238 Loc. cit.

NEURO-PARALYTIC OPHTHALMIA.—In 1822, Herbert Mayo239 showed that section of the fifth nerve within the cranium produces insensibility of the eye; and Charles Bell240 in 1830, while recognizing this fact, maintained that "when that sensibility is destroyed, although the motions of the eyelids remain, they are not made to close the eye, to wash and clear it, and consequently inflammation and destruction of that organ follow." Since that time the subject has been a favorite theme with both clinicians and physiologists, but opinions as to its cause have been a good deal divided. While, perhaps, a majority, with Bell,241 Snellen,242 Kondracki,243 Gudden,244 Senftleben,245 and others, hold that the inflammation of the cornea is of traumatic origin, many writers—amongst whom may be mentioned Longet,246 Graefe,247 Meissner,248 Schiff,249 and Eckhard250—assert that it is caused by the impaired action of the trophic fibres of the nerve; and again others, such as Ferrier,251 Balogh,252 and Buchmann,253 maintain that the inflammation is peripheral, consequent upon the drying of parts of the cornea. Clinically, soon after the occurrence of complete palsy of the trigeminus, there is an interstitial punctate keratitis, which makes the cornea so cloudy that the motions of the iris are with difficulty observed, this being accompanied by conjunctival and ciliary injection. The symptoms, especially where the paralysis is incomplete, are often much alleviated by maintenance of careful closure of the lids and repeated washing of the eye, which protects the enfeebled tissue from the action of foreign bodies. Success is not, however, always obtainable, for occasionally, even with the most complete protection of the eye, eventual sloughing of the cornea cannot be prevented. This is not a usually-accepted doctrine, but the writer is convinced254 of its truth by a case seen within a week of the commencement of the disease, in which the cornea was not yet ulcerated, where the most sedulous care in cleansing the eye and protecting it from external irritants did not prevent the necrosis and perforation of the central part of the cornea. Since then other cases of similar import have been published. Quaglino255 gives an instance where complete ptosis shielded the eye from all gross insults, but where, nevertheless, a central slough of the cornea formed. Laqueur256 also found that the cornea sloughed in spite of the most careful protection. In all other cases where the cornea is exposed to air and external irritants, as in lagophthalmos or excessive exophthalmos, the case is quite different, the consequent inflammation being much better borne. While this is a fact more or less familiar to all clinicians, it is nowhere better shown than in the case of Horner,257 where there was caries of the petrous portion of the temporal bone and complete paralysis of the facial nerve. Two years later the trigeminus was attacked, and then for the first time ulceration occurred in the hitherto sound cornea. Hirschberg258 describes neuroparalytic keratitis and panophthalmitis consequent upon a neurectomy of the infraorbital nerve, and quotes Langenbeck as relating a similar case after section of the supraorbital nerve.

239 Anat. and Physiol. Commentaries, London, 1822, No. 2, p. 5.

240 Nervous System of the Human Body, London, 1830, p. 207.

241 Loc. cit.

242 Virchow's Archiv, Bd. xiii. S. 107, 1850.

243 Nagel's Jahresbericht (Lit. 1873), p. 266.

244 Idem.

245 Virchow's Archiv, Bd. lxv. Heft. 1, pp. 69-99.

246 Anatomie et Physiologie du Système nerveux, t. ii. p. 161, Paris, 1842.