Bruxism in Movement Disorders: A Comprehensive Review

Bruno Ella, DDS, PhD,1,2 Imad Ghorayeb, MD, PhD,1 Pierre Burbaud, MD, PhD,2,3 &
Dominique Guehl, MD, PhD2,3
1
Department of Odontology and Buccal Health, Bordeaux University Hospital, Bordeaux, France
2
Department of Clinical Neurophysiology, Bordeaux University Hospital, Bordeaux, France
3
Institute of Neurodegenerative Disorders, Bordeaux University, Bordeaux, France

Keywords
Bruxism; basal ganglia; movement disorders.
Correspondence
Bruno Ella, University—Odontology and
Buccal Health, 16-20 cours de la Marne
Bordeaux 33082, France.
E-mail: tsir.ella@wanadoo.fr.
The authors have not received any funding or
grant for this work from organizations or
foundations.
The authors deny any conflict of interest.
Accepted December 29, 2015
doi: 10.1111/jopr.12479
Abstract
Bruxism is an abnormal repetitive movement disorder characterized by jaw clenching
and tooth gnashing or grinding. It is classified into two overlapping types: awake brux-
ism (AB) and sleep bruxism (SB). Theories on factors causing bruxism are a matter
of controversy, but a line of evidence suggests that it may to some extent be linked
to basal ganglia dysfunction although so far, this topic has received little attention.
The purpose of this article was to review cases of bruxism reported in various move-
ment disorders. The biomedical literature was searched for publications reporting the
association of bruxism with various types of movement disorders. As a whole, very
few series were found, and most papers corresponded to clinical reports. In Parkin-
sonian syndromes, AB was rarely reported, but seems to be exacerbated by medical
treatment, whereas SB is mainly observed during non-REM sleep, as in restless leg
syndrome. AB is occasionally reported in Huntington’s disease, primary dystonia, and
secondary dystonia; however, its highest incidence and severity is reported in syn-
dromes combining stereotypies and cognitive impairment, such as Rett’s syndrome
(97%), Down syndrome (42%), and autistic spectrum disorders (32%). Taken as a
whole, AB seems to be more frequent in hyperkinetic movement disorders, notably
those with stereotypies, and is influenced by anxiety, suggesting an involvement of
the limbic part of the basal ganglia in its pathophysiology.

Bruxism has been defined as an oral habit consisting of involun-
tary rhythmic or spasmodic non-functional gnashing, grinding,
or clenching of teeth that is different from the chewing move-
ments of the mandible and which may lead to occlusal trauma.1
Given the limitations regarding current definitions for bruxism,
it has been defined as a repetitive jaw-muscle activity charac-
terized by clenching or grinding of the teeth and/or by bracing
or thrusting of the mandible.2 Bruxism can be classified into
two overlapping types: awake bruxism (AB) and sleep brux-
ism (SB).2,3 Phenomenologically, important differences appear
between them: AB is a semi-voluntary “clenching” activity
influenced by stress and anxiety4 whereas SB is a stereotyped
movement disorder occurring during sleep and thus correspond-
ing to a form of parasomnia.5
Based on self-questionnaires in the absence of direct mea-
surements, the diagnosis of bruxism remains subjective in most
studies. The presence of comorbid conditions in selected pop-
ulations may act as a confounding variable for the assessment
of bruxism prevalence at the community level. An overlap be-
tween AB and SB was estimated in one out of five patients in
the general population.6 The estimates are commonly based on
findings from a few large-scale epidemiologic surveys, which
suggests that self-reported tooth grinding during sleep has a
prevalence of 13% ± 3% in the general adult population, is
unrelated to sex, and decreases in elderly people.5 Two studies
reported a prevalence of AB of 22% to 31% in adults, with
a higher rate among females and younger subjects. In adults
aged over 60 years, only 3% of subjects seem to be aware of
frequent grinding. Because polysomnography (PSG), a costly
test, is needed to confirm the diagnosis of SB, it is difficult to
conduct cross-sectional studies in the population.
Theories on the peripheral factors causing bruxism are a
matter of controversy in the current literature. A consensus is
emerging that they only play a minor role, and that central
mechanisms might be involved, particularly the basal ganglia
network. The purpose of this article was to review the exist-
ing literature concerning the association between bruxism and
movement disorders.
Methods
Various descriptions of abnormal movements in the oro-
mandibular area have been reported in patients suffering from
movement disorders: “involuntary” chewing-like movements,
oromandibular myoclonus or dystonia, excessive swallowing,
oral tardive dyskinesia, mandibular Parkinsonian tremor and

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various types of tics.7 Thus, the search for “mean cut-off”
criteria for differentiating bruxism from other oromandibular
movements is not easy. On the whole, bruxism, orofacial
dystonia, and/or dyskinesia can be considered as involuntary
hyperkinetic motor disorders that affect the orofacial region.8
To document the link between bruxism and movement
disorders, we systematically searched PubMed using the term
bruxism and one of the following items: Parkinson’s disease
(PD), Parkinsonian syndromes, Huntington’s disease (HD),
choreo-acanthocytosis, dystonia, dyskinesia, Tourette’s syn-
drome (TS), restless leg syndrome (RLS), obsessive-compulsive
disorders, anxiety, attention-deficit hyperactivity disorder
(ADHD), Rett’s disease, Down syndrome, autism spectrum
disorders, and brain lesions. Sleep disorders, botulinum toxin,
and pharmacological treatments were also searched.
Results
We identified 44 papers in which the term bruxism was asso-
ciated with the predefined keywords, but only 37 papers were
relevant (Table 1), of which 17 corresponded to single clinical
reports.
Parkinsonian syndromes
Awake bruxism has seldom been reported in patients with PD or
in multiple-system atrophy, progressive supranuclear palsy, and
cortico-basal degeneration.9 Sleep bruxism was not mentioned
in several recent studies dealing with sleep disorders in PD,
most focusing on REM sleep disorders.10 However, we identi-
fied nine papers reporting bruxism in Parkinsonian syndromes.
Three corresponded to case reports of AB,11-13 and one men-
tioned bruxism as a potential indication for botulinum toxin
treatment.14 A severe wearing-off facial dystonia associated
with severe tonic spasms of masseter muscles firmly closing
the jaw and leading repeatedly to dental fractures was reported
in a PD patient.15 We found only one case of AB in a patient
with multi-system atrophy.9 The only cohort study examining
the incidence of AB in a geriatric population including 45 PD
patients, reported a low incidence (2%) of AB16 similar to that
in the general population of the same age (3%), whereas higher
rates were observed in patients with fronto-temporal dementia
(27%) and hydrocephalus (24%).16 A relatively high prevalence
of bruxism (30%) in PD was, however, reported in another co-
hort study, but this enquiry relied on a structured questionnaire
administered by telephone interview.17 The nature of AB or SB
and the conditions of its appearance (in ON or OFF medication
state) were unclear, and there was no clinical examination. In a
recent paper, rhythmic masticatory muscle activity, a marker of
SB, was found during non-REM sleep both in PD patients with
RBD (PD-RBD) and in patients with idiopathic RBD (iRBD).18
Taken as a whole, these data suggest that AB is rare in PD and
that SB can be observed during non-REM sleep, as in the gen-
eral population.
Awake bruxism can be induced or exacerbated by chronic
dopamine treatments.11 On the other hand, L-dopa and
dopamine agonists can reduce sleep bruxism both in PD patients
and normal subjects,19 supporting the idea that awake and sleep
bruxism might have different pathophysiological mechanisms.
600 Journal of Prosthodontics 26 (2017) 599–605 
Ella et al
Finally, two pilot single-photon-emission computed tomogra-
phy studies suggested an abnormal side imbalance in striatal
D2 receptor expression associated with SB, reinforcing the link
between dopamine and the pathophysiology of bruxism.20
Choreic syndromes
Huntington’s disease (HD) is a hereditary neurological dis-
ease related to the degeneration of the medium spiny cells
of the striatum, clinically characterized by abnormal involun-
tary movements, behavioral disturbances, cognitive dysfunc-
tion, and psychiatric symptoms. We found only four papers
reporting bruxism in HD. Its incidence seem to be low, as sug-
gested by data collected in a series of 59 symptomatic HD pa-
tients, where only one patient (1.7%) complained of bruxism.21
However, when bruxism occurs, it is frequently severe. Nash
et al22 described a 50-year-old woman admitted to their care
unit with a diagnosis of HD who complained of teeth grind-
ing and severe jaw pain. Louis and Tambone21 documented
a patient with HD who had had a history of mild nocturnal
bruxism as early as the age of 25 years, bruxism being exac-
erbated by the onset of HD. Tan et al23 reported three severe
cases of bruxism in young HD patients. In their first case,
tooth grinding became so pronounced that the loud sounds dis-
turbed other family members. In their third case, tooth grinding
was markedly aggravated after the neuroleptic treatment was
started. Finally, a case of HD mimicking Tourette’s syndrome
(TS) was reported by Alonso et al24 The patient had multiple
motor tics since his teenage years, and associated vocal tics and
bruxism; however, this patient also suffered perinatal hypoxia
and the relation between HD and bruxism is questionable. Al-
though rhythmic mandibular movement and tongue biting are
common in patients with chorea-acanthocytosis syndromes,25
bruxism per se has not been reported so far.
Primary dystonia
Primary dystonia is a hyperkinetic syndrome characterized
as cramps, task-specific or occupational spasms, or labeled
psychogenic.26 To date, there are relatively few papers re-
porting bruxism in primary dystonia. In a pilot study, Watts
et al17 investigated bruxism in 79 patients (28 men, 51 women)
with cranial-cervical dystonia. Sixty-two of them (78.5%), 22
men and 40 women, had bruxism. About 25% of patients with
bruxism had associated dental problems including temporo-
mandibular dysfunction (TMD) (21%) and tooth wear (5%).
AB and SB concerned 58% and 12% of patients, respectively.
The prevalence of bruxism evaluated on a structured ques-
tionnaire administered by telephone was much higher in the
cranial-cervical dystonia patients than in healthy subjects.17 In
a recent study dealing with sleep disturbances in dystonia (27)
including two groups of dystonic patients (n = 111 for cervical
dystonia; n = 110 for blepharospasm), an incidence of 28% and
18% of SB, respectively, was reported. Patients with cervical
dystonia had a significantly higher rate of bruxism than con-
trols. The diagnosis of SB relied on a questionnaire. Among
the patients with bruxism, 18% and 28% of them suffered
from blepharospasm and cervical dystonia. In cervical dysto-
nia, the Pittsburgh Sleep Quality Index (PSQI) was significantly
higher in patients with RLS and SB. In two other studies, the
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Ella et al Bruxism in Movement Disorders

Table 1 Reported cases of bruxism in movement disorders

Movement disorders
(authors, year published) Population Bruxism features

Parkinsonian syndromes
Magee, 197011 n=1 AB associated with face, lip, and tongue dyskinesia in MD
Durham et al,199312 n=1 Use of a bruxism splint to correct bruxism, diminution of pain
Srivastava et al, 200213 n=1 AB as presenting feature of PD
Sheffield and Jankovic, 200714 BTx for the treatment of PD features including bruxism
Kwak et al, 200915 n = 45 AB in a population of hospitalized geriatric patients, incidence 2% in PD
Watts et al, 199916 n = 100 AB, telephone enquiry, incidence 30%, no clinical examination
Abe et al, 201317 n = 15 SB during REM sleep in PD, higher in PD vs. controls but not in patients
without PD but having REM-related SB
Lobbezoo et al, 199719 n = 10 SB, L-dopa resulted in a significant decrease in the average number of bruxism
episodes per hour of sleep in PD
Wali, 20049 n=1 Asymmetric AB in a 51 y-o patient with multi-system atrophy (MSA)
Tan, 200023 n=1 AB in the context of a severe off-period facial dystonia in PD
Chorea
Nash et al, 200422 n=1 AB in a women with HD improved by BTx, no effect of haloperidol
Louis, 200121 n=1 AB, appeared at the age of 25 before HD symptoms, worsened after it
Tan et al, 200023 n=3 Three cases of severe AB in young HD patients, improved by BTx
Louis, 200121 n=1 Low incidence of AB in a cohort of 50 HD patients (2%)
Alonso et al, 200424 n=1 Huntington’s disease mimicking Tourette’s syndrome
Primary dystonia
Paus et al, 201127 n = 111 SB, incidence 28% in CD, correlated with sleep disorders
n = 110 SB, incidence 18% in BL, higher in women
Watts et al, 199917 n = 79 Bruxism, incidence 78% (74% in OMD, 55% in BL; 34% in CD, AB [58%] and
SB [12%])
Singer and Papapetropoulos, 200628 n = 23 AB in OMD (17%), higher in jaw-closure than in jaw opening dystonia
Psychomotor disorders
Friedlander and Cummings, 199231 NS Tourette’s syndrome, AB
Bimstein et al, 200832 n = 25 Higher rate of AB and toothache in ADHD patients
Ghanizadeh, 200833 n = 32 AB in ADHD patients correlated with defiant behavior
Retless legs syndrome
Ahlberg et al, 200540 NS SB, linked to stress
Dickoff, 201341 NS SB, responses to dopamine
Van der Zaag, 201438 n = 17 SB, periodic limb movement index higher in patients with SB
Lavigne and Montplaisir, 199439 n = 60 SB in 8%, higher severity in smokers
Lavigne et al, 20034 n = 303 SB in about 16% of subjects with RLS
Secondary bruxism
Winocur et al, 200343 NS Review on drug-induced bruxism, AB mainly
Sankhla et al, 199824 n = 27 Mixed bruxism in 30%, higher in primary than post-trauma OMD
Tan et al, 200450 n=1 AB. Stroke. Lesion in the right thalamus and bilateral caudate
Kim et al, 200652 n=1 Delayed onset continuous bruxism with olivary hypertrophy (basilary syndrome)
Munoz et al, 200459 n=1 Severe bruxism in a case of dentatorubropallidoluysian atrophy with severe
white matter involvement
Tison et al, 199251 n=1 Permanent bruxism in a case of Whipple’s disease
Fitzgerald et al, 199053 n = 32 Review on Rett’s syndrome, 97% of AB
El Khatib et al, 201454 n = 100 Review on autism spectrum disorders, 30% of AB
DeMattei et al, 200755 n = 55 Series of autism spectrum disorders, 44% of AB
Lopez-Perez et al, 200756 n = 86 Series of Down syndrome, 42% of AB, associated with chromosomal
abnormalities (mosaı̈cism)
Bell et al, 200257 n = 49 Series of Down syndrome, 32% of reported bruxism of whom 27 AB and 36%
SB but clenching, chewing, tapping were not considered
Paesani et al, 201347 n=1 Severe bruxism secondary to a pineal cavernoma. Electrophysiological study
showing sensitization of the nociceptive fibers
Meletti et al, 200458 n=1 Continuous bruxism (AB and SB) in a patient with temporal lobe seizures
Review on nocturnal frontal lobe epilepsy

n: sample size; NS: non-specified; AB: awake bruxism; SB: sleep bruxism; RLS: Restless legs syndrome; ADHD: attention-deficit-hyperactivity disorder; TS:
Tourette’s syndrome; PD: Parkinson’s disease ; CD: cervical dystonia; BL: blepharospasm.

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association of AB and oromandibular dystonia was slightly
higher28,29 (17% for Singer and Papapetropoulos; 23% for
Sankhla et al) than in the general population (13%).2
Essential tremor
No report has been made so far in this context.
Psychomotor disorders
Tourette’s syndrome (TS) is a familial neurodevelopmental dis-
order affecting up to 1% of school-age children.30 It is defined
as the chronic presence of both multiple motor tics and one or
more vocal/phonic tics.30 Very few papers report on the asso-
ciation of TS and dental disorders.31 However, many orofacial
tics and compulsive behaviors seen in this disorder including
tooth grinding, tongue-, jaw-, and lip-biting, as well as many
other forms of self-mutilation that may cause destructive oral
lesions. Moreover, the neuroleptic drugs used to treat the syn-
drome may adversely induce secondary tardive dyskinesia with
buccolingual choreiform movements; however, to our knowl-
edge there is no cohort report of typical cases of bruxism in
TS. We found, as previously mentioned,24 only one atypical
case associated with HD. On the other hand, several papers re-
ported AB in children with attention-deficit/hyperactivity dis-
order (ADHD), but its incidence remains unclear.32,33 Bruxism
is also frequently found in patients with obsessive compulsive
or anxiety disorders.34-36
Restless legs syndrome
Restless legs syndrome (RLS) is a common chronic and dis-
abling sensorimotor disorder clinically characterized by un-
comfortable and unpleasant sensations associated with an urge
to move the affected legs. The symptoms are typically present
at rest, become worse at night and are partially and temporar-
ily relieved by movements.37 During sleep, most patients with
RLS show periodic limb movements (PLMS) characterized by
periodic episodes of involuntary repetitive and highly stereo-
typed extension of the big toe and dorsiflexion of the ankle
with occasional flexion of the knee and hip. Few studies have
questioned the association of sleep bruxism and RLS and, so
far, there is no agreement as to whether SB is more preva-
lent in RLS than in the general population.38-40 In a pioneering
Canadian study, between 14.5% and 17.3% of the subjects who
reported subjective RLS-related symptoms also reported SB.
Conversely, 9.6 to 10.9% of the tooth grinders reported RLS-
related symptoms.39 In one open study, bruxism and periodic
leg movements were observed in 80% of the patients during
non-REM sleep.41 Among the 41% of dopamine-responding
RLS patients, 86% were also improved for bruxism. Even
though these results should be confirmed by a double-blind
study, they suggest that SB may be associated with RLS and
could be a dopamine-responsive movement disorder.41 In two
pilot studies, PLMS were synchronous to slowing of the corti-
cal activity as measured by the spectral analysis of the EEG,42
suggesting that periodic changes in the level of cortical activa-
tion might modulate abnormal motor behavior in sleep, such
as rhythmic masticatory muscle activity. In line with this view,
it can be hypothesized that bruxism may be related to simi-
602 Journal of Prosthodontics 26 (2017) 599–605 
Ella et al
lar dysfunction at the trigeminal nucleus where sensorimotor
information is processed.4
Drug-induced bruxism
The association between drugs and bruxism was beyond the
scope of this study since this topic has been already reviewed
in a previous paper.43 It is likely that the neurotransmitter
dopamine may be involved to some extent in the pathophys-
iology of bruxism since it is frequently observed in patients
receiving long-term treatment with dopamine receptor antago-
nists, sometimes leading to acute or tardive dyskinesia.43 Both
are related to hypersensitivity of DA post-synaptic receptors,
mainly of the D2 type, at the striatal level.43 Bruxism is also
triggered or exacerbated by many other drugs acting on the
dopaminergic system (dopaminergic agonists, cocaine, and am-
phetamines). Taken as a whole, this is a strong argument for the
involvement of the dopaminergic system in the pathophysiol-
ogy of awake bruxism. Drugs acting on the serotoninergic sys-
tem (tricyclic antidepressants and selective serotonin reuptake
inhibitors) are also reported to influence bruxism, although less
frequently than those acting on the dopamine system. Since the
above-mentioned review, three papers have been published.44-46
As a whole, no epidemiological data indicate the rate of bruxism
in tardive dyskinesia or dystonia except from clinical reports in
schizophrenic patients.44
Secondary bruxism
Secondary bruxism would appear after brain lesions identified
on MRI or eventually after peripheral trauma. We can men-
tion the case of oromandibular dystonia (OMD). Usually, it
is primary, but in some cases it may follow peripheral injury.
In a cohort study (n = 48) comparing clinical features of pa-
tients with peripherally induced OMD and primary OMD, a
rate of 23% of bruxers was reported.29,47 Most exhibited both
awake and sleep bruxism. Bruxism was less frequent in post-
traumatic than in primary OMD, but the rate of bruxism in
OMD was not very different from that observed in the gen-
eral population. Edentulous orodyskinesia (ED) is a neglected
source of aimless oral movements that may be confused with
tardive dyskinesia.48 Some authors reported that edentulous-
ness may increase the risk of neck and trunk dyskinesias,49 but
the relation with bruxism remains unclear.
Documented focal lesions of the central nervous system lead-
ing to bruxism are rare. Tan et al50 reported an elderly man
presenting an acute episode of tooth grinding and jaw clench-
ing associated with dysarthria. His bruxism worsened during
the day and abated during sleep. An MRI and angiography ex-
amination revealed a recent infarct in the right thalamus and
chronic lacunar infarcts in the bilateral caudate nuclei. Con-
tinuous bruxism has been also mentioned in a single case of
Whipple’s disease associated with mesencephalic lesions.51,52
In this rare genetic disease described in female subjects, vol-
umetric reductions are observed throughout the brain, mainly
in the dorsal parietal gray matter with diffuse reductions in
the subcortical white matter. In a cohort study of 32 patients,
bruxism was the most common hyperkinetic abnormality, being
reported in 97% of patients.53 It occurred chiefly during day-
time and was only rarely seen during sleep, leading the authors
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Ella et al
to interpret bruxism as a form of oro-mandibular dystonia. In
a recent study, self-injurious behavior and bruxism were found
to be more frequent in children with autism spectrum disorder
(32%) than in controls (2%).54,55 The symptomatology is also
particularly frequent in Down syndrome, with a prevalence of
42%56 and high levels of tooth wear.57 Lastly, rhythmic jaw
movements indistinguishable from typical bruxism could be a
semeiological feature observed during epileptic seizures, such
as temporal lobe attacks.58
Discussion
The first takeaway from this review is that few papers have
reported bruxism in movement disorders. Many are based on
clinical reports, and we lack large epidemiological surveys tak-
ing into account the precise type of bruxism (awake or sleep
bruxism or both), the clinical status (e.g., on and off status in
PD), and the effect of drugs on bruxism in these patients.
In Parkinson’s disease,59 AB is not commonly reported, sug-
gesting that it a rare feature of the disease; however, this topic
has so far received little attention because this non-specific
symptom of the disease may appear as a minor problem in
comparison with other motor and cognitive symptoms. That
said, it seems clear that drugs acting on the dopaminergic sys-
tem promote AB in human patients,43 and preclinical studies
in rodents have shown that repetitive stimulation with apomor-
phine, a D2 agonist, can induce a non-functional masticatory
activity. Moreover, the number of bruxism cases reported in pa-
tients treated by dopamine antagonist43 support a putative role
of dopamine, and consequently of the striatum, in the patho-
physiology of AB. On the other hand, although sleep disorders
are frequent in PD, SB is reported infrequently and mainly ob-
served during non-REM sleep in the minutes before transition
to REM sleep. It could be related to micro-arousals, associated
with a rise in autonomic cardiac and respiratory activity, an
event repeated 8 to 14 times per hour of sleep.4,6 The fact that
bruxism and PLM are frequently observed during non-REM
sleep supports the view that both represent a form of non-REM
sleep disorder; however, the incidence of PLMS in PD does not
seem to be significantly higher than in the general population.
On the other hand, bruxism is commonly reported in a num-
ber of hyperkinetic syndromes including dystonia, chorea, and
levodopa-induced dyskinesia. The few cases reported in Hunt-
ington’s disease were characterized by their severity. Interest-
ingly, the somatotopy of striatal lesion in some HD patients has
been proposed to explain the occurrence and severity of their
bruxism.23 Above all, the most severe and frequent forms of AB
are observed in pathological conditions combining stereotyp-
ies and cognitive impairment, such as Rett’s syndrome, Down
syndrome, and autistic spectrum disorders.54
The hyperkinetic feature of AB is also partially supported
by the fact that drugs promoting the dopaminergic and sero-
toninergic systems increase it.43 Thus, the classification of AB
into a given type of hyperkinetic syndrome remains a matter
of debate. The frequent association between bruxism and oro-
mandibular dystonia, and their location in the lower facial area,
has led previous authors to consider that bruxism could be a
form of oromandibular dystonia. On the other hand, the phe-
nomenological features of AB (i.e., consisting of repetitive and
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Bruxism in Movement Disorders
focal mandibular movements, unrelated to specific actions, its
potential control by willpower, and high incidence and severity
in diseases characterized by limb stereotypies) suggest that this
movement disorder could more likely be a form of oromandibu-
lar stereotypy. The relation with anxiety is also a critical fea-
ture of AB, the symptomatology being clearly influenced by
personality trait in the general population,35,36 suggesting an
involvement of the limbic components of the basal ganglia in
its pathophysiology.
The role of the basal ganglia network in the pathophysiology
of bruxism remains speculative. The basic pattern of rhyth-
mic jaw movements produced during mastication is generated
by a neuronal network located in the brainstem and referred
to as the masticatory central pattern generator (CPG).60 The
latter involves mostly neurons in the vicinity of the trigemi-
nal system, capable of producing rhythmic network activity.4,60
The CPG receives a large amount of both descending (central)
and sensory (peripheral) afferents. The sensory inputs come
from periodontal receptors, jaw muscle spindles, mucosal re-
ceptors, and skin receptors. This region is the only cortical area
whose stimulation can elicit rhythmic jaw movements. Many
subcortical areas are also known to influence mastication and/or
to project to the trigeminal complex. They include the amyg-
dala, the hypothalamus, the anterior pretectal nucleus, the red
nucleus, the periaqueductal grey, the raphe nuclei, the cere-
bellum, and various parts of the basal ganglia.4,60 In addition,
most of the frontal cortical areas projecting to the CPG in turn
receive inputs from the basal ganglia through thalamo-cortical
projections.
In bruxism, the normal alternating pattern between jaw-
opening muscles and jaw-closing muscles is disrupted, and
co-activation of both is observed.4,6 Such impairment in the se-
lection of muscular pattern during action is observed in diseases
involving the basal ganglia, such as dystonia. A functional im-
pairment of the trigeminal-basal ganglia networks controlling
the mandibular musculature has been evoked, but the mech-
anism involved requires further physiological investigations;
however, in hyperkinetic syndromes associated with AB, the
cortico-striatal network might be altered because of functional
immaturity (e.g., Tourette’s syndrome), cortical atrophy (e.g.,
dementia, Down syndrome, and Rett’s syndrome),61 or be-
cause of a major dysfunction of the striatum (dystonia, chorea,
levodopa-induced dyskinesia, tardive dyskinesia, or dystonia).
In these conditions, there could be either an impaired cortical
control of the CPG through the direct pathway and/or dimin-
ished inhibitory control exerted by the basal ganglia on the CPG
through the pallido-reticular projections. Our knowledge of the
pathophysiology of SB seems to be better, and we refer the
reader to several detailed and excellent reviews on this topic.4,6
However, the weak evidence we found for an association be-
tween SB and movement disorders will certainly require further
investigations.
Conclusion
As a whole, neurologists should be aware of bruxism in order
to prevent its negative consequences on oromandibular func-
tions and the stomatognathic system. On their own, dentists
need to be able to refer patients to a neurologist for diagnosis,
603
Bruxism in Movement Disorders
management, and common coverage. Thus, a multidisciplinary
clinical assessment is desirable for the care of these patients
and in selecting those who may benefit from prosthodontic
treatment and/or botulinum toxin injections.
Acknowledgments
We thank Ray Cooke for his comments on the manuscript.
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