Father and son show the full clinical picture of the EEC syndrome with clefting, lobster-like deformities of the hands and ectodermal dysplasia with tear duct atresia and aplasia of the meibomian glands with defective tear film. During childhood, the main handicapping features are the clefting and the hand deformities with their respective multiple operative revisions. During early adulthood, however, the ocular problems become the predominantly handicapping aspects of the EEC syndrome; due to the ectodermal dysplasia, vascularized corneal scarring develops. Tearing and secondary inflammation due to lacrimal duct atresia has to be treated by early dacryocystorhinostomy. As secondary infections promote the development of corneal scars, one should not postpone the operation too long. Infections have to be treated promptly by local antibiotics. Because of the aplasia of the meibomian glands, artificial tear substitution should be given on a regular basis to support the defective tear film. Thus, the development of vascularized corneal scars can perhaps be delayed. Once corneal scarring has developed, perforating keratoplasty has a poor prognosis due to the ectodermal dysplasia, the absence of the meibomian glands and the defective tear film. Three factors lead to the formation of vascularized corneal scars: recurrent infections of lid margins and conjunctiva due to obstructed tear ducts; defective tear film with insufficient lipid phase due to the aplasia of the meibomian glands; and primary corneal epithelial defects in the course of the generalized ectodermal dysplasia.

All patients who underwent a bone marrow transplantation for leukaemia need to be followed up closely to estimate the level of GvHD they are in. This applies especially to those patients who are treated according to the regimen of adaptive immune therapy. A close cooperation of oncologists and ophthalmologists during adaptive immune therapy is mandatory, as the ophthalmologist can provide important information to help to grade the level of GvHD, judging by the morphological picture at the slit lamp.

For the first time this report describes the histopathological findings 2 months after retinal-tack implantation in a human eye. A stainless-steel tack was implanted to seal a small retinal tear during vitrectomy because of severe proliferative diabetic retinopathy in a 38-year-old man. By gross examination the enucleated eye showed a total retinal detachment except at the site where the tack had been implanted. Histologically a fibrovascular tissue proliferation arising from the choroid had grown into the adjacent retina at the tack site. No inflammatory reaction, pigment epithelium proliferation or glial-cell proliferation attributable to the tack were observed.

These findings provide further evidence of early oculomotor involvement in ALS, e.g. prior to respiratory failure and prior than previously suspected. Oculomotor impairment may occur in both the peripheral and the bulbar type of ALS.

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