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Objective: Discussion of clinical symptoms and differential diagnosis of blepharospasm and treatment with botulinum A toxin. Blepharospasm is an involuntary spasmodic contraction of the eyelids. Within a few years 35%-70% of the patients becomes severely disabled., Design: Prospective, open study., Setting: Academical Medical Centre, Amsterdam., Method: In the period 1985-1992 we have seen 85 patients with blepharospasm. Of these 69 were treated with botulinum toxin, a total of 436 treatments, with a mean dose of 25 IU for each eye., Results: The cause of blepharospasm was unknown in 71 patients. Secondary blepharospasm occurred in: peripheral facial palsy (one patient), herpes zoster infection of the trigeminal nerve (2), brain infarct (1), use of neuroleptics (2), progressive supranuclear palsy (2), Shy-Drager syndrome (1), kernicterus (1), and morbus Sjögren (4). There were 18 patients with autoimmune diseases. 77 (91%) patients had a (very) severe form of blepharospasm. Electromyographic registration revealed a dysfunction of M. levator palpebrae in 7 patients. More than 70% of the patients were free of symptoms for a mean period of two months after each treatment. Local side effects were seen in 61 (14%) of the 436 treatments: ptosis, haematoma, dry eyes, and diplopia., Conclusion: Blepharospasm is a disabling disease and occurs sometimes in association with other neurological and ophthalmological diseases. Botulinum A toxin is a safe and effective therapy. Electrophysiological investigation is important in the differential diagnosis; it is unnecessary to do CT or MRI routinely.

At the Academic Medical Center of the University of Amsterdam the results of treatment of hemifacial spasms (HFS) with botulinum toxin type A were evaluated in a pilot study. Five men and 21 women with HFS were treated with toxin injections. The mean age was 65 years. Most patients were referred from other centers and had been previously treated without success with various medications or with surgical treatment. Treatment took place at the outpatient department. The toxin was injected into the M. orbicularis oculi at the medial and lateral sides of the upper and lower lids. The total dose varied between 6 and 16 LD50. Patients were reinjected on demand. All patients except for one reported satisfying improvement of their spasm. The onset of the beneficial effect was 1-2 days after the injection and the effect lasted about 3 months. All patients were re-examined 1 to 2 weeks after each treatment and showed reduction or disappearance of synkinesias. No systemic side effects occurred and local complications were mild and transient. We conclude that local injection of botulinum toxin appears to be a successful alternative in the current treatment of hemifacial spasm.