Abstract
Neuroparalytic keratitis is regarded as a trophoneurosis caused by injury of the Gasserian ganglion or nerves emanating from it or of the ciliary ganglion. Recently we succeeded in the experimental production of neuroparalytic keratitis through the injection of one cc. of 80% alcohol into the rabbit's orbita. 1 Immediately after the retrobulbar injection of alcohol the cornea loses its sensitivity and in 24 hours the corneal epithelium begins to exfoliate. This usually is associated with more or less profuse discharge from the cul-de-sac and chemosis of the bulbar conjunctiva. Keratitis of various degrees develops in the course of 3-7 days after the injection. In some cases this process is aggravated by the ulceration of the cornea characteristic of neuroparalytic keratitis. Out of 34 experiments done in connection with this study, neuroparalytic keratitis failed to develop only in 4 instances.
Among the hypotheses on the pathogenesis of this disease, one supports the bacterial origin of the affection. Davies and Hall 2 found a pseudo-diphtheritic type of bacillus in human eyes affected with neuroparalytic keratitis to which they attributed the specific etiological rôle. Other authorities are of opinion that neuroparalytic keratitis is due to a secondary infection of the eye, the resistance of which has been diminished by the trophic disturbance of the nervous supply of the organ.
The readiness with which neuroparalytic keratitis can experimentally be produced in the rabbit's eye has offered means of investigating the question of the bacterial origin of this disease and the probable diminution of the resistance of the injured eye to bacterial infection. We at first determined the normal bacterial flora of the rabbit eyes using blood agar plates for culturing the content of the cul-de-sac. It was found that the cultures were constantly negative.
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