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Evaluation of stato-kinetic dissociation

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EVALUATION OF STATO-KINETIC DISSOCIATION USING EXAMINER-INDEPENDENT AUTOMATED PERIMETRIC TECHNIQUES

JAN SCHILLER,1 JENS PAETZOLD,1 REINHARD VONTHEIN² and

ULRICH SCHIEFER1

1Department II, University Eye Hospital Tübingen; 2Department of Medical Biometry, University of Tübingen; Tübingen, Germany

Introduction

In 1917, Riddoch1 first described the phenomenon of dissociation in the perception of kinetic and static stimuli. He assumed that this stato-kinetic dissociation (SKD) is limited to lesions of the occipital cortex and that it is a poor prognostic sign if SKD is absent. However, in 1971 Zappia et al.2 showed that the Riddoch phenomenon is neither pathognomonic for occipital lobe or optic radiation lesions, nor does it carry the prognostic significance Riddoch attached to it. Since then several studies have shown that SKD appears in nearly all pathologies affecting the visual pathway, and even in healthy persons.5-11 Safran and Glaser3 suggested that kinetic stimuli are processed by the transient (magnocellular) nerve fibers, while static stimuli are processed by sustained (parvocellular) neural mechanisms. Hence, SKD may reflect greater damage to cells of the parvocellular system than to cells of the magnocellular system,3,4 and evaluation of SKD may lead to a better understanding of any underlying pathology. Therefore, the aim of this study was to develop a semi-automated, almost examiner-independent, procedure for evaluating and quantifying SKD along the border of various visual field defects.

Methods and subjects

Fifteen patients with advanced, stable visual field defects of three different origins (retinitis pigmentosa, glaucoma, and lesions of the posterior pathway) were evaluated with kinetic and static perimetric methods. All examinations were carried out using the Tübingen Computer Campimeter (TCC),12,13 using a high resolution true-color video display unit (Calibrator, Barco Inc., Kortrijk, Belgium). With the help of the

Address for correspondence: Jan Schiller, University Eye Hospital Tübingen, Department II, Schleichstrasse 12–16, D-72076 Tübingen, Germany. Email: janschiller@gmx.de

Perimetry Update 2002/2003, pp. 75–81

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

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Fig.1a. In an initial session, the location of the scotoma border is estimated by conventional manual kinetic and static perimetry. Each rhomb labels a kinetic or static threshold. b. Kinetic vector arrangement. The gray arrows are vectors to evaluate the scotoma border, the black ones are vectors to measure individual response time. c. Static vector arrangement. Each static ‘vector’ consists of five static stimulus locations with an interstimulus distance of 1.5°. d. Results of the automated kinetic examination. Each stimulus was presented six times in random order. Each white dot represents a local kinetic threshold (mean), each black box represents a related parameter for dispersion (SD). Patients’ responses are corrected for mean individual response time. e. Results of the automated static examination. Each stimulus was presented six times in random order. Additionally, 4% false-positive catch trials were presented. Local thresholds were estimated as the position on a vector assuming a probit model. Dispersion was assessed by evaluating the steepness of the ‘frequency-of-seeing curve’ at the position of the static threshold located. f. Scotoma borders evaluated by the automated kinetic (white dots and black broken line) and automated static examination (gray boxes and gray broken line). The arrow marks the reference position from where automated evaluation of SKD is started (see Fig. 2).

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TCC, visual fields can be examined up to 34° eccentricity in the horizontal and up to 25° eccentricity in the vertical meridian. Stimulus characteristics for all examinations

– manual as well as automated perimetry – were an angular stimulus subtense of 26' with a luminance of 110 cd/m² and a background luminance of 10 cd/m².

In an initial session, the border of the scotoma was roughly estimated by manual kinetic and static perimetry (Fig. 1a). In the manual kinetic mode, angular velocity of the stimuli was about 2-3°/sec, and in the static mode, stimulus presentation duration was about 200 msec.

Based on these results, two individually adjusted perimetric sets of vectors were constructed – one for the automated static, the other for the automated kinetic examination. Kinetic vectors were defined by their start and end locations. For each examination, a kinetic set consisted of 16 to 24 vectors (each 6° in length), which started approximately 2-3° within the scotoma and crossed the scotoma border almost perpendicularly. In the kinetic mode, four to eight additional vectors were presented in healthy parts of the visual field in order to estimate the individual response time (Fig. 1b). Each static examination vector (6° in length) consisted of five stimulus locations in a linear arrangement. The distance between two stimulus locations on such a vector was 1.5° (Fig. 1c). The static set of vectors consisted of the same number of vectors as the kinetic set and, in most cases, had the same orientation. (In cases of considerable local SKD, the location of the vectors was modified.) In the subsequent automated examination, each stimulus was presented six times in random order in the kinetic as well as in the static mode.

Patients’ responses on automated kinetic perimetry were corrected for mean individual response time, estimated by the four to eight response time vectors. A ‘local kinetic threshold’ (mean) and a related parameter for dispersion (SD) were assessed (Fig. 1d). During the automated static part of the test, local thresholds were estimated as the position on a vector assuming a probit model. Dispersion was assessed by evaluating the steepness of the ‘frequency-of-seeing curve’ at the position of the static threshold located (Fig. 1e).

Local SKD was evaluated by the distance between automatically estimated kinetic and related static scotoma border (Fig. 1f). SKD was defined as positive when the static scotoma was larger than the kinetic, otherwise it was negative. Individual SKD was quantified along the scotoma border by subdividing each linear connection between two kinetic or two static thresholds into 20 equidistant points. The individual SKD was assessed by estimating the shortest distance between one of these points (e.g., on the connection of two static thresholds) and a corresponding (in this example, kinetic) threshold on the other ‘bank’. This procedure was performed with each point on each scotoma line (Fig. 2).

Results

Figure 3 shows a patient (female; 57 years) with arcuate glaucomatous visual field defects in the upper and lower hemifield, who demonstrated severe visual field loss on routine static perimetry (Tübingen automated perimeter: threshold-oriented, slightly supraliminal automated perimetry, 30° visual field). Examinations with the TCC revealed only moderate SKD with a minimum of -0.1° (local negative SKD) and a maximum of 1.8°.

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Fig. 2. Automated evaluation and visualization of SKD. Each y-value represents the local SKD, each dot (kinetic) or box (static) the position of an estimated threshold. The broken lines are not just connections between these thresholds. Each linear distance between two neighboring thresholds is subdivided into 20 additional locations from where SKD is estimated. The black line shows calculated SKD based on the kinetic scotoma border, while the gray one is based on the static scotoma border. The arrow marks the reference position from where automated evaluation of SKD is begun (see Fig. 1f).

All patients showed various SKDs along the scotoma border. The maximum local positive SKD of all patients examined was 13.5°. Eight patients showed a local negative SKD (maximum -1.2°). Both methods revealed considerable interand intraindividual ‘fluctuations’ along the scotoma border.

Discussion

A major drawback in evaluating SKD has been the need to use two different perimetric devices in order to measure the exact static and kinetic borders. This limits the comparability of results and makes it difficult to quantify the extent of SKD. Furthermore, by using manual kinetic perimetry, several examiner-dependent effects have to be considered, e.g., response times of the patient and examiner, and stimulus velocity.14-17 In addition, in case of manual stimulus presentation, the angular velocity of the stimuli is not constant and the examination result largely depends on the examiner’s skill and experience.

With the method presented here, the above-mentioned disadvantages are avoided. By using the TCC, the examiner has the opportunity to choose the vector location and to ensure that each scotoma border is crossed close to the perpendicular. Each kinetic stimulus is moved with a constant angular velocity.18-21 Moreover, in the automated

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Fig. 3a. Results of conventional static perimetry (Tübingen automated perimeter) in a patient with glaucoma. The gray box marks the region of interest, which is being examined. b. Manual static and kinetic examination with the TCC. c. Results of the automated kinetic examination. d. Results of the automated static examination. e. Kinetic and static scotoma borders. The arrow marks the reference position from where evaluation begins (see Fig. 3f). f. Visualization of SKD. Note: Scaling in this graph is adapted to the individual examination result and may differ from scaling of other SKD visualization graphs!

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kinetic part, thresholds are corrected for mean individual response time.

 

By using the same perimetric device for performing static and kinetic perimetry,

local SKD can be measured and quantified.

 

However, the use of a campimetric device has limited this evaluation to the central

part of the visual field, <34° of eccentricity. The techniques to examine SKD in the peripheral field are in the process of being transferred to the Octopus 101 perimeter (Haag-Streit, Bern, Switzerland). At the present time, this perimeter is the only commercially available ‘full-field’ cupola instrument that enables the transfer of the methods described above.

References

1.Riddoch G: Dissociation of visual perceptions due to occipital injuries, with especial reference to appreciation of movement. Brain 40:15-57, 1917

2.Zappia RJ, Enoch JM, Stamper R, Winkelman JZ, Gay J: The Riddoch phenomenon revealed in nonoccipital lobe lesions. Br J Ophthalmol 55:416-420, 1971

3.Safran AB, Glaser JS: Statokinetic dissociation in lesions of the anterior visual pathways. Arch Ophthalmol 98:291-295, 1980

4.Wedemeyer L, Johnson CA, Keltner JL: Statokinetic dissociation in optic nerve disease. In: Heijl A (ed) Perimetry Update 1988/1989, pp 9-14. Amsterdam/Berkeley/Milano: Kugler & Ghedini Publ 1989

5.Finkelstein JI, Johnson LN: Relative scotoma and statokinetic dissociation (Riddoch’s phenomenon) from occipital lobe dysfunction. Trans Pennsylvania Acad Ophthalmol Otolaryngol 41:789-791, 1989

6.Osako M, Casson EJ, Johnson CA, Huang P, Keltner JL: Statokinetic dissociation: analysis of spatial and temporal characteristics by perimetry. In: Mills RP, Heijl A (eds) Perimetry Update 1990/1991, pp 129-134. Amsterdam/New York: Kugler Publ 1991

7.Katsumori N, Bun J, Shirabe H, Mizokami K: Statokineic dissociation in glaucomatous peripheral visual damage. In: Mills RP, Heijl A (eds) Perimetry Update 1990/1991, pp 503-507. Amsterdam/ New York: Kugler Publ 1991

8.Hudson C, Wild JM: Assessment of physiologic statokinetic dissociation by automated perimetry. Invest Ophthalmol Vis Sci 33(11):3162-3168, 1992

9.Gandolfo E, Rossi F, Ermini D, Zingirian M: Early perimetric diagnosis of glaucoma by stato-kinetic dissociation. In: Mills RP, Wall M (eds) Perimtery Update 1994/95, pp 271-276. Amsterdam/New York: Kugler Publ 1995

10.Gandolfo E: Stato-kinetic dissociation in subjects with normal and abnormal visual fields. Eur J Ophthalmol 6(4):408-414, 1996

11.Krastel H, Auffarth GU, Glaser N, Beitzinger M, Alexandridis E: Häufigkeit und Ausprägung des Riddoch-Phänomens (stato-kinetische Dissoziation) in der Perimetrie bei Netzhaut-, Sehnervund cerebralen Erkrankungen. Ophthalmologe 93(Suppl 1):152, 1996

12.Schiefer U, Stercken-Sorrenti G: Ein neues Rauschfeldkampimeter. Klin Mbl Augenheilk 202:6063, 1993

13.Wabbels B, Schiefer U, Treutwein B, Benda N, Strecken-Sorrenti G: Automated perimetry with bright and dark stimuli. German J Ophthalmol 4:2217-221, 1995

14.Fankhauser F: Kinetische Perimetrie. Ophthalmologica 158:406-418, 1969

15.Schiefer U, Schiller J, Selig B, Dietrich TJ, Flad M, Stumpp F et al: How does reaction time depend on eccentricity and luminance of kinetic targets? A [video-] campimetric study in young normal volunteers. Invest Ophthalmol Vis Sci 40:71, 1999

16.Schiller J, Selig B, Dietrich TJ, Becker ST, Stumpp F, Dietz K et al: Does direction of linear target motion influence reaction time? A campimetric study using automated kinetic stimuli. Invest Ophthalmol Vis Sci 40:845, 1999

17.Schiefer U, Strasburger H, Becker ST, Vonthein R, Dietrich TJ, Schiller J et al: Reaction time in automated kinetic perimetry: effects of stimulus luminance, eccentricity, and movement direction. Vision Res 41(16):2157-2164, 2001

18.Schiefer U, Schiller J, Paetzold J, Dietrich TJ, Vonthein R, Besch D: Evaluation ausgedehnter

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Gesichtsfelddefekte mittels computerassistierter kinetischer Perimetrie. Klin Mbl Augenheilk 218:1320, 2001

19.Schiefer U, Schiller J, Dietrich TJ, Besch D, Paetzold J, Vonthein R: Evaluation of advanced visual field loss with computer-assisted kinetic perimetry. In: Wall M, Mills RP (eds) Perimetry Update 2000/2001, pp 131-136. The Hague: Kugler Publ 2001

20.Goldmann H: Grundlagen exakter Perimetrie. Ophthalmologica 109(2/3):57-70, 1945

21.Goldmann H: Ein selbstregistrierendes Projektionskugelperimeter. Ophthalmologica 109(2/3):7179, 1945

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