January 28, 1905


Author Affiliations

Clinical Professor of Ophthalmology and Otology, Johns Hopkins University; Ophthalmic and Aural Surgeon to the Johns Hopkins Hospital and to the Baltimore Eye, Ear and Throat Charity Hospital. BALTIMORE.

JAMA. 1905;XLIV(4):284-287. doi:10.1001/jama.1905.92500310028001g

Thirty years ago, it is safe to say, there was but one view held as to the genesis of sympathetic ophthalmitis. The doctrine of Mackenzie that the optic nerve played the chief rôle in the transference of the inflammation from the exciting to the sympathizing eye, had been universally abandoned, and the view that the pathologic changes in the secondarily affected eye were the product of an influence—an influence of a reflex character—transmitted to it through the ciliary nerves, was as universally accepted. This view, which had been suggested by Mackenzie as an alternative but improbable explanation of the phenomena of sympathetic inflammation, and had been advanced previously by Tavignol, in 1845, was first brought prominently forward by Heinrich Müller, who published his conclusions—based on pathologico-anatomic observations—in 1858. His theory gained converts rapidly, and among those who accepted it, and who soon became its

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