Original Paper
Eur Neurol 1999;42:4951
Gabapentin as Treatment for
Hemifacial Spasm
Fabio Bandini Luca Mazzella
Department of Neurological Sciences and Neurorehabilitation, University of Genoa, Italy
Key Words
Hemifacial spasm W Gabapentin
Abstract
Hemifacial spasm, a life-long condition characterized by
involuntary unilateral contractions of the facial muscles,
is a disabling disorder often resulting in patient irritation
and social embarassment. Its probable etiology is neu-
rovascular compression of the facial nerve at its root exit
zone. The current medical treatment consists of either
baclofen or anticonvulsant drugs, with limitation due to
side effects or low efficacy. In recent years botulinum
toxin injection and microvascular decompression of the
facial nerve have been shown to be highly successful.
However, both procedures share some complications
and require special techniques. We present 5 patients
affected by hemifacial spasm who responded well to the
novel anticonvulsant drug gabapentin. Gabapentin was
administered at a dose ranging from 900 to 1,600 mg dai-
ly, with rapid and clear improvement of spasms and
absence of any remarkable adverse effects. Our findings
suggest that gabapentin may be an effective treatment
for patients with hemifacial spasm with a very good ratio
of therapeutic effects to side effects when compared with
other drugs currently used.
1999 S. Karger AG, Basel
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Received: October 12, 1998
Accepted: February 23, 1999
Introduction
Hemifacial spasm (HFS) is a chronic condition charac-
terized by paroxysmal unilateral facial muscle contrac-
tions. The disorder is believed to involve the facial nerve,
and it is often due to microvascular compression of the
nerve by a blood vessel. HFS usually affects both upper
and lower parts of the face, but patients are commonly
more concerned about closure of the eyelid than contrac-
tions of the cheek. The disorder usually results in patient
irritation, social embarrassment and esthetic deformity.
The contractions in HFS are intermittent, but tend to be
sustained when they appear. Electromyography usually
shows some facial nerve denervation and ephaptic con-
duction.
The current pharmacological management of HFS in-
cludes baclofen, carbamazepine, clonazepam and other
antiepileptic drugs (AEDs). However, both baclofen and
AEDs often produce intolerable adverse effects, and new
potentially effective drugs are needed.
Gabapentin (GBP) is a novel AED with a good safety
profile and a presumed mechanism of action involving
GABAergic activities. Although GBP was initially devel-
oped for cotreatment of epilepsy, it has been shown to
have therapeutic properties in a wide number of neurolog-
ical disorders, which include neuropathic pain [1], mi-
graine [2], acquired pendular nystagmus [3], spasticity [4],
and bipolar disorder [5].
Here we report 5 consecutive patients with HFS who
were successfully treated with GBP (table 1).
Dr. Fabio Bandini
Laboratorio di Neuro-Oftalmologia
Dipartimento di Scienze Neurologiche e di Neuroriabilitazione
Universit di Genova, Via A. De Toni 5, I16132 Genoa (Italy)
Tel. +39 010 353 7040, Fax +39 010 354 180, E-Mail bandif16@tn.village.it
 Table 1. Clinical summary of 5 patients with HFS treated with gabapentin
Patient Sex Age HFS side
No. years
1 F 61 Right
2 M 34 Right
3 M 75 Left
4 M 42 Left
5 F 55 Right
Case Reports
Patient 1
A 61-year-old woman with an unremarkable neurological history
started complaining of intermittent involuntary contractions of her
right facial muscles, particularly of the eyelid. Physical and neurolog-
ical examinations were entirely normal, apart from the intermittent
and frequent twitching of the right orbicularis oculi and oris (at the
rate of about 45/min). Laboratory tests were normal. Magnetic reso-
nance image (MRI) of the brain and brainstem auditory evoked
responses (BAERs) showed no abnormalities. She was given GBP,
starting with 400 mg/day, increased weekly to 800 and 1,200 mg/day.
Her spasm started improving after the 1,200-mg daily dose was
reached, with a reduction in the contraction frequency and intensity
by 7080%. She did not complain of any adverse effect. After 3
months the improvement was still present.
Patient 2
A 34-year-old man was seen for intermittent contractions of his
right facial muscles. His symptoms started when he was 31 and pre-
vious treatment with carbamazepine (600 mg/day) was soon inter-
rupted due to the occurrence of remarkable side effects (dizziness,
nausea and vomiting). His past medical history was unrevealing.
Physical and neurological examinations were normal except for the
right HFS (2030 spasms/min). Laboratory data, brain MRI and
BAERs were normal. GBP was started at a dose of 900 mg/day and
increased to 1,200 mg/day in the 2nd week. There was very good
improvement in the HFS, with a reduction in the frequency of con-
tractions by 6070%. The improvement was still significant after 4
months of treatment.
Patient 3
A 75-year-old man with hypertension had a 7-month history of
sporadic tonic spasms of the left eyelid. Initially the spasms were
mostly activated by smiling and grimacing, and the patient chose not
to receive any medication. After 2 months the left eyelid spasm wor-
sened, involving the left inferior facial muscles and also occurring at
rest. Neurological examination revealed a left HFS, clinically charac-
terized by tonic spasms with a frequency of 1015/min. Laboratory
tests showed only a mild increase in blood glucose. MRI scan showed
multiple small lacunar lesions in the white matter of the brain, but no
abnormal signal intensities were noted in the posterior fossa. BAERs
were normal. GBP was introduced (1,200 mg/day) with a consistent
improvement in the left HFS (about 23 spasms/min). The patient
complained of mild somnolence; however, he did not interrupt the
treatment. A follow-up of 5 months showed a stable benefit on HFS.
50 Eur Neurol 1999;42:4951
MRI scan Dose Results Follow-up Adverse events
mg/day months
Normal 1,200 Improved 3 None
Normal 1,200 Improved 4 None
Normal 1,200 Improved 5 Somnolence
Normal 1,600 Improved 4 Giddiness
Not done 900 Improved 6 None
Patient 4
A 42-year-old man noted the subtle onset of involuntary intermit-
tent contractions of the left facial muscles, initially limited to the
eyelid. His past medical and neurological histories were negative.
Examination revealed frequent spasms of the left facial muscles,
especially of the orbicularis oculi (at a rate of 1525/min). The
remainder of the neurological examination was normal. He also had
normal results on chemistry profile, MRI of the brain and BAERs.
He was given GBP 1,200 mg/day. His HFS partially improved and
the dose was increased to 1,600 mg/day. At this dosage there was
complete control of the spasms. The patient complained of a mild
giddiness, which fortunately decreased in the following days. After 4
months, improvement persisted.
Patient 5
A 55-year-old woman had a 3-year history of right HFS. She had
been treated with several medications, including baclofen, clonaze-
pam and carbamazepine. Baclofen was ineffective. Clonazepam,
though partially successful, was interrupted because of the occur-
rence of severe drowsiness. Carbamazepine (800 mg/day) proved
effective, but with important side effects, such as ataxia and vomit-
ting. In view of these discouraging results carbamazepine was tapered
and GBP was introduced, beginning with 300 mg/day and gradually
increasing up to 900 mg/day. A remarkable (7080%) improvement
was noted after 1 week of treatment. The patient did not undergo
brain MRI because of claustrophobia. Neurological examination,
laboratory data and BAERs were normal. After a 6-month follow-up,
improvement persisted and the patient did not complain of any side
effects.
Discussion
The etiology and pathogenesis of HFS are not known
with certainty. When it does not follow facial palsy, it is
often due to a neurovascular compression of the facial
nerve in the posterior fossa, close to the brainstem. The
blood vessel involved may be the anterior inferior cerebel-
lar, posterior inferior cerebellar, the acoustic, or the inter-
nal auditory arteries. Ephaptic transmission and ectopic
excitation are the main mechanisms hypothesized to be
responsible for the spasm [6]. Hyperexcitability of the
motor nucleus of the facial nerve is also postulated [7].
Bandini/Mazzella
 The common drugs available for the disorder are
baclofen, orphenadrine, phenytoin, carbamazepine, clon-
azepam and other AEDs, including felbamate [8]. Gross
[9] suggested pizotifen as an effective medication. In
recent years new techniques have been developed for the
treatment of HFS. Botulinum toxin injection has been
reported to be very effective and safe [10], and HFS may
occasionally spontaneously resolve after botulinum thera-
py. However, botulinum toxin injection has some pitfalls
regarding cost, difficulty, and several adverse effects, such
as facial weakness, blurred vision, diplopia, dry eye, ptosis
and lid edema [10]. Local doxorubicin chemomyectomy
has also been reported to be an effective treatment for
HFS [11]. However, local skin inflammation is still an
unresolved complication of this procedure. Microvascu-
lar decompression of the seventh nerve is widely accepted
as an excellent long-term treatment of HFS [12]. How-
ever, a possible recurrence of symptoms within 2 years
[13] and some complications (ipsilateral deafness, facial
weakness) have been reported with this technique [12,
14].
GBP is a novel AED with a partially unexplained
mechanism of action. It does not have direct activity on
common GABAA or GABAB receptors or uptake carriers
[15]. However, GBP influences GABA metabolism, en-
hancing GABA synthesis (by increasing activity of glu-
tamic acid decarboxylase) and decreasing GABA degra-
dation (by inhibiting GABA transaminase) [15]. GBP also
increases GABA turnover [16] and promotes GABA re-
lease [17].
It is thus conceivable that GBP reduced HFS in our
patients by increasing GABA levels, with a possible reduc-
tion in either ephaptic transmission or hyperexcitability
of the motor nucleus of the seventh nerve. It proved effec-
tive in reducing facial spasms in all the patients at a dose
ranging from 900 to 1,600 mg/day. At these dosages GBP
was well tolerated: patient 3 complained of mild somno-
lence, and patient 4 reported transient giddiness. How-
ever, in both patients there was no need to discontinue
therapy.
To our knowledge there is only a single reported use of
GBP for the control of HFS in the available literature
[18]. Caution is obviously needed to draw any conclusion
from a study on just 5 patients. We are also aware that the
measures of GBP effectiveness were based on a subjective
scale and on patients judgement. However, the rapid and
clear improvement and the absence of any remarkable
side effect indicate GBP as a promising agent for the phar-
macotherapy of HFS, and an alternative treatment for
those patients in whom both botulinum toxin injection
and surgery are not suitable options. The long-term dura-
tion of the salutary effects has still to be determined.

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