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Original Paper

Eur Neurol 1999;42:4951 Received: October 12, 1998

Accepted: February 23, 1999

Gabapentin as Treatment for

Hemifacial Spasm
Fabio Bandini Luca Mazzella
Department of Neurological Sciences and Neurorehabilitation, University of Genoa, Italy

Key Words Introduction

Hemifacial spasm W Gabapentin
Hemifacial spasm (HFS) is a chronic condition charac-
terized by paroxysmal unilateral facial muscle contrac-
Abstract tions. The disorder is believed to involve the facial nerve,
Hemifacial spasm, a life-long condition characterized by and it is often due to microvascular compression of the
involuntary unilateral contractions of the facial muscles, nerve by a blood vessel. HFS usually affects both upper
is a disabling disorder often resulting in patient irritation and lower parts of the face, but patients are commonly
and social embarassment. Its probable etiology is neu- more concerned about closure of the eyelid than contrac-
rovascular compression of the facial nerve at its root exit tions of the cheek. The disorder usually results in patient
zone. The current medical treatment consists of either irritation, social embarrassment and esthetic deformity.
baclofen or anticonvulsant drugs, with limitation due to The contractions in HFS are intermittent, but tend to be
side effects or low efficacy. In recent years botulinum sustained when they appear. Electromyography usually
toxin injection and microvascular decompression of the shows some facial nerve denervation and ephaptic con-
facial nerve have been shown to be highly successful. duction.
However, both procedures share some complications The current pharmacological management of HFS in-
and require special techniques. We present 5 patients cludes baclofen, carbamazepine, clonazepam and other
affected by hemifacial spasm who responded well to the antiepileptic drugs (AEDs). However, both baclofen and
novel anticonvulsant drug gabapentin. Gabapentin was AEDs often produce intolerable adverse effects, and new
administered at a dose ranging from 900 to 1,600 mg dai- potentially effective drugs are needed.
ly, with rapid and clear improvement of spasms and Gabapentin (GBP) is a novel AED with a good safety
absence of any remarkable adverse effects. Our findings profile and a presumed mechanism of action involving
suggest that gabapentin may be an effective treatment GABAergic activities. Although GBP was initially devel-
for patients with hemifacial spasm with a very good ratio oped for cotreatment of epilepsy, it has been shown to
of therapeutic effects to side effects when compared with have therapeutic properties in a wide number of neurolog-
other drugs currently used. 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).

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Table 1. Clinical summary of 5 patients with HFS treated with gabapentin

Patient Sex Age HFS side MRI scan Dose Results Follow-up Adverse events
No. years mg/day months

1 F 61 Right Normal 1,200 Improved 3 None

2 M 34 Right Normal 1,200 Improved 4 None
3 M 75 Left Normal 1,200 Improved 5 Somnolence
4 M 42 Left Normal 1,600 Improved 4 Giddiness
5 F 55 Right Not done 900 Improved 6 None

Case Reports Patient 4

A 42-year-old man noted the subtle onset of involuntary intermit-
Patient 1 tent contractions of the left facial muscles, initially limited to the
A 61-year-old woman with an unremarkable neurological history eyelid. His past medical and neurological histories were negative.
started complaining of intermittent involuntary contractions of her Examination revealed frequent spasms of the left facial muscles,
right facial muscles, particularly of the eyelid. Physical and neurolog- especially of the orbicularis oculi (at a rate of 1525/min). The
ical examinations were entirely normal, apart from the intermittent remainder of the neurological examination was normal. He also had
and frequent twitching of the right orbicularis oculi and oris (at the normal results on chemistry profile, MRI of the brain and BAERs.
rate of about 45/min). Laboratory tests were normal. Magnetic reso- He was given GBP 1,200 mg/day. His HFS partially improved and
nance image (MRI) of the brain and brainstem auditory evoked the dose was increased to 1,600 mg/day. At this dosage there was
responses (BAERs) showed no abnormalities. She was given GBP, complete control of the spasms. The patient complained of a mild
starting with 400 mg/day, increased weekly to 800 and 1,200 mg/day. giddiness, which fortunately decreased in the following days. After 4
Her spasm started improving after the 1,200-mg daily dose was months, improvement persisted.
reached, with a reduction in the contraction frequency and intensity
by 7080%. She did not complain of any adverse effect. After 3 Patient 5
months the improvement was still present. A 55-year-old woman had a 3-year history of right HFS. She had
been treated with several medications, including baclofen, clonaze-
Patient 2 pam and carbamazepine. Baclofen was ineffective. Clonazepam,
A 34-year-old man was seen for intermittent contractions of his though partially successful, was interrupted because of the occur-
right facial muscles. His symptoms started when he was 31 and pre- rence of severe drowsiness. Carbamazepine (800 mg/day) proved
vious treatment with carbamazepine (600 mg/day) was soon inter- effective, but with important side effects, such as ataxia and vomit-
rupted due to the occurrence of remarkable side effects (dizziness, ting. In view of these discouraging results carbamazepine was tapered
nausea and vomiting). His past medical history was unrevealing. and GBP was introduced, beginning with 300 mg/day and gradually
Physical and neurological examinations were normal except for the increasing up to 900 mg/day. A remarkable (7080%) improvement
right HFS (2030 spasms/min). Laboratory data, brain MRI and was noted after 1 week of treatment. The patient did not undergo
BAERs were normal. GBP was started at a dose of 900 mg/day and brain MRI because of claustrophobia. Neurological examination,
increased to 1,200 mg/day in the 2nd week. There was very good laboratory data and BAERs were normal. After a 6-month follow-up,
improvement in the HFS, with a reduction in the frequency of con- improvement persisted and the patient did not complain of any side
tractions by 6070%. The improvement was still significant after 4 effects.
months of treatment.

Patient 3
A 75-year-old man with hypertension had a 7-month history of Discussion
sporadic tonic spasms of the left eyelid. Initially the spasms were
mostly activated by smiling and grimacing, and the patient chose not The etiology and pathogenesis of HFS are not known
to receive any medication. After 2 months the left eyelid spasm wor-
with certainty. When it does not follow facial palsy, it is
sened, involving the left inferior facial muscles and also occurring at
rest. Neurological examination revealed a left HFS, clinically charac- often due to a neurovascular compression of the facial
terized by tonic spasms with a frequency of 1015/min. Laboratory nerve in the posterior fossa, close to the brainstem. The
tests showed only a mild increase in blood glucose. MRI scan showed blood vessel involved may be the anterior inferior cerebel-
multiple small lacunar lesions in the white matter of the brain, but no lar, posterior inferior cerebellar, the acoustic, or the inter-
abnormal signal intensities were noted in the posterior fossa. BAERs
nal auditory arteries. Ephaptic transmission and ectopic
were normal. GBP was introduced (1,200 mg/day) with a consistent
improvement in the left HFS (about 23 spasms/min). The patient excitation are the main mechanisms hypothesized to be
complained of mild somnolence; however, he did not interrupt the responsible for the spasm [6]. Hyperexcitability of the
treatment. A follow-up of 5 months showed a stable benefit on HFS. motor nucleus of the facial nerve is also postulated [7].

50 Eur Neurol 1999;42:4951 Bandini/Mazzella

The common drugs available for the disorder are tamic acid decarboxylase) and decreasing GABA degra-
baclofen, orphenadrine, phenytoin, carbamazepine, clon- dation (by inhibiting GABA transaminase) [15]. GBP also
azepam and other AEDs, including felbamate [8]. Gross increases GABA turnover [16] and promotes GABA re-
[9] suggested pizotifen as an effective medication. In lease [17].
recent years new techniques have been developed for the It is thus conceivable that GBP reduced HFS in our
treatment of HFS. Botulinum toxin injection has been patients by increasing GABA levels, with a possible reduc-
reported to be very effective and safe [10], and HFS may tion in either ephaptic transmission or hyperexcitability
occasionally spontaneously resolve after botulinum thera- of the motor nucleus of the seventh nerve. It proved effec-
py. However, botulinum toxin injection has some pitfalls tive in reducing facial spasms in all the patients at a dose
regarding cost, difficulty, and several adverse effects, such ranging from 900 to 1,600 mg/day. At these dosages GBP
as facial weakness, blurred vision, diplopia, dry eye, ptosis was well tolerated: patient 3 complained of mild somno-
and lid edema [10]. Local doxorubicin chemomyectomy lence, and patient 4 reported transient giddiness. How-
has also been reported to be an effective treatment for ever, in both patients there was no need to discontinue
HFS [11]. However, local skin inflammation is still an therapy.
unresolved complication of this procedure. Microvascu- To our knowledge there is only a single reported use of
lar decompression of the seventh nerve is widely accepted GBP for the control of HFS in the available literature
as an excellent long-term treatment of HFS [12]. How- [18]. Caution is obviously needed to draw any conclusion
ever, a possible recurrence of symptoms within 2 years from a study on just 5 patients. We are also aware that the
[13] and some complications (ipsilateral deafness, facial measures of GBP effectiveness were based on a subjective
weakness) have been reported with this technique [12, scale and on patients judgement. However, the rapid and
14]. clear improvement and the absence of any remarkable
GBP is a novel AED with a partially unexplained side effect indicate GBP as a promising agent for the phar-
mechanism of action. It does not have direct activity on macotherapy of HFS, and an alternative treatment for
common GABAA or GABAB receptors or uptake carriers those patients in whom both botulinum toxin injection
[15]. However, GBP influences GABA metabolism, en- and surgery are not suitable options. The long-term dura-
hancing GABA synthesis (by increasing activity of glu- tion of the salutary effects has still to be determined.


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Gabapentin and Hemifacial Spasm Eur Neurol 1999;42:4951 51

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