TREATMENT AND PROGNOSIS. — The treatment for glioma of the retina is re moval of the eyeball at the earliest mo ment, with so much of the optic nerve as can be readily taken with it. If the growth has reached the third stage the removal of the whole contents of the orbit is necessary. Without complete extirpation of the tumor it always causes death. After early removal of the eye about one-third of the cases remain per manently free from the disease. But only the lapse of a sufficient period of time, at least three years, can give posi tive assurance that there will be no re currence.
Optic neuritis, papillitis, or choked disk is an inflammation of the ocular end of the optic nerve. It is important as a symptom of the diseases which cause it, and on account of the atrophy and impairment of vision which are liable to follow it.
SvmProms.—The essential symptoms, hypenemia and swelling, are only dis coverable by the ophthalmoscope. Hy peraemia at first causes the optic disk to appear redder, and more uniform in color than normal. At the same time exudation causes blurring or complete obscuration of its outlines; so that the location of the disk may only be recog nized by the convergence to it of the larger retinal vessels. As the inflamma tion advances, the swelling becomes greater; and measurement of their re fraction with the ophthalmoscope shows that the vessels at the centre of the disk are pushed forward into the vitreous. With the increased swelling the small vessels become separated by exudate, and the general color of the disk be comes more gray. The individual vessels, greatly enlarged and tortuous, appear and disappear in the swelling. The prin cipal branches of the retinal arteries are small from compression at the point of entrance to the eye; and from com pression at the point of exit the veins are swelled, dark, and tortuous. 1-Icem orrhages occur mostly on or near the disk. Vision may not be noticeably im paired. It may remain practically nor mal, even with great swelling. When impairment of vision does occur, it is rather a sign of optic atrophy secondary to the neuritis, or of involvement of the visual centres or optic tract within the cranium. The course of the disease is essentially chronic, sometimes lasting for many months, or even several years, when caused by a slowly-growing tumor. Ulti mately, if the patient lives long enough, the swelling becomes paler and dimin ishes, and the process passes over into one of optic atrophy. Commonly both eyes are affected, although often one earlier or more severely than the other.
Monocular neuritis may occur from cold, rheumatism, or local causes.
The diagnosis rests on the ophthal moscopical appearances above described. In a severe case these cannot be mis taken. But a commencing neuritis may easily be confused with the hypermia and slight haziness of the disk, often seen with eye-strain, and in rare cases protrusion and haziness exist as a con genital anomaly. In these doubtful cases repeated observations must be made. At this stage neuritis is progressive, the swelling and the alterations of the ves sels increasing, while conditions with which it might be confused remain un changed for a long period. Subsiding neuritis, which might also be overlooked, is likely to be attended with impairment of vision, especially with irregular con traction of the field of vision; and with opacity of the nerve-head hiding its deeper details, pigment - disturbances about the disk, and opacity of the walls of the retinal vessels or irregularities in their calibre.
—A mild form of optic neuritis may arise from eye-strain. Syphilis, rheumatism, lead poisoning, Bright's disease, and exten sion of inflammation from adjoining structures may cause it. But the larger number of cases are due to organic dis ease of the brain and its membranes, especially tumor, meningitis, and ab scess. Its connection with intracranial disease has been the subject for much speculation. The principal theories to account for it are: 1. That the inflam mation reaches the nerve-head by direct extension from within the cranium, either through the nerve-trunk or along its sheath. 2. That the inflammation is due to "choking of the disk" by intra cranial pressure, transmitted by the veins or the lymph-spaces around the nerve to its point of entrance into the eyeball, where the sheath of the nerve is usually found dilated. 3. That the inflammation of the nerve-head arises through a nerve-influence controlling its nutrition and originating in afferent nerves distributed to the cerebral me ninges. 4. That toxic substances make their way along the lymph-spaces sur rounding the optic nerve from the cranial cavity to the nerve-head, where they excite inflammation. Neither of these theories seems consistent with all the facts, and it is probable that vari ous influences contribute to the result. Relief of intracranial pressure is often followed by improvement in the neuritis, and Deyl suggests that the pressure may act by "choking" the central retinal artery and vein where they enter the optic nerve back of the eye.