, 1977). Some amount of bruxing or nonfunctional tooth

contact is normal during sleep (Powell, 1965) and many

authorities believe that all people engage in transient

bruxing at some time.

The various health-care disciplines involved with

bruxist patients have undertaken etiological research and











have brought to bear their own concepts in explaining the

behavior. Therefore, a large literature on empirical

correlates of bruxism exists and there are several "theories

of bruxist behavior." An exhaustive review of the various

theories is not presented here and no attempt at theoretical

arbitration is made. This follows from several

considerations. First, a comprehensive summary of the very

complex theoretical state of affairs is beyond the present

scope. Second, the empirical knowledge is limited and

support of particular theoretical formulations is weak.

Third, activities of diagnosis and treatment do not derive

from theoretical considerations, except at a general level.

Nadler (1957) arranged the correlates of bruxism into

four categories that included local/dental,

psychological/emotional, systemic, and occupational factors.

Glaros and Rao (1977) organized theories of bruxism into

three categories that subsumed local/mechanical,

psychological, and systemic/neurophysiological factors.

Scharer (1974) organized theories of bruxism into three

categories that involved neural, internal, and external

factors. These expository schemes impose categories that do

not exist as actually separate clusters of causes. Bruxism

is a behavior that results from multiple, interacting causes

that cut across these domains of variables (Rugh, 1976).

The categories below were used solely for purposes of

clarity.








5


Dental Theories
Some early dentists wrote that bruxism is caused by

anatomical factors such as missing or elongated teeth.

Contemporary views have shifted toward occlusal interference

as an etiological factor. There are various opinions about

which kinds of occlusal interference produce bruxing

(Carlsson & Droukas, 1984), but most dentists would agree

that "any occlusal interference may trigger bruxism"

(Ramfjord & Ash, 1983, p. 181).

There are reports of experiments in which various

occlusal interference were produced experimentally while

bruxing was monitored concurrently. For instance, Barghi,

Rugh, and Drago (1981) recorded nocturnal masseter activity

among five adult humans before, during, and after 10-15

days, during which a lateral deflection of the mandible was

produced with a crown. However, the results from studies of

this type have been inconclusive. Barghi et al. (1981), for

example, found that the nocturnal EMG activity of two

subjects dropped, one increased, and two remained unchanged

when the crown was in place. Hence, the consensus among

dentists that occlusal interference trigger bruxing is

overly simplistic.

Psychological Theories
Psychological theories of bruxism are derived from two

intellectual traditions. One is the tradition of











personology or personality theories. The other is the

tradition of psychosomatics.

Personality Theories

Psychoanalytic writers have suggested that bruxism is a

result of unconscious mental forces. For example, bruxism

might reflect repressed oral aggression (Forsberg, 1956;

Pond, 1968; Ramadan, 1970; Shapiro & Shannon, 1965; Walsh,

1965), or attempted gratification of oral needs (Frohman,

1931, 1932; McCartney, 1951; Ross, Bentley, & Greene, 1953;

Sumner, 1949). It is not scientifically productive to view

bruxing as related to unconscious mental forces, because the

psychodynamic theories are not disconfirmable.

There is a large literature on personality traits among

patients who suffer from craniomandibular disorders related

to bruxing. Some authors have described these patients as

passive-dependent and frustrated, while others have

described them as perfectionistic, domineering, and striving

to appear normal (Lefer, 1972; Moulton, 1955, 1966). Recent

investigations with the Minnesota Mutiphasic Personality

Inventory (MMPI) suggest that many patients with

craniomandibular disorders show conversion or depression

profiles (cf. Eversole, Stone, Matheson, and Kaplan, 1985).

For at least three reasons, however, the value of

personality-trait measures in understanding bruxism remains

in doubt. There is no agreement in the literature regarding

the nature of abnormal personality as it occurs in bruxist











populations. Studies have not found consistent personality

differences between craniofacial pain patients and "normal"

controls (Reding, Zepelin, & Monroe, 1968; Solberg, Flint, &

Brantner, 1972). Relevant studies have used subjects with

various craniomandibular disorders and only some of them

were bruxers.

Psychophysiological Theories

Bruxism can be conceptualized as a psychophysiological

or stress-related disorder. The following evidence is

required to confirm this view: (a) that stress and negative

emotions can lead to exaggerated activity in the muscles of

mastication; (b) that bruxers manifest greater masseter EMG

under stress than do nonbruxers; and (c) that there is a

correlation between stressful events and bruxing.

All three requirements are supported by some empirical

evidence. Yemm (1968, 1969, 1971, 1972) has demonstrated

that anxiety and frustration can produce increased masseter

and temporalis muscle activity. Rao and Glaros (1979) showed

that bruxists had higher baseline masseter EMG levels and

greater masseter EMG response to experimental stress than

did nonbruxists. Rugh and Solberg (1976) have used

ambulatory EMG monitoring devices to show that daytime

stress correlates with nocturnal bruxing.

Interactive Theories
While many dentists believe that occlusal interference

can produce bruxing (Christensen, 1970; Lindquist, 1972;











Ramfjord, 1961), it is known that some bruxers have no

interference and that some patients with interference do

not brux (Olkinura, 1969; Robinson, Reding, Zepelin, Smith &

Zimmerman, 1969; Schwartz, 1958). Accordingly it has been

argued that occlusal interference participate as

interacting factors in complex multifactor etiologies

leading to the behavior. Ramfjord and Ash (1983) for

example, suggested that "a variable tolerance level to

occlusal interference exists and that this tolerance level

may be altered by psychic stress affecting the tonus

activity in the jaw muscles" (p.81).

Only recently have researchers attempted to study
interference in interaction with other variables that

influence bruxing. Evidence from one controlled experiment

suggests that occlusal factors can interact with situational

stress to influence diurnal clenching (Bichajian, 1984).

However, the multifactor theory of bruxism needs massive

empirical fleshing out to be of significant value.

Sleep Theories
Laboratory research has provided several hypotheses

about relationships between bruxing and sleep activities.

Reding, Rubright, Rechstaffen, and Daniels (1964)

hypothesized that bruxing is associated with dreaming.

Satoh and Harada (1973) hypothesized that bruxing is











associated with arousal during sleep and with transitions

toward lighter sleep stages. There are several reports

suggesting that bruxing is associated with periods of body

movement and rapid-eye-movement or REM sleep stages (Powell,

1965; Reding, Zepelin, & Robinson, 1968).

As with the other etiological literatures on bruxing,

much work remains before the roles of sleep activities will

be known confidently. The bulk of evidence does suggest,

however, that at least some nocturnal bruxing is associated

with arousal phenomena (Rugh & Ware, 1986).













THE ASSESSMENT OF BRUXISM

The occurrence of bruxism can be evaluated by

monitoring and recording the behavior itself and by

measuring its effects on the intraoral environment.

Typically psychologists have evaluated bruxing behavior and

dentists have evaluated its stomatognathic consequences.

Various methods are reviewed here.

Dental Signs
The most obvious dental signs of bruxism are unique

wear patterns on the teeth. These are flat and highly

polished occlusal surfaces termed bruxofacets (Xhonga,

1977). The formation of wear facets is facilitated by the

presence during grinding of extremely small particles of

enamel that actually function as a gritty polish (Ramfjord &

Ash, 1983). Bruxing sometimes produces wear through the

enamel and can lead to exposure of the tooth pulp. Faceting

due to bruxism sometimes takes the form of sharp cuspal

edges and sometimes appears as cupping of the teeth or as

concave depressions.

Extreme wear of the teeth can result in occlusal

disharmony. Among the features of occlusal disharmony that

dentists assess are unilateral mastication, bite

discrepancies, locked bite, and sounds emanating from the

TMJ (Alling & Mahan, 1977).











Persons who brux excessively might exhibit well

developed or bulging masseter muscles. Nocturnal bruxing

can involve extended periods of masseteric hypertonicity

that, in turn, lead to the observed muscular hypertrophy

(Meklas, 1971; Posselt, 1968).

Hyperactivity of the masticatory muscles can result

also in various facial pains. Bruxist patients report

sometimes that the elevator muscles feel tired or painful,

especially in the morning (Alling & Mahan, 1977). Affected

teeth might be tender to percussion or hyperresponsive to

thermal changes (Dubner et al., 1978).

Intraoral Telemetry

Brewer and Hudson (1961) were able to quantify patterns

of tooth contacts by using miniaturized radio transmitters

fitted into complete dentures. Later, intraoral telemetry

systems were developed that used radio transmitters small

enough to fit into parts of bridges that substitute for

absent teeth (Glickman, Haddad, & Roeber, 1971).

In a telemetry system the transmitter consists of an

oscillator circuit, a battery power supply, and a

multilayered switch. The unit is embedded in a pontic

replacing a molar, and is activated when the switch makes

contact with a pinpoint gold inlay on the cusp of an

opposing tooth. Signals are emitted at frequencies, that

vary according to the part of the switch that makes contact.

The signals then are picked up by an antenna, and fed











through receivers and an oscillograph (c.f. Glickman,

Pameijer, Roeber, & Brion, 1969).

Miniaturized radio transmitters were developed to study

occlusal relationships. Scott and Ash (1966), however,

developed transmitters that were capable also of registering

the force of tooth contacts. Powell (1965) succeeded in

studying tooth contacts during sleep in seven nonbruxing

patients. Hence intraoral telemetry seems to be adaptable

to the study of bruxing.

Audible Grinds

Patients who brux report frequently that they were

unaware of the habit until a spouse or roommate told them of

grinding sounds. These sounds have been used by researchers

to measure bruxing behavior. In one approach grinding

sounds are microphonically recorded, amplified, and hand

scored on a polygraph record (Reding, Zepelin, Robinson,

Zimmerman, & Smith, 1968).

The second approach utilizes an automated tape

recorder. In one variation of this approach the recorder is

constructed to record at preset intervals. For instance, it

may record for 1.5 minutes every 15 minutes. In another

variation of this approach the recorder is activated by a

sound operated relay. In both cases the tapes are later

replayed and scored for brux frequencies (Heller & Strang,

1973).











Using audible grinding sounds to measure bruxing is

problematic. Automated tape recordings that sample the

nights at preset intervals are potentially unrepresentative

and time consuming to score. Sound operated relays on tape

recorders do not provide for real time analysis of bruxing

episodes (McGlynn et al., 1985). A major problem is that

audible sounds are associated only with ecentric bruxism.

Centric bruxism does not appear to generate a characteristic

noise (Reding, Zepelin, Robinson, Zimmerman, & Smith, 1968).

Bruxscore Monitor
The bruxscore monitor (Forgione, 1974) is a thin

plastic plate with imbedded microdots. It is molded to

conform to the occlusal surfaces and is worn at night.

Bruxing is quantified by counting missing dots.

The original appliance was composed of four differently

colored plastic sheets laminated to a total thickness of

0.02 inches. Microdots were printed in edible ink on each

plastic surface. The dots were 1/180 inches in diameter,

fitting 120 dots per inch in a pattern of 14,400 dots per

square inch. The appliance is worn by the subject during

sleep then examined and scored under a microscope.

Mejias and Mehta (1982) developed an index of bruxism

for use with the bruxscore monitor. In brief, the numbers

of dots ground away after one week are tallied. For example

if two dots are ground away from one plastic surface, then a

score of 2 would be recorded. Depending on where the score











falls within the author's norms, he or she is classified as

a non-bruxer, a mild-bruxer, a moderate-bruxer, or a

severe-bruxer.

There are several problems with the bruxscore index in

its current form. For example, the procedure used to

develop norms for the index has not been published.

Additionally, the exact process used to construct the device

itself has never been described. Finally, use of the

bruxscore monitor raises the issue of reactivity of

measurement. A device that is placed in the oral cavity can

influence the very behavior that the device is intended to

measure.

Notwithstanding the problems just described,

investigators have used the bruxscore monitor in several

treatment outcome studies. Heller and Forgione (1975)

compared massed negative practice (below) with automated

relaxation training (below) and found that neither technique

reduced bruxism significantly. Mejias and Mehta (1982)

studied short-term splint therapy and found that bruxing

decreased immediately after therapy.

Electromyography
During any muscle fiber contraction a minute electrical

potential is discharged and dissipated into the surrounding

tissue. If surface electrodes are attached properly over a

muscle, then the cumulative electrical activity of the

muscle bundles can be quantified in terms of total voltage.











Typically this voltage is on the order of microvolts or

thousandths of volts. Measuring the electrical activity of

muscles is called electromyography (EMG).

Currently EMG recording is the most common method of

assessing bruxism. This approach is possible because there

is a high correlation between muscle activity and EMG levels

and because muscle activity during bruxism is generally

greater than is muscle activity during mastication. In

fact, EMG recording can be used to measure bruxist behavior

at microvolt levels completely outside the ranges found for

functional oral motor behaviors (Dubner et al., 1978;

Solberg, Clark, & Rugh, 1975).

It is possible to employ EMG assessment procedures in a

variety of settings including the laboratory, clinic, home,

or work environment. Some procedures for naturalistic

recording are discussed here. There are several EMG devices

on the market that amplify, filter, integrate and record EMG

activity. Each device should be evaluated for usefulness

based on the criteria of expense, portability, and ease of

operation (Burger & Rugh, 1978).

Solberg and Rugh (1972) developed the first portable

device for EMG monitoring. It is about the size of a pack

of cigarettes. A tone sounds via an earphone each time the

subject's EMG level exceeds a preset level. The patient

writes down the time and the activity or situation when

he/she hears the tone.











The first portable EMG recorder is the same size and

shape as the monitor (Burger & Rugh, 1983). Unlike the

monitor, the recorder actually stores electrical activity

above a minimum (e.g. 20 microvolt) threshold. A digital

reading is noted by the subject at the end of a recording

period and written on a log. The digit is a function of the

signal amplitudes, frequencies, and durations. The EMG

recorder is much more sophisticated than the monitor. Even

so it has limitations. The integrated digital data fail to

discriminate an intense short duration response from a less

intense long duration response in terms of

microvolt/seconds. In brief, the single value is vague.

A portable EMG recorder that might overcome some of the

limitations of earlier equipment is currently being

developed by James G. Lee, F. D. McGlynn, and the author. In

general, the frequencies and amplitudes of electrical

impulses above an adjustable microvolt threshold are

continuously recorded on minicassette tapes (Dowdell,

Clarke & Kardachi, 1976). In addition, a high precision

crystal clock marks the tape at intervals so as to permit

real time recording. The amplifiers and clock are housed in

the standard minicassette player case.

At the beginning of each recording period the subject

simply inserts a tape into the player, attaches the

electrodes over the belly of the masseter, records the time,

and activates the player. The subject later returns the











collection of tapes and the recorded activity on each is

played into wave form analysis peripherals contained within

an IBM-PC computer. The data are analyzed and stored in the

computer.

Data obtained with the unit provide for fine-grain

assessment of the number of separate bruxing episodes per

night, the duration of individual episodes, and the average

EMG amplitude over individual episodes. In addition, the

typical times bruxing episodes occur during the night for an

individual are known (McGlynn et al., 1985; Cassisi,

McGlynn, & Mahan, in press).













AVAILABLE TREATMENTS FOR NOCTURNAL BRUXISM

The professions of clinical psychology and dentistry

both have methods for treating bruxist patients. Therapy by

professionals from either or both groups might be called for

in any individual patient. Dental and psychological

approaches to the problem are reviewed generally in the two

narratives that follow. Then uses of nocturnal wake-up

alarms are reviewed in more detail.

Dental Therapies
Drug Therapy

The benzodiazepines, and other muscle relaxants, are

used frequently for controlling extreme cases of bruxism.

Typically a small dosage is prescribed before bed (Alling &

Mahan, 1977). The precise mechanisms of action for these

drugs are unknown. Rugh (1978) reported a representative

evaluation of diazepam effects on masseter muscle activity

before, during, and after use of a 5 mg. dose for seven

nights. Nocturnal EMG activity decreased dramatically

during the drug period, but overactivity returned soon after

discontinuation of drug therapy. Similar findings have been

reported in the literature consistently (Ramfjord & Ash,

1983).

Occlusal Equilibration

Equilibration is defined as the permanent adjustment of

occlusion with grinding techniques. Equilibration follows a











more or less standard course of events. The procedure is

explained to the patient. Next, impressions and casts are

made of the patient's teeth. The upper and lower casts are

then mounted on an adjustable articulator, and interference

to smooth gliding contact between them are noted as the

"jaws" of the articulator are moved about. Finally, the

patient's teeth are marked and the interference are ground

down in a manner so as to maximize remaining tooth surface.

Dentists report high rates of success using

equilibration and some laud occlusal therapies as highly

successful treatments for bruxism (Ramfjord & Ash, 1983).

However, replicable treatment effects on bruxing have not

been shown, because researchers have not characterized

fundamental aspects of the behavior accurately. In

addition, the possibility exists that clinically beneficial

effects from equilibration derive to an important degree

from placebo or nonspecific influences in the overall

treatment context (Greene & Laskin, 1972; Goodman, Greene, &

Laskin, 1976). Hence, there is a clear need for further

investigation (cf. Clark, Beemsterboer, Solberg, & Rugh,

1979).

Occlusal Appliances

Occlusal appliances (variously called bite splints,

night guards, occlusal splints, etc.) are used frequently in

the treatment of bruxist patients. The appliances are

fabricated in acrylic from articulator-mounted castings of











the patient's dentition and are retained in the mouth by

wire or hard acrylic clasps. The purpose of splints include

functionally removing occlusal interference and preventing

occlusal contacts between maxillary and mandibular teeth

(Kass & Tregaskes, 1978)

Patients treated with splints report clinical

improvement in 70 to 90 percent of the cases. However,

methodological shortcomings are apparent in the clinical

research reported to date (McGlynn & Cassisi, 1985; Okeson,

Moody, Kemper, & Calhoun, 1983). In addition, the research

shows mixed results for therapeutic efficacy, including some

reports describing all possible outcomes (Cassisi, McGlynn,

& Mahan, in press).

Psychological Therapies
Diverse psychological treatments for bruxism have been

reported. They range from insight-oriented psychotherapy

and hypnosis to biofeedback and behavioral conditioning.

Components of psychological therapies for which some

meaningful treatment-outcome data exist are reviewed below.

Muscular Relaxation Training

Progressive relaxation training (Jacobson, 1938)

teaches patients the skill of voluntary-muscle relaxation.

It entails: (a) subdividing the skeletal musculature into a

number of discrete muscle sub-groups, (b) presenting

instructions which will produce easily detectable tension

alternating with relaxation in each of the muscle











sub-groups, and (c) suggesting that the patients focus

attention on how differing sensations arise from tense

versus relaxed muscles (see Bernstein & Borkovec, 1973).

Muscular relaxation has been used as a component

treatment in several multiple-treatment experiments having

to do with bruxing. Heller and Forgione (1975), for

example, compared relaxation training to massed negative

practice (below) as a treatment among 27 patients clinically

and radiographically diagnosed as bruxers. Relaxation had

no impact on a bruxscore monitor definition of bruxing.

Moss, Hammer, Adams, Jenkins, Thompson, and Haber (1982),

for another example, used relaxation training as one

component in a relaxation-feedback treatment of bruxing for

a 29-year-old female patient with a 3-year bruxing history.

Relaxation had no effect on an EMG definition of bruxing.

Extensive reports in the literature attest to the

tension-reducing effect of relaxation training when it is

done correctly (cf. Jacobson, 1938). Progressive relaxation

is used frequently to treat conditions such as insomnia,

tension headache, and spasm-related pain. No application of

relaxation to bruxist patients involved clinically sound

relaxation training procedures. Therefore, the utility of

progressive relaxation in some cases of bruxism has not been

ruled out.

Massed Negative Practice

Dunlap (1932) suggested that repetitive, voluntary

practice to the point of fatigue might reduce habits such as











nailbiting and tics. Yates (1958) presented a

neobehavioristic learning theory account of how such an

effect might be achieved. The first use of "massed negative

practice" as a treatment for bruxism was reported at about

the same time.

Successful use of massed practice in individual case

studies of bruxist patients has been reported by Wolpe

(1958) and Ayer and Gale (1969). Each patient was taught to

perform six series of daily trials in which five 1-minute

periods of voluntary clenching were alternated with 1-minute

periods of rest. Patient- and spouse-reports of bruxing

cessation were used as the measure of treatment success.

Ayer and Levin (1973) treated 14 nocturnal bruxists

using massed-practice clenching. A 14-day massed-practice

protocol prompted six daily series of self-monitored

voluntary clenchings in which five, 5-second clenches were

separated by 1-minute rest periods. Self- and

spouse-reports of grinding were used as measures of bruxism.

Eleven of 14 patients stopped bruxing within 9 days. Ayer

(1976) used the same massed practice protocol to treat 33

nocturnal bruxists. He found approximately 25 percent of

patients to have ceased the behavior through a 1-year

follow-up. Self-reports of grinding were used to measure

bruxing.

As noted previously, Heller and Forgione (1975)

compared massed practice to muscular relaxation training as

treatment among 27 patients clinically and radiographically











diagnosed as bruxers. The protocol of Ayer and Levin (1973)

was replicated. Massed practice had no impact on the

behavior as assessed by a bruxscore monitor.

Rugh (1976) compared massed-practice clenching to

controlled gum chewing and to placebo exercises as

treatments for bruxing among 20 TMJ patients. Eight of the

patients used a 10-14 day massed-practice protocol that

entailed six daily sessions of vigorous clenching. Massed

practice did produce significant reductions in nocturnal

bruxing according to an EMG measure.

Various conceptualizations of massed-practice effects

on nocturnal bruxing have been offered by Rugh (1976).

These conceptualizations include a combination of aversive

punishment, stress reduction, homeostasis, and "response

sensitization." Thus therapeutic effects from massed

practice protocols can be explained by theories of differing

systematic origins. However, the weak literature on massed

practice treatment for bruxing and the antiquated theories

concerning massed practice mechanisms call for caution in

endorsing the approach.













EMG-ACTIVATED ALARM THERAPY
As noted, the basic purpose of the present research was

to evaluate EMG-based feedback alarms for the treatment of

nocturnal bruxing. Hence, the present section considers in

detail the research reported to date in which response

produced signals have been used to modify nocturnal bruxist

behavior. Emphasis is placed on research that has made use

of signals triggered by facial EMG activity.

Early Research
DeRisi (1970) studied three bruxist subjects in their

own homes. Equipment was developed that recorded bruxing

episodes with a pressure transducer that was implanted in a

silastic mouthpiece and that presented a loud tone

contingent upon rhythmic or lengthy pressure registration.

The alarm did not produce enduring behavior change according

to three intrasubject (ABA) experiments. However, the use

of the mouthpiece raised an important methodological issue.

The masticatory system is reactive to disruptions in

the relationships between tooth surfaces. As described

earlier, some dentists have suggested that the modification

of gliding contacts between maxillary and mandibular teeth

can increase or decrease rates of bruxing activity.

Therefore, any effects from the nocturnal alarm in DeRisi's

(1970) experiments might have been confounded in unknown











ways by the presence of the mouthpiece itself within the

oral cavity.

Heller and Strang (1973) treated one bruxist patient in

her home. In this case, equipment was developed via which

audible grinding sounds activated a voice operated relay

that sounded an alarm. Use of the alarm reduced audible

grinding according to an intrasubject (ABAB) design. More

importantly, a second methodological problem was raised.

Descriptions of the various topographies of nocturnal

bruxing have not been adequate. Self-report data (Glaros,

1981) and the author's clinical experience suggest, however,

that a large proportion of nocturnal bruxing takes the form

of prolonged clenching. Since clenching produces no

transducible sound, alarm contingencies based on audible

grinding will be incomplete for some patients. Heller and

Strang (1973) noted also that some grinding sounds were

recorded below the trip threshold of their voice-operated

relay.

Contemporary Research
The basis for modern bruxing alarm systems was

established by Solberg and Rugh (1972) who used recordings

of facial EMG activity to define bruxing. There are three

reasons why this approach is beneficial. First, as noted

earlier, the muscular forces associated with bruxing are

generally above those associated with functional oral-motor

behaviors such as swallowing (Dubner et al., 1978; Solberg











et al., 1975). Therefore, bruxing should be relatively easy

to identify electromyographically. Second, surface

recording does not entail any incursion into the oral

cavity, hence eliminating confounds from the effects of

occlusal changes. Third, EMG recording identifies silent

clenching as well as audible grinding provided that suitable

instrumentation is used. The remainder of this section

reviews the literature in which facial EMG-triggered alarms

have been used to modify nocturnal bruxing.

Clinical Trials of Feedback Alarms

Kardachi and Clarke (1977) used an EMG-correlated tone

to treat a series of nine nocturnal bruxist patients 19 to

38 years of age. Bruxing feedback was provided by an

audible tone that varied in pitch according to the intensity

of muscular activity. EMG data were recorded with a small

tape player that was activated and driven by bruxing

activity (Dowdell et al., 1976). The tapes provided a

measure termed the total count which was a function of

bruxing duration and intensity.

Bruxing was recorded for seven baseline nights for most

subjects. This was followed by the use of biofeedback for

an equal period. Nights were not consecutive in either the

baseline or feedback phases. Presentation of the mean

bruxing units recorded for each subject during baseline and

feedback phases showed reduced bruxing in eight of the nine

patients. Reductions were fairly uniform across seven of











these eight patients. The authors suggested that the counts

reflected reduced durations of bruxist episodes, not reduced

frequencies.

Rugh and Johnson (1981) described the application of an

EMG-activated tone in treating five nocturnal bruxist

patients 20-39 years of age. Bruxing was defined by

unilateral masseter EMG signals of at least one second

duration with 20 microvolts (peak to peak) or greater

activity. Bruxing episodes were counted with a small chart

recorder fitted into a briefcase to render it more portable.

The charts were hand scored so as to yield frequency and

duration data. Bruxing feedback consisted of a 700 Hz, 300

mW tone temporally contingent on bruxing. Data were

collected for at least 10 baseline nights. Feedback was

provided subsequently for at least eight nights.

Presentations of the mean bruxing frequencies and durations

for each subject showed obvious reductions in bruxing

durations as a function of auditory bruxing feedback. As

was reported by Kardachi and Clarke (1977) there were no

reductions in bruxing frequencies.

Some have interpreted the absence of feedback effects

on bruxing frequencies to mean that feedback paradigms are

devoid of "learning." In turn, this consideration has

prompted efforts to enhance the durability of feedback

effects by awakening patients during bruxing episodes. The

first report of work along these lines was presented briefly











by Beemsterboer, Clark, and Rugh (1978). Recordings of

cumulative masseteric EMG activity above 20 microvolts were

obtained from six subjects for 12 nights before and 10

nights after a two-week period of nocturnal alarm feedback.

During the feedback period subjects were told to become

fully awake following alarm soundings. They were given a

performance task that required three to five minutes of

wakefulness. Uniformly significant decreases in each

subject's nightly mean suprathreshold masseter activity from

before to after treatment were noted. The authors concluded

that nocturnal auditory feedback must be combined with an

arousal task in order to promote long term reductions in

bruxist behavior.

Auditory feedback coupled with an arousal task was

studied and reported in more detail by Clark, Beemsterboer,

and Rugh (1981). Cumulative recordings of masseteric EMG

activity above 20 microvolts were obtained from 10 subjects

for 10-12 nights before and 7-14 nights after a two-week

period of alarm treatment. During the treatment each

subject received auditory feedback upon emitting a

moderately hard biting force which was defined separately

for each subject. The auditory signal served further to

prompt subjects to get out of bed, cross the room, and

record the time and sleep quality at the time of wakening.

Comparisons before and after treatment showed significant

decreases in nightly mean suprathreshold masseter activity











among nine of 10 patients. Marked reductions in the numbers

of self-monitored awakenings during treatment were noted

also by the authors. These data appeared to indicate that

the treatment package effectively reduced bruxing for up to

two weeks after its withdrawal.

The reports just-reviewed suggest that auditory

feedback of bruxing during sleep has differential effects

depending on the use of a contingent arousal task. However,

this observation is based on comparisons between trials in

which the variables of feedback and of feedback-plus-arousal

instructions were studied separately. There are two reports

describing work in which the effects of feedback and of

feedback-plus-arousal instructions were studied within the

same experiment.

The first is a report by Funch and Gale (1980) who

modeled their experiment on that of Rugh and his colleagues

with respect to experimental variables such as bruxing

feedback and arousal task requirements. A 27-year-old

female patient was used in two baseline-treatment-baseline

experiments that were separated by two months and were

followed by a final baseline assessment one month later.

Baseline and treatment phases lasted for 10 consecutive

nights. In the first experiment feedback was provided

following Rugh and Solberg (1975). In the second experiment

feedback was paired with arousal task instructions following

Beemsterboer et al. (1978). The results reported by Funch











and Gale (1980) differed from earlier results in three ways.

First, durations of bruxist activity following the

feedback-alone phase increased markedly over baseline

levels. Second, durations of bruxist activity following

feedback-plus-arousal instructions increased over baseline

levels as did bruxing durations following feedback alone.

Finally, the feedback conditions brought about reduced

frequencies as well as reduced durations of bruxing during

treatment.

The second report comparing alarm treatment with and

without arousal instructions was provided by Moss et al.

(1982). They described the treatment of a 30-year-old

female with a seven year history of nocturnal bruxing. This

study manipulated feedback-plus-arousal and feedback alone

by sometimes requiring and sometimes not requiring manual

termination of the feedback signal. In addition the

variable of feedback termination was crossed sequentially

with the variable of quality/loudness of the feedback signal

itself. Feedback in the form of a soft tone had no

meaningful impact on bruxing frequencies or durations either

with or without the manual reset contingency. Loud buzzer

feedback that required manual termination demonstrably

reduced both the frequencies and durations of bruxist

episodes. The effects of loud buzzer feedback alone were

evaluated for only two nights.











Funch and Gale (1980) noted that intrasubject research

is clearly problematic from the standpoint of generalizing

results to other patients. Variability in the data reported

by Moss et al. (1982) rendered some of their phase durations

too short to meet the requirements of intrasubject

replication design logic. Finally, a number of potentially

important variables differed between these two intrasubject

experiments and the other studies reviewed in this section

of the narrative. On the whole the larger literature about

clinical trials suggests that alarms per se reduce bruxing

durations, while alarms plus arousal task instructions

reduce both durations and frequencies.

Laboratory Studies of Feedback Alarms

Three relevant studies have been conducted in sleep

laboratory settings. Wagner (1981) combined home based

recording with laboratory work to evaluate nocturnal alarm

treatment. The patient was a 26-year-old female with a

lengthy history of nocturnal grinding. Bruxing frequency in

the home setting was quantified for 60 nights by spouse

recordings of nightly grinding sounds on an 11-point scale

that ranged from 0 (no grinding) to 10 (grinding throughout

the night). A Coulbourn Instrument Modular System was used

to amplify, filter (90 Hz low cut, 500 Hz high cut), and

integrate ENG activity in the laboratory. Bruxing

frequency, intensity, and duration were quantified for six

nights with this device. The resulting signal was sent to a











threshold trigger, and to a recorder that cumulated seconds

of suprathreshold activity, as well as to the polygraph.

Bruxing was defined as activity above five microvolts

(integral average). Three seconds of quiescent EMG

recording were required to tally separate bruxing episodes.

When bruxing occurred during treatment, the threshold

trigger sounded an alarm until bruxing ceased. The alarm

was "loud enough to disturb the subject's sleep, but not so

loud as to startle or frighten the subject" (Wagner, 1981,

p. 88). The subject was told that relaxing her jaw would

stop the tone.

The protocol began with 24 nights of home baseline

recording and two nights of laboratory baseline recording.

These 26 nights were followed by a single night of alarm

treatment in the laboratory. The single treatment night was

followed by 14 nights of home recording that, in turn, were

followed by a second treatment night in the laboratory.

Finally there were 26 nights of "follow-up" recording, 24 in

the home and two in the laboratory.

Despite having only two nights of alarm treatment in

the laboratory, four nights of EMG monitoring demonstrated

reductions of 50 to 65 percent between baseline and

"follow-up" for bruxing frequencies and durations,

respectively. The spouses' ratings for 60 nights showed

reduced variability and average reductions in the 11-point











rating scale from 3 before treatment to 0.5 during

"follow-up."

Piccione, Coates, George, Rosenthal and Karzmark

(1982) used a nocturnal alarm coupled with a task requiring

wakefulness to treat two bruxist patients both at home and

in a sleep laboratory. The first subject was a 50-year-old

female who had been bruxing 29 years. The second subject

was a 44-year-old female who had been experiencing morning

jaw fatigue for three years and who had often awakened with

her teeth clenched tightly. Bruxing rates and durations in

the home were assessed using the ambulatory equipment and

parameters developed by Rugh and his colleagues (described

previously). Bruxing rates and durations in the laboratory

were assessed with a Grass Model 7D polygraph that amplified

and filtered (10 Hz low cut, 75 Hz high cut) bilateral

masseter EMGs. There were three criteria for defining

bruxism; amplitude, duration and rhythmicity. The amplitude

criterion was at least 20 microvolts. The duration

criterion was 0.5-1.5 seconds. The rhythmicity criterion

was three incidents of criterional amplitude and duration

separated by return to baseline EMG for 2.5 seconds or less.

Bruxing episodes were scored for number of bruxes and for

total suprathreshold duration. Bruxes during treatment

phases produced a contingent alarm and arousal-task.

Instructions were identical to those reported by

Beemsterboer et al. (1978).












Both subjects were exposed to alternating baseline and

treatment phases (ABAB) of two to three weeks duration. One

subject lagged behind the other by approximately a week.

Each subject slept in the laboratory for up to three nights

per week during baseline and treatment phases. The

investigators were also interested in the effects of alarm

treatment on sleep, so laboratory assessment of EMG was

accompanied by polysomnographic characterization of sleep

stages using standard methods and definitions (Rechtschaffen

& Kales, 1968).

The results did not replicate prior research using

feedback alarms plus arousal task instructions. One

subject's bruxing was not reduced significantly during the

first treatment period. Subsequently, there was a marked

rebound during the "return-to-baseline" period and the

second treatment period served only to reduce the rebound to

just above the original baseline levels. The other

subject's, bruxing increased slightly from the original

baseline through the treatment period. Subsequently, there

was a further increase during the "return-to-baseline" phase

and it dropped to the original baseline level during the

second period of treatment. These results were similar for

bruxing frequency and duration measures. In sum, the alarm

treatment protocol failed to affect bruxing favorably. In

addition, there were signs of negative effects on sleep

duration, at least initially during treatment. The authors











discussed the possibility that sleep deprivation could have

changed the depth and duration of sleep stages as treatment

progressed.

Purzycki, Harsh, and Badia (1986) conducted a

laboratory study of nocturnal bruxing that compared feedback

alone to feedback-plus-arousal instructions. They also

characterized the effect of feedback on selected sleep

variables. Two subjects were recruited via a newspaper

advertisement. The first was a female 22 years of age with

a lengthy history of nocturnal bruxing and of unsuccessful

intervention by dentists. The second was a female 26 years

of age with a lengthy bruxing history.

A Narco six-channel physiograph and a Coulbourn Hi-Gain

Bioamplifier/Coupler were used to quantify bruxing. The

amplified signal was filtered with a 150 Hz low cut, 1.0 kHz

high cut bandpass filter. Bruxing events were detected via

a bipolar comparator that served also to trigger feedback

during treatment periods. Bruxing events were defined as

EMG above 30 microvolts for 0.5 seconds or longer that

followed prior events by at least one second. Bruxing

frequency and duration data were digitized and printed on a

continuous tape. Subthreshold EMG events from 20-29

microvolts were handled similarly.

The subjects were exposed to baseline, "feedback,"

"feedback/awake," and baseline phases for 17 to 20 nights.

There were at least three nights per phase. Phase shifts











were made following true intrasubject replication design

logic (Johnston & Pennypacker, 1980). The "feedback"

condition consisted of diurnal pre-training to produce and

escape a 65 db tone via increasing then decreasing

masseteric activity. Next the 65 db tone was presented

contiguously with bruxing during sleep. The

"feedback/awake" condition consisted presenting an 87 db

tone contingent upon nocturnal bruxing. The 87 db tone

could be stopped only by manually closing a microswitch that

was located above the bed. The subjects were told to stay

awake for two minutes after alarm soundings and intercom

instructions were used to assist in maintaining wakefulness.

Bruxing was differently affected by the "feedback"

condition across the two subjects. For the first subject

the 65 db feedback reduced suprathreshold EMG to 50 percent

of baseline duration while increasing subthreshold EMG

durations nearly fivefold. For the second subject the 65 db

feedback did not reduce suprathreshold EMG durations as

compared to baseline levels.

The "feedback/awake" condition affected bruxing by the

two subjects differently also. For the first subject the

manually terminated 87 db tone reduced dramatically the

duration and frequency of suprathreshold EMG and failed to

change subthreshold values from baseline levels. For the

second subject the manually terminated tone was associated

with a significant increase in suprathreshold EMG duration.











Since the tone was failing to produce two-minutes of

wakefulness for the second subject, the experimenter began

entering the sleep area at tone terminations and turning on

a lamp. He also prompted the subject to prop herself on her

elbows for two minutes. This additional procedure produced

bruxing decreases similar to those displayed by the first

subject during her last treatment period.

In the last baseline, the first subject demonstrated

brux frequencies equal to and durations longer than those

observed in the original baseline assessment. The second

subject demonstrated similar results. Unlike the earlier

report by Piccione et al. (1982), there were no signs that

alarm therapy affected sleep staging. The percentages of

time in REM and NREM stages were equivalent across all

conditions.

In summary, the protocol used by Wagner (1981) appeared

to have awakened the subject and to have reduced both

durations and rates of bruxing. The alarm-plus-arousal

approach reported by Piccione et al. (1982) altered the

EEG-defined sleep staging of two subjects but did not reduce

their bruxing durations or rates. The alarm-plus-arousal

paradigm used by Purzycki et al. (1986) did not appear to

change sleep staging but did reduce bruxing durations and

frequencies when the two subjects were awakened fully.

These results are less consistent than the results of

clinical trials. Despite the "laboratory" context, these











investigations also were less methodologically rigorous than

were some of the clinical studies.

Comparisons of Feedback Alarms
With Other Treatment Approaches

Three experiments have been published in which

EMG-based alarms were compared directly to other means of

modifying nocturnal bruxing. Kardachi, Bailey, and Ash

(1978) compared EMG-correlated auditory feedback to

noncontingent tones, to occlusal adjustment, and to mock

occlusal adjustment as treatments for 16 nocturnal bruxers

18-39 years of age.

Bruxing was monitored for all groups as reported by

Kardachi and Clarke (1977). Masseter EMG was recorded

unilaterally. Activity above 100 microvolts was amplified

then stored on a small tape recorder in the form of duration

and intensity counts.

For two groups, bruxing during sleep was recorded for

seven nights before and seven nights after occlusal or mock

occlusal treatments. For two other groups, bruxing was

recorded during sleep for seven nights before, during, and

after auditory feedback or noncontingent tone treatments.

In addition, bruxing among subjects who received either

occlusal adjustment or true EMG feedback, was recorded for

several nights approximately three months after the

experiment. True auditory feedback of masseter activity was











contingent on activity above a 100 microvolt threshold.

This treatment continued nightly for one week. The

noncontingent tone treatment consisted of auditory signals

from three to seven seconds in duration presented six to

eight times per hour. This control "treatment" also

continued nightly for one week. Occlusal adjustment was

performed in accordance with standard dental practice. Mock

occlusal adjustment consisted of grinding nonopposing and

nonsupporting tooth surfaces minimally. Four subjects who

were identified clinically as nonbruxists were evaluated

also for seven nights.

True auditory feedback of suprathreshold

masseter/temporalis EMG activity produced a 70 percent

average reduction in bruxing during treatment. However,

this reduction was followed by an immediate return to

baseline levels among three of the four subjects when

treatment was withdrawn. The noncontingent or false

feedback produced no meaningful change from baseline bruxing

activity among four subjects. The effects of occlusal

adjustment were more complex. Two subjects showed immediate

increases in bruxing followed by short-term reductions to or

below the baseline levels. Two subjects showed immediate

decreases in bruxing followed by short-term returns to

baseline levels. Mock equilibration produced slight

reductions in bruxing for all four subjects. The four

nonbruxist subjects bruxed much less than did the other 16

subjects. The three-month follow-up of bruxing demonstrated











that one subject who had received occlusal adjustment and

one who had received auditory feedback showed 50 percent

less activity than had been shown before treatment. The

authors suggested that the effect of auditory feedback in

reducing suprathreshold EMG activity appeared to be more

consistent than was the effect of occlusal adjustment.

Casas, Beemsterboer, and Clark (1982) compared

nocturnal alarms to stress-management training, to nocturnal

alarms plus stress-management training, and to no treatment.

Sixteen bruxers who averaged 29 years of age served as

subjects. Bruxing was monitored as in the study reported by

Clark et al. (1981). The protocol entailed recording

bruxing during sleep for approximately ten nights before and

ten nights after each experimental treatment.

Four subjects received the nocturnal alarm treatment

described by Clark et al. (1981). This treatment included

their arousal task instructions and it continued nightly for

two weeks.

Four subjects received stress management training that

had components of both cognitive behavioral (Beck, 1976) and

clinical biofeedback (Budzynski & Stoyva, 1973) approaches.

There were four, weekly, individual treatment sessions of 60

minutes in duration. Each had the threefold purpose of

teaching the subjects (1) to identify stressful situations

and correlated cognitions, (2) to counter the aversive

cognitions with private self-efficacy statements, and (3) to











relax with EMG assisted biofeedback training of the arm and

facial muscles.

Four subjects received the four-week stress management

training protocol to which the nocturnal

alarm-plus-arousal-task treatment was added during the third

week. A wait-list control group of four subjects was used

also.

Differences in mean suprathreshold EMG activity from 10

nights before to 10 nights after treatment showed

significant bruxing reductions in all three groups of

treated subjects. These changes were not different but were

consistently larger than changes among the four untreated

subjects. Casas et al. (1982) concluded that stress

management and nocturnal alarm approaches both are

appropriate.

The third comparison of nocturnal alarms with other

approaches was reported by Moss et al. (1981). The patient

was a 29-year-old female who reported a three year bruxing

history. The effects of loud buzzer feedback requiring

manual termination were compared with those of muscular

relaxation training and with those of baseline constraints.

The feedback contingency was associated with dramatically

reduced bruxing frequencies and durations, while muscular

relaxation training had no effect.

The results of the three treatment comparisons suggest

that nocturnal alarm approaches are competitive with the








42


other approaches that are available for managing nocturnal

bruxing. This conclusion is not surprising given the modest

effects that have been reported in the larger literature on

dental approaches to the problem (cf. McGlynn et al., 1985;

Okeson et al., 1983).













PURPOSES OF THE EXPERIMENT

The exhaustive review of the literature provided above

suggests that alarm therapy is a promising approach for the

treatment of bruxism. There remain significant research

questions at all levels of inquiry. Below are the questions

that were asked in this experiment along with the rationales

for asking them.

One conclusion reached in previous studies is that full

arousal following alarm soundings increases the efficacy of

therapy. However, different methods to promote wakefulness

have been used. At one extreme, investigators have merely

instructed the patients to record the time and quality of

sleep following alarm soundings (Beemsterboer et al., 1978).

At the other extreme, investigators have actually entered

the sleep environment and tapped on the shoulder of the

subject following alarm soundings (Purzycki et al., 1986).

Neither approach is entirely satisfactory.

Two previous studies have included a manipulation that,

in principle, provides a practical solution to the problem

of requiring arousal following alarm soundings (Moss et al.,

1981; Purzycki et al. 1986). This is the inclusion of a

manual reset switch on the alarm itself. Using this

approach, the tone sounds continuously following a brux

episode until a motor escape response is emitted.












The manual escape manipulation has only been studied in

three subjects to date. The primary purpose of this study

was to evaluate the efficacy of EMG-activated alarm therapy

with manual reset as a treatment/management package for

reducing rates of nocturnal bruxing.

Several studies have reported that bruxism levels

following alarm protocols have actually increased above

those found before treatment (Funch & Gale, 1980; Piccione

et al., 1982). If one likened this treatment to operant

punishment (DeRisi, 1970), such effects would be viewed as

mirroring a behavioral contrast effect (Reynolds, 1961).

A second purpose of this study was to evaluate the

occurrence of post-treatment rebound or "contrast" following

alarm therapy.

As noted, one method of promoting wakefulness following

alarm soundings has been to instruct subjects to monitor

data such as time of night. Clark et al. (1981) have used

these records of alarm soundings as an adjunct dependent

measure. This raises a third question of interest. Since

the sleep records are obtained as a matter of course, might

such records be used to monitor the course of brux frequency

across successive nights? In the present experiment nightly

diaries were kept in addition to alarm counts made

automatically and unobtrusively in the apparatus. The

third purpose of the study was to compare self-monitored











alarm counts with automatically recorded alarm counts so as

to evaluate the former as a data acquisition mode.

The potential risks and contraindications of alarm

therapy procedures have rarely been discussed in prior

reports. This is surprising given that the treatment

disrupts sleep and, while controversial, there is a very

large literature arguing about the adverse effects of sleep

fragmentation (Bonnet, 1985; Pearlman, 1982). No previous

study has included measures of diurnal fatigue in patients

undergoing nocturnal alarm treatment. The fourth purpose of

this study was to evaluate the impact of alarm therapy on

reports of daily sleepiness, fatigue and vigor.

The fifth and final purpose of this study was to

examine relationships between bruxism and facial pain or

discomfort. This purpose is ancillary because facial pain

patients were not used as subjects. Nonetheless, an attempt

was made to evaluate the controversial relationship between

nocturnal bruxism and subclinical muscular

soreness/discomfort.

Previewed briefly, subjects were recruited via public

notices and by word of mouth. Ten heavy bruxers were

selected from 18 individuals who presented. Subjects were

evenly divided into two groups whose experimental

participation differed only in the sequence of 14 day

no-treatment and treatment phases. Nightly brux-episode

frequency, and the daily ratings of vigor, fatigue,








46


sleepiness, anxiety, and facial pain were taken throughout

the study. In addition, nightly self-monitored alarm counts

and automated alarm-counts were recorded during treatment

phases.














METHOD

Subjects

Individuals who suspected they were bruxing were

solicited and screened. These included various health

center employees, students, and acquaintances. They were

recruited with notices that were placed on various health

center bulletin boards, and in the mail boxes of the third

and fourth year dental students. (See Appendix A for copy

of notice.) During recruitment, individuals were asked if

their dentist had indicated a diagnosis of bruxing, if their

roommates had reported overhearing grinding sounds during

the night, and if they had experienced facial pain/muscular

soreness. If there was an affirmative answer to any of

these questions, the individual was given an informed

consent document. After the potential subjects signed the

informed consent document they entered the screening phase.

In return for their participation during the screening

phase, individuals were paid $10.00. In return for

participation in the study, subjects were paid $50.00, and

given the opportunity to purchase an EMG-activated alarm at

reduced cost.

Activities during the screening phase included a

structured dental exam (Appendix B), three nights use of the

EMG monitor (described below), and completion of a Screening

Questionnaire (Appendix C). Criteria for inclusion in


-47











the study included confirmation by the dentist of

characteristic wear facets, no observed dental infection,

and demonstrable bruxing during the three night screening

phase. While not criterional, masticatory muscle soreness

on palpation and hypertrophy of the masseter muscles were

noted during the dental exam.

Twelve of the 18 individuals who presented met the

inclusion criteria. Of the 12, one subject dropped-out

following the death of a close family member. Another

subject completed the study, but was excluded because it was

learned that she had taken muscle-relaxant medication at

various times. All subjects were requested to refrain from

other treatments during screening and during the study.

The dental exam and the Screening Questionnaire also

were structured so as to allow a comprehensive description

of the subjects in terms of demographic variables and dental

status. Six females and four males served. The average age

of the male subjects was 25. The average age of the female

subjects was 32. On average the subjects reported having

been aware of the habit for 7.5 years. Three of the males

and five of the females reported facial pain/discomfort.

Two of the subjects had received an occlusal splint

treatment for the problem. The demographic data are

presented in Table 1.










49






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Instrumentation

EMG activity was recorded via three electrodes (two

reference, one ground) with 40 mm leads. Bard pregelled, 10

mm diameter, disposable, ECG electrodes were used (reorder

number #160340). Exact placement of the electrodes on the

face followed the standard masseter site described in

Lippold (1967). The electrodes are fitted with

surgical-tape adhesive collars. In addition, strips of 25

mm wide Micropore Hypoallergenic Surgical Tape were placed

over the attached electrodes. One was placed over the two

active electrodes, one was placed over the ground, and one

over the wire leads on the subject's neck. During pilot

work it was determined that electrode stability was enhanced

when the leads were looped over the ear-lobe prior to taping

them down. Appendix D illustrates the electrode placement

and contains the written instructions given to each subject

during monitoring phases.

A detailed description of the EMG-activated

alarm/monitor is in preparation. The device can function as

a portable EMG-activated nocturnal alarm, or by disabling

the alarm, the device can function as a portable EMG

response-episode monitor. The following information about

the device is available.

The alarm/monitor is contained within a 12 cm x 20 cm x

30 cm plastic box that weighs 411 gm. The internal

components of the alarm/monitor are an amplifier, a











gain/threshold control, a comparator, a Schmitt trigger, an

alarm disabling jumper switch, a piezo buzzer (75dB/meter

mini), an EMG response counting chip, and an alarm response

counting chip. External components are an on/off switch, an

alarm reset switch, a momentary data display push button,

and an LED data display. A flow-chart of the system is

presented in Figure 1, and a schematic diagram of the device

is presented in Appendix E.

The gain/threshold adjustment was set so that a 100

microvolt (integral average) signal of .25 seconds duration,

would trigger the alarm. In order to set and calibrate the

device, a constant independently measured criterion

microvolt value was inputted through the electrode leads.

The recessed threshold screw was then turned

counterclockwise until the alarm sounded.

The following method was used to produce independently

measured criterion values with which to validate the

apparatus. A voltage output of preset frequency was

produced by a signal generator (Wavetek 4 MHz Function

Generator Model 182A). This equipment allowed precise

adjustment to the 150 Hz frequency that was used for all

tests except the bandpass. However, because the signal

generator did not provide scaling of voltage, its output was

interfaced with a bioamplifier and digital integrator.

A one volt output from the signal generator was stepped

down by a factor of 1000 by using a simple two resistor

























ENABLE
ALARM
COUNTER


DISPLAY


Figure 1: Flow-Chart of the Alarm/Monitor











network (100,000 ohm in series with 100 ohm). Appendix E

illustrates the configuration schematically. The output

from the resistor network (now on the order of microvolts)

was then split and one signal was input into a bioamplifier

(Autogen 1700 Feedback Myograph, bandpass 20 Hz to 1 KHz),

while the other was input into the alarm/monitor. The

instantaneous output from the bioamplifier was connected to

an Autogen 5100 Digital Integrator/Wave Form Analyzer which

allowed digital display of the microvolt amplitude (1 sec,

integral average) that was being input to the alarm/monitor.

Using this system, the frequency of the input was

varied and the functional bandpass of the alarm/monitor was

determined. From 10 Hz to 550 Hz the device sounded

reliably to a 100 microvolt, 2 second signal.

After the threshold of the alarm/monitor was adjusted

using the method described above, the signal generator was

adjusted to several values above criterion. The output from

the signal generator was set to the gated mode. One hundred

2-second trials at each of five suprathreshold levels (105,

107, 109, 111, and 113 microvolts) were inputted to the

alarm/monitor and resulted in 100 percent correct alarm

soundings. Then one hundred 2-second trials at each of five

subthreshold levels (95, 93, 91, 89, 87 microvolts) were

inputted to the alarm/monitor. These trials resulted in 100

percent correct rejection. Taken together, the above











results indicate that the alarm/monitor has adequate

performance characteristics for experimental use.

No differences in the performance of the alarm/monitor

were detected when it was tested in and out of the alarm

mode. The device was tested out of alarm mode by depressing

the read button and observing increments in the

response-episode count function.

Measures

Response-Episode Count

The response-episode counting function of the device is

activated whenever the device is turned-on. It tallies a

response-episode after EMG/microvolt activity exceeds the

preset threshold for .2 seconds or more and returns to

subthreshold levels for at least one second. The

response-episode count is read from the second of two

columns of ten LED lights located on the face of

alarm/monitor. The count is recorded by the subject in the

morning before detaching and turning the device off. The

subject activates the display by pushing a button marked

"read." Both columns of the light array are then activated.

The lights that are illuminated are recorded by the

subject on the Morning Questionnaire (see Appendix F)

contained within the Daily Supply Book (see below). The

response-episode count is encoded into a binary numbering

system such that illuminated lights represent "l's" and











nonilluminated lights represent "O's." Therefore, a

continuous response-episode count is available up to 1024.

The recorded response count was later decoded with the

aid of the calculating function of the IBM PC-standard

computer software Sidekick, version 1.56 by Borland

International Inc., Scotts Valley, California. This

function provides for binary to decimal transformations with

a single key stroke.

Alarm Frequency Count

The first column of ten LED lights on the monitor

displays the count of alarm soundings. This count

increments by one at the onset of an alarm sounding. This

count is also encoded, as is the response-episode count to a

limit of 1024. When the contingent alarm function of the

device is disabled and the device is in the monitoring mode,

this column of lights is left free to vary with incidental

contact of the manual reset switch. Additionally, subjects

were not informed about the meaning of the LED until the

debriefing at the end of the study. They were initially

instructed that the entire light array is the measure of

"how much they brux."

Self-Monitored Alarm Frequency Count

During treatment subjects were instructed to record on

a Nightly Alarm Record (Appendix G) the times when the alarm

sounded. They were instructed to place the record in an

area that could be reached conveniently from the bed and to











make sure that the chosen place was flat, and close to a

light. They were instructed also to acquire an illuminated

clock. Pretreatment instructions explained that

consistently timing the alarm soundings was important to the

project. The instructions explained also that individuals

who "wake-up fully following alarm soundings appear to

respond much better to treatment."

Sleepiness, Vigor, and Fatigue Measures

Daytime sleepiness was assessed via self-reports on the

Stanford Sleepiness Scale or SSS (Hoddes, Dement, & Zarcone,

1972; for review see Carskadon, 1982). This seven-item

scale sound psychometrically and it correlates significantly

with behavioral measures of sleepiness such as the Sleep

Latency Test (Magee, Harsh, Badia, Revis, & Purvis, 1986).

The SSS was taken in the evening as one of the Nighttime

Questionnaires (see Appendix H) and in the morning as part

of the Morning Questionnaire.

Fatigue and vigor were measured with the corresponding

subscales from the Profile of Mood States or POMS (McNair,

Lorr, & Droppleman, 1981). The standard POMS form available

from the Educational and Industrial Testing Service, San

Diego, California, was page 2 of the Nighttime

Questionnaire. At least six independent factor analytic

studies have been reported that identify fatigue and vigor

as mood factors on the POMS (Eichman, 1978; McNair, Lorr, &

Droppleman, 1981). The vigor factor is defined by adjectives











suggesting a mood of vigorousness and high energy. The

fatigue factor represents a mood of weariness, inertia and

low energy. While negatively related, these two subscales

appear do not appear to be opposite extremes of a single

bipolar factor. The POMS has been used to investigate the

effects of sleep deprivation in several studies (Freidmann,

Globus, Huntley, Mullaney, Naitoh, & Johnson, 1977; Johnson,

1982, p. 129).

The instructions of the POMS were modified to read "HOW

HAVE YOU BEEN FEELING DURING TODAY," instead of "HOW HAVE

YOU BEEN FEELING DURING THE PAST WEEK INCLUDING TODAY."

McNair et al. (1981) reported replicating the the original

factor structure with a similar instructional change.

Anxiety Measure

The POMS has a tension-anxiety factor among the six

factors produced reliably by factor analytic work. This is

a factor related to heightened musculoskeletal tension and

observable motor manifestations of anxiety. Since the POMS

provides information on this construct and it is

theoretically related to bruxism, the tension-anxiety factor

was scored and used in subsequent exploratory analyses.

Facial Pain/Discomfort Ratings

Facial pain/discomfort ratings were made on an

adaptation of the visual analog scale (VAS) developed by

Scott and Huskisson (1976). The VAS in this study was a 10

cm line which is taken to represent the continuum of facial











muscle comfort to severe facial pain. One extreme was

defined as "Comfortable/No Pain". The other extreme was

defined as "Pain As Bad As It Could Be." The subject was

asked to mark the line at a point corresponding to the

severity of his or her pain at the moment. The VAS ratings

were made on the Morning Questionnaire (Appendix F).

The distance of the mark from the end of the scale was

taken to represent the subjects pain severity. This method

has proven to be a simple, robust, sensitive, and reliable

approach to assessing pain (Huskisson, 1983).

Daily Supply Book

The Daily Supply Book was a one-inch looseleaf

notebook. The front pocket contained instructions for

either the Brux-Monitor, or the Brux-Alarm (see Appendix I).

These instructions reviewed the daily procedures. Behind

these instructions was the original informed consent form,

which overviewed the experiment as a whole. Two vinyl

pencil/pen pouches were contained in the front of the ring

binder of the notebook. The first pouch contained seven

disposable 70 percent isopropyl alcohol prep pads. The

second contained seven reclosable (Ziplock) sandwich bags

each containing three disposable electrodes. Following the

two pouches on the ring binder were the forms that had to be

completed daily. Each day's supply was separated by a

plastic tabbed manila notebook divider. The first sheets

for all days were the Nighttime Questionnaires (containing











space to write bedtime, the SSS, and instructions to

continue on the next page where the POMS was located). This

was to be completed before retiring.

During alarm treatment, the next page contained

instructions and the Nightly Alarm Record form for recording

alarm soundings. This form contained numbered spaces to

record the time for up to 93 alarm soundings.

The last form for all subjects was the Morning

Questionnaire. This contained instructions and spaces to

record the monitor readings from the previous night. It

contained also spaces to record the time of awakening, the

VAS, and the SSS.

Procedure and Experimental Protocol

In the first meeting, or telephone contact, with each

potential subject the investigator said: "Psychologists

often successfully treat bruxism by providing patients with

an alarm that they wear when asleep. If they brux, the

alarm sounds a warning tone that wakes the person up and

signals them to stop. We want to determine the

effectiveness of this type of therapy for bruxism. First we

want to determine if you are a good prospect for this type

of therapy. Thus, we will need for you to wear a monitoring

device for three nights. It will measure how much you

clench and grind your teeth. You will be paid $10.00 for

this screening. If we can use you in the study, and if you

do volunteer, it will involve up to four weeks of your time











and quite a bit of effort from you. To repay you for the

effort, we will provide you with the alarms free of charge

for the period of the study. Also, on completion of the

study we will pay you $50.00. If the alarms turns out to be

helpful, you will be provided one at the end of the study at

a 25 percent reduction in cost, or $150.00. If you are

interested, please read this informed consent form. It

tells you about the details."

After signing the informed consent form, the subjects

were trained to use the monitoring function of the the

alarm/monitors, and to use a three day version of the Daily

Supply Book. All individuals were instructed in skin

preparation with alcohol prep pads, and electrode placement.

Each subject was required to demonstrate proper application

and use of the monitor on two successive occasions before

the start of the screening phase.

During the three day screening period all potential

subjects were evaluated by a Dentist in the University of

Florida Dental Occlusion and Facial Pain Center. (All

patients were seen by Michael Henry, D.D.S., a second year

pain-center resident.) He followed an abridged version of

the clinic's standardized examination that incorporated the

three criteria mentioned previously. On the basis of this

exam he did or did not make a diagnosis of bruxism.

Individuals who met the criteria during screening and

during the dental exam were considered as subjects. They












were assigned randomly to groups with an equal group-size

restriction.

There were two groups that differed only in the

sequencing of no-treatment and alarm-treatment conditions.

The first group received 14-days of baseline, followed by

14-days treatment. The second group received 14-days of

treatment, followed by 14-days of baseline. Figure 2

overviews the experimental design.



Group 1: Alarm Therapy No-Treatment
EMG (EMG Monitoring)
Screening
All
Volunteers
Group 2: No-Treatment
(EMG Monitoring) Alarm Therapy
3 days 14 days 14 days

Figure 2: Overview of the Experimental Design



During the first meeting following screening, subjects

either were shown how to use the alarm function of the

alarm/monitors or they were told to continue monitoring as

in the screening phase. Subjects were then given a

seven-day version of the Daily Supply Book appropriate to

their condition. An appointment for three to four days

later was then made in order to change batteries in the

alarm/monitor. In addition, subjects were informed that the

investigator would contact them in two days in order to

ensure that the procedures had been explained properly. The











investigator called subjects at least twice weekly

throughout the study to prompt adherence and to troubleshoot

problems.

The second meeting was brief. Batteries were changed,

and an appointment to take place seven-days after the first

meeting was made.

At the third meeting, the first Daily Supply notebook

was collected and new ones provided. Batteries were changed

again, but this time all devices were reevaluated with the

calibration procedure described above. No threshold drift

was detected. A fourth meeting three to four days later was

held in order to change batteries.

Seven-days following the third meeting, a fifth meeting

was held to collect materials and check calibration. During

this meeting the alarm mode was switched to that appropriate

for the opposite experimental condition. Some subjects

received instructions in operating the alarm mode of the

alarm/monitor. For other subjects, the monitoring

procedures were reviewed.

Over the following 14-day period four meetings were

held exactly as in the first phase, to change batteries,

check calibration, troubleshoot, and give the seven-day

Daily Supply Book. Additionally, during the last meeting,

subjects were debriefed about the meaning of the

light-display, and shown a graph of their total nightly brux












episodes throughout the study. They were paid at this time

as well.

Data for one to two nights in one or both phases were

missing for four subjects. This happened for several

reasons. In some cases the subject forgot, or was unable to

comply. In other cases, the batteries failed, or the

electrodes fell off during the night. Phases were extended

for appropriate numbers of nights for these four subjects in

order to compensate for the missing data.














RESULTS

The questions of interest are reviewed below. The

overview is followed by the relevant statistical analyses

and results.

1.) The average nightly brux-episode frequency during

the no-treatment and treatment conditions were compared

within and between groups. The question of interest was

whether EMG-activated alarm therapy would reduce the

frequencies of bruxing episodes. Based on previous

literature the directional prediction was made that

brux-episode frequencies during alarm-treatment phases would

be lower than during no-treatment (baseline) phases.

2.) The average nightly brux-episode frequencies

during a phase preceding treatment were compared with those

during a phase following treatment. Based on the literature

the prediction was made that bruxing following alarm therapy

would exceed bruxism preceding alarm therapy. Because this

is a between-group comparison and only five subjects were

included in each group, this was a tentative prediction.

The prediction was tentative also because "rebounds"

following alarm therapy have not been observed uniformly.

3.) The nightly self-monitored alarm count and the

automated alarm count during treatment phases were compared

for all subjects during the alarm phases. The prediction











was that self-monitored alarm frequency would be lower than

automatically recorded alarm frequency. This is an informal

prediction based on anecdotal reports (Piccione et al.,

1982) that subjects sometimes sleep through alarm soundings.

4.) The average daily sleepiness, fatigue, and vigor

ratings during alarm treatment and baseline phases were

compared for both groups. This is exploratory work that

involves no prediction. A neutral stance is adopted because

the untoward effects of sleep deprivation are not

overwhelming in the literature (Johnson, 1982) and because

there is no guarantee that the present alarm-therapy package

will work sufficiently to constitute a de facto sleep

deprivation paradigm.

5.) A comparison was made of morning facial pain and

discomfort ratings during the treatment and no-treatment

phases. The tentative prediction was that alarm therapy

would reduce the intensity of facial pain insofar as it did

reduce bruxing rates. Therefore ratings on the VAS would be

lower for subjects while they were undergoing alarm therapy.

Impact of Treatment
The group mean hourly brux frequencies during screening

are presented in Table 2. The 30 nightly brux frequency

values from the screening phase were subjected to a 2

(groups) x 3 (days) repeated-measures Analysis of Variance

(ANOVA; BMDP Statistical Software Manual, 1983). This

analysis yielded no significant effects when tested at the












Table 2. Means and Standard Deviations for the Nightly Brux
Responses Per Hour by Group during Screening,
Phase 1, and Phase 2.


Screening Phase 1 Phase 2
M SD M SD M SD

(Baseline) (Treatment)
Group 1 2.3 1.6 2.2 2.6 0.9 0.8


(Treatment) (Baseline)
Group 2 3.4 2.4 0.7 0.8 1.5 2.1




.15 level. Hence there was no evidence that the groups

differed before treatment and no effort was made to

incorporate pretreatment differences into the logic of

subsequent analyses. This finding also justified

comparisons between groups. The ANOVA summary is presented

in Table J-l. Comparisons within groups were made as well,

and they are described following the between-groups

findings.

Average hourly brux frequency for each group during

each phase are shown also in Table 2 and in Figure 4. The

280 nightly brux frequency values were subjected to a 2

(groups) x 2 (phases) x 14 (days) repeated-measures ANOVA.

The ANOVA summary is presented in Table J-2. This analysis

yielded significance for the Group x Phase Interaction

(F=6.18, df=1/8, p<.05). This finding justified additional

post-hoc analyses to identify where the significance

occurred.















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Figure 3: Brux Frequency By Condition and Group.











First, the 140 nightly brux frequency values from Phase

1 were subjected to a 2 (groups) x 14 (days)

repeated-measures ANOVA. The ANOVA summary is presented in

Table J-3. This analysis yielded significance for the Group

Main Effect (F=14.19, df=1/8, p<.01). Inspection of the

means in Table 2 indicates the direction of the significant

difference. The group receiving alarm therapy displayed

lower brux frequencies than did the group who monitored

without the alarm.

Next the 140 nightly brux frequency values from Phase 2

were subjected to a 2 (groups) x 14 (days) repeated-measures

ANOVA. The ANOVA summary is presented in Table J-4. This

analysis failed to yield significant effects. Hence the

significant Group x Phase Interaction in the initial ANOVA

mirrors the finding that significant between-group

differences occurred during Phase 1, but not during Phase 2.

The 140 nightly brux frequency values from the two

treatment phases were subjected to a 2 (groups) x 14 (days)

repeated-measures ANOVA. This ANOVA summary is presented in

Table J-5. The analysis failed to yield significance for

any effect.

The 140 nightly brux frequency values during no

treatment and during treatment within Group 1 were subjected

also to a 2 (conditions) x 14 (days) repeated-measures

ANOVA. This ANOVA summary is presented in Table J-6. It

yielded significance for the Condition Main Effect (F=11.63,












df=1/8, p<.01). Table 2 indicates directionality. Subjects

bruxed less frequently during treatment than during no

treatment. Visual inspection of the graphs of nightly brux

frequency per hour for subjects 1 through 5 (see Appendix K)

indicates that four of the five subjects replicated the

group effect. Only Subject 3 failed to demonstrate a

convincing response to treatment.

The 140 nightly brux frequency values during treatment

and during no treatment within Group 2 were subjected also

to a 2 (conditions) x 14 (days) repeated-measures ANOVA.

This ANOVA summary is presented in Table J-7. It failed to

yield significance for any effect. Visual inspection of the

graphs of nightly brux frequency per hour for subjects 6

through 10 (see Appendix K) indicates that four of the

subjects remained at brux frequency levels observed during

treatment. Subject 8 appears to have returned to

pretreatment levels during the no-treatment period.

Evidence Concerning
Rebound Effects

In order to examine the data for evidence of a rebound

effect following a period of treatment the 140 nightly brux

frequency values from the two no-treatment phases were

subjected to a 2 (groups) x 14 (days) repeated-measures

ANOVA. This ANOVA summary is presented in Table J-8. It

failed to yield significance for any effect. Therefore, no

evidence for a "rebound" or a relatively high posttreatment

bruxing frequency was found.












Self-Monitored Versus
Automated Alarm Count

The mean self-monitored alarm-count and the mean

automated alarm-count for each subject are reported in Table

3. The 140 nightly self-monitored alarm-counts and 140



Table 3. Mean Self-Monitored Alarm-Count (SMAC) and
Automated Alarm-Count (AAC) for the 14 day
treatment phase by Subject.


Subject # SMAC AAC % of AAC


1 .9 3.8 23
2 1.6 3.9 41
Group 1 3 1.8 5.3 34
4 3.1 7.9 39
5 6.0 13.3 45

6 1.2 1.2 100
7 3.6 4.4 82
Group 2 8 6.9 8.6 80
9 0.3 0.9 33
10 2.4 8.0 30

Average %50



automated alarm-counts were subjected to a 2 (methods) x 14

(days) repeated-measures ANOVA. This ANOVA summary is

presented in Table J-9. This analysis yielded significance

for the Method Main Effect (F=4.52, df=l/18, p<.05).

Collapsing across all subjects the mean self-monitored count

was 50 percent of the automated-count. Inspection of the

average for all subjects on Table 3 reveals that

self-monitored alarm-count varied from 23 percent of the

automated-count in subject 1, to 100 percent in subject 6.












Effects of Treatment on
Vigor, Fatigue, Sleepiness,
Anxiety and Pain

Group mean vigor, fatigue, sleepiness, anxiety, and

pain ratings by phase and group are displayed in Table 4.



Table 4. Means and Standard Deviations for the Daily
Ratings of Fatigue, Vigor, Sleepiness, Tension,
and Pain by Group during Phase 1 and Phase 2.


Group 1 VIG
FAT
SSS(AM)
SSS(PM)

ANX

PAIN


Group 2 VIG
FAT
SSS(AM)
SSS(PM)

ANX

PAIN


Phase 1
M SD

(Baseline)
14.1 7.2
5.0 4.1
3.5 1.1
2.0 1.1


5.3

4.6


2.7

6.4


(Treatment)
15.1 6.4
6.9 5.2
3.1 1.2
1.9 0.9


6.7

5.4


4.5

8.8


Phase 2
M SD

(Treatment)
13.7 7.6
6.4 4.7
3.0 1.2
2.0 0.9


6.2

3.7


4.1

5.5


(Baseline)
15.3 7.0
6.4 6.3
2.9 1.0
2.0 0.8


5.2

5.2


3.6

7.8


Note. VIG=Vigor subscale from the Profile of Mood States
(R=0-32); FAT=Fatigue subscale from the Profile of Mood
States (R=0-28); SSS=Stanford Sleepiness Scale (R=0-7);
ANX=Anxiety subscale from the Profile of Mood States
(R=0-36); PAIN=Visual Analog Scale of Facial Muscle
Pain/Discomfort (R=0-100).











Visual inspection revealed only small differences in

means between groups and phases. However, visual inspection

pointed also to small variances. Therefore, the various

data were subjected to separate ANOVAs. A repeated-measures

Multivariate Analysis of Variance approach was rejected as

unduly complex, given the appearance of nondifferent values

in Table 4.

Initially, 2 (groups) x 3 (days) repeated measures

ANOVAs were performed on each of the five sets of 30 values

acquired from the 10 subjects during the three-day

screening. No significant effects were produced by any of

the five analyses. Hence, pretreatment values for vigor,

fatigue, sleepiness, anxiety, and pain were viewed as

nondifferent.

Next, separate 2 (groups) x 2 (phases) x 14 (days)

repeated-measures ANOVAs were done within each of the five

sets of self-report data. For the variables of vigor,

fatigue, sleepiness, and pain these analyses produced no

significant effects (see Appendix J-10, J-ll, J-12, and

J-13).

The ANOVA summary for anxiety ratings is presented in

Table J-14. This analysis yielded a significant Group x

Phase Interaction (F=6.77, df=1/8, p<.05). As is shown in

Row 5 and Row 11 of Table 4 lower mean anxiety ratings were

obtained during baseline phases than during treatment.













DISCUSSION
The narrative below discusses the results of the

experiment as they are related to the experimental purposes

described earlier. In each section an attempt is made to

delineate implications of the results and directions for

future research. Also included is a narrative about

theoretical explanations of alarm-therapy mechanisms.

Future research is discussed in that connection as well.

Impact of Treatment

The experiment reported here supports the conclusion

from prior research that EMG-activated alarm therapy can

reduce nocturnal bruxism (Beemsterboer et al., 1978; Casas

et al. 1982; Clark et al., 1981; Kardachi & Clarke, 1978;

Rugh & Solberg, 1975). Specifically, it strengthens the

literature (Moss et al., 1981; Purzycki et al., 1986) in

which manual termination of a nocturnal alarm was included

in intrasubject replication protocols. This conclusion is

based on several comparisons. The comparison between groups

during the first phase shows that subjects who received

alarm therapy had significantly lower rates of bruxing than

did untreated subjects. In addition, the comparison across

phases within Group 1 showed that subjects had significantly

higher bruxing rates during no treatment than during

subsequent alarm therapy. Therefore, both between- and

within-group comparisons support the efficacy of the alarm











therapy protocol. Finally, graphic data for each subject in

Group 1 showed the overall effect in four of the five

participants.

Notwithstanding the encouraging results, additional

research is needed to define the boundary conditions of

successful alarm therapy packages with bruxist individuals.

Larger samples of subjects are required. Classifications of

bruxist subjects according to differing bruxing etiologies

will be valuable as etiological data become available.

Variations in the fine grain of alarm-therapy protocols will

be of interest also as the "mechanisms" of alarm therapy

effects become known.

Evidence Concerning
Rebound Effects
As noted earlier, several studies have found that

post-treatment bruxing actually increased above

pre-treatment bruxing when alarm therapy was used (Funch &

Gale, 1980; Piccione et al. 1982). No similar effect was

seen in the present results even though the experimental

design afforded several opportunities for it to occur.

The research reported by Piccione et al. (1982) is weak

methodologically in several respects (Mealiea & McGlynn,

1986). Funch and Gale (1980), in turn, used only one

subject. Hence, relatively greater confidence can placed in

the data reported here. However, the issue should be viewed

as open to continuing investigation.












Beemsterboer et al. (1978) proposed originally that

wakefulness following alarm soundings should increase

maintenance of treatment effects. Neither Piccione et al.

(1982) nor Funch and Gale (1980) provided for wakefulness

following alarm soundings. Alarm-contingent wakefulness

could be an important determinant of rebound phenomena

associated with alarm therapy protocols. Thus, alarm

features such as the manual reset switch constitute one

important domain for further study. Research might begin by

pitting manual-reset alarm therapy against the more common

paradigm in which instructions for wakefulness are provided

to subjects.

Self-Monitored Versus
Automated Alarm Count

The validity of some previous conclusions about alarm

therapy effects is doubtful owing to the assumption that

subjects self-monitor accurately (Clark et al., 1981).

Hence, an important purpose of the present study was to

characterize the degree to which subjects were able to

self-monitor alarm sounds during the night. The comparison

between self-monitored and automated counts of alarm

soundings revealed very large differences.

The above finding suggests that instructions to

self-monitor alarm soundings during the night are an

insufficient means of tracking the course of alarm therapy.

It draws into question those reports of successful alarm











therapy in which self-monitored alarm records constituted a

mode of treatment evaluation (Clark et al., 1981).

Additional contingencies are needed to provide more reliable

self-monitoring. In the meantime, research should make use

of automated alarm records.

Effects of Treatment on
Vigor, Fatigue, Sleepiness,
and Anxiety
As noted earlier, no discussion of the risks or

contraindications of alarm therapy exists in the literature.

This is surprising given that the treatment disrupts sleep

intentionally. Some laboratory research has investigated

the effect of alarms on sleep staging. One study has

suggested that alarm therapy does influence sleep staging

(Piccione et al., 1982), while another found no effect on

sleep staging (Purzycki et al., 1986). However, no previous

study has examined diurnal sleepiness or mood ratings in

patients undergoing alarm treatment.

No evidence was found here that ratings of sleepiness,

vigor, or fatigue were influenced by alarm treatment. This

benign effect occurred even though the alarm protocol did

produce frequent arousals during the night. However, the

present treatment lasted only two weeks. The very real

possibility exists that maladaptive effects on sleepiness

and/or mood reports would be seen with continuation of

treatment. Hence, a high priority area for future research











is the effects of longer therapy durations on this domain of

variables.

Caution is prompted also by the present findings

concerning self-reported anxiety on the POMS. Subjects

reported higher levels of anxiety during treatment phases

than during baseline phases. Even though anxiety ratings

for all subjects remained far below normatively significant

levels, they should not be ignored. Several post hoc

explanations for this effect exist, but they need not be

explored until the result is replicated.

For the time being studies should proceed with added

caution. Informed consent should require statements about

the possibility of moderately increased anxiety during

treatment.

Effects of Treatment
on Facial Pain

No reductions in daily ratings of facial pain were

found during alarm treatment. The trend was in the

direction of lowered ratings during and following treatment,

but it was not significant. While eight of the subjects

reported a history of facial pain and headaches, only two

had sought treatment. Therefore, they constitute a

subclinical pain population.

The question of whether alarm therapy can reduce some

facial pains remains to be answered by research. Only two

studies have used alarms with facial pain patients (Rugh &











Solberg, 1977; Clarke & Kardachi, 1977) and neither

quantified pain ratings or bruxist behavior systematically.

Theoretical Explanations of
Alarm Effects
Detailed versions of various theories concerning alarm

effects have not been presented because clinical outcome

research has not derived from theoretical considerations.

However, future research could benefit from a better

integration of theoretical assumptions with experimental

problems. Hence, a theoretical narrative is offered in

closing here.

DeRisi (1970), and Heller and Strang (1973) proposed

two orthodox theoretical explanations for why alarm therapy

reduces bruxing. DeRisi (1970) described his work as an

extension of Azrin's work on avoidance conditioning within

the operant paradigm (Azrin, 1958, Azrin & Holz, 1966).

Heller and Strang (1973), in turn, briefly cited a

connection with the work of Mowrer and Mowrer (1938) and the

Pavlovian tradition.

Alarm therapy is relatively straightforward when

conceptualized within the operant paradigm. If the

probability of a bruxist response decreases after contingent

tone presentation, then the tone is a punishing stimulus.

Procedures via which a patient learns to first escape then

avoid a punishing stimulus are referred to as avoidance

conditioning.











An operant analysis of bruxing accesses a large

literature on punishment parameters and predicts the

posttreatment return of bruxing in the absence of a

reinforced competing response (Walters & Grusec, 1977).

Also, such an analysis suggests potentially beneficial

modifications to alarm therapy protocols. One obvious

modification is to schedule alarm soundings intermittently

so as to enhance the durability of punishment effects

(Finley, Rainwater, & Johnson, 1982).

A specific problem for an operant analysis of alarm

therapy effects on bruxing involves whether to construe them

as reflecting punishment or passive avoidance. In general,

competing conceptualizations and research with operant

analyses are likely to be relatively unproductive insofar as

the operant analysis generically is incomplete.

The classical conditioning model of alarm therapy

effects is somewhat more complicated. The alarm serves as

an unconditioned stimulus (UCS) for the response (UCR) of

awakening. The UCS is presented repeatedly in temporal

proximity with masseteric muscle tension. In time,

therefore, the muscle tension becomes a conditioned stimulus

(CS) for awakening (CR).

There are several shortcomings with the Pavlovian

model. In general respondent conditioning is a procedural

paradigm, not an explanatory structure. Thus if

alarm-therapy effects are said to result from respondent











conditioning, then the task becomes that of explaining

respondent conditioning. Not only is the task of explaining

respondent acquisition complex (Delprato & McGlynn, 1984),

but also it draws attention away from the problem of

interest; namely describing variables that influence

alarm-therapy outcomes. Furthermore, the Pavlovian model of

the Mowrer and Mowrer (1938) work is now recognized as

incomplete (Lovibond, 1964, 1972). Hence, drawing parallels

between alarm-therapy for bruxing and the bell-and-pad

treatment of enuresis does not strengthen Pavlovian

interpretations of alarm therapy effects generally.

There are specific problems with a respondent analysis

as well. For example, the CS (bruxing) is also the response

to be eliminated. For the CS to elicit awakening, the

problematic response must occur. In a sense, this model

predicts that the response will never be totally eliminated.

The claim that alarm therapy is analogous to the Mowrers'

(1938) treatment for nocturnal enuresis is specifically

flawed as well. The Mowrers' argued that the bell and pad

worked because the alarm (UCS) was paired with bladder

fullness (CS). After repeated pairings, the CS alone would

be sufficient to elicit arousal from the subject.

Problematically, there is no analogous antecedent for

bruxism. Bladder fullness might sometimes be part of an

arousal/bruxing pattern of behavior. But, as noted earlier,

the Pavlovian view of alarm therapy effects is not











applicable even in such a situation because it does not

account satisfactorily for the events of bell-and-pad

treatment outcomes.

Research within the Pavlovian construction of

alarm-therapy effects would identify precursors to bruxing

that reliably occur within an ideal conditioning window of

.2 to 2 seconds before the response (Kimble, 1961). Then

the alarm would be paired with such precursors. Probably

more effective treatments could be based on work along these

lines. Nonetheless, excessive or sole reliance on a

Pavlovian view of the problem should be avoided for the

various reasons mentioned.

To varying degrees the nocturnal alarm paradigms

represent the larger continuum of biofeedback treatment.

The most representative are procedures in which EMG activity

initiates and terminates actual analog feedback of

suprathreshold values (Kardachi & Clarke, 1977). The least

representative are procedures in which suprathreshold EMG

activity initiates a constant signal that is terminated by

some psychomotor performance that is not related to bruxing

itself (Purzycki et al., 1986). There are a half dozen or

so theoretical models of how biofeedback treatments result

in efficacious outcomes (for a review see Raczynski,

Thompson, & Sturgis, 1982). Despite some overlap (Black,

Cott, & Pavloski, 1977) these models can supplement the

traditional learning approaches such as those just discussed











in suggesting experimental variables and interpreting

experimental results (Mealiea & McGlynn, 1986). Allowances

can be made for unique features and procedural nuances in

the nocturnal alarm paradigms.

Notwithstanding the experimental guidance that is

afforded by learning and biofeedback theories, a

comprehensive program of research on nocturnal

feedback-alarm effects should be guided also by etiological

theories of bruxism itself. In this connection, a major

domain of interest has to do with variables related to

sleep.

There is a literature comprised of a dozen or so

studies in which nocturnal bruxing was studied in relation

to EEG-defined sleep staging. The most impressive work in

the area suggests that bruxing is differentially associated

with REM sleep (Clarke & Townsend, 1984) and with

transitions between sleep stages (Satoh & Harada, 1972,

1973). Some recent work suggests that bruxing during REM

and NREM sleep might differ fundamentally (Rugh & Ware,

1986). In any event, relatively stable relationships

between nocturnal bruxing and sleep phenomena probably do

exist. Hence research on the effects of alarm-feedback

paradigms on sleep variables is likely to be beneficial, as

is research on treatment efficacy as a function of sleep

phenomena. The work of Piccione et al. (1982) and Purzycki

et al. (1986) constitutes preliminary effort. A high








84


priority area for research in the near future should entail

use of manual reset feedback alarms under conditions of

night long polysomnographic recording.

























APPENDICES









APPENDIX A


SUBJECT RECRUITMENT NOTICE


g 'U
ni


Do

-eBI~


You Grind Your

eth While Yu'-

Sleep?


Is Your Face Sore When You Wake Up?
Have Roommates Told You That They
Hear You Grinding Your Teeth When
You Sleep?
Have Dentists Told You That Your
Teeth Are Worn?
Excessive grinding and clenching is called bruxism.
Bruxism may lead to serious problems such as tooth wear,
facial pain, and damage to the jaw joints. We are
studying a treatment for bruxism and we are looking for
individuals who have this problem. In addition to free
treatment, volunteers will earn money for participating.

Earn Money


Free


Treatment


For more information call Mr. Jeff Cassist
at 377-2883 between 5:00 p.m. and 10:00 p.m.,
or stop by room D6-11 in the dental tower
during weekdays.


aim___ 1110















APPENDIX B

STANDARDIZED DENTAL SCREENING EXAM








DENTAL OCCLUSION AND FACIAL PAIN CENTER U. OF FLORIDA
COLLEGE OF DENTISTRY

NAME: DATE:

ADDRESS:
street city county state zip

TELEPHONE: AGE: DATE OF BIRTH: SEX: M F

OCCUPATION/EMPLOYER: BUS. PHONE:

REFERRED BY:
name street address

TELEPHONE:
city state zip

Allergies:

Tobacco: Yes_ No Cigs_ Pipe_ Smokeless_ Amount

Alcohol: Yes_ No_ Type/Amount

Accident or trauma: Yes No When What

Arthritis: Yes No Comment

Head, neck swelling: Yes No Facial Asymmetry: Yes_ No

EAR:Hearing loss Hyperacusis_ Tinnitus_ Pain_ Stuffy_ Drainage_

SPEECH PROBLEMS: (such as persistent horseness) Yes_ No

Comment:



HEADACHE: Yes No VascularMuscular Migraine Cluster_ AM_ PM

Right_ Left_ Hours per day_ Comment



ORAL PATHOLOGY: Yes No Comment:

TONGUE: Abnormal: Yes No

GINGIVA: Abnormal: Yes No

LYMPHNODE: Abnormal: Yes No


























JOINT LAXITY: 1 tight; 2 = normal; 3 = loose

Wrist: Rt. Lft. Elbow: Rt. Lft. Other:

----------------- ---------- ---------

Right TMJ Left PAIN SCALE Right Musculature Left
0 = NO PAIN
Pain, lat. 1 MILD Masseter, super.
2 MODERATE
Pain, post. 3 SEVERE Masseter, deep.

Pain, vert. Masseter, trig. pt.

Click, open Masseter, insert.

Click, close ___ Temporalis, ant.

Click, ipsilat __ Temporalis, post.

Click, contra ___Temporalis, insert.

Crep., vert. __Trapezius, ant.

Crep., ipsilat ___ Trapezius, insert.

Crep., contra Splenius Capitis

ROM: open with pain mm. SCM, insert.

open w/o pain mm. SCM, middle

deviation Digastric, ant.

R mm lat. move L mm. Digastric, post.

protrusive mm. pain:Yes_ No ___ Lateral pterygoid

SMedial pterygoid

Right VASCULAR Left COMMENT:

Carotid

Facial

STemporal


SIGNIFICANT DENTAL WORK: Ortho


Rest


-Surg Perio Endo










89










PREVIOUS TREATMENT: Medical Occ adj _TMJ Surg Splints

Comment:

BRUX, CLENCH, other habit: Yes No_ Day_ Night_ Other

OCCLUSAL FUNCTION: Angle Class: Tooth code: 11-18 21-28
41-48 31-38
Teeth missing: Replaced with:

Wear facets: Mobile teeth#, class:

Percussion response:

Crossbite: R L Teeth# Crossover#

Slide: Lat. Dev. R L Vert. Dev. Ant. Dev.
LATERAL EXCURSIONS

Work<------------- Balance------------->Work Prot--------V--------
Right Left Right Left


DIAGNOSIS: Noxious occlusion

Myofascial pain

Bruxism

Joint derangement















APPENDIX C


SCREENING QUESTIONNAIRE






DEPARTMENT OF CLINICAL PSYCHOLOGY
AND THE
DENTAL OCCLUSION AND FACIAL PAIN CENTER


Date


__ State Zip


Phone (where to


reach you during the day and evening):


We are asking you to help us get to know you and your problem
better by filling out this questionnaire at your first appointment.
This information will be held in strict confidence and will not be
released to others without your specific written permission. We know
this form is long and will take time, but the information is very
important in helping us determine the correct diagnosis and factors
that may contribute to the problem. It will be used to help provide
you with the best and most comprehensive care. Thus, it is to your
ultimate benefit to answer the questions by yourself as accurately and
sincerely as possible.

Please read each question carefully and answer by writing
clearly, circling carefully, or marking distinctly. We appreciate the
time you will spend in answering these questions carefully.

1.) HOW DID YOU FIND OUT ABOUT THIS TREATMENT PROGRAM?


2.) YOUR PRESENT OCCUPATION

3.) SPOUSE'S PRESENT OCCUPATION


4.) GENDER: MALE


FEMALE (5.) BIRTHDATE _/_/


6.) HEIGHT (feet,inches)

7.) WEIGHT (pounds)

8.) RACE (circle:) White Black Indian Asian
Hispanic Other
9.) MARITAL STATUS (circle:) Single Married Widowed Divorced
Separated Remarried


Name

Address


City