| OCR Text |
Show Journal of Neuro- Ophthalmology 16( 2): 107- 109, 1996. 11996 Lippincott- Raven Publishers, Philadelphia Hemifield Slide Diplopia from Altitudinal Visual Field Defects Mark S. Borchert, M. D., Simmons Lessell, M. D., and William F. Hoyt, M. D. We report two cases in which heteronymous, altitudinal visual field defects resulted in loss of fusion and transient overlap of preserved hemifields. This phenomenon resulted in complaints of diplopia similar to that described as " hemifield" slide previously described by temporal hemianopsias. These cases illustrate that generalized loss of fusion, and not the particular type of hemianopic field defect, is responsible for the symptoms known as hemifield slide. Key Words: Hemifield slide- Diploplia- Visual field defects. Manuscript received April 18, 1995; accepted April 25, 1995. From the Division of Ophthalmology, Childrens Hospital Los Angeles, and Department of Ophthalmology, University of Southern California School of Medicine, Los Angeles, California, U. S. A. ( M. S. B.); Department of Ophthalmology, Massachusetts Ear and Eye Infirmary, Boston, Massachusetts, U. S. A. ( S. L.); and Department of Ophthalmology, University of California San Francisco, San Francisco, California, U. S. A. ( W. F. H.). Address correspondence and reprint requests to Dr. Mark S. Borchert, Division of Ophthalmology, Childrens Hospital Los Angeles, 4650 Sunset Blvd., MS88, Los Angeles, CA 90027, U. S. A. Some patients with bitemporal hemianopias will experience doubling of images along a vertical median strip because of overlap of the two nasal fields ( 1). This phenomenon, designated hemifield slide by Kirkham ( 2), should also occur in patients who have a superior altitudinal visual field defect in one eye and an inferior defect in the other. We have encountered two examples. CASE REPORTS Casel An 81- year- old man, well but for hypertension, underwent bilateral cataract extraction for visual impairment. However, not only was his vision unimproved after surgery, but he also noticed that he had visual field defects in each eye. Since then he had experienced numerous episodes of doubling of images in which the second image was just above the object of regard. He estimated that the objects were separated by about six inches at six feet. Neuro- ophthalmic evaluation five years later showed that his best- corrected Snellen visual acuities were 20/ 200 right eye and 20/ 25 left eye. There was marked dyschromatopsia in the right eye ( Ish-ihara), but the left eye had normal color vision. Tangent screen examination ( Fig. 1) revealed a dense inferior altitudinal defect in the field of the right eye and a dense superior altitudinal defect in the field of the left eye. He was aphakic with full-sector iridectomies. There was no evident defect in lid or ocular motility. Both discs were atrophic. Erythrocyte sedimentation rate, complete blood count, and plain skull radiographs showed no abnormalities. Bilateral nonarteritic anterior ischemic optic neuropathy was the putative diagnosis. 207 108 M. S. BORCHERT ET AL. o. s. O. D. FIG. 1. Tangent screen visual field evaluation at a distance of 2 m reveals dense heteronymous altitudinal field defects to hand movements. Case 2 A 50- year- old man with chronic lymphocytic leukemia had three or four days of blurred peripheral vision in his left eye. An ophthalmologist found no abnormalities on examination. Four months later he noticed painless " clouding" of vision of his left eye. This was followed by a stepwise decline in his visual field over the succeeding two months. When reexamined there was cupping of both optic discs and bilateral visual field defects. Visual function remained stable, but he developed episodic binocular vertical and horizontal doubling of images when viewing distant objects and constant splitting of images with horizontal diplopia in the inferior hemifield while reading. Neuro- ophthalmic examination was conducted nine months after his visual symptoms had begun. His Snellen visual acuity was 20/ 15 right eye and 20/ 25 left eye. There was marked bilateral dyschro-matopsia ( Ishihara). Goldmann perimetry ( Fig. 2) showed a partial inferior altitudinal visual field defect in the right eye. The left eye had only a preserved inferior island of vision with a sharp edge at the horizontal meridian. There was a left relative afferent pupil defect. The only ocular motor abnormality was a small comitant exodeviation at near. Applanation intraocular pressure was 14 mm Hg in each eye. Both discs were pathologically cupped and pale. Magnetic resonance scanning of the brain and orbits gave normal results. The putative diagnosis was normal tension glaucoma. Within eight months the diplopia disappeared with loss of vision in the left eye. DISCUSSION Transient binocular diplopia associated with heteronymous hemianopic field defects without ocular motor paresis was first described in 1929 by Kubie and Beckmann in eight of 41 patients with pituitary tumors ( 3). All of their cases had horizontal diplopia, and one also had vertical diplopia. They attributed the problem to decreased central acuity in one eye and attempted perimacular fixation with that eye. Subsequently, Bardram described the symptom in 15 of 90 similar patients and attributed the problem to central vision loss with secondary divergence ( 4). However, one of his cases had preserved central vision in both eyes. Chamlin et al. noted diplopia without extraocu- 13ft/ X \ . s^^ \ / I K ) / / / \^ yS \ s ^ * t\ wZ / / / pC^ / ^ \ / 10 I 0 I o ^ tfo elo « Io to jfc r JX 5 \ \ \ \ j^< r \ v ^ ^ *) 7i \ \ \ ^ \ \ , x ^ ^ / l / ' \ Js\ \ XX^ s/ 1/ * 3,0 \ \ ^\ Xr^ /^^-~ Y. 220X. ^ K / ^ - - ^ / \ • \ i u y--_ j_ /-^ 9 \ l y^ v \> 9 M 7 \ / \ 1. / \ / ^ \ , / \ \ \ i/ Xs M \ K/ 0\ i\ o B| O a ^ k I \ J S N. / / r-~~\/\ V / \ / a /\ y J^\ y\ o ~ T \ o j \ < D T ( r / 31S l35< j M J- ) T 23 » \ 130 • lo « p ^ ^ IOC 90 / i \/ * / \ J * 0sV / V / * \\ * V ™ * \ T 9 \ 9 \/ i , ^ 1 / 1 i t / jf^ ) T\\/ M \ o A ° T ^ « a / 7D 60 ]>£>^ o in >\° TA^ A30 ^ V\ x V-- A16 la ( 1 1 s J • 9 « 0 U / 1 z348 j f y/ 330 y^ 31B OS. OD. FIG. 2. Goldmann perimetry reveals a partial inferior altitudinal field defect in the right eye. There is a dense superior altitudinal field defect with sparing of an island of vision interiorly in the left eye. J Neuro- Ophthalmol, Vol. 16, No. 2, 1996 HEMIFIELD SLIDE FROM ALTITUDINAL FIELD DEFECTS 109 lar muscle paresis in three of 156 cases of suprasellar tumors ( 5). They also attributed the complaint to central vision loss in one eye and image recognition in noncorresponding points of the preserved paracentral field. In 1968, Elkington described diplopia in 84 of 170 patients with bitemporal hemianopsia without ocular motor paresis ( 6). He was the first to attribute the complaint to " difficulty in accurately registering the image in each eye," rather than parafoveal fixation in one eye. Subsequently, Nachtigaller and Hoyt detailed the sensory phenonomena that occur when separation, overlap, or vertical slip of preserved heteronymous hemifields occurs with minor shifts in ocular alignment ( 1). They described overlap of the preserved nasal hemifields accompanying exotropia resulting in complaints of diplopia only within a central vertical strip. They also described the subjective, vertical, splitting of images that occurs with vertical misalignment of the eyes and consequent misregistration of the preserved hemifields. Later, Kirkham coined the term " hemifield slide" to describe this phenomenon. The mechanism of hemifield slide is uncertain. At issue is whether hemifield slide is due simply to generalized loss of binocular fusion or whether the complete separation of afferents from the two eyes into separate hemispheres, as occurs in chiasmal syndromes, results in a unique propensity for loss of inter ocular alignment. Neither of our cases had substantial overlap of corresponding retinal points despite the fact that patient 2 had considerable preservation of the affected hemifield of one eye. This partial hemifield preservation resulted in horizontal diplopia interiorly along with splitting of images centrally due to an exodeviation while reading. On the other hand, patient 1 had loss of central vision in the right eye along with inferior field loss in that eye. Since his fixation was with the left eye, he presumably experienced hemifield slide as a duplication above the image of regard whenever there was a relative hypotropia of the right eye. These cases suggest that overlap of preserved visual fields, and not a particular type of heteronymous hemianopia, is responsible for reduplication of images in hemifield slide. Both of the patients described in this report had symptoms that could be considered as hemifield slide. However, to our knowledge, these are the first reported cases in which the phenomenon can be attributed to heteronymous altitudinal field defects. We suspect that this relates to the paucity of cases with heteronymous altitudinal field defects rather than the propensity to maintain precise ocular alignment in such cases. In fact/ these were the only two cases of heteronymous altitudinal field defects that could be found in a review of all cases of ischemic optic neuropathy or optic atrophy in the neuro- ophthalmic records of Massachusetts Eye and Ear Infirmary. REFERENCES 1. Nachtigaller VH, Hoyt WF. Storungen des Seheindruckes bei bitemporaler Hemanopsie und Verschiebung der Seh-achsen. Klin Monatsbl Augenheilkd 1970; 156: 821- 36. 2. Kirkham TH. The ocular symptomatology of pituitary tumours. Proc R Soc Med 1972; 65: 517. 3. Kubie LS, Beckmann JW. Diplopia without extra- ocular palsies, caused by heteronymous defects in the visual fields associated with defective macular vision. Brain 1929; 52: 317. 4. Bardram MT. Oculomotor pareses and non- paretic diplopia in pituitary adenomata. Acta Ophthalmol 1949; 27: 225. 5. Chamlin M, Davidoff LM, Feiring EH. Ophthalmologic changes produced by pituitary tumors. Am ] Ophthalmol 1995; 40: 353. 6. Elkington SG. Pituitary adenoma: preoperative symptomatology in a series of 260 patients. Br J Ophthalmol 1968; 52: 322. / Neuro- Ophthalmol, Vol. 16, No. 2, 1996 |
