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Latanoprost in hemifacial spasm
Prostaglandins & other Lipid Mediators 67 (2002) 27–30
Latanoprost in hemifacial spasm Luc Crevits*, Maarten Goethals, Niels Libbrecht, Koen Paemeleire Department of Neurology, Neuro-Ophthalmology Unit, Ghent University Hospital, Ghent, Belgium Received 28 July 2001; accepted 13 August 2001
Abstract An empirical observation that the prostaglandin derivate latanoprost quited facial spasms in patients with glaucoma prompted us to study latanoprost in non-glaucomatous patients with hemifacial spasms [HFS]. This explorative trial followed an open-label, prospective treatment design. At short term, most patients showed no or only mild improvement and subsequently needed therapy with Botulinum toxin A. Although these results are not impressive, latanoprost could be considered as an interesting alternative in the treatment of patients with HFS and with concomitant glaucoma. A role for prostaglandins in the trigeminofacial reflex is hypothesised. © 2002 Elsevier Science Inc. All rights reserved. Keywords: Hemifacial spasms; Prostaglandin; Latanoprost; Therapy; Trial
1. Introduction Hemifacial spasm [HFS] is characterised by involuntary twitching and spasm of the facial muscles on one side. Apart from some specific causes, the aetiology is presumed to be a compression of the facial nerve at the root exit zone by an aberrant blood vessel [1]. HFS is a chronic disorder with social and functional implications. Local injection of Botulinum toxin A in the facial muscles has been found effective [2] and has become the gold standard therapy. Botulinum toxin A, however, is very expensive and should only be given by experienced physicians. Paresis of the extraocular eye muscles, eyelids and facial muscles are well known side effects [3]. The clinical effect lasts only for some months requiring repeated injections, considered inconvenient by many patients. In addition, 3–5% of patients
* Corresponding author. Tel.: ⫹32-9-2404539; fax: ⫹32-9-2404971. E-mail address: [email protected] (L. Crevits). 0090-6980/02/$ – see front matter © 2002 Elsevier Science Inc. All rights reserved. PII: S 0 0 9 0 - 6 9 8 0 ( 0 2 ) 0 0 1 6 8 - X
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Table 1 Patient no
Gender
Age [yrs]
Side of HFS
Prior therapy
First clinical evaluation of the effect of latanoprost after
Effect
Further therapy
1 2 3 4 5 6
F F F F F F
67 68 55 49 72 64
left right left bilat. left left
Botulinum None None Acupuncture Clonazepam Botulinum
6 4 6 9 9 6
⫺ ⫹ ⫹/⫺ ⫺ ⫹/⫺ ⫹
7
M
52
left
Botulinum 8 weeks Carbamazepine
Botulinum Nihil Botulinum Botulinum Botulinum Latanoprost/ anticholinergic drug Botulinum
weeks weeks weeks weeks weeks weeks
⫺
HFS ⫽ hemifacial spasms; Bilat ⫽ bilateral; Effect ⫹ ⫽ sufficient; ⫹/⫺ ⫽ mild; ⫺ ⫽ none.
have been reported to stop responding after several administrations, probably due to antibody formation [4]. It was observed empirically that the ocular hypotensive drug latanoprost [0,005% eye drops] quieted facial spasms in patients with glaucoma. This observation (not published) prompted us to try latanoprost in non-glaucomatous patients with HFS.
2. Material and methods This trial followed an open-label, prospective treatment design. The study population consisted of seven patients presenting with HFS. Demographic and clinical data are summarised in Table 1. Six women and one man ranging in age from 49 to 72 years agreed to participate in this explorative trial. All patients underwent a complete neurologic examination, including a cerebral MRI-scan with focus on the basal ganglia and the facial nerve. None of the patients had a prior history of facial palsy. Although one patient [no 2] exhibited an acoustic neurinoma and a loop of the vertebral artery was seen in another patient [no 5], compression of the facial nerve could not be visualised in any patient. Finally, all cases were classified as primary, “idiopathic” HFS. Five of the patients had already undergone a therapy for HFS in the past. Patients were prescribed one drop of 0,005% latanoprost in the eye on the affected facial side each morning for at least 4 weeks. Clinical efficacy was assessed semi-quantitatively through self-reporting by patients. Categories included sufficient, mild or no improvement.
3. Results Three patients reported no improvement whatsoever. Two other patients had experienced mild improvement, but HFS was still interfering with their social lives. These five patients were treated with Botulinum toxin A after a latanoprost trial of at least 6 weeks. HFS was quieted sufficiently by latanoprost in two patients. In one of them [patient no 2], latanoprost
L. Crevits et al. / Prostaglandins & other Lipid Mediators 67 (2002) 27–30
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was stopped after 4 weeks with only minimal residual HFS not necessitating any further treatment. In the other good responder [patient no 6], the clinical effect diminished after 8 months of continuous latanoprost treatment and an anticholinergic drug was associated. 4. Discussion Latanoprost, a prostaglandin derivative, has been shown to be efficacious in glaucoma by increasing the uveoscleral outflow of aequous humour, thus lowering the intraocular pressure [5]. It seems to have no adverse effect on the optic nerve head and peripapillary retinal blood flow [6]. Latanoprost is not associated with clinically significant respiratory side effects [7] but cardiovascular disorders have been reported in post-marketing surveys [8]. Latanoprost can cause increased pigmentation of the iris and periorbital tissue, and hyperpigmentation and growth of the eyelashes [9]. These side effects have not been observed in our patients. Based on the empirical observation of a favourable effect on facial spasms of latanoprost as a treatment for glaucoma, we studied the effect in 7 non-glaucomatous HFS patients in a prospective, explorative trial with the intention to treat. HFS was diagnosed as primary or “idiopathic” in all cases. In particular, there was no history of previous facial palsy and compression of the facial nerve could not be demonstrated. At short term, most patients showed no or only mild improvement and subsequently needed Botulinum toxin A. In 2 patients latanoprost was sufficient to control the complaints. In one of these good responders, HFS remained quited after stopping latanoprost, in another the positive effect remained for 8 months. The subjective evaluation of the results can be questioned. However, the functional and social outcome are the treatment criteria handled for HFS in clinical practice. Certainly, there are serious limitations to an open trial performed in seven patients. Controlled, randomised double blind trials for extended periods would be required to verify our findings in a larger group of patients and to establish the place of latanoprost in the treatment of HFS and blepharospasm. Although the present results are not very impressive, we suggest to consider latanoprost as an alternative therapy for HFS or blepharospasm in patients with concomitant glaucoma. The mode of action of latanoprost in HFS is unknown. The effect could hardly be ascribed to lowering of the ocular pressure in patients without glaucoma. Analogous to the possible role of sensory feedback in dystonia [10], latanoprost could alter some sensory afferents and therefore modulate central processing resulting in lowering of the excitability of the facial nucleus through the trigeminofacial reflex. However, since the effect on the HFS lasted the whole day and latanoprost known to be long acting, was administered only once a day it seems likely that there was a pharmacological impact apart from the sensory input. We hypothesise that latanoprost applied topically to the eye could interfere with the trigeminofacial reflex by a prostaglandin effect. References [1] Wilkins RH. Hemifacial spasm: A review. Surg Neurol 1991;36:251–77. [2] Jankovic J, Brin MF. Therapeutic uses of botulinum toxin. N Engl J Med 1991;324:1186 –94.
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L. Crevits et al. / Prostaglandins & other Lipid Mediators 67 (2002) 27–30
[3] Yoshimura DM, Aminoff MJ, Tami TA, Scott AB. Treatment of hemifacial spasm with botulinum toxin. Muscle Nerve 1992;15:1045–9. [4] Elston JS. The management of blepharospasm and hemifacial spasm. J Neurol 1992;239:5– 8. [5] Watson PG, the Latanoprost Study Group. Latanoprost—two years experience of its use in the United Kingdom. Ophthalmology 1998;105:82–7. [6] Seong GJ, Lee HK, Hong YJ. Effects of 0,005% latanoprost on optic nerve head and peripapillary retinal blood flow. Ophtalmologica 1999;213:355–9. [7] Hedner J, Svedmyr N, Lunde H, Mandahl A. The lack of respiratory effects on the ocular hypotension drug latanoprost in patients with moderate-steroid treated asthma. Surv Ophtalmol 1997;41(Suppl 2):S111–S115. [8] Anonymous. Cardiovascular disorders due to latanoprost eye drops? Prescrire Int 1999;41:85. [9] Selen G, Stjschantz J, Resul B. Prostaglandin-induced iridial pigmentation in primates. Surv Ophthalmol 1997;41(Suppl 2):S125–S128. [10] Hallett M. Is dystonia a sensory disorder? Ann Neurol 1995;38:139 – 40.
Latanoprost in hemifacial spasm Luc Crevits*, Maarten Goethals, Niels Libbrecht, Koen Paemeleire Department of Neurology, Neuro-Ophthalmology Unit, Ghent University Hospital, Ghent, Belgium Received 28 July 2001; accepted 13 August 2001
Abstract An empirical observation that the prostaglandin derivate latanoprost quited facial spasms in patients with glaucoma prompted us to study latanoprost in non-glaucomatous patients with hemifacial spasms [HFS]. This explorative trial followed an open-label, prospective treatment design. At short term, most patients showed no or only mild improvement and subsequently needed therapy with Botulinum toxin A. Although these results are not impressive, latanoprost could be considered as an interesting alternative in the treatment of patients with HFS and with concomitant glaucoma. A role for prostaglandins in the trigeminofacial reflex is hypothesised. © 2002 Elsevier Science Inc. All rights reserved. Keywords: Hemifacial spasms; Prostaglandin; Latanoprost; Therapy; Trial
1. Introduction Hemifacial spasm [HFS] is characterised by involuntary twitching and spasm of the facial muscles on one side. Apart from some specific causes, the aetiology is presumed to be a compression of the facial nerve at the root exit zone by an aberrant blood vessel [1]. HFS is a chronic disorder with social and functional implications. Local injection of Botulinum toxin A in the facial muscles has been found effective [2] and has become the gold standard therapy. Botulinum toxin A, however, is very expensive and should only be given by experienced physicians. Paresis of the extraocular eye muscles, eyelids and facial muscles are well known side effects [3]. The clinical effect lasts only for some months requiring repeated injections, considered inconvenient by many patients. In addition, 3–5% of patients
* Corresponding author. Tel.: ⫹32-9-2404539; fax: ⫹32-9-2404971. E-mail address: [email protected] (L. Crevits). 0090-6980/02/$ – see front matter © 2002 Elsevier Science Inc. All rights reserved. PII: S 0 0 9 0 - 6 9 8 0 ( 0 2 ) 0 0 1 6 8 - X
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L. Crevits et al. / Prostaglandins & other Lipid Mediators 67 (2002) 27–30
Table 1 Patient no
Gender
Age [yrs]
Side of HFS
Prior therapy
First clinical evaluation of the effect of latanoprost after
Effect
Further therapy
1 2 3 4 5 6
F F F F F F
67 68 55 49 72 64
left right left bilat. left left
Botulinum None None Acupuncture Clonazepam Botulinum
6 4 6 9 9 6
⫺ ⫹ ⫹/⫺ ⫺ ⫹/⫺ ⫹
7
M
52
left
Botulinum 8 weeks Carbamazepine
Botulinum Nihil Botulinum Botulinum Botulinum Latanoprost/ anticholinergic drug Botulinum
weeks weeks weeks weeks weeks weeks
⫺
HFS ⫽ hemifacial spasms; Bilat ⫽ bilateral; Effect ⫹ ⫽ sufficient; ⫹/⫺ ⫽ mild; ⫺ ⫽ none.
have been reported to stop responding after several administrations, probably due to antibody formation [4]. It was observed empirically that the ocular hypotensive drug latanoprost [0,005% eye drops] quieted facial spasms in patients with glaucoma. This observation (not published) prompted us to try latanoprost in non-glaucomatous patients with HFS.
2. Material and methods This trial followed an open-label, prospective treatment design. The study population consisted of seven patients presenting with HFS. Demographic and clinical data are summarised in Table 1. Six women and one man ranging in age from 49 to 72 years agreed to participate in this explorative trial. All patients underwent a complete neurologic examination, including a cerebral MRI-scan with focus on the basal ganglia and the facial nerve. None of the patients had a prior history of facial palsy. Although one patient [no 2] exhibited an acoustic neurinoma and a loop of the vertebral artery was seen in another patient [no 5], compression of the facial nerve could not be visualised in any patient. Finally, all cases were classified as primary, “idiopathic” HFS. Five of the patients had already undergone a therapy for HFS in the past. Patients were prescribed one drop of 0,005% latanoprost in the eye on the affected facial side each morning for at least 4 weeks. Clinical efficacy was assessed semi-quantitatively through self-reporting by patients. Categories included sufficient, mild or no improvement.
3. Results Three patients reported no improvement whatsoever. Two other patients had experienced mild improvement, but HFS was still interfering with their social lives. These five patients were treated with Botulinum toxin A after a latanoprost trial of at least 6 weeks. HFS was quieted sufficiently by latanoprost in two patients. In one of them [patient no 2], latanoprost
L. Crevits et al. / Prostaglandins & other Lipid Mediators 67 (2002) 27–30
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was stopped after 4 weeks with only minimal residual HFS not necessitating any further treatment. In the other good responder [patient no 6], the clinical effect diminished after 8 months of continuous latanoprost treatment and an anticholinergic drug was associated. 4. Discussion Latanoprost, a prostaglandin derivative, has been shown to be efficacious in glaucoma by increasing the uveoscleral outflow of aequous humour, thus lowering the intraocular pressure [5]. It seems to have no adverse effect on the optic nerve head and peripapillary retinal blood flow [6]. Latanoprost is not associated with clinically significant respiratory side effects [7] but cardiovascular disorders have been reported in post-marketing surveys [8]. Latanoprost can cause increased pigmentation of the iris and periorbital tissue, and hyperpigmentation and growth of the eyelashes [9]. These side effects have not been observed in our patients. Based on the empirical observation of a favourable effect on facial spasms of latanoprost as a treatment for glaucoma, we studied the effect in 7 non-glaucomatous HFS patients in a prospective, explorative trial with the intention to treat. HFS was diagnosed as primary or “idiopathic” in all cases. In particular, there was no history of previous facial palsy and compression of the facial nerve could not be demonstrated. At short term, most patients showed no or only mild improvement and subsequently needed Botulinum toxin A. In 2 patients latanoprost was sufficient to control the complaints. In one of these good responders, HFS remained quited after stopping latanoprost, in another the positive effect remained for 8 months. The subjective evaluation of the results can be questioned. However, the functional and social outcome are the treatment criteria handled for HFS in clinical practice. Certainly, there are serious limitations to an open trial performed in seven patients. Controlled, randomised double blind trials for extended periods would be required to verify our findings in a larger group of patients and to establish the place of latanoprost in the treatment of HFS and blepharospasm. Although the present results are not very impressive, we suggest to consider latanoprost as an alternative therapy for HFS or blepharospasm in patients with concomitant glaucoma. The mode of action of latanoprost in HFS is unknown. The effect could hardly be ascribed to lowering of the ocular pressure in patients without glaucoma. Analogous to the possible role of sensory feedback in dystonia [10], latanoprost could alter some sensory afferents and therefore modulate central processing resulting in lowering of the excitability of the facial nucleus through the trigeminofacial reflex. However, since the effect on the HFS lasted the whole day and latanoprost known to be long acting, was administered only once a day it seems likely that there was a pharmacological impact apart from the sensory input. We hypothesise that latanoprost applied topically to the eye could interfere with the trigeminofacial reflex by a prostaglandin effect. References [1] Wilkins RH. Hemifacial spasm: A review. Surg Neurol 1991;36:251–77. [2] Jankovic J, Brin MF. Therapeutic uses of botulinum toxin. N Engl J Med 1991;324:1186 –94.
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L. Crevits et al. / Prostaglandins & other Lipid Mediators 67 (2002) 27–30
[3] Yoshimura DM, Aminoff MJ, Tami TA, Scott AB. Treatment of hemifacial spasm with botulinum toxin. Muscle Nerve 1992;15:1045–9. [4] Elston JS. The management of blepharospasm and hemifacial spasm. J Neurol 1992;239:5– 8. [5] Watson PG, the Latanoprost Study Group. Latanoprost—two years experience of its use in the United Kingdom. Ophthalmology 1998;105:82–7. [6] Seong GJ, Lee HK, Hong YJ. Effects of 0,005% latanoprost on optic nerve head and peripapillary retinal blood flow. Ophtalmologica 1999;213:355–9. [7] Hedner J, Svedmyr N, Lunde H, Mandahl A. The lack of respiratory effects on the ocular hypotension drug latanoprost in patients with moderate-steroid treated asthma. Surv Ophtalmol 1997;41(Suppl 2):S111–S115. [8] Anonymous. Cardiovascular disorders due to latanoprost eye drops? Prescrire Int 1999;41:85. [9] Selen G, Stjschantz J, Resul B. Prostaglandin-induced iridial pigmentation in primates. Surv Ophthalmol 1997;41(Suppl 2):S125–S128. [10] Hallett M. Is dystonia a sensory disorder? Ann Neurol 1995;38:139 – 40.