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Ординатура / Офтальмология / Учебные материалы / Uveitis Text and Imaging Text and Imaging Text and Imaging 2009

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Figure 13G3: Birdshot chorioretinopathy. ICGA after discontinuation of immunosuppression. No recrudescence of choroiditis was seen

Figure 13H: Birdshot chorioretinopathy. Visual field 5 months after reintroduction of immunosuppressive therapy (azathioprin) showing again recovery of a quasi normal visual field

include enlargement of the blind spot. Typically, the scotomata increase in size within days to weeks, although progression of visual field defects has been

Figure 14: A 30-year-old woman presented with rapid loss of peripheral field in the left eye 15 months prior (AZOOR). (A) Fundus photograph of the left eye showing extensive pigment change in inferior fundus. (B) Incomplete superior arcuate defect with enlarged blind spot corresponding to fundus changes

documented up to 6 months after the onset of symptoms.24

In the acute annular outer retinopathy variant of AZOOR, photopsia may not be a presenting symptom. In the first published case, the patient experienced sudden onset of a scotoma. A circular ring of graywhite retinal opacification was seen in the superotemporal fundus of the left eye, with narrowing of the retinal vessels within the ring.25

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TOXOPLASMOSIC RETINOCHOROIDITIS

Visual field loss arising as a result of toxoplasma retinochoroiditis, particularly when the focus of inflammation is within one disc diameter of the optic disc is poorly documented in the literature. In a retrospective consecutive case series, Schlaegel26 reported the Goldmann field findings in 60 eyes; 35 percent showed a field defect within 5° of fixation, with 27 percent being paracentral (from 6° to 13°), and 38 percent being peripheral. Analysis of whether the field defect was absolute or relative or whether it broke out to the periphery was not reported, and many of the eyes had active uveitis at the time of inclusion.

Stanford and coworkers27 showed that absolute field defects were seen in 31 eyes. In approximately half of these there was breakout to the periphery, but in the other half the field defect remained localised to correspond to the area of the scar. There was no difference in the size of the scar with respect to whether defects were absolute or relative; however, absolute defects occurred when the scar was close to the optic nerve head. As might be expected the average mean defect was more important for absolute compared to relative defects. Almost all (9/10) scars within one disc diameter of the optic nerve head gave rise to absolute defects with breakout to the periphery (Figures 15A and B).

ACUTE MACULAR NEURORETINOPATHY (AMN)

Acute macular neuroretinopathy (AMNR) is a rare condition first described in 1975 by Bos and Deutman.28 It is characterized by a sudden mild central vision loss, photopsia and red-brown wedge-shaped lesions in the macular region with corresponding scotoma in the central visual fields. The condition may be associated with the use of oral contraceptives or with a recent febrile illness. Patients with AMN generally present with either unilateral or bilateral disturbance or loss of central vision and/or acute central or paracentral scotoma (Figure 16). These visual field (VF) defects correspond to petaloid macular lesions, best seen with red-free or infrared (IR) light.29

NEURORETINITIS

Perimetry most often reveals a central or cecocentral scotoma, but other “optic nerve-type” field defects

Figure 15: Toxoplasmic retinochoroiditis.27 Color fundus photograph of the right eye (A) showing the area of retina with old toxoplasma scars. FASTPAC Humphrey 24/2 visual field

(B) showing an absolute defect with breakout to the periphery

may occur, including arcuate and altitudinal defects or generalized constriction.30,31

COMPLICATIONS OF UVEITIS

Visual field examination is useful to detect some complications of uveitis. Amsler grid may show metamorphopsia in patients with cystoid macular edema (Figure 17), subretinal fluid in association with choroidal neovascular membrane (Figure 18) or

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Figure 16: Acute macular neuroretinopathy.29 (A) Humphrey automated VF (AVF) 10–2 TT shows U- shaped paracentral Scotoma. (B) Color fundus photograph shows brown petaloid macular lesions best seen on red-free (C) and IR images (D)

Figure 17: Late phase fluorescein angiogram (A) shows cystoids macular. Amsler grid (B) shows metamorphopsia

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Figure 18: Ocular histoplasmosis. Fundus photograph (A) shows juxtapapillary choroidal neovascularization with subretinal fluid extending under the fovea in a patient with ocular histoplasmosis. Amsler grid (B) shows Dark or gray area corresponding to a positive scotoma

exudative macular detachment in Vogt-Koyanagi- Harada (VKH) disease (Figure 19), and sympathetic ophthalmia. Central or cecocentral scotomas are seen as dark areas (positive scotomas) in patients with optic neuritis or with retinal vascular occlusions (Figures 20 and 21).

The Humphrey visual field is useful in various uveitides including those associated with retinal

Figure 19: Vogt-Kyanagi-Harada disease. Fluorescein angiogram (A) shows multifocal serous retinal detachment, Goldmann perimetry (B) shows cecocentral scotoma and constriction of isopters

vasculitis as in Behcet’s disease,32,33 Toxoplasma retinitis and serpiginous choroiditis with associated branch retinal vein or artery occlusions,34 ischemic optic neuropathy as in herpes zoster35 and in Rickettsia conorii infection,36 inflammatory bowel disease,37 syphilis,38 acute posterior multifocal placoid pigment epitheliopathy,39 infiltrative disorders of the optic nerve as in sarcoidosis.

SUMMARY: DISORDERS WITH VISUAL FIELD DEFECTS

1.Acute idiopathic blind spot enlargement (AIBSE)

2.Multiple evanescent white dot syndrome (MEWDS)

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Figure 20: Behcet’s disease. Left eye of a 46-year-old Caucasian male with Behcet’s disease showing an infarct in the papillo-macular bundle (A) and corresponding Amsler grid

(B)

3.Multifocal choroiditis (and panuveitis) (MFC)

4.Serpiginous choroiditis

5.Birdshot chorioretinopathy (BC)

6.Acute retinal pigment epitheliitis (ARPE)

7.Punctate inner choroidopathy (PIC)

8.Subretinal fibrosis and uveitis syndrome (SFU)

Figure 21: Rickettsia conorii infection. Color fundus photograph (A) shows branch retinal artery occlusion. Goldmann perimetry (B) shows paracentral scotoma corresponding to the white macular lesion

9.Acute zonal occult outer retinopathy (AZOOR) and acute annular outer retinopathy

10.Toxoplasmic retinochoroiditis

11.Acute macular neuroretinopathy (AMN)

12.Diffuse unilateral subacute neuroretinopathy – late stage (DUSN)28

13.Complications of uveitis:

a.Optic neuropathy:

Multiple sclerosis with intermediate uveitis and optic neuritis

Sarcoid optic nerve granulomas

Ischemic optic neuropathy with inflammatory bowel disease or infectious disease

b.Cystoid macular edema

c.Choroidal neovascularization

d.Exsudative macular detachment

e.Retinal vascular occlusions

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REFERENCES

1.Tasman W, Jaeger EA. Duane’s Ophthalmology. The ultimate reference for residents. Philadelphia, Lippincott Williams and Wilkins, 2006.

2.Traquair HM. Introduction to clinical perimetry. London, Kimpton 1927.

3.Anderson DR. Perimetry with and without automation. 2nd ed. St Louis: CV Mosby Co., 1987.

4.Armaly MF. The size and location of the normal blind spot. Arch Ophthalmol 1969;81:192-201.

5.Scott GI. Traquair’s clinical perimetry. St Louis, 7th ed. CV Mosby Co., 1957.

6.Harrington DO, Drake MV. The visual fields. A text book and atlas of clinical perimetry. St Louis, 6th ed. CV Mosby Co., 1990.

7.Barton JS, Benatar M. Field of vision: A Manual and Atlas of Perimetry. New Jersey, Humana Press, 2003.

8.Sit AJ, Medeiros FA, Weinreb RN. Short-wavelength automated perimetry can predict glaucomatous standard visual field loss by ten years. Semin Ophthalmol 2004;19:122-4.

9.Siy Uy H, Sha Chan P. Multiple evanescent white dot syndrome. In: Foster CS, Vitale AT, (Eds): Diagnosis and treatment of uveitis. Philadelphia, WB Saunders Co., 2002, 767-71.

10.Singh K, de Frank MP, Shults WT, Watzke RC. Acute idiopathic blind spot enlargement. A spectrum of disease. Ophthalmology 1991;98:497-502.

11.Volpe NJ, Rizzo JF, Lessell S. Acute Idiopathic Blind Spot Enlargement Syndrome: A Review of 27 New Cases. Arch Ophthalmol 2001;119(11):59-63.

12.Khorram KD, Jampol LM, Rosenberg MA. Blind spot enlargement as a manifestation of multifocal choroiditis. Arch Ophthalmol 1991;109:1403-7.

13.Reddy CV, Brown J Jr, Folk JC, et al. Enlarged blind spots in chorioretinal inflammatory disorders. Ophthalmology 1996;103:606-17.

14.Brown JJr, Folk JC. Multifocal choroiditis, punctuate inner choroidopathy, and other related conditions. In Guyer DR, Yanuzzi LA, Chang S, et al (Eds): Retina, Vitreous, Macula. Vol. 1. Philadelphia, WB Saunders Co., 1999;614-30.

15.Chisholm IH, Gass JD, Hutton WL. The late stage of serpiginous (geographic) choroiditis. Am J Ophthalmol 1976;82:343-51.

16.Weiss H, Annesley WH Jr, Shields JA, et al. The clinical course of serpiginous choroidopathy. Am J Ophthalmol 1979;87:133-42.

17.Gordon LK, Monnet D, Holland GN, et al. Longitudinal cohort study of patients with birdshot chorioretinopathy. IV. Visual field results at baseline. Am J Ophthalmol 2007; 144(6):829-37.

18.De Courten C, Herbort CP. Potential role of computerized visual field testing for the appraisal and follow-up of birdshot chorioretinopathy. Arch Ophthalmol 1998; 116:1389-91.

19.Thorne JE, Jabs DA, Kedhar SR, et al. Loss of visual field among patients with birdshot chorioretinopathy. Am J Ophthalmol 2008;145:23-8.

20.Krill AE, Deutman AF. Acute retinal pigment epitheliitis. Am J Ophthalmol 1972;74:193-205.

21.Park CH, Raizman MB. Punctate inner choroidopathy. In: Foster CS, Vitale AT, (Eds): Diagnosis and treatment of uveitis. Philadelphia, WB Saunders Co., 2002,806-12.

22.Rojas B. Subretinal fibrosis and uveitis syndrome. In: Foster CS, Vitale AT, (Eds): Diagnosis and treatment of uveitis. Philadelphia, WB Saunders Co., 2002;797-805.

23.Palestine AG, Nussenblatt RB, Chan CC, et al. Histopathology of the subretinal fibrosis and uveitis syndrome. Ophthalmology 1985;92:838-44.

24.Wu H. Acute zonal occult outer retinopathy. In: Foster CS, Vitale AT, (Eds): Diagnosis and treatment of uveitis. Philadelphia, WB Saunders Co., 2002;813-6.

25.Gass JD, Stern C. Acute annular outer retinopathy as a variant of acute zonal occult outer retinopathy. Am J Ophthalmol 1995;119:330-4.

26.Schalagel TF Jr, Weber JC. The macula in ocular toxoplasmosis. Arch Ophthalmol 1984;102:1153-5.

27.Stanford MR, Tomlin EA, Comyn O, et al. The visual field in toxoplasmic retinochoroiditis. Br J Ophthalmol. 2005; 89:812-4.

28.Bos PJ, Deutman AF. Acute macular neuroretinopathy. Am J Ophthalmol 1975;80:573-84.

29.Corver HD, Ruys J, Kestelyn-Stevens AM, et al. Two cases of acute macular neuroretinopathy. Eye 2007;21:1226-9.

30.Lee AG, Brazis PW. Clinical Pathways in NeuroOphthalmology: An Evidence-Based Approach. New York, 2nd ed. Thieme 2003;63-72.

31.Gass JD, Scelfo R. Diffuse unilateral subacute neuroretinitis. J R Soc Med 1978;71(2):95-111.

32.Garcher C, Bielefeld P, Desvaux C, et al. Bilateral loss of vision and macular ischemia related to Behcet disease. Am J Ophthalmol 1997;124:116-7.

33.Scouras J, Koutroumanos J. Ischaemic optic neuropathy in Behcet’s syndrome. Ophthalmologica 1976;173:11-8.

34.Haefliger E, Muller O. Branch artery occlusion due to focal necrotizing retinitis probably caused by toxoplasmosis. Klin Monatsbl Augenheilkd. 1980;176:613-8.

35.Borruat FX, Herbort CP. Herpes zoster ophthalmicus. Anterior ischemic optic neuropathy and acyclovir. J Clin Neuroophthalmol 1992;12:37-40.

36.Khairallah M, Zaouali S, Ben Yahia S, et al. Anterior ischemic optic neuropathy associated with Rickettsia conorii infection. J Neuroophthalmol 2005;25:212-4.

37.Heuer DK, Gager WE, Reeser FH. Ischemic optic neuropathy associated with Crohn’s disease. J Clin Neuroophthalmol 1982;2:175-81.

38.Belin MW, Baltch AL, Hay PB. Secondary syphilitic uveitis. Am J Ophthalmol 1981;92(2):210-4.

39.Kirkham TH, Ffytche TJ, Sanders MD. Placoid pigment epitheliopathy with retinal vasculitis and papillitis. Br J Ophthalmol 1972;56:875-80.

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B. Microperimetry in Inflammatory

Chorioretinal Diseases

Edoardo Midena, Elisabetta Pilotto

INTRODUCTION

Fundus-perimetry (or fundus-related perimetry) is the diagnostic technique which allows to exactly correlate, in real time, the sensitivity threshold of any individual point of the retina with the ophthalmoscopic aspect of the same point. It also documents the location and stability of fixation. Fundus-perimetry is also, and probably better, known as microperimetry, a term introduced when scanning laser ophthalmoscope (SLO) allowed, for the first time, to easily and reliably document the above mentioned correlation. In this chapter, the term microperimetry is used as a synonym of the more precise fundus perimetry, because it is better known among both clinics and researches.

Fundus perimeters are designed to provide a direct correlation between retinal sensitivity threshold and retinal lesions. An ideal device should provide: visualization of the stimulus location on the fundus image, a range of different stimuli and visual targets, and an objective mean of recording fundus image and sensitivity threshold.

The earliest fundus perimeter was a modified direct ophthalmoscope (Visuscope, Oculus), with a cross in the middle of illuminated field, to be used as fixation target. The central cross is clearly projected onto the retina when the fundus is brought into focus. The cross, moved over the fundus, is used to “macroscopically” determine the function of a given retinal area, simply asking the patient if he sees or not the central cross.1 The aiming beam of an argon laser photocoagulator was also proposed as a useful tool to test the function of discrete retinal areas. Using a biomicroscopy contact lens, the area of the retina stimulated by the aiming beam can be directly observed and the examined subject is asked to report if he sees or not the projected laser beam.2 Beside ocular hazards related to the use of a laser beam to test retinal function, the major limitations of the this device were: elevated brightness of both retinal illumination (to allow fundus examination) and stimulating

aiming beam, and fixed size and shape of the retinal stimulus. Moreover, with both previoulsy mentioned techniques recording of the location of the stimulus is performed separately, using a fundus camera.

Different types of fundus cameras have been also proposed to record simultaneously fundus image and stimulus location directly.3,4 This technique was again mainly limited by the high luminance levels required by a conventional fundus camera, a limitation overwhelmed only by the introduction of infrared (IR) fundus camera.5-9 IR illumination allows minimal, if any, retinal stimulation while offering enough irradiance to obtain a fundus image. However, these instruments still had several defects: first, image quality was poor because of the lack of contrast using IR illumination and conventional optics; second, there was not direct digital interface with a computer, making analyses of results a time-consuming procedure. Calibration and standardization were difficult and finally, only a limited range of stimuli and background intensities were available.

The introduction of scanning laser ophthalmoscope (SLO) fundus-perimetry completely modified not only the imaging documentation of macular disorders, but also the functional one. For the first time, the exact site of fixation (and its stability) and the sensitivity of selected retinal areas (under real-time fundus control) were determined.10-13 SLO microperimetry allowed to: investigate macular function, relating it exactly to macular morphology; monitor the (functional) natural history of macular disorders, and quantify the beneficial or detrimental effects of any local or systemic treatment on macular function.14-20 But, SLO microperimetry did not allow for fully automatic examinations and follow-up. Moreover, SLO microperimeter never underwent a real technological (hardware and software) improvement. SLO microperimeter is no more commercially available.

Recently, a new fully automatic microperimeter (fundus-perimeter) has been introduced into clinical practice (Micro Perimeter 1, MP1, Nidek, Japan).21,22

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This instrument allows for a fast, reliable functional fundus-related examination of fixation and scotoma characteristics in patients affected by retinal and choroidal diseases, with topographic accuracy and test–retest reliability, even when visual acuity is poor and fixation is unstable and eccentric.23 Threshold values with the Micro Perimeter 1 are reproducible, but comparison with Octopus perimetry is controversial.24 The development of MP1 microperimeter has dramatically expanded the application microperimetry in clinical practice, providing relevant information on functional changes in several macular and extramacular disorders.25-28

MP1 MICROPERIMETER

MP1 microperimeter performs automatic fundus perimetry, using an electronic eye tracking system for automatic correction of eye movements, and allows precise automatic follow-up examinations irrespective of baseline fixation. The following specifications refer to the MP1-Professional (fundus) microperimeter (Figure 1). MP1 microperimeter consists of: main hardware including projection and acquisition system; desktop PC elaborating data and results, and dedicated software.

ACQUISITION SYSTEM

An infrared light is generated by an infrared (IR) source and is conveyed to the retina of the examined eye. The retinal image is then acquired by a black and

Figure 1: Microperimeter MP1 (Nidek, Japan)

white IR CCD camera (resolution 768 × 576 pixels) at 25 Hz (1 image every 40 ms). The system is also equipped with a color fundus camera (which may be also used independently as a non mydriatic fundus camera) which is used to acquire fundus color images at a resolution of 1392 × 1040 pixels. The field of view of the instrument is 45 degrees. The operator is assisted in maintaining a correct working distance by Purkinje bright spots created by infrared rays reflected onto the cornea. The working distance (from the camera lens to the examined eye) is set at 47.1 mm. The instrument has a correcting system for refractive errors, ranging from -12.5 to +16 diopters.

PROJECTION SYSTEM

An internal liquid crystal display (6.5" LCD, 640 x 480 pixels) acts as projection system, this is the reason why this technique has been named liquid crystal display microperimetry. The projecting images are optically conjugated with the IR camera CCD sensor. The optical conjugation between the displayed pattern and the acquired fundus image brings to a 1:1 relationship between a given point of the projection plane and a certain point of the retina, imaged through the CCD. Any pattern that can be produced by the computer and displayed on its video monitor can also be displayed simultaneously in the MP1 liquid crystal display.

PRELIMINARY STEPS

MP1 microperimetry is a mesopic test, and each tested eye should undergo a short time (5 to 10 minutes) adaptation before beginning the examination, assuming no prior exposure to bright sun or fundus photography, which needs longer adaptation. Main room lights should be off, with room illumination close to that of the stimulus screen. The operator should know uncorrected and best corrected visual acuity, and refractive error of subject under examination.

MICROPERIMETRY TEST

The patient should sit comfortably in front of the instrument. The not tested eye is patched. The patient is asked to fixate on the previously selected target inside the instrument. The operator performs the alignment phase with the IR camera that displays fundus details in real time. Microperimetry, when

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performed by an expert examiner, can be done through a pupil as small as 3 mm in diameter, and this is particularly useful in patients where mydriasis is contraindicated. Notwithstanding, a 4 mm pupil diameter is recommended in order to achieve both an ideal image and high test quality . However, mydriasis does not significantly influence test results. Each stimulus consists of a short presentation of a selected luminance test in the LCD background. The patient reports the perception of a stimulus by pushing a button. This signal is counted as a ‘seen’ stimulus. The absence of signal is a ‘not seen’ stimulus. Light stimuli range from 0 to 20 dB, on a 1 dB step scale. The reduction of differential light threshold is reported as dense (or absolute) scotoma when stimuli are not seen at the brightest stimulus intensity (0 dB). The tested area which shows a reduced differential light threshold, compared to age-relate normal theshold, is recorderd as relative scotoma. At the end (or at the beginning) of the examination, the operator can acquire a color fundus photograph. This image is then aligned with the IR reference frame (using an electronic dedicated procedure), so that functional results (fixation area and sensitivity map) are overlapped automatically onto the color fundus image. This represents a relevant advantage for the clinicians who can directly compare functional data with colored fundus details, compared to SLO microperimeter where comparison was possible only with IR (black and white) fundus image.16

AUTOMATED TRACKING SYSTEM

The MP1 software contains an automatic tracking system of eye movements. This system evaluates in each acquired frame the X and Y shifts of the fundus details compared to a baseline reference frame and continuously corrects stimulus location according to the current fundus position. This is performed in real time during the acquisition: the time for frame tracking is less than the time between two consecutive frames (25 Hz). The algorithm is based on the application of a normalized greyscale correlation technique inside a region of interest (ROI) of 128 × 128 pixels. Tracked images are acquired only by the IR camera. This system has a mean tracking accuracy of 0.08 degrees (4.9 arc minutes), with a maximum of 0.21 deg (12.8 arc minutes) along the horizontal axis, and 0.08 deg

(4.9 arc minutes) with a maximum of 0.21 deg (12.4 arc minutes) along the vertical axis.

To achieve a satisfying contrast between details within ROI, which is necessary for the tracking system, higher levels of infrared illumination than the default level has to be used. This may cause a reduction of the IR image quality used during the examination.

BACKGROUND

According to the manufacturer, the LCD background may be varied: monochromatic of given color, white, red or full white (for reading test). Compared to conventional white-on-white perimetry, the standard background used for microperimetry is a white background with luminance set at 1.27 cd/m2 (= 4 asb).

FIXATION TARGET

The software offers different choices for the fixation target: size and shape may be varied according to the patient’s visual acuity and macular functional and anatomical characteristics. The most frequently used fixation target is a single cross (Figure 2). It may be varied in size (1°-20°), thickness and color. The standard cross is red and set at 100 asb in luminance. The single full cross is also suggested in subjects with central scotoma involving the fovea, but who have developed a preferred retinal locus (PRL) and a relative stable fixation. To increase test accuracy, it’s possible to use the four crosses or a ring as paracentral fixation target (Figure 3). Thus, subjects with relatively

Figure 2: A single cross used as a target in MP1 microperimetry

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Figure 3: A ring used as a target in MP1 Microperimetry

unstable fixation and without a preferred retinal locus are facilitated to maintain their fixation onto the center as stable as possible. The four crosses target is used as paracentral fixation target (similar to that used in SLO microperimetry) in subjects with recent macular scotoma involving the fovea and without a stable PRL. The patient is asked to gaze at the (ideal) center of the four crosses. This paracentral target presents a major limitation: one or more crosses may disappear during examination because they are projected onto the macular scotoma. And patient’s fixation movements may become wider and fixation profile irregular. The four crosses may be customized in size (1°-20°), thickness, distance (0°-20°) and color. The standard four crosses are red and set at 100 asb in luminance. The ring target is also used as an alternative paracentral fixation target in subjects with recent macular scotoma involving the fovea and without an eccentric PRL. Compared to the four crosses, even if the ring may be partly involved in the macular scotoma it commonly maintains a more stable fixation by the filling-in phenomenon. The ring may be integrated by four straight lines crossing the ring at selected points and pointing toward the center of fixation. We suggest to use a small ring (1 deg or 0.5 deg) when the clinician is interested in evaluating foveal differential light threshold without any target interference, as by the central cross. The ring may be customized in radius (0.5°-20°), thickness and color. The standard ring is red and set at 100 asb in luminance.

STIMULI

Stimulus intensity may be varied in 1 dB steps (0.1 log steps) between 0 dB and 20 dB. 0 dB (400 asb, 127 cd/ m2) represents the instrument’s maximum stimulus luminance, and 20 dB (4 asb, 1.27 cd/m2) the minimum stimulus luminance. The stimulus size may be varied according to Goldmann stimulus standard: from size I to V ( from 6.5 to 104 min/arc). Many investigators have focused their attention on the influence of stimulus variables on perimetric threshold values, whereas the influence of stimulus variables on perimetric resolution power has been less emphasized. The influence of stimulus size on microperimetric resolution power is important because microperimetry is frequently used in detecting tiny scotomas in the central visual field (i.e macular holes and pseudoholes).

The blind spot normally subtends approximately 5° horizontally and 7.5° vertically in the visual field. There is only a slight difference in the delimitation of the blind spot between Goldmann stimulus size I and II. This is probably due to the small diameter of these stimuli. For Goldmann III stimulus size, however, smoothing of the borders of the blind spot occurs.29 Goldmann III stimulus size is the most commonly used target size in standard automated perimeters and in SLO microperimeter, and also in MP1 microperimetry, because of its higher reliability from a topographic point of view. Normal database of MP1 microperimetry have been collected using this target size. Goldmann I stimulus size may be used in detecting and delineating very small scotomas, such as those due to macular hole. Stimulus shape (even figures, etc.) may be also customized according to the examiner’s choice.

The duration of each stimulus may be varied from 100 ms to 2000 ms. Because the maximum time over which temporal summation can occur in normal eyes is supposed to be completed at 100 ms (Bloch law) , the most used presentation time is between 100 and 200 ms. Differential light threshold values with the MP1 do not change irrespective to 100 ms and 200 ms stimulus time presentation.

THRESHOLD STRATEGIES

According to the clinical situation, several standard psychophysical threshold strategies are available: