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We treated four patients with essential blepharospasm, receiving botulinum A toxin, in whom, although they had no preexisting blepharoptosis, a concurrent bilateral acquired blepharoptosis developed. Since the blepharoptosis did not improve after the period of time during which the effects of botulinum A toxin would have been expected to resolve (2 to 10 weeks), we judged that its development was unrelated to the toxin. We propose, rather, that the stretching, attenuation, disinsertion, or dehiscence of the upper eyelid levator muscle caused by the blepharospasm were at least partly responsible for the onset of the blepharoptosis. To ensure appropriate treatment in these cases, careful clinical evaluation is required to differentiate the two conditions.

A family with autosomal dominant congenital cataracts was studied to determine clinical variability. A total of 159 relatives was ascertained; 17 affected and 19 normal individuals were evaluated and their blood sampled for inclusion in the linkage analysis. The disease was compatible with normal to mildly decreased visual acuity until adult life in all affected except the product of a consanguineous marriage of affected first cousins who was born with bilateral microphthalmos and dense congenital cataracts, attributed to homozygosity of the cataract gene. There were no extraocular abnormalities; the patient was of normal intelligence. Twenty-three markers were typed, 18 of which were informative. Linkage could be excluded for all 18 markers at short distances.

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