Anterior ischemic optic neuropathy in type I diabetes.

Anterior ischemic optic neuropathy (A.I.O.N.) may cause optic disc edema in type-I diabetes. A.I.O.N. affects diabetic patients of all ages. Such optic neuropathy is more likely to become bilateral in diabetics than in the non-diabetic subjects. A 41-year-old diabetic insulin-dependent woman presented A.I.O.N. in RE; 5 years later, the same affection occurred in LE. The clinical course was relatively benign in both eyes, with good functional restitution. The patient was treated by high doses of Sodium Salicylate and Sulfinpyrazone. The pathogenesis of optic disc edema in type-I diabetes is, according to Hayreh (1981), ischemia of different grade in the district of the posterior ciliary arteries: microangiopathy, rheological anomalies and atherosclerotic added lesions produce a variability of clinical pictures of increasing seriousness. Our case has an intermediate position in such a continuous spectrum. The VEP supported the diagnosia of A.I.O.N.

Unusual association of Eales disease with multifocal neurological deficit.

A man who had suffered from Eales disease at the age of 20 presented an acute Brown-Séquard spinal syndrome when he was 30, followed shortly after by paralysis of the right abducens and recurrent laryngeal nerves. Steroid treatment apparently relieved the myelopathy while the neurological deficits have remained unchanged for the past 14 years. In view of the clinical and CSF findings the neurological deficits are attributed to the same disease process as that underlying the peripheral retinal abnormalities characteristic of Eales disease rather than to multiple sclerosis.

Beneficial effect of botulinum A toxin in blepharospasm: 16 months' experience with 16 cases.

After introducing the problem of blepharospasm, we report our experience on treatment with purified botulinum A toxin in 16 cases of blepharospasm, symptomatic in two and essential in 14, than had not responded to drugs. The changes in intensity and frequency of spasm after treatment were evaluated on a clinical scale and by review of videotapes. The beneficial effect appeared within a week in most patients, lasting from 6 to 28 weeks (mean 13), and reached the maximum at the third-seventh week. Mild spasms and female patients responded better. Repeated injections were followed by better response to the drug. Complications, exclusively local, were represented by transient corneal exposure, ptosis, lacrimation or diplopia.

Use of botulinum toxin in Meige's disease.

Four patients with severe Meige's disease (blepharospasm-oromandibular dystonia) have been treated, after having given an informed consent, by local injections of purified botulinum toxin type "A". Previous systemic therapy with anticholinergics, dopamine antagonists and other drugs had been unsuccessful in all these subjects. Each patient was treated by saline solution injected with the same method as botulinum toxin, just once. The self-evaluation of patients and the clinical evaluation that some of us- unaware of the kind of therapy which had been performed- gave to the symptoms on the basis of videotapes, for each session of injection, showed that the injections of botulinum toxin are effective in the treatment of such disorder. The duration of the beneficial effect was slightly shorter in these patients than in patients with blepharospasm treated by the same method.