Journal of the California Dental Association

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Hemifacial Spasm: A Case Report and Review of

Literature

Mariela Padilla, Robert Alcala Utsman & María José Brenes Castillo

To cite this article: Mariela Padilla, Robert Alcala Utsman & María José Brenes Castillo (2017)
Hemifacial Spasm: A Case Report and Review of Literature, Journal of the California Dental
Association, 45:7, 361-364, DOI: 10.1080/19424396.2017.12222472

To link to this article: https://doi.org/10.1080/19424396.2017.12222472

Published online: 07 Mar 2023.

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 spasm
C D A J O U R N A L , V O L 4 5 , Nº 7

Hemifacial Spasm: A Case

Report and Review of Literature
Mariela Padilla, DDS, MEd; Robert Alcala Utsman, DDS;
and María José Brenes Castillo, DDS

A B S T R A C T A hemifacial spasm is characterized by the presence of tonic or clonic,

intermittent and involuntary unilateral contractions of the muscles supplied by the
facial nerve, usually around the eyes, cheeks, mouth and neck. A case is presented in
a patient with twitching in the right lower eyelid with irradiated pain in the temple
and upper lid edema. Causative factors and management strategies are emphasized to
enhance the recognition and understanding of this condition.

AUTHORS

Mariela Padilla, DDS,
MEd, is the assistant
director of online programs
at the Herman Ostrow
School of Dentistry of USC.
Conflict of Interest
Disclosure: None reported.
Robert Alcala Utsman,
DDS, is an assistant
professor and director of
research at Universidad
Latinoamericana de Ciencia
y Tecnología (ULACIT) in
San José, Costa Rica.
Conflict of Interest
Disclosure: None reported.
A
María José Brenes
hemifacial spasm is a
Castillo, DDS, is a
graduate of Universidad
condition characterized by the
Latinoamericana de Ciencia presence of tonic or clonic,
y Tecnología (ULACIT) and intermittent and involuntary
works in private practice in unilateral contractions of
Costa Rica.
the muscles supplied by the facial nerve,
Conflict of Interest
Disclosure: None reported.
usually starting around the eyes before
progressing to the bottom of the cheek,
mouth and neck.1 Although it affects
mostly females, there are reports of the
condition in males. The condition has
been reported mainly on the left side
with a progressive evolution starting in
the orbicularis oculi and orbicularis oris
muscles.2,3 These symptoms can be motor
or nonmotor, producing movements and
autonomic signs. The intensity of this
disorder can vary and intensify with factors
such as stress, intense light and masticatory
movements. On average it affects people
around the age of 44 and incidence has
been reported in 9.8–11/100,000 persons.4,5
The cause seems to be of neuronal
origin and is most often attributed
to compression of the facial nerve or
damage to the brain stem. In cases where
there is a confirmed lesion, treatment is
decompression or removal of structures.
However, sometimes no specific cause is
identified. This complicates the therapeutic
approach, which should be directed to
the recovery of function and aesthetics.6
Other conditions reported as causative
agents are the aneurysm spasm,7 occupying
masses8 and neuronal hyperactivity.9–10
Dentists have a role in the diagnostic
process due to the possibility that the
initial symptoms are related to discomfort
and dysfunction of the jaws. Additionally,
episodes of spasm can cause damage
to oral tissue, making the dentist an
important part of the treatment plan.
The purpose of this article is to review
the signs and symptoms, as well as
management of hemifacial spasms. This
case of a nonspecific cause is presented
to enhance understanding of hemifacial
spasms and the treatment approach.
J U LY 2 0 1 7 361
 spasm
FIGURE 1A .
FIGURES 1. The pictures show an interval of two seconds, where the patient goes from open eyes to a sudden
twitch of the right eye. (Patient consented to the use of these photos.)
Case Report
E.C.F. is a 62-year-old male who was
seen at the Orofacial Pain Clinic, Dentus
Group in Costa Rica. His chief complaint
was a twitching in the right lower eyelid
(FIGURES 1A, 1B ), with irradiated pain
in the temple and upper lid edema that
he had experienced for four years but
that had worsened the last two years.
Imaging studies (CAT scan and MRI)
were noncontributory. The cranial nerves
examination showed a CNII with smooth
extraocular movements, no double vision
and CNIII, CNIV and CNVI within
normal limits. There was equal pupil
reaction to light. CNV had symmetrical
and normal response to light touch and
pinprick with normal motor function.
Regarding facial expression, there was
lacrimation and ptosis in the right eye
and asymmetrical pull of the upper lip
on the right side. The patient’s forehead
was flat. There was a reduction of hearing
of the right side, which was confirmed
by audiometry. Palatal elevation was
equal and the uvula was located at the
midline. His finger-nose coordination was
normal. His masticatory muscles were not
tender to palpation, range of jaw motion
was normal and there were no intraoral
lesions. The differential diagnosis
included benign essential blepharospasm,
362 J U LY 2 01 7
FIGURE 1B .
Bell’s palsy, trigeminal neuralgia, damage
in the facial nerve and cluster-tic
syndrome. However, based on the clinical
presentation and evolution, a diagnosis
of hemifacial spasm was favored because
he had had episodic pain accompanied
by ptosis and twitching of the eye.
He had been treated by a neurologist
and an otolaryngologist and had
pharmacotherapy (carbamazepine
200mg qid, pregabalin 150 mg hs,
sodium valproate 500 mg hs, clonazepam
0.5 mg hs, lorazepam 1 mg hs), but
the medications were discontinued
either because of the side effects at the
indicated doses or because the patient
got no relief. He also received a series
of three botulinum toxin injections
four months apart in the temporalis and
orbicularis oculi. No significant changes
with these approaches were reported.
Considering the possible contribution
of the autonomous nervous system, a
calcium channel blocker (verapamil 160
mg) was prescribed together with a muscle
relaxant (cyclobenzaprine, 10 mg hs) to
address the stress-triggered contraction.
A series of four physical therapy sessions
were performed, including the use of
electric stimulation, ultrasound and facial
massage. None of the described treatments
produced a change in the symptoms.
C D A J O U R N A L , V O L 4 5 , Nº 7
The case was presented in a
roundtable session of neurologists,
and a decompression surgery was
recommended considering the possibility
of compression of the trigeminal root
not evident in the MRI of the cranial
region. However, considering the risks
of the surgery and the uncertainty of
the results, the patient declined this
procedure. In order to help the patient
with the episodic twitching, biofeedback
intervention was suggested with the
hope of him being able to control
his musculature. The patient is now
under the care of the psychologist.
Discussion
As in this case and many others, the
causes of the disease are not clear and
may be multiple,11 including vascular
compression, movement disorders,
neuronal demyelination and the
presence of other diseases. One of the
most common theories is that the facial
nerve is pressed by blood vessels at the
level of output from the nerve to the
central nervous system.12 This etiology
is also supported by other studies.13
Castiglione et al.8 state the facial nerve
compression is by the lower anterior
cerebellar artery, although one must
rule out a pathological condition.
Another possible cause of facial nerve
compression has been linked to a
blood defect in the sensory root of
the nerve.14 An alternative theory
is the possibility of artery and vein
compression at the spinal cord level.15
Genetic and psychological factors
have also been linked to hemifacial
spasms,14 and in this case there was
no family history reported. In cases
with atypical features, psychogenic
etiologies should be considered.14
Although the patient in this case
reported no psychogenic conditions,
the psychological impact of this

condition is very important because the
patient tends to move away from daily
activities as a result of functional and
aesthetic alterations that occur with the
spasms.16 Interference with social life
has been reported in up to 90 percent
of the cases, leading to isolation and
depression.17 In this case, the patient
reported an impact on social and
daily activities because of the spasms
that could occur at any moment. For
example, if a spasm occurred when
he was driving he would have to pull
over because his vision was affected.
There was a documented
coexistence of hemifacial spasms with
migraine headaches among the cases
reported in the literature. Spasms can
behave as activators thus complicating
the management of headaches;
however, they are not a causal element
if one has predisposing features.18
The patient in this case did not have
migraine or other headache issues.
As with any medical condition,
the diagnosis process should include
history, clinical examination and
the use of additional diagnostic
tools. In this case, a bone scan and
neuroimaging enabled us to rule out
potential underlying conditions that
were unremarkable in the findings. In
the case of a hemifacial spasm, other
imaging tools can be useful. Functional
magnetic resonance imaging can
detect changes in neuronal activity.
Voxel-based morphometry can assess
changes in gray matter, thalamus,
putamen and dorsolateral spinal
region, which are areas that have
an impact on motor control.19
Treatment depends on the
diagnosis and identification of causal
or etiological elements. In general,
hemifacial spasms are addressed with
surgical options, radio frequency,
pharmacotherapy, a behavioral
approach and complementary or
alternative techniques. In this case,
pharmacotherapy was one of the
first lines of treatment, although
medications tend not to be effective
long-term treatments of hemifacial
spasms. Baclofen, clonazepam,
carbamazepine, gabapentin, phenytoin
or orphenadrine are considered
first-line medications that may be
used to provide transient relief.20,21
Membrane stabilizers or drugs
related to gamma aminobutyric
acid (such as carbamazepine and
Interference with social
life has been reported
in up to 90 percent of the
cases, leading to isolation
and depression.
gabapentin), which can be used as
both monotherapy and complementary
to other techniques, have been
described as an alternative therapy.21,6
Botulinum toxin is also reported as an
alternative therapy, but its effectiveness
is limited in controlling symptoms.4 It
has been indicated that after application
of botulinum toxin, there is an
improvement ranging from eight days
to 14.8 weeks in approximately 73.7
percent of patients.22 The most common
adverse effects reported were erythema (5
percent), facial asymmetry (3.6 percent),
ptosis (3.4 percent) and diplopia (3.2
percent), which are conditions that
sometime accompanied hemifacial
spasms from the start.5 It is important
to point out that the botulinum toxin
effect is temporary; the procedure must
C D A J O U R N A L , V O L 4 5 , Nº 7
be repeated periodically. In this case,
pharmacotherapy has been ineffective
in managing the patient’s symptoms.
Microvascular decompression is
the surgical treatment of choice for
hemifacial spasm. It is considered a
safe and effective alternative, although
complications as a result of the
procedure include facial paralysis and
hearing loss.2,3,7,23 Other techniques
have been reported that separate
the vessels, such as placing Teflon
between the vein and facial nerve.
This procedure generally improves
the condition, but there is a lengthy
recovery time of up to 10 months.15,24,25
Sometimes it is necessary to repeat
these procedures because of small
vessels that are not identified in
the first approach.26 Improvement
because of these surgical procedures
can last up to five years.9 The use of
radiofrequency is another alternative
that damages the nerves directly by
reducing their firepower. This approach
is considered conservative and has
been described for refractory spasms
and in cases where decompression
surgery has not been efficient.27
Complementary therapies, such as
acupuncture, biofeedback and facial
massage, have also shown benefits.18,28
Biofeedback interventions using
electromyography have suggested that
the length of the spasms are reduced
but not the frequency.28 Although
there are insufficient data on its
effectiveness, it has been observed
that individuals whose symptoms have
greater severity are the ones who tend
to seek these alternatives. However, in
this case physical therapy, including
the use of electric stimulation,
ultrasound and facial massage, was
unsuccessful. The biofeedback and
psychological intervention results
in this case are too early to tell.
J U LY 2 0 1 7 363
 spasm
Conclusions
In the case presented, the patient
had experienced hemifacial spasms for
more than four years. The necessity of
implementing a detailed history and
comprehensive examination with the
adjunctive diagnostic instruments, such
as radiographic imaging, cannot be
overemphasized. Imaging studies have
been noncontributory and treatments
to date unsuccessful. The cause in this
case, although not clear, appears to be
of neuronal origin. In these cases, it is
important that dentists have knowledge
of the treatment and diagnostic
processes to correctly guide patients. ■
ACKNOWLEDGMENT
The authors thank Dr. Robert Merrill for taking the time off his
trip to Costa Rica to give his input on this case.
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