The document provides an overview of electro-diagnostic tests, specifically electroretinography (ERG), electrooculography (EOG), and visual evoked potential (VEP), detailing their physiological bases and recording protocols. It discusses the origins of ERG waveforms, clinical applications for diagnosing retinal disorders, and factors influencing test results. Additionally, it outlines the EOG's method of evaluating retinal function and the VEP's role in assessing visual system functionality beyond the retina.

1. ELECTRO-DIAGNOSTIC TESTS ( ERG, EOG, VER ) Dr. Ankit M. Punjabi DOMS (final year) Dept. of Ophthalmology, KIMS Hospital Bangalore, Karnataka, INDIA Email: drankitalways@gmail.com

2. ERG Electric potential generated by retina in response to stimulation of light. First recorded by Frithiof Holmgren (1865) In humans by Dewar (1877) Extensive work thereafter by Riggs (1941)

3. ERG waves ( a, b, c ) ‘ a’ is negative wave. Amplitude is from baseline to trough & implicit time is from onset of stimulus to trough of ‘a’ wave ‘ b’ is large positive wave. Amplitude is trough of ‘a’ to peak of ‘b’ & implicit time is from onset of stimulus to peak of ‘b’ ‘ c’ is lower amplitude, prolonged +ve wave less imp

4. ERG

5. ERG ‘ a’ origin  photoreceptors ‘ b’ origin  Muller’s cells + bipolar cells. Mainly from Muller’s in response to increase (ECF) K + in bipolars ‘ c’ origin  RPE Oscillatory potentials (small wavelets on ascending limb of ‘b’) from amacrine cells

6. Physiologic basis of ERG a wave – - Light falling – Hyperpolarisation - Outer portion of photoreceptor – positive - Inner portion - negative - Blue dim flash - Rod ERG - Bright red light - Cone ERG

7. Physiologic basis of ERG b wave- - Muller cells – modified astrocytes - No synaptic junction - Respond to potassium concentration - Change in membreane potential - Cells provide b wave from rods and cones - Oscillatory potential

8. Physiologic basis of ERG C wave – - RPE – in response to rod signals only - Direct contact of rod cells with RPE

9. Amplitude Implicit time

10. Recording protocol Full mydriasis 30 min dark adaptation Rod response / scotopic blue/dim white Max. combined response / scotopic white Oscillatory potentials 10 min of light adaptation Single flash cone response / photopic white flash 30 Hz flicker

11. ERG recording Electrodes  active, reference, ground Ganzfeld bowl stimulator Signal averager Amplifier Display monitor Printer

13. Factors influencing ERG 1 . Stimulus – - a wave increase in size - b wave reaches maximum - Shortening of latency of peaks . Flickering light – cone response only

14. Factors influencing ERG 2 . Recording equipment - 3. Dark adaptation – - ERG increases in size - b wave becomes slower 4. Age and sex – - small ERG within hr of birth , declines in adults - Larger in females than males

15. Cone Rod ERG In light adaptation 6-8 million cones tested In dark- additional 125 million rods contribute In dark adaptation initial 6-8 min majority of response is from cones Orange-red stimulus  cone + rod response White flicker at 30 Hz with intensity constant only cones respond. As the freq increases ‘b’ amplitude decreases

16. Separation of cone & rod ERG For clinically useful information Cone ERG  flickering stimulus 30-70 Hz (rods upto 50 Hz) Rod ERG  in dark adaptation / blue light

17. ERG recording Normal Waveforms  Rod response / scotopic blue / dim white are usually smoother, dome shaped. Initial –ve ‘a’ wave is not seen & is hidden by ‘b’. Longer implicit time. Only rods contribute

18. ERG recording Max combined response / scotopic white flash / mesopic response is a deep ‘a’ wave with tall ‘b’. Longer implicit, larger amplitudes. Both rods & cones contribute

19. ERG recording Oscillatory potentials  Single flash cone response / photopic white flash  small ‘a’ & ‘b’ waves. Waveforms are more peaked with shorter implicit & smaller amplitude. Cone function 30 Hz flicker multiple peaked waveforms. Cone function 4 5

20. Clinical Applications 1. Diagnosis and prognosis of retinal disorders – a. Retinitis pigmentosa b. Diabetic retinopathy c. Retinal detachment d. Vascular occlusions of retina e. Toxic and deficiency status

21. Clinical Applications 2.To assess retinal function when fundus examination is not possible - Corneal opacities - Dense cataract - Vitreous haemorrhage

22. EOG

23. EOG Measurement of resting potential of eye Which exist between cornea and back of the retina during fully light adapted and Fully dark adapted conditions.

24. EOG First discovered by Du Bois-Raymond (1849) Riggs (1954) & Francois worked extensively Arden & Fojas discovered importance of ratio Records overall mass response only.

25. EOG recording Dilate (>3 mm) Skin electrodes near both canthi of BE Ground electrode at forehead. Lighted room 3 fixation lights 15 o apart (dim, red) Looks left & right with 30 o excursion at rate of 15—20 rotations per minute .

26. EOG recording

27. EOG recording Base line. Keep lights on for 5 min Turn off the lights. Record for 15 min in dark adapted state Turn on the lights. Record for 15 min in light adapted state Recordings sampled at 1 min intervals Response decreases progressively during dark adaptation

28. EOG Potentials decrease progressively reaching lowest value called ‘dark trough’ in 8-12 min Light insensitive part of EOG Switch on  record in light adapted state Progressive increase in potential, peak is called ‘light peak’ in 6—9 min Light sensitive part of EOG

29. EOG

30. Arden’s ratio Light peak / dark trough X 100 >180% Normal 165—180% Borderline <165% Subnormal Difference of >10 % in BE is significant Good pt cooperation is required

31. Light sensitive – [ Light peak ] - Contributed by rods and cones B) Light insensitive – [ Dark trough ] - Contributed by RPE , Photoreceptors inner nuclear layer 2 components of EOG

32. EOG Indications Best dystrophy  markedly reduced with Arden ratio is less than 120% Butterfly pattern dystrophy Chloroquine toxicity Stargardt’s dystrophy

33. Visually Evoked Potential (Response) VEP / VER

34. Visual evoked potential Gross electrical signal generated at visual cortex in response to visual stimuli Impulses carried to visual cortex via visual pathway Recorded by EEG It is the only objective technique to assess clinical and functional state of visual syst.beyond retinal ganglion cells.

35. Types of VEP Pattern VEP (checker-board patterns on TV monitor) Flash VEP (diffuse flash light for uncooperative subjects)

36. VEP Un-dilated pupils. Sit 1 meter from monitor Electrodes in midline at forehead, vertex & occipital lobes 2-3 different checker sizes are shown Recording is done

38. VEP Normal waveform Pattern VEP has initial –ve ( N 1 )  +ve( P 1 )  second –ve ( N 2 ) wave Positive wave – 70 100 ms Negative wave – 100 – 130 ms Positive wave - 150 –200 ms Flash VEP is complex. 2 positive & 2 negatives.

41. VEP Indications Un-explained visual loss Optic neuritis Multiple sclerosis Compressive ON lesions Cortical blindness Amblyopia Glaucoma

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