NATURAL COURSE OF HOMONYMOUS VISUAL FIELD DEFECTS AS A FUNCTION OF LESION LOCATION, PATHOGENESIS AND SCOTOMA EXTENT

M. BAUR,1 E. ROHLFS,1 G. MAGNUSSON,1 R. BURTH,1 R. VONTHEIN2 and U. SCHIEFER1

1Department of Neuro-Ophthalmology, University Eye Hospital; 2Department of Medical Biometry, University of Tübingen; Tübingen, Germany

Introduction

Hemianopia does not always represent absolute and permanent visual loss – sometimes visual function improves spontaneously.1,2

Purpose

In this study, our aim was to describe the natural course of homonymous visual field defects over time and to determine the influence of underlying pathogenesis, location of the lesion, scotoma pattern, patient’s age, and eccentricity of affected test points3-6 on spontaneous recovery.

Patients and methods

We screened the perimetry database of the department for 30° visual field data, recorded between January 1997 and November 2000, obtained with automated threshold oriented slightly supraliminal white-on-white static grid perimetry using the Tübingen Automated Perimeter (TAP).

We analyzed visual field examinations of 65 patients, 36 males and 29 females, aged between 14 and 85 years, recorded within one year of the initial examination (Fig. 1).

Homonymous visual field defects were caused by vascular lesions (37 cases), tumors (eight cases), inflammation (five cases), and other causes (15 cases), e.g., trauma,

Address for correspondence: Matthias Baur, MD, University Eye Hospital, Department of NeuroOphthalmology, Schleichstrasse 12-16, 72076 Tübingen, Germany. Email: matthias.baur@gmx.net

Perimetry Update 2002/2003, pp. 365–370

Proceedings of the XVth International Perimetric Society Meeting, Stratford-upon-Avon, England, June 26–29, 2002

edited by David B. Henson and Michael Wall

© 2004 Kugler Publications, The Hague, The Netherlands

Fig. 1. Age distribution divided by gender.

surgery, or no lesion found. Thirty-three lesions were located in the occipital cortex, 19 in the optic radiation, and 13 in other locations, e.g., LGN, tract. The proportion of vascular lesions increases in the posterior portions of the visual pathway (Fig. 2). We found 21 hemianopias, 23 large sector scotomas (greater than one quadrant), eight quadrantanopias, and 13 small sector scotomas (smaller than one quadrant).

We used a multiple logistic regression model to estimate the odds of a test point being seen versus an absolute defect, regarding the following factors: pathogenesis, location of the lesion, scotoma pattern, patient’s age, eccentricity of affected test points – and interactions between these factors.

Results

The probability of a test point being seen versus not being seen is about the same for lesions in both the occipital cortex and the optic radiation (Fig. 3). Visual field defects due to a lesion in ‘another location’ start with a lower probability and show a steeper increase over time but do not reach the level of those in the occipital cortex or optic radiations.

With regard to pathogenesis, the course of the probability is very similar in visual field defects resulting from a vascular lesion or a tumor, although the tumor group starts worse and stays worse (Fig. 4). The ‘other causes’ show a steep increase.

When looking at different scotoma patterns, the probability of a test point being seen versus an absolute defect improves a little over time in hemianopias and large sector scotomas, whereas in small sector scotomas, and especially in quadrantanopias, the probability gets worse (Fig. 5).

Looking at the upper and lower part of the visual field, the course of the probabili-

Fig. 2. Distribution of different pathogeneses depending on the location of the lesion.

Fig. 3. Course of the probability of a test point being seen versus not being seen in homonymous visual field defects comparing different locations of the causative lesion.

ties is rather similar, ending up at the same level, although the upper half starts slightly worse (Fig. 6).

In young patients, the increase of the probability of a test point being seen versus an absolute defect is quite distinct, whereas it becomes more gentle with increasing age until there are no changes at all in patients older than about 70 years of age (Fig. 7). This is true of homonymous visual field defects due to a lesion in the occipital cortex or in the optic radiation.

With regard to eccentricity, the probability of a test point being seen versus not

Fig. 4. Course of the probability of a test point being seen versus not being seen in homonymous visual field defects comparing different underlying pathogeneses.

Fig. 5. Course of the probability of a test point being seen versus not being seen in homonymous visual field defects comparing different scotoma patterns.

being seen rises more steeply in eccentricities >10° than in the central visual field over a time period of one year, but as it is already initially higher in the central visual field, probabilities remain higher in the center (Fig. 8). We found this for all locations, but most obviously in visual field defects resulting from a lesion in the occipital cortex.

→

Fig. 8. Course of the probability of a test point being seen versus not being seen in homonymous visual field defects (due to lesions in the occipital cortex) depending on the eccentricity of the test point. The probabilities are again color-coded – the lighter the gray, the higher the probability.

Fig. 6. Course of the probability of a test point being seen versus not being seen depending on the test point location being in either the upper or lower half of the visual field.

Fig. 7. Course of the probability of a test point being seen versus not being seen in homonymous visual field defects (due to lesions in the occipital cortex) depending on patients’ age. The probabilities are color-coded – the lighter the gray, the higher the probability.

Conclusions

The chances of the recovery of a homonymous visual field defect are more likely in the central visual field than in the periphery. With increasing age, the chances of recovery decline; this effect is more profound in homonymous visual field defects resulting from a lesion in the occipital cortex than from a lesion in other parts of the postchiasmal visual pathway.

References

1.Pambakian ALM, Kennard C: Can visual function be restored in patients with homonymous hemianopia? Br J Ophthalmol 81:324-328, 1997

2.Zihl J, Von Cramon D: Visual field recovery from scotoma in patients with postgeniculate damage: a review of 55 cases. Brain 108:335-365, 1985

3.Fujino T, Kigazawa K, Yamada R: Homonymous hemianopia: a retrospective study of 140 cases. Neuro-Ophthalmology 6:17-21, 1986

4.Trobe JD, Lorber ML, Schlezinger NS: Isolated homonymous hemianopia: a review of 104 cases. Arch Ophthalmol 89:377-381, 1973

5.Huber A: Homonymous hemianopia. Neuro-Ophthalmology 12:351-366, 1992

6.Smith JL: Homonymous hemianopia: a review of one hundred cases. Am J Ophthalmol 54:616-623, 1962