According to Foerster, temporal hemianopia always develops slowly without any concomitant paralytic symptoms: it does not have constant boundaries, and is now progressive and again retrogressive. He cites cases which he has observed for years where at first small negative scotoma appeared just outside of the fixation-point, and increased till there was a total loss of the temporal fields. The line of division between the blind and seeing sides of the field of vision is not sharply defined and not accurately vertical. In some cases there is a gradual invasion of the sound side. Although it is usually assumed that some pressure in the anterior or in the posterior angle of the chiasm is the cause, yet the writer does not know of any post-mortem examination of a case. Mauthner205 gives short histories of 23 cases of temporal hemianopia, besides 11 cases relating to nasal hemianopia (or, according to his classification, hemianopia heteronyma medialis) from various authors, in most of which the ophthalmoscope showed either the presence of a neuritis or an atrophy of the nerve. There were two autopsies in the cases of nasal hemianopia related by Mauthner—those of Schule and Knapp—one of which showed an enlargement of the third ventricle and infundibulum, with atrophy of the nerves, and the other a high degree of ætheromatous degeneration of arteries at the base of the brain. Any cause which would produce simultaneous pressure on the outer angles of the commissure would give rise to nasal hemianopia. Little is known regarding hemianopia above or below the horizontal line: both Mackenzie and Graefe mention its occurrence, and Knapp, Schoen, and Mauthner give interesting cases. The writer has seen a case in a woman of fifty-five years otherwise apparently in good health. The upper part of each field was wanting, and the line of division ran slightly above the fixation-point, it being nearly horizontal. The optic nerves did not present any marked departure from their normal appearance, and central vision was fair (20/x1). The only autopsy of a case of superior hemianopia with which the writer is familiar is that reported by Russell,206 in which there was a tumor involving the bones of the base of the cranium. The patient had upper hemianopia, confined to the right eye, followed by total blindness, coming on first in the right and then in the left eye. Genuine binocular hemianopia of the superior or inferior variety is probably produced by some symmetrical affection of the optic nerves between the chiasm and the eyes.
205 Gehirn und Auge, 1881, pp. 373-381.
206 Med. Times and Gazette, No. 47, 1873 (rep. Nagel's Jahresbericht, 1873, p. 361.)
In apparently healthy individuals transient hemianopia is not an unfrequent occurrence, and may either develop with or without other cerebral symptoms. It is usually followed or accompanied by headache, or more rarely by vertigo, tinnitus aurium, difficulty of speech, etc. Even in intelligent patients, who have not been drilled by their medical adviser to carefully analyze their symptoms, it is not recognized as half-vision, but here, as in the permanent variety of the affection, it is described as a dimness or blindness of the eye on the side in which the field of vision is defective. Some cases of transient hemianopia are accompanied by peculiar zigzag flickerings of light in the defective portions of the field of vision, which have given it the name of scotoma scintillans. We are fortunate in having an accurate description of this form of the affection by so competent an observer as Foerster, who has frequently experienced it in his own person. In his case the phenomena last from fifteen to twenty-five minutes, and commence with the appearance of dimness in both eyes, which gradually increases to a defect of the field of vision lying to one side of the fixation-point. This is soon followed by a flickering which commences in a zone around the scotoma, and increases centrifugally until it assumes the form of an arc with the convexity outward, the flickering rarely extending beyond the vertical line which separates the two halves of the field of vision. When it has reached the outer limits of the field, it generally diminishes and fades away. From a consideration of the celebrated case of Wollaston, it is probable that transient hemianopia may be caused by some temporary congestion of a brain tumor, but in the majority of instances it is certainly allied to functional disorders like migraine. Transient hemianopia has been observed in several members of the family of one of the writer's patients, all of whom are subjects of consecutive neuralgic headaches. Leber has observed the same thing. Brewster and Quaglino have attributed it to a retinal anæmia, but a careful ophthalmoscopic examination in two well-marked cases (that of Foerster and one related by Mauthner) failed to show any retinal changes. In some cases the well-marked hemianopic character of the attack speaks for its intracranial origin, which may be temporary derangement of the circulation, possibly in the optic tracts. Dianoux tells us that in his case the attack could be cut short by keeping the head down between the legs. In some of the cases which the writer has seen it may be cut short by a liberal dose of whiskey.
Affections of the Third Pair.
While a few words on the pathology of the third and sixth nerves tend to throw light on our knowledge of cerebral localization, they will also spare a good deal of needless repetition in the detailed discussion of the eye symptoms which accompany many well-marked diseases. Complete paralysis of the third nerve may be caused by pressure on its filaments at the base of the brain without other symptoms. Where it occurs with hemiplegia of the opposite side of the body and other cerebral symptoms, it is usually due to pressure on the nerve where it runs beneath the cerebral peduncle: according to Nothnagel,207 this localization of the disease is still more certain when paralysis of the facial and hypoglossal nerves exists on the same side as the hemiplegia (that is, on the side opposite to the third-pair paralysis). Hughlings-Jackson208 remarks that the symptoms are only positively diagnostic of a lesion in the neighborhood of the peduncle when they appear simultaneously, but when they are concentric to each other they may be due to an affection of the cranium. Ollivier and Little209 have each related a case where this group of symptoms has not originated in any lesion in the peduncle, but has been caused by an abscess of the middle and posterior lobes, which secondarily involved these parts.
207 Topische Diagnostik der Gehirnkrankheiten, p. 198, 1879.
208 In Russell Reynolds's System of Medicine, vol. ii., 1872.
209 Robin, Des Troubles oculaires dans les Maladies de l'Encephale, p. 95.
DOUBLE THIRD-PAIR PARALYSIS.—Double third-pair paralysis is rare, but might be produced by any cause acting on both peduncles. Kohts gives a case where such paralysis was caused by a tumor of the size of a cherrystone limited exactly to the posterior tubercles of the quadrigeminal body. Nothnagel remarks that paralysis of corresponding branches of the third pair point to the corpora quadrigemina as the seat of lesion. On the other hand, Panas210 relates a case of absolute immobility of the eyes where the only demonstrable lesion at the autopsy was a meningo-encephalitis in the lower part of the cerebellum. Robin describes a case of double third-pair paralysis where there were ptosis and dilatation of the pupils, with a loss of all power to move the eyes except downward and outward. The diagnosis was that of an interpeduncular syphilitic gumma: there was complete recovery. In the above case it is interesting to note that while the paralysis of the left eye occurred previous to that of the right, the eye last attacked was the first to regain its motions.