We examined 19 eyes of 12 patients who had undergone penetrating keratoplasty utilizing the Castroviejo square graft technique. The visual acuities at the time of examination for inclusion in the study ranged from 20/30 to counting fingers. Of the 19 original square grafts, eight were judged clear centrally with varying degrees of peripheral stromal haze, and one was hazy. The remaining eight failed with varying degrees of irreversible corneal edema. The eight corneas obtained following repeat penetrating keratoplasty were studied with light and electron microscopy. The donor/recipient corneal stromal lamellae were continuous at the graft-host junction, particularly in the mid-stromal area. Disruptions in Descemet's membrane were present at the wound; transmission electron microscopy revealed differences in the composition of Descemet's membrane between the graft and the host. Two additional square grafts had failed, and the patients were awaiting keratoplasty. Nine of the 19 grafts were judged functionally clear, with six of the nine requiring contact lens correction.

Of nine patients (five men and four women, 25 to 55 years old) with localized orbital neurofibromas, only one had other systemic findings consistent with neurofibromatosis. The neurofibromas originated from sensory nerves of the orbit, producing gradual proptosis with expansion of the orbital walls in most cases. Mild orbital discomfort occurred in some patients. Preoperative and postoperative anesthesia in the distribution of the involved sensory nerves was also encountered. Five patients had multiple tumors within the same orbit. Four patients had tumors or a pedicle of the tumor extending into the superior orbital fissure. Two patients were initially thought to have fibrotic pseudotumors. Surgical excision is the treatment of choice for these tumors.

Rabbits received nonpenetrating central corneal knife wounds. Immediately after wounding, a single 2.5 or 5.0 micron dose of mesodermal growth factor (MGF) was applied topically to the wound. Controls were treated with saline. Electron microscopic studies compared the healing responses of the control and treated animals over a 7-day period. MGF was a potent nitrogen for keratocytes in rabbit corneas. The single dose enhanced fibroblast proliferation and metabolic activity. Control wounds were not healed after 7 days, whereas those of treated animals showed complete healing.

A 51-year-old man received cyclophosphamide, vincristine, procarbazine and prednisone in the treatment of a small-cell undifferentiated lymphoma. Two years later, he developed a rapidly progressive neurological syndrome characterized by a decline in alertness, deafness, blindness and paraplegia. Examination of his eyes revealed severe hemorrhagic chorioretinitis. Leg weakness was thought to be due to transverse myelopathy at a thoracic level. He had a grand mal convulsion and died from terminal bronchopneumonia.

Fifteen corneal buttons were removed at keratoplasty from patients with keratoconus who had previously undergone thermokeratoplasty (TKP). The buttons were studied with light microscopy, in an attempt to analyze the type of changes produced by TKP. The principal histologic findings in patients with retarded epithelial healing (8 of 15) included epithelial thinning, bullous keratopathy, thickening of the epithelial basement membrane, and frequent destruction of Bowman's membrane. More severely affected patients showed asceptic stromal necrosis and fibrinous iritis with hypopyon. A poor visual result in patients with normal epithelial healing (7 of 15) was caused by superficial stromal scarring or persistent inflammatory infiltrate. Vascularization was seen in only one patient.

A patient sustained mild bilateral alkali burns of the cornea following ocular exposure to a commercial hair straightening preparation. This compound and three other products all had an alkaline pH which was not reduced to neutrality by the neutralizer provided. Corneal alkali burns similar to those seen in our patient were produced in experimental animals after brief exposure. Histologic changes were primarily limited to the cornea. The warning against ocular exposure printed on the containers or package insert is not sufficiently emphatic to protect the consumer.

A patient with a contributory history of stromal herpes presented with a severe hypopyon and multiple corneal infiltrates. Culture of corneal scrapings grew out a species of Alternaria, a generally nonpathogenic fungus. The presence of hyphae and budding yeast forms in the keratoplasty specimen gave further confirmation to the diagnosis.

The condition of a 4-year-old boy who developed conjunctivitis, urethral discharge, and arthritis was diagnosed as Reiter syndrome. Conjunctival cultures for bacteria, viruses, andMycoplasmespecies grew no organisms. Recovery was complete within one month. While Reiter syndrome is rare in children, ophthalmologists should be aware of the possibility of its occurrence in them.

In 1928, von Gierke described a small group of young patients who showed mas­ sive deposition of glycogen in their liver and kidneys at autopsy. A few years later, Pompe reported the case of a child who died with glycogen deposits in many organs as well as in skeletal muscle. Subsequently, Cori, Hers, and others have identified the inherited enzyme deficiency responsible for these and other disorders of glycogen metabolism. Pompe's disease (type II glycogenosis) results from absence of the enzyme alpha 1-4 glucosidase (acid maltase). Abnormal depo­ sition of glycogen is found in cardiac and skeletal muscle, liver, kidney, thyroid, and spleen. Because of the wide distribution of abnormal glycogen deposits, Pompe's disease is also referred to as generalized glycogeno­ sis. The light and electron microscopic changes in Pompe's disease have been thor­ oughly studied in skeletal and cardiac muscle and in other organs. Cogan was the first to observe deposits of glycogen in the mural cells of the retinal vessels in patients with Pompe's disease. Toussaint described the light microscopic ocular changes in a fivemonth-old infant with type II glycogenosis. He found deposits of glycogen in retinal ganglion cells, in mural cells of the retinal vessels, and in the smooth and striated mus­ cle fibers of the eye. Their illustrations of the rectus muscle showed a complete disap-