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The Journal of Craniomandibular & Sleep Practice

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Bruxism and Cranial-cervical Dystonia: Is There a

Relationship?

Maureen Wooten Watts M.D., Eng-King Tan M.D. & Joseph Jankovic M.D.

To cite this article: Maureen Wooten Watts M.D., Eng-King Tan M.D. & Joseph Jankovic M.D.
(1999) Bruxism and Cranial-cervical Dystonia: Is There a Relationship?, CRANIO®, 17:3,
196-201, DOI: 10.1080/08869634.1999.11746095

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196$03.00/0, THE
JOURNAL OF
CRANIOMANOIBULAR
PRACTICE,
Copyright© 1999
by CHROMA, lnc.
Manuscript received
October 29, 1998; revised
manuscript received
January 27, 1999; accepted
March 20, 1999
Address for reprint requests:
Dr. Joseph Jankovic
Professor of Neurology
Department of Neurology
Baylor College of Medicine
6550 Fannin, Suite 1801
Houston, Texas 77030
email: JosephJ@bcm.tmc.edu
• BEHAVIORAL SCIENCES
Bruxism and Cranial-cervical Dystonia: Is There a
Relationship?
Maureen Wooten Watts, M.D.; Eng-King Tan, M.D.; Joseph Jankovic, M.D.
ABSTRACT: To characterize the relationship between bruxism and dystonia, 79 patients (28 men and
51 women) with cranial-cervical dystonia were studied. Sixty-two patients (78.5%), 22 men and 40
women, had bruxism. The mean age at onset of dystonia in patients with bruxism was 52.4 ± 12.6 years
(range 14-80), similar to patients with cranial-cervical dystonia without bruxism. lnvoluntary oro-
mandibular movements (46 patients) and blepharospasm (34 patients) were the most common initial
symptoms among patients with dystonia. About one-fourth of bruxism patients had associated dental
problems inclüding TMD (21 %) and tooth wear (5%). A majority (58%) of the bruxism patients had diur-
nal bruxism and 12% had noctumal bruxism. The bruxism patients were compared to 100 patients with
Parkinson's disease (PD), cervical dystonia, cranial dystonia, and normal controls, respectively. The
prevalence of bruxism was much higher in the cranial-cervical dystonia patients when compared to
normal controls (P<0.001 ); however, this difference was not significant between other diseased groups
and controls. Medications and botulinum toxin injections, used in the treatment of focal dystonia also pro-
vided effective relief of bruxism.
ruxism is a diurnal or nocturnal parafunctional
B activity including clenching, grinding, bracing
and gnashing of the teeth. It is a source of many
dental and neuromuscular problems, including tooth
wear, periodontal disease, hypertrophy of the masticatory
muscles, headaches, and temporomandibular disorders. 1·4
Es ti mates of the pre valence of bruxism in the adult popu-
Dr. Maureen Wooten Watts obtained lation have varied between 5% to 96%, 5· 7 and about 15%
her M.D. degree from the University of
Ari:ona Co/lege of Medicine in 1985.
of children have bruxism. 8 Bruxism is usually transient in
She completed her neurology residency children and resolves with eruption of the secondary den-
at Bav/or Co/lege of Medicine, Houston, tition.9·10 The wide variation in the prevalence rate may be
Texas and is certified in the American
Board of Neuro/ogy and Psychiatry. Her
explained by the differences in diagnostic criteria and in
chief interests include genera/neurology, the demographies of the surveyed populations.
movement disorders and neurophysiology. Bruxism is an important public health problem because
Dr. Watts is a member of the American
Academy of Neurology and is present/y in
of its high prevalence and frequently associated compli-
private practice in Dallas, Texas. cations. Furthermore, the quality of li fe in bruxers, espe-
cially those with pain, is also affected. 11 Fischer, et al., 12
in their study of personality characteristics in chronic
bruxers, found them to exhibit shyness, rigid ways, and
"inferiority complex." The pathogenesis of bruxism is
unknown, but abnormal emotional states and stresses are
thought to precipitate or exacerbate the disorder.l3-Js
Occlusal discrepancies (e.g., malocclusion) have been
postulated to be a cause of bruxism.9· 16·17 One hypothesis
196
WATTS ET AL.
is that muscle reflex receptors elicit contraction of the jaw
muscles as a result of stimulation from improper teeth
contacts, but this has not been proven. 18·19 Other reported
etiologies include drugs such as amphetamines, lev-
odopa, fenfluramine, dopaminereceptor blocking agents, 20-
24 selective serotonin reuptake inhibitors, 25 -27 and alcohol. 28
Bruxism has also been associated with idiopathie or post-
traumatic oromandibular dystonia, 29 hemifacial spasm,3o
post anoxie brain damage, 31 coma, 32 cerebellar damage, 33
Rett's syndrome, 34 Whipple's disease, 35 and the mentally
retarded. 36 Bruxing behavior is also more common among
those with craniomandibular disorders such as temporo-
mandibular joint dysfunction (TMD). 3738 Bruxism tends
to occur more often in stage two sleep and with arousal,
though it has been reported in ali stages of sleep. 39
However, patients with severe symptoms of nocturnal
bruxism are more likely to have it in REM sleep. 40
Lavigne, et al. 41 in a survey of 2,019 adults, found smok-
ers to have more tooth-grinding episodes during sleep
than nonsmokers.
As bruxism is frequently associated with disorders of
the central nervous system (CNS), CNS mechanisms may
be the underlying cause in these cases. One common
CNS cause of bruxism encountered in our Movement
Disorders Clinic is cranial dystonia, a neurologie syn-
drome dominated by sustained muscle contractions that
can cause involuntary eye closure (blepharospasm),
facial and tongue contractions and involuntary jaw open-
ing, deviation and jaw closure with trismus and brux-
ism. 42 Th us bruxism may re suit from spasmodic (dystonie)
muscle contractions, involving the masseter and tempo-
ralis muscles. It is often associated with other forms of
cranial dystonia including blepharospasm and oro-
mandibular dystonia. 29 ·43 Electrophysiologic studies in
patients with jaw closing spasm have provided additional
evidence that bruxism is a form of focal dystonia. 44 The
purpose of this study is to characterize the relationship
between bruxism and cranial-cervical dystonia.
Materials and Methods
The records of 79 patients, 28 men and 51 women,
with cranial-cervical dystonia consecutively evaluated at
the Bay lor College of Medicine, Movement Disorders
Clinic during a five-year period were reviewed. The
demographie and clinical data were entered into a rela-
tional database. Cranial-cervical dystonia patients were
those patients with involuntary, sustained, repetitive and
patterned contractions or movements involving the upper
face, mouth, eyes, tongue, pharynx, vocal cords and neck.
Ali patients with cranial-cervical dystonia were carefully
evaluated regarding bruxism. We defined bruxism as a
JULY 1999, VOL. 17, NO. 3
BRUXISM AND DYSTONIA
diurnal or nocturnal parafunctional activity including
clenching and/or grinding of the teeth. This is similar to
the definition given by the American Academy of
Orofacial Pain. 45 Supporting evidence of bruxism,
although not required for the diagnosis, include tooth
wear, masseter (temporal) hypertrophy, and soreness,
tenderness and stiffness in masticatory muscles on awak-
ening. Patients were categorized as having diurnal brux-
ism (while awake), nocturnal bruxism (while asleep), or
both. Patients who were classified with nocturnal brux-
ism had to have their history corroborated by bed partners
or family members. Due to the cost factor, no sleep
polysomnography was carried out. TMD was defined as
either persistent or recurrent pain in the temporo-
mandibular joint area.
A second part of this study involved a structured ques-
tionnaire administered in person or by telephone inter-
view of randomly selected groups of patients and normal
controls to determine the pre valence of bruxism in those
populations. One hundred patients with Parkinson's dis-
ease, cervical dystonia, and cranial dystonia, respec-
tively, were surveyed. One hundred spouses of sorne of
the patients served as "normal" controls. The interviewer
was unaware of the neurologie diagnosis of the subject.
The correctness of the response was later verified by one
of the investigators who interviewed a random sample
of ten subjects in each group. The questionnaire was
designed to elicit prevalence and duration of teeth clench-
ing and grinding during the day and during sleep.
Questions regarding possible exacerbating factors for
bruxism, such as emotional states, were included as were
questions about associated symptoms including tooth
wear, sore jaws, difficulty chewing, headaches, earaches,
jaw popping or clicking, tooth sensitivity, TMD, and dif-
ficulty opening the mouth. Subjects were also questioned
about previous history of trauma to the head and mouth
region, and the presence of involuntary movements of the
mouth andjaw.
Statistical tests of differences in characteristics of
patients were performed using the Fischer's Exact Test or
the Chi-Square test for contingency tables. Statistical
significance is defined when p<0.05.
Results
Of 79 patients with cranial-cervical dystonia, 62
(78.5%), 22 men and 40 women, had definite bruxism
and 17 (21.5% ), six men and eleven women, did not.
Similar to other patients with cranial-cervical dystonia
whose mean age at onset was 54.0 years (13.7, range
6-86), the mean age at onset of dystonia in patients with
bruxism was 52.4 years (±12.6, range 14-80) (Table 1).
THE JOURNAL OF CRANIOMANDIBULAR PRACTICE 197
BRUXISM AND DYSTONIA WATTS ET AL.

The most common initial symptoms in cranial dystonia
patients with and without bruxism were oromandibular
dystonia and blepharospasm. Tardive dystonia was sig-
nificantly more common in patients with bruxism than in
those without (p<0.05).
In the 62 patients with bruxism, the mean duration of
symptoms of clenching and/or grinding was 54.7 ± 97.4
months (Table 1). Approximately a quarter of ali patients
in this group had associated dental problems, primarily
TMD and tooth wear. Evidence of TMD included corn-
plaints of jaw soreness, jaw popping or clicking, diffi-
culty chewing, and a reported diagnosis of TMD by a
dentist. About one-half (58%) of the patients had diurnal
bruxism and 12% had nocturnal bruxism. Twelve
patients ( 19%) had oromandibular and dental procedures
including splinting, grinding or capping of the teeth,
mandibular implants, electrical stimulation of the mas-
seter muscles, tooth extractions, and wiring of the jaws.
In contrast, among the nonbruxism patients, only one
(6%) had a diagnosis of TMD, and two (12%) had oro-
mandibular and dental surgery.
In the survey of 100 normal control subjects and 100
diseased controls (PD, cranial, and cervical dystonia),
there was a higher percentage of clenching and/or grind-
ing in the PD, cervical dystonia and cranial dystonia
groups as compared to the control group. However, this
difference was not statistically significant (Table 2). A
larger portion of patients in the PD, cervical and cranial
dystonia groups noted jaw popping or clicking, difficulty
chewing and involuntary movements of the jaw and
mouth. The cervical and cranial dystonia patients seemed
to have more difficulty with mouth opening and had
more jaw surgery.
There was a significant difference of prevalence
of bruxism between patients with cranial-cervical dysto-
nia and normal controls (62179 vs. 21/100, p<O.OOl)
(Tables 1 and 2).
Of the 62 patients with bruxism, 23 were treated with
botulinum toxin injections into their masseter muscles.
Eight of the 12 (67%) with adequate follow-up reported
improvement in teeth grinding and/or clenching, leading
to functional improvement in speech and swallowing.
However. five patients reported transient complications
of dysphagia and local swelling during the course of
treatment. The mean dosage of botulinum toxin used was
about 50 units, with a mean active duration of 13 weeks.

Table 1
Bruxism in Patients with Cranial-cervical Dystonia
Patients wlbruxism Patients w/o bruxsim
Total patients= 79 N =62 (78.5%) N = 17 (21.5%)
No. % No. %
Female/male ratio 40/22 65/35 11/6 65/35
Mean age at onset of dystonia (yrs.) 52.4±12.6
Mean duration of symptoms (mos.) 54.7±97.4
Diagnosis at evaluation
Oromandibular dystonia 46 74 15 88
Blepharospasm 34 55 7 41
Lingual dystonia 23 37 6 35
Cervical dystonia 21 34 6 35
Palatopharyngeal dystonia 5 8 0 0
Spasmodic dysphonia 3 5 1 6
Tardive dystonia* 27 44 1 6
Tremor (upper limbs) 19 31 3 18
Severity of dystonia at evaluation
Moderate w/disability 45 73 16 94
lncapacitating 12 19 1 6
Moderate w/o disability 5 8 0 0
Family history of dystonia in
first degree relative 9 15 2 12
Associated dental problems
TMD 13 21 1 6
Tooth wear 3 5 0 0
Oromandibular or dental surgery 12 19 2 12
* < 0.05

198 THE JOURNAL OF CRANIOMANDIBULAR PRACTICE JULY 1999, VOL. 17, NO. 3
 WATTS ET AL. BRUXISM AND DYSTONIA

Table 2
Survey of Bruxism and Associated Symptoms
Normal PD Cervical dystonia Cranial dystonia
Number 100 100 100 100
Mean age (yrs) 59.8±11.4 67.7±9.4 53±11.8 62.9±10.2
Bruxism 21 30 27 28
(teeth grinding
and/or clenching)
Tooth wear 16 26 24 34
Jaw soreness 18 13 26 19
Difficulty chewing* 6 19 21 30
Headaches 25 18 21 25
Earaches 7 4 14 11
Jaw pop/click* 17 27 42 29
Sensitive teeth 26 22 21 26
Difficulty opening
mouth 4 4 18 12
TMD 4 3 9 8
Jaw surgery 0 0 3 3
lnvoluntary movements
of jaw/mouth* 0 16 19 44
*p < 0.05

Discussion ences because bruxism occurred with LHA stimula-

In this study of 79 patients with cranial-cervical
dystonia, 62 (78.5%) patients with bruxism were identi-
fied. These patients reported grinding and/or clenching
their teeth and had tendemess and/or hypertrophy of the
masseter muscles on clinical examination. Oromandibular
dystonia was the most common diagnosis in the pa-
tients with bruxism, and over 90% of them had
moderate or incapacitating dystonia. Approximately
25% of the bruxism patients had associated dental prob-
lems such as TMD and tooth wear, and 19% also re-
ported previous oromandibular and dental procedures.
Patients with no bruxism had Jess dental complica-
tions (Table 1).
In a survey of randomly selected controls, we found
that 21% clenched and/or ground their teeth. The preva-
lence of bruxism in the con trois was lower than in patients
with PD, cervical and cranial dystonia, but this was not
statistically significant. Bruxism is frequently associated
with dystonia and hence, both may share similar patho-
physiology. No CNS structures associated with teeth
grinding have thus far been identified. Animal studies
have suggested sorne of its possible underlying mecha-
nisms. Stimulation of limbic structures such as amygdala
and the lateral hypothalamic area (LHA) or the jaw area
of the motor cortex produced bruxing behavior in rab-
bits.46 The investigators postulated that bruxism could
possibly result from a Joss of inhibitory cortical influ-
tion on! y when the cortex was ablated. Gnawing behavior
in rats can be enhanced by release of endogenous
dopamine 32 and manipulation of the dopaminergic system
causes bruxism in humans. 20•23 Gomez, et al., 47 measured
nonfunctional masticatory activity in a rat mode! by the
degree of incisai attrition. They showed that repeated
stimulation of the dopaminergic system with apomor-
phine, a dopamine receptor agonist, led to enhancement
of nonfunctional masticatory activity, and the severity of
apomorphine-induced oral behavior was positively
correlated with an increase in incisai attrition rate.
Pharmacologie evidence also suggests that a central
dopaminergic system may be implicated in the patho-
physiology of sleep bruxism. Using Single-Photon
Emission Computed Tomography (SPECT), Lobbezo, et
al. 48 demonstrated that abnormal side distribution in
striatal D2 receptor binding is associated with sleep brux-
ism. Bruxing behavior occurs primarily during transition
from sleep to wakefulness at which time dopaminergic
neurons exert their excitatory effects on cortical and
limbic jaw motor areas. 49
Besides the dopaminergic system, the norepinephric
(NE) system may be also involved. For instance, the mas-
seteric reflex in anesthetized cats is enhanced by NE and
by the NE agonist, phenylephrine. 50.5 1 Microinfusions of
NE produced dose-dependent increases in the amplitude
of the elicited reflex response and this response was
blocked by pretreatment with the alpha-1-adrenergic

JULY 1999, VOL. 17, NO. 3 THE JOURNAL OF CRANIOMANDIBULAR PRACTICE 199
BRUXISM AND DYSTONIA
antagonist, prazosin. The masseteric reflex was also
elicited when cats were exposed to various environmental
stimuli known to activate NE neurons and could be
blocked with alpha-1-adrenergic antagonists. Recently,
propranolol has been reported to alleviate bruxism, pro-
viding additional support for the involvement of the
adrenergic system. 52 Alterations in NE have been impli-
cated in the pathogenesis of dystonia and elevated levels
of NE have been found in the midbrains of patients with
dystonia, including one with bruxism.s3.s 4
Various therapies have been reported for bruxism
including hypnosis, muscle relaxation exercises, aversion
therapy, psychotherapy, drugs, biofeedback, splinting,
and massage, but not ali of these have been found to be
consistently effective. 55 -6° Clinical studies have demon-
strated the potential usefulness of drugs like amytripty-
line,61 propranolol, 52 ·62 bromocriptine63 and levodopa64 in
alleviating sleep bruxism.
The retrospective nature of our study did not allow us
to evaluate accurately the effects of various therapies on
bruxism. However, sorne patients with cranial-cervical
dystonia improved with clonazepam, trihexyphenidyl or
tetrabenazine. Botulinum toxin injections into abnor-
mally contracting muscles have been found to provide
the most effective relief of spasm.31.65.66
We recognize the shortcoming of using self-reporting
of bruxism in the second part of the study. However, this
should not totally invalidate our results. To date, there
have been no validated methods of assessment for the
diagnosis of bruxism, and historical data from patients
and their family members is still an important component
of the diagnosis. Age matched spouses of patients were
chosen as controls because they were more likely to be
aware of symptoms of bruxism. We believe they were
more likely to over-report than under-report their bruxing
behavior, which may in part account for the Jack of robust
difference between the control group and the other dis-
eased population (Table 2). The large difference in the
prevalence rates between the patients with cranio-cervi-
cal dy,;tonia and controls, and the large numbers of
patients and controls involved, also reduced the risk of
spurious results.
In summary, this study demon strates a significantly
higher prevalence rate of bruxism in patients with
cranio-cervical dystonia compared to controls without
dystonia. This suggests that bruxism may be an important
clinical component of this type of dystonia or, alterna-
tively that dystonia may cause or exacerbate the bruxing
behavior. Cranio-cervical patients with bruxism are more
likely to have dental complications than those without.
Lastly, botulinum toxin injections provide the most effec-
tive relief to patients with severe bruxism.
200 THE JOURNAL OF CRANIOMANDIBULAR PRACTICE
WATTS ET AL.
Our study highlights the possible relationship between
bruxism and dystonia, and also draws attention to the
need for close monitoring of dental problems in patients
with dystonia. Further studies are needed to investigate
the pathophysiologic differences between the severe
involuntary bruxism of central origin and the milder
bruxism seen in normal controls.
Acknowledgement
We would like to thank C. Contant, Ph.D., K. S.
Schwartz, P.A., and W. Clemence for their technical
assistance.
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Dr. Eng-King Tan received his M.D. degree from the National
University of Singapore in 1989. He completed his internai medicine
residency and obtained his MRCP (UK) in 1995. ln 1998, he completed
his neuro/ogy residency in Singapore and then received a govemment
scholarship to continue training in movement disorders under Dr. Joseph
Jankovic at the Parkinson 's Disease Center and Movement Disorders
Clinic, Bay/or Colle ge of Medicine. Dr. Tan is a junior member of the
American Academy of Neurology.
Dr. Joseph Jankovic received his M.D. degree from the University of
Arizona in 1973, completed an intemship at Bay/or College of Medicine,
and received his neurologica/ training at the Neurologicallnstitute,
Columbia University, New York. He is the immediate past president of
the International Movement Disorder Society and past president of the
Houston Neurological Society. His chief interest is Parkinson 's Disease
and related movement disorders, including dystonia and dyskinesias. He
has conducted numerous clinical trials and published over 500 original
articles, chapters and other communications. Dr. Jankovic has also
served on the editorial boards of various journals including "Neurology
and Movement Disorders" and is afel/ow of the American A cademy of
Neurology.
THE JOURNAL OF CRANIOMANDIBULAR PRACTICE 201