Journal of the Neurological Sciences 217 (2004) 229 – 232
www.elsevier.com/locate/jns

Short communication

Severe bruxism following basal ganglia infarcts: insights
into pathophysiology
Eng-King Tan a,b,c,*, Ling-Ling Chan d, Hui-Meng Chang a,b
a

Department of Neurology, Singapore General Hospital, Outram Road, Singapore 169608, Singapore
b
National Neuroscience Institute, Singapore
c
Singhealth Research, Singapore
d
Department of Diagnostic Radiology, Singapore General Hospital, Outram Road, Singapore 169608, Singapore
Received 30 June 2003; received in revised form 19 September 2003; accepted 15 October 2003

Abstract
Bruxism characterized by clenching and grinding of teeth can lead to toothwear, headaches and depression. While bruxism has been
associated with a number of neurological diseases, it has not been highlighted following cerebral infarction.
An elderly man presented with an acute onset of tooth grinding and jaw clenching associated with dysarthria. His bruxism was worse
during the day and resolved during sleep. He had frequent jaw aches, headaches and swallowing difficulty. Examination demonstrated the
presence of dysarthria with jaw clenching and tooth grinding, producing persistent high pitch and loud squeaky sounds. A magnetic
resonance imaging and angiography examination revealed a recent infarct in the right thalamus. In addition, chronic lacunar infarcts were
present in the bilateral caudate nuclei with severe basilar artery stenosis. He was successfully treated with botulinum toxin.
We discuss the pathophysiologic mechanisms of bruxism associated with basal ganglia infarcts. Dysfunction of the efferent and/or afferent
thalamic or striatopallidal tracts may play a role in bruxism. Early recognition of bruxism following stroke could reduce unnecessary
suffering since the condition can be effectively treated.
D 2003 Elsevier B.V. All rights reserved.
Keywords: Thalamic infarct; Bruxism; Botulinum toxin

1. Introduction
Bruxism refers to the presence of diurnal or nocturnal
parafunctional activity such as clenching, grinding, bracing
and gnashing of the teeth [1]. Its reported prevalence in the
adult population is highly variable, presumably from differences in diagnostic criteria [1– 5]. Severe bruxism can cause
tooth damage, temporomandibular disorders, swallowing
and speech difficulties, headaches and depression. Such
problems can complicate stroke rehabilitation. Bruxism
has been observed in brain injuries, neurodegenerative
diseases and mental retardation, though the exact etiology
of nocturnal bruxism, the most common type in the general
population, remains unknown [1– 5].

* Corresponding author. Department of Neurology, Singapore General
Hospital, Outram Road, Singapore 169608, Singapore. Tel.: +65-63265003; fax: +65-6220-3321.
E-mail address: gnrtek@sgh.com.sg (E.-K. Tan).
0022-510X/$ - see front matter D 2003 Elsevier B.V. All rights reserved.
doi:10.1016/j.jns.2003.10.003

Pathophysiologic studies suggest underlying dopaminergic system dysfunction [2 –4]. We highlight the first report
of a patient who developed severe bruxism following a
recent thalamic and chronic caudate infarcts, and discuss the
involvement of the basal ganglia in the pathogenesis and the
role of botulinum toxin in modifying the course of bruxism.
We also draw attention to the observation that bruxism
following basal ganglia strokes maybe an unrecognized
complication.

2. Case report
The patient, a 64-year-old man with a long history of
hypertension and hyperlipidemia, had presented with nonvertiginous dizziness and left-sided weakness. Neurological
examination revealed mild dysarthria and left hemiparesis of
grade 4+/5. A brain magnetic resonance imaging and
angiography (MRI/A) examination showed lacunar infarcts
in the head of both caudate nuclei, both external capsules

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and left lentiform nucleus, with severe basilar artery stenosis
(Fig. 1, upper row). He was anticoagulated with warfarin
with gradual resolution of his neurologic symptoms.
About one and a half years later, he presented with an
acute onset of tooth grinding and jaw clenching associated
with dysarthria. Initially, he could voluntarily suppress these
jaw movements for a few seconds, but subsequently these
movements progressed in severity to the extent that they
became constant and persistent during the day. The loud
grinding sounds created much distress to him and his family
members. He also complained of frequent jaw aches and
headaches. His bruxing episodes disturbed his swallowing
and he was socially embarrassed and depressed. However,
the bruxism usually resolved during sleep and he had no
early morning jaw pain. There was no previous or family
history of bruxism, no history of psychiatric illness or
exposure to neuroleptics, antidepressants, sedative or anxiolytic medications or drugs of abuse.
Neurologic examination demonstrated the presence of
jaw clenching and tooth grinding, producing persistent high
pitch and loud squeaky sounds. There was no significant
masseter hypertrophy but some degree of tooth wear was
present. There were no involuntary orolingual movements
or evidence of movement disorders elsewhere. He had no

Fig. 1. Consecutive axial T2-weighted images demonstrating lacunes in
both external capsules and caudate head nuclei (upper row). MRI 1.5 years
later shows interval new right anteromedial thalamic lacunar infarct on T1weighted and T2-weighted images (lower row).

focal neurological deficits, except for dysarthria. A repeat
MRI/A revealed an interval new lacunar infarct in the right
thalamus (Fig. 1, lower row).
He was initially treated with clonazepam with little
improvement of his bruxism. The patient was subsequently
treated with DysportR (Speywood Biopharm, UK), where
25 units were injected at two to three sites intramuscularly
into each side of the masseter muscles. Within a month, the
patient reported some improvement of his bruxism. A
second injection with DysportR (50 units per side) 3
months later provided greater relief to his symptoms.
Subsequently, he required lesser botulinum toxin (BTX)
injections as the severity of his bruxism without treatment
was much improved.

3. Discussion
To our knowledge, this is the first report of severe
bruxism associated with cerebral infarction. Our patient’s
bruxism was most likely precipitated by the acute thalamic
infarct and/or contributed by the chronic caudate infarcts for
the following reasons: (1) his bruxism onset was acute; (2)
there were no previous or family history of bruxism and
movement disorders; (3) he had no other neurological and
systemic illness, or drug exposure to possibly account for
his symptoms; (4) MRI showed a new thalamic infarct
compared with baseline scans; and (5) the diurnal pattern
of his bruxism with no nocturnal symptoms was compatible
with the clinical description of secondary bruxism, different
from the common variety of bruxism, which happened
during sleep [1– 5].
The pathophysiology of bruxism is still debated. Older
theories such as occlusal discrepancies with reflex contraction of the jaw muscles have frequently been challenged
[1,2]. It is possible that there exists a central ‘‘bruxism
generator’’ complex, which helps modulate the interactions
of the motor, limbic and autonomic systems, and control the
pattern of bruxism [2]. The theory of dopaminergic dysfunction in bruxism patients can be supported by some of
the following observations: (1) reports of bruxism in
patients with Huntington’s disease [6] and cranio-cervical
dystonia [4]. A higher than expected frequency of bruxism
and jaw movements have also been reported in Parkinson’s
disease compared to controls [4]. (2) Clinical efficacy of
dopaminergic drugs such as bromocriptine and levodopa in
alleviating bruxism [7 – 9]. (3) Induction of non-functional
masticatory activity in rats by repeated stimulation of the
dopaminergic system with apomorphine [10]. (4) Demonstration of an abnormal side imbalance in striatal D2
receptor expression on functional imaging in patients with
nocturnal bruxism [11].
The thalamus, which receives afferents from the striatum,
is the main gateway of the motor outflow tracts from the
basal ganglia. Sensory afferents from the trigeminothalamic
tract also terminate in the thalamus. The right thalamic

E.-K. Tan et al. / Journal of the Neurological Sciences 217 (2004) 229–232

infarct in our patient was predominantly within the territory
of the paramedian thalamic – subthalamic arteries. A review
of the literature shows that infarcts within this area are
associated with a change of consciousness, neuropsychological and vertical gaze disturbances [12]. None of these
signs were found in our case. Delayed onset movement
disorders such as tremor and dystonia have been reported
with thalamic and other static brain lesions [12 –14]. A
syndrome of complex movement disorders have also been
described in infarcts of the postero-lateral and paramedian
thalamus, presumably by disruption of the motor outflow
tracts to the motor cortex [15].
How could thalamic or caudate infarcts possibly cause
bruxism? In animal studies, stimulation of the limbic
structures or the jaw area of the motor cortex can produce
bruxism [16]. In our patient, it is likely that dysfunction of
the afferent and/or efferent pathways to the thalamus as a
result of the infarct lead to a disruption of the normal
interplay of neuronal circuits connecting the striatum,
thalamus, subthalamus and cerebral cortex. This in turn
created a loss of inhibition of the higher cortical control on
the trigeminal motor nuclei located in the pons. The
thalamic infarct could also be a triggering event for the
bruxism in a background of dopaminergic dysfunction as a
result of the chronic caudate infarcts. Transcranial magnetic stimulation studies in human subjects during different
biting tasks have demonstrated that the corticotrigeminal
projections to masseter are bilateral, with a stronger
contralateral projection [17]. This can explain why a right
thalamic infarct in the patient could lead to bruxism
involving both masseters. In support of this, animal studies
have also showed that inputs from the premotor area to the
trigeminal nuclei and their connections within the pontine
reticular formation are bilateral but with ipsilateral preponderance. The neuronal circuits within the pontine reticular
formation and the trigeminal and facial nuclei play an
integral part in oral motor behavior [18,19]. The caudate
infarcts could result in variable disruption of both the
direct and indirect striato-pallidal pathways leading to an
altered thalamocortical drive.
It remains speculative why thalamic or striatal infarctinduced bruxism appears rare, though a genetic predisposition cannot be discounted. It is possible that the cause and
effect of bruxism in stroke patients may be unrecognised
especially if the onset of bruxism happened weeks or months
after a stroke, or the cause be attributed to dental malocclusion or neuroleptic drugs. Alternatively, it could also be that
bruxism following thalamic or basal ganglia strokes are
relatively mild in most patients, and hence the awareness of
this problem is low.
The effectiveness of BTX in severe bruxism has been
highlighted previously [5,20]. However, interestingly, we
observed that the toxin lessened the baseline severity of
bruxism after only one to two courses of treatment in our
patient. It is conceivable that BTX could alter the propioceptive input to the thalamic nuclei, and hence disrupt the

231

higher cortical efferent input to the trigeminal motor
nucleus.
In conclusion, we highlighted an unusual case of severe
bruxism associated with recent thalamic and chronic caudate
infarcts. Dysfunction of the thalamic or striatopallidal tracts
may play a role in the pathogenesis of this condition. Early
recognition of bruxism can reduce unnecessary suffering as
it can be effectively treated. A prospective case control
study would be useful to address the prevalence of bruxism
following strokes.

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