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Blepharospasm – one of the most successful treatment applications β0ToxinA®

The age of onset is usually around 60, but the symptoms may present when a person is still in his/her thirties.

Most people develop blepharospasm without any warning symptoms. It may begin with a gradual increase in blinking or eye irritation. Some people may also experience fatigue, emotional tension, or sensitivity to bright light. As the condition progresses, the symptoms become more frequent and easily recognizable: spasmodic uncontrollable winking and seizures, the eyelids remaining shut for unusually long periods and no longer responding to signals from the brain. In the most advanced phases/stadi, patients may develop spasms so severe to turn them functionally blind and impair everyday activities. Blepharospasm may decrease or cease while a person is sleeping or concentrating on a specific task. This neurological pathology can be isolated or occur in combination with dystonic movements of other muscles in several syndromes, the most frequent being Meige syndrome or idiopathic oromandibular dystonia. Mild eyelid ptosis is the most common complication (10 to 40% of cases).

The causes of blepharospasm are complex and multiple. Current medical research suggests that the condition is induced by a defect in a large network of brain cells. There are areas in the base of the brain, in the basal ganglia, the midbrain, and/or the brainstem, that regulate and coordinate blinking. An abnormality from an unknown origin in a central control centre in the network may be responsible for it. However, it is unlikely that a single defect in any of these areas may be the primary cause of the disorder, and several factors probably contribute to its development. In rare cases, A role may be played by heredity. Or it can be induced by drugs, such as those used to treat Parkinson's disease.

Many therapeutic approaches have been tested with inconstant, often unsatisfactory, and sometimes even dangerous, results. Before the advent of botulinum toxin, the most effective drug therapy were anticholinergic agents, which resulted in the improvement of symptoms in about 20% of treated patients. Also myorelaxants and neuroleptics, levodopa, dopaminergic agonists, benzodiazepines and tricyclic antidepressants were used, with improvement in isolated cases.

The most severe situations were treated surgically, in the early to mid nineteen hundreds, with radical procedures options to de-bulk the facial nerve or even cut it completely (alcohol injections, neurectomy). In the early '80s surgeons started performing a full myectomy procedure in which the muscles that close the eyelid are extirpated, while currently the trend is for a limited or partial myectomy procedure. Unfortunately, spasms often relapse after some time.

Many studies and clinical trials, especially conducted in the '80s and '90s in the USA, Europe, Australia, and Japan, have proved that botulinum toxin A injections, by blocking the release of acetylcholine in the neuromuscular junction and thus
inducing a "deliberate paralysis" of the spasmed muscles, represent an excellent alternative to medical and surgical therapy, so much so that nowadays they are the treatment of choice for primary blepharospasm, and blepharospasm associated with dystonia, including VII nerve disorders in patients aged 12 years and older. This treatment was approved in December 1989 by the U.S. Food and Drug Administration (FDA), and is currently licensed in the United Kingdom, and in several other countries.

The safety, effectiveness, and simplicity of this therapy is constant and the treatment offers from total to partial relief to almost all patients (from 78 to 90% depending on the source) with orbicularis oculi spasm, eyelid forced closure, and eyebrow spasm, and even those with blepharospasm resistant to other forms of therapy, or with relapse after surgery.

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Table of the muscles to be injected in the treatment of blepharospasm.

Several studies have by now proved that the position of the injection sites around the orbicularis oculi muscle influences the effectiveness and side effects of botulinum toxin treatment for patients with blepharospasm. Often, two injections are administered into the upper eyelid and one injection into the lower eyelid. However, it has been noted that two further injections (of the same dose) into the pretarsal portion (adjacent to the opening of the pupil) of the orbicularis oculi muscle of the upper lid significantly increased the number of successful treatments (95% instead of 80%) and also helped patients with combined blepharospasm and involuntary levator palpebrae inhibition who responded poorly to standard treatment. Injecting the brow, inner orbital, and outer orbital hadinstead a shorter duration of effects.

The clinical results show that minute doses should be injected, about 1-5 U per muscle. Yet further studies and trials are being undertaken to test whether pretarsal injections would require an even lower dosage. Once an effective dosage has been reached, increasing the dose further does not prolong the duration of effect.

Satisfactory results with often complete spasm relief are obtained in many cases after only two days from the treatment. And the mean symptom-free interval is of 3 to 6 months.

Results of second and third injections are similar to the first in rapidity of onset and duration of effect. With time, treatments seem to cause the atrophy of the orbicularis oculi muscle and therefore a permanent effect.

No systemic toxic reactions are present, local complications are few, mild, and transient. The most common secondary effects are ptosis (21%), superficial punctuate keratitis (6%), and eye dryness (6%). As diplopia may occur most commonly from injection of the lower eyelid, and surgical relief of blepharospasm is often achieved by excision of only some upper eyelid muscles, avoiding injection of toxin in the medial two thirds of the lower eyelid is recommended.

References:

  • No authors listed, Botulinum toxin therapy of eye muscle disorders. Safety and effectiveness. American Academy of Ophthalmology. Ophthalmology. 1989 Sep;Suppl:37-41.
  • Aramideh M, Ongerboer de Visser BW, Brans JW, Koelman JH, Speelman JD. Pretarsal application of botulinum toxin for treatment of blepharospasm. J Neurol Neurosurg Psychiatry. 1995 Sep;59(3):309-11.
  • Behbehani AA. [Surgical therapy of blepharospasmus gravis] [Article in German] Laryngorhinootologie. 1989 Jan;68(1):19-22.
  • Elbaz D. [Treatment of blepharospasm and facial hemispasm with botulinum toxin. Apropos of 58 injections in 22 patients] [Article in French] Ann Otolaryngol Chir Cervicofac. 1994;111(3):141-4.
  • Frueh BR, Felt DP, Wojno TH, Musch DC. Treatment of blepharospasm with botulinum toxin. A preliminary report. Arch Ophthalmol. 1984 Oct;102(10):1464-8.
  • Frueh BR, Nelson CC, Kapustiak JF, Musch DC. The effect of omitting botulinum toxin from the lower eyelid in blepharospasm treatment. Am J Ophthalmol. 1988 Jul 15;106(1):45-7.
  • Grandas F, Elston J, Quinn N, Marsden CD. [Pharmacologic, surgical and infiltration of botulin toxin treatment in blepharospasm] [Article in Spanish] Neurologia. 1989 Jul-Aug;4(6):194-9.
  • Kalra HK, Magoon EH. Side effects of the use of botulinum toxin for treatment of benign essential blepharospasm and hemifacial spasm. Ophthalmic Surg. 1990 May;21(5):335-8.
  • Price J, Farish S, Taylor H, O'Day J. Blepharospasm and hemifacial spasm. Randomized trial to determine the most appropriate location for botulinum toxin injections. Ophthalmology. 1997 May;104(5):865-8.
  • Price J, O'Day J. Efficacy and side effects of botulinum toxin treatment for blepharospasm and hemifacial spasm. Aust N Z J Ophthalmol. 1994 Nov;22(4):255-60.
  • Roggenkämper P, Laskawi R. Die Therapie des essentiellen Blepharospasmus. in: R. Laskawi und P. Roggenkämper (Hrsg.): Botulinum-Toxin-Therapie im Kopf- Halsbereich. Urban & Vogel München 2004.
  • Saraux H. [Treatment of blepharospasm and facial hemispasm by injection of botulinum toxin] [Article in French] J Fr Ophtalmol. 1988;11(3):237-40.
  • Tsoy EA, Buckley EG, Dutton JJ. Treatment of blepharospasm with botulinum toxin. Am J Ophthalmol. 1985 Feb 15;99(2):176-9.
  • Wang J, Lin S, Zhang X. [Blepharospasm and hemifacial spasm treated with botulinum A toxin injection] [Article in Chinese] Zhonghua Er Bi Yan Hou Ke Za Zhi. 1998 Oct;33(5):291-3.

To learn more about this condition, you can visit the website of Benign Essential Blepharospasm Research Foundation (BEBRF): http://www.blepharospasm.org/

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