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Electrophysiological tests

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Visual evoked Potential, ERG , EOG in Ophthalmology

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Electrophysiological tests

  1. 1. Electrophysiological tests Presenter : Dr. Reshma Peter Moderator : Dr. Prabhakar
  2. 2. Electrophysiological methods of examination involve the recording of bioelectric potentials that arise during the neural processing of visual information by the various elements of the afferent visual pathways. The various methods include 1.ERG (Electroretinogram)  Ganzfeld full field  Focal  Pattern  Multifocal 2.EOG (Electro-oculogram) 3.VEP/VER (Visual Evoked Potential/Response) • Pattern • Flash
  3. 3. International Society for Clinical Electrophysiology of Vision (ISCEV) Standardised the protocols for performing electrophysiological tests (1989) Ensures uniformity and comparability between labs
  4. 4. History Du Bois-Raymond (1849)-1st discovered EOG Frithiof Holmgren (1865)-1st recorded that alteration in electric potential occurs when light is thrown on retina Dewar (1877)- 1st recorded ERG In humans Einthoven and Jolly (1908)-separated the ERG response into 3 components: a-wave, b-wave and c-wave Riggs(1941)-introduced practical recording contact lens electrode in humans
  5. 5. Riggs (1954) and Francois (1956)worked extensively and popularized EOG  Arden & Fojas (1962)-discovered importance of ratio Ragnar Granit (1967) demonstrated the physiology of th e receptor potential of each component of the ERG- Nob el prize winner Sutter and Tran (1992)- developed multifocal ERG
  6. 6. Anatomy
  7. 7. ELECTRORETINOGRAM  Response recorded by placing electrodes on the surface of eye  The recorded response is weak and needs to be amplified  Recorded data can be stored and analyzed on a computer Recording of the electrical response of the retina to light stimulus which may be a flash of light or a light pattern under different states of light adaptation
  8. 8. useful diagnostically in differentiating certain retinal diseases It is the composite of electrical activity from the photoreceptors, Muller cells & RPE.
  9. 9. BASIC PRINCIPLE OF ERG  Sudden illumination of retina.  Simultaneous activation of all the retinal cells to generate the current  Currents generated by all the retinal cells mix, then pass through vitreous & extra cellular spaces.  High RPE resistance prevents summated current from passing posteriorly.  The small portion of the summated current which escapes through the cornea recorded as------------
  10. 10.  ‘b wave’ :  ‘positive’ (upward) wave  from bipolar cells and Muller cells  reflects bipolar cell activity.  ‘Oscillatory potentials ‘:  Small rippling currents in b wave Ascending limb  3 or more wavelets  produced by Amacrine cells in inner plexiform layer.  ‘a wave’ :  ‘negative’ (downward) wave  Arises from photoreceptors  reflects photoreceptor function  Late receptor Potential
  11. 11.  ‘C wave ‘–  Prolonged positive wave  Low Amplitude  Not used clinically as it is considerably slower  Arises from RPE – in response to rod signals only  Represents metabolic activity of Pigment epithelium
  12. 12. Physiologic basis of ERG a wave Summation of potential change along length of photoreceptors (Light falling on photoreceptor cells) Hyperpolarisation of photoreceptor Cornea negative a wave is recorded as negative wave FLASH STIMULUS Outer portion positive Inner portion negative
  13. 13. Blue dim flash striking dark adapted eye - Rod ERG Bright red light striking light adapted eye - Cone ERG
  14. 14. Rhodopsin consists of Opsin and 11 cis retinal activates Transducin (bound to GTP) Activates PDE Reduced cGMP light 11cis retinal all trans retinal Photo activated rhodopsin(Metarhodopsin II) PDE cGMP GMP
  15. 15. Reduced cGMP Closure of Na + channels Decreased release of neurotransmitter RECEPTOR POTENTIAL Which marks the beginning of the nerve impulse Hyperpolarisation (local graded potential)
  16. 16. STEP 1 OPSIN ACTIVATION STEP 2 OPSIN ACTIVATES TRANSDUCIN WHICH ACTIVATES PDE STEP 3 CYCLIC GMP DECLINES ; GATED Na+ Channels CLOSE STEP 4 RATE OF NEUROTRANSMITTER DECLINES
  17. 17. b wave- Large positive wave. Arises from Muller cells in bipolar cell layer, representing the activity of bipolar cells. Muller cells – modified astrocytes with no synaptic junction Light strike a photoreceptor trigger the On- and Off- Bipolar cells extracellular K+ changes (K+ is released in amounts related to incident light intensity) Trigger Müller cell membrane potential changes linear with extracellular K+ Bipolar cell depolarization
  18. 18. Thus b wave Is dependant on electrical activity originating within Photoreceptor layer - Muller Cells provide b wave from rods and cones Oscillatory Potential  Seen on photopic light adapted b wave  produced by Amacrine cells in inner plexiform layer.  Reflect feedback circuits in inner retina  Disappear in cone dysfunction syndromes  Selectively abolished in animals by clamping retinal circulation and in humans aft er CRAO and in severe diabetic retinopathy Because the ratio of Rods vs Cones is about 13:1, scotopic B-wave is a measure of the respons e from the Rod system, especially for dim flash
  19. 19. C wave Generated from RPE cells in response to rod signals only as rod cells are in direct contact with apical end of RPE cells while cones do not appear to make such contact
  20. 20. ERG arises from parts of retina distal to the ganglion cells Thus a normal ERG may be recorded from an eye with advanced optic atrophy Provided that the outer layers of retina are intact
  21. 21.  a wave Amplitude is measured from baseline to the trough of a wave  b wave amplitude is measured from trough of the a wave to the peak of the b wave  The implicit time is the time from onset of stimulus onset to the peak of a or b response. considering only a and b wave duration of ERG response is less than ¼ second  Latency is the time interval between onset of stimulus and beginning of a wave response .(Normally 2msec)
  22. 22. PHOTOPIC NEGATIVE RESPONSE (PhNR) In flash erg Phnr is the negative wave following the “b” wave Amplitude of phnr is measured from the baseline to the trough o f the negative wave This wave is believed to originate from the ganglion cell layer of th e retina and is earliest affected in glaucoma and appears before visual field defects
  23. 23. Recording protocol  Dark room with non-reflecting walls  FFA, Fundus photography should be avoided  Dilate the pupil with mydriatic to maximize the light entering the eye and minimize the interference from pupil contraction  Dark adapt > 20 minutes to maximize the rod responsiveness  Connect the electrodes:  Corneal electrodes on eyes  Reference electrode on forehead  Ground on ear  Rod response with scotopic blue/dim white light  Max. combined response with scotopic white light  Oscillatory potentials  10 min of light adaptation  Single flash cone response with photopic white flash  30 Hz flicker
  24. 24. BURIAN-ALLLEN CORNEAL CONTACT LENS ELECTRODES :  Multiple use electrode, not commonly used nowadays.  Placed over the cornea after topical anesthesia.  Advantages :  Come in different sizes so can be used for most of the eyes.  They can be used for years.  Disadvantages :  Expensive.  Can be uncomfortable for some due to the large size of the speculum attached. ELECTRODES USED IN ERG
  25. 25.  JET DISPOSABLE ELECTRODE :  Small monopolar, hard contact lens electrode which is placed over cornea.  Requires skin electrode as reference electrode which is placed on forehead.  Single use electrodes & quite expensive.
  26. 26.  HK LOOPS :  Plastic coated, pliable wire electrode.  Placed in lower fornix.  Can be used in unco-operative patients such as young children & patients with ocular  trauma.
  27. 27.  DTL ELECTRODE :  Fine silver nylon fiber electrode with white adhesive disc at either end.  Silver fiber is placed in palpebral sac & discs are attached to canthi to secure the electrode.  Single use electrode & quite expensive,
  28. 28.  MAYER’S GOLD PLATED ELECTRODE :  Gold foil electrode.  For Single use.  Placed in lower fornix with gold comi ng in direct contact with eye.
  29. 29.  SKIN ELECTRODES :  Silver chloride cup electrodes used as gro und or reference electrodes.  Used especially in patients with ocular tr auma where other electrodes coming dir ectly in contact with eye cannot be used.  Sensitive to facial movements so of limite d value in crying children.
  30. 30. Recording protocol Full pupillary dilatation 30 minutes of dark adaptation Rod response Maximum combined response Oscillatory potentials 10 minutes of light adaptation single flash cone response 30 Hz flicker
  31. 31. Recording Electrode Amp. Reference Electrode Computer Ear Ground Electrode ERG Recording Setup Ganzfeld Dome ERG Response
  32. 32. ISCEV Standard for full-field clinical electroretinography
  33. 33. ISCEV ERG Protocol: Step #1 “Rod Response”  Patient is dark adapted  there is no background light when ERG is recorded  The response is “Scotopic”  A dim flash stimulus (-24 dB), 0.01cd s m-2 with minimum interval of 2s between flashes  activates Rod photoreceptor cells but not Cones  Only B-wave response is recorded  Useful for the evaluation of Rod function Scotopic - 24 dB Flash Scotopic - 24 dB Flash -200 -100 0 100 200 300 -200 -100 0 100 200 300 0 50 100 150 200 Electroretinogram 1:(µV)Od2:(µV)Os milliseconds
  34. 34. ISCEV ERG Protocol: Step #2 “Maximal Response”  Patient remains dark adapted, so the response is also Scotopic  Standard flash stimulus (0 dB), 3 cd s m-2 with minimum interval of 10 s between flashes  activates both Rods and Cones  The response contains both A-wave and B-waves  In normal retina, this stimulus intensity elicits the maximal respons e Scotopic 0 dB Flash Scotopic 0 dB Flash -500 -250 0 250 500 -500 -250 0 250 500 0 50 100 150 200 Electroretinogram 1:(µV)Od2:(µV)Os milliseconds
  35. 35. ICSEV ERG Protocol: Step #3 “Oscillatory Potentials”  Same stimulus as Step #2 also elicits Oscillatory Potentials (OPs),using high and low pass filters  OP s ride on the ascending B-wave  frequency range of 100-160 Hz  Affected by retinal ischemia: Diabetics, CRVO have reduced OP Amplitude  OP Amplitude predicts high-risk diabetic patients -500 -250 0 250 500 -100 -50 0 50 100 0 25 50 75 100 125 150 Electroretinogram 1:(µV)Od2:(µV)Od milliseconds Filtered ERG Unfiltered ERG
  36. 36. ICSEV ERG Protocol: Step #4 “Cone Response”  The patient is exposed to background light (30 cd/m2) for at least 10minutes a nd then stimulated with a standard flash (0 dB) of 3 cd s m-2 with minimum interval of 0.5s between flashes  “Photopic” response  Rod photoreceptors are bleached by the background light, so response from R ods is suppressed  The response is mainly from Cone photoreceptors 1 2 1 2 Photopic 0 dB Flash Photopic 0 dB Flash -100 0 100 200 300 -200 -100 0 100 200 0 50 100 150 200 Electroretinogram 1:(µV)Od2:(µV)Os milliseconds
  37. 37. ICSEV ERG Protocol: Step #5 “Flicker Response”  Flicker stimulation (15-60 Hz) at the standard intensity white stimulus (0 dB) of 3 cd s m-2 with flash rate of 30 stimuli per second  elicits photopic response  The B-wave from Cones is recorded, primarily inner retinal response  Applications: Retinal Ischemia; cone and rod-cone disorders 1 2 Photopic 0 dB 30 Hz Photopic 0 dB 30 Hz Ampl.: 132.7 µV, Latency: 32.8 ms Ampl.: 135.2 µV, Latency: 32 ms -100 -50 0 50 100 -100 -50 0 50 100 0 50 100 150 200 250 Electroretinogram 1:(µV)Od2:(µV)Os milliseconds
  38. 38. 1 Dark-adapted 0.01 ERG A rod-driven response of bipolar cells 2 Dark-adapted 3 ER G Combined responses arising from photor eceptors and bipolar cells of both the rod an d cone systems; rod dominated 3 Dark-adapted 3 osc illatory potentials Responses primarily from amacrine cells 4 Dark- adapted 10 E RG Combined response with enhanced a-waves ref lecting photoreceptor function 5 Light-adapted 3 ER G A cone-driven response of bipolar cells 6 Light- adapted 30 Hz flicker ERG A sensitive cone-pathway-driven response McCulloch, Daphne L., et al. "ISCEV Standard for full-field clinical electroretinography (2015 update)." Docum
  39. 39. Diagnose: Retinitis Pigmentosa and other inherited retinal degenerations Congenital and acquired night blindness Inflammatory conditions Vitamin A deficiency Manage: Diabetic Retinopathy Central and Branch Vein or Artery Occlusion Monitor retinal toxicity of drugs such as Plaquenil, Quinine, Cisplatin, Vigabatrin To assess retinal function when fundus examination is not possible Corneal opacities Dense cataract Vitreous haemorrhage Prognosis: Ocular trauma Detached Retina Clinical Applications –
  40. 40. A non recordable flash ERG is an ominous sign for visual prognosis. Disorders result in a completely extinguished ERG Leber’s congenital amaurosis Severe retinitis pigmentosa Retinal aplasia Total detachment of retina Ophthalmic artery occlusion Advanced stage of rod– cone dystrophy Gyrate atrophy Choroideremia Autoimmune retinopathy
  41. 41. Factors influencing ERG Physiological :  Pupil  Age - small ERG within hr of birth declines in adults  Sex-Larger in females than males  Ref. Error  Diurnal Variation  Dark adaptation  anesthesia Limitation of Full Field ERG - Unless 20% or more of the retina is affected with a diseased state the ERGs are usually normal Artifacts :  Blinking  Tearing  eye movements  air bubbles under electrode. Instrumental :  Amplification  Gain  Stimulus  electrodes
  42. 42. EYE MODEL BASED IN EOG (BIDIM-EOG) Bi Dimensional Bi Polar Model
  43. 43. PATTERN ERG • Measure of macular function and generalized bipolar cell function. • most common stimulus : Checkerboard stimulus composed of white and black squares • PERG generation requires physiological integrity of anatomically present RGCs • Reduction of PERG amplitude reflect the reduced activity of dysfunctiona l RGCs • reflects inner retina activity under light-adaptation. • should be used in combination with a traditional light-adapted luminance ERG to have an index of outer retina function • an important tool to monitor the onset and the progression of RGC dysfunction in optic nerve disease. Example:- Glaucoma, optic neuritis, ischemic optic neuropathy, and mitochondrial optic neuropathy
  44. 44. Principle : Net retinal illumination remains constant. Only a redistribution of the pattern of light and dark areas is made  17” monitor from a distance of 1 meter  stimulus field is 15 °  150 stimuli for signal averaging at a frequency of 1 pulse per second  Central fixation is necessary.  Refraction to be corrected  Use temporal fossa for reference electrod e, and forehead for ground electrode.  Recording electrode: DTL or Gold Foil Elec trode (no lens electrode)
  45. 45. The normal pattern electroretinogram : – N35- a small negative component with a peak time occurring around 35 ms; – P50- a prominent positive wave emerging around 50 ms – N95- a wide negative wave around 95 ms
  46. 46. Can help differentiate Macular from Optic nerve related pathologies in Macular diseases:- The P50 component was shown to be altered in all patients with retinal and macular diseases in Optic nerve disease:- N95 component was abnormal in 81% of patients with diseases of the optic nerve. The P50 component remain normal.
  47. 47.  MFERG tests ERG activity in individual small retinal areas in central 30° area  Erich Sutter used binary m-sequences to extract hundreds of focal ERGs from a single electrical signal.  Stimulation is provided by video display  Sophisticated algorithms extract the response of each retinal area from the overall recording  Photopic test (cone function)  Response amplitude related to cone density.  Typically, stimulus areas are scaled to provide equal response. Multifocal ERG (MFERG): Mapping of Retinal Function
  48. 48. MFERG: The Concept Recordin g Electro de Amp. Referenc e Electro de Computer Ear Ground E lectrode Stimulus on high-qua lity video monitor
  49. 49. MFERG: The Individual Response and 3-Dimensional Display Blind spot Foveal peak 3D display of ERG response densityFocal ERG from each retina area
  50. 50. MFERG: Map And Focal • Analyze summarized ERG responses from different regions • Analyze the overall response from the central retina area of 50 - 600 view angle
  51. 51. • Small scotomas can be mapped and quantified • 61 or 103 focal ERG responses can be recorded from the cone-driven retina. • 20-30 degrees to each side of the fovea
  52. 52.  Dilate patient’s pupil with a mydratic  No dark adaptation is necessary.  Refractive correction is recommended but not required.  Recording using Burian-Allen or DTL electrode on the eye, a reference electrode (only for DTL) a ground electrode  The test is composed of several segments, 10 - 30 seconds each  Total recording time is 5 - 10 minutes per eye  It is critical that patient is staring at the fixation during recording; the eye can be monitored using a fixation camera  Eye or body movement will distort the recording, and the segments shou ld be repeated if there is too much noise MFERG: Recording Procedure
  53. 53.  Diagnosing macular disease: ARMD, others  Retinal toxicity (Plaquenil and other drugs)  AZOOR (Acute Zonal Occult Outer Retinopathy)  Macula vs optic nerve in unexplained visual loss  Early diagnosis of retinal disease: Many retinal disorders affect small areas in early stages Diabetic retinopathy Retinitis pigmentosa MFERG: Applications
  54. 54. Additional Tests Very bright flash (+25dB) for pre-operative evaluation In Dense cataract and Vitreous hemorrhage Photopic Negative Response ERG Test condition: Dilated, photopic test Stimulus: Red Flash on Blue Background Generated by retinal ganglion cells Early glaucoma evaluation On/Off Response ERG Test condition: Dilated, photopic test Stimulus: Red Flash on Blue Background Looking at On and Off Bipolar Cells responses Inner retina dysfunction
  55. 55. S-Cone ERG Test condition: Dilated, photopic test Stimulus: Blue Flash on Amber background Generated by S-Cone Photoreceptors Enhanced S-Cone Syndrome Scotopic Threshold response ERG Test condition: Dilated, scotopic test Stimulus: Series of flash of increasing intensity starting from below thres hold (starting intensity is species dependent) Double Flash ERG Stimulus: Bright Flash followed by medium flash
  56. 56. Electrooculogram Measurement of resting potential of eye Which exist between cornea and back of the retina During fully light adapted and Fully dark adapted conditions Records overall mass response only.  Records the “Corneo-Fundal Potential”  Measures function of Retinal Pigment Epithelium (RPE)
  57. 57. Mainly derived from the response of retinal pigment epithelium (RPE) to retinal illumination Amplitude of potential changes with retinal illumination over a period of mi nutes • Dark: smaller potential • Light: larger potential • The potential decreases for 8–10 min in darkness. • Subsequent retinal illumination causes an initial fall in the standing po tential, followed by a slow rise for 7–14 min (the light response). • These phenomena arise from ion permeability changes across the basal RPE membrane.
  58. 58. EOG recording  Arrangement to make the eyes light adapted with a bright long duration stimulus  Dilate (>3 mm) with mydriatic  Skin electrodes near both canthi of BE  Ground electrode at forehead.  3 dim , red fixation lights 15o apart  Looks left & right with 30o excursion at rate of 15—20 rotations per minute.  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 1- 1+ 2- 2+
  59. 59. • Calibration of the signal • Gazing at consecutively at two different fixation points located at known angle apart and recording the concomitant EOGs . • Skin electrodes on both sides of an eye the potential can measure th e potential by having the subject move his or her eyes horizontally a s et distance .
  60. 60. After training the patient in the eye movements, the lights are turned off. About every minute a sample of eye movement is taken as the patient is asked to look back and forth between the two lights . After 15 minutes the lights are turned on and the patient is again asked about a minute to move his or her eyes back and forth for about 10 seconds. Typically the voltage becomes a little smaller in the dark reaching its lowest potential after about 8-12 minutes, the so-called “dark trough”. When the lights are turned on the potential rises, the light rise, reaching its peak in about 10 minutes. When the size of the "light peak" is compared to the "dark trough" the relative size should be about 2:1 or greater . A light/dark ratio of less than about 1.7 is considered abnormal.
  61. 61. Arden’s ratio >180% Normal 165—180% Borderline <165% Subnormal Difference of >10% in BE is significant Good pt cooperation is required Arden Ratio = maximum height of light peak (LP) x 100 minimum height of dark trough (DT)
  62. 62. 2 components of EOG A)Light sensitive – [ Light peak ] - Contributed by rods and cones B) Light insensitive – [ Dark trough ] - Contributed by RPE , Photoreceptors ,inner nuclear layer Three phases are typically recorded in EOG The pre-adapt light phase is to standardize the standing potential, taking 1-5 min. The dark-adapt phase is to “discharge” the standing potential, taking 10 - 20 min. The light phase is to “recharge” the standing potential, taking 4 - 10 min. The test takes about 30 - 40 min in total. Recording of both eyes are recommended to save time
  63. 63. Indications 1. Best’s Disease (Best’s Vitelliform Macular Dystrophy)  markedly redu ced with Arden ratio is less than 120% 2. Butterfly pattern dystrophy 3. Chloroquine toxicity 4. Stargardt’s dystrophy 5. Retinal pigmentary degenerations 6. Chorioretinal dystrophies (e.g. choroideremia)
  64. 64. ‘visually evoked response (VER)’ or ‘cortical potentials’.  It is the electrical response of the brain to sudden app earance / disappearance / change of visual stimulus.  Like EEG, VEP is detected by placing surface electrode s at scalp which can be placed anywhere, but should always include posterior occipital area. VISUALLY EVOKED POTENTIALS (VEP)
  65. 65. 1. Pattern VEP (checker-board patterns on TV monitor) 2. Flash VEP (diffuse flash light for uncooperative subjects) TYPES OF VEP
  66. 66. • Gross electrical signal generated at visual cortex in res ponse to visual stimuli • Impulses carried to visual cortex via visual pathway recorded by EEG • It is the only objective technique to assess clinical and functio nal state of visual system beyond retinal ganglion cells • Measures function of visual pathway: fovea, optic nerve, prim ary visual cortex
  67. 67.  Pupils are un-dilated .  Patient seated about 1 meter from monitor  Electrodes in midline at forehead, vertex & occipital lobes Procedure
  68. 68.  The occipital electrode (Inion) lies near visual area thus called as reference electrode.  The vertex electrode is placed over non visual area which detects minimu m activity in response to visual stimulation is called as active electrode.  The 3rd electrode is placed over forehead is called ground electrode. VEP ELECTRODES
  69. 69.  The stimulus shown flash of light (diffuse light spot, annulus ) patterned stimulus (illuminated checkerboard)  The stimuli are repetitively presented at random within a short period of ti me. Eg. 1 cycle/second for 100 seconds.  Normally use pattern stimulus (less variability) Alternating grating, sinusoid, or checkerboard pattern Stimulus may be full field or hemi-field  Signals at visual cortex are recorded
  70. 70. Normal waveform Pattern VEP has initial –ve (N1) +ve(P1)second –ve (N2) wave Positive wave – 70 100 ms Negative wave – 100 – 130 ms Positive wave - 150 –200 ms Flash VEP is complex. 2 positive & 2 negatives.
  71. 71.  Amplitude of VEP : Height of the potential of P100 wave. Predominantly affected in ischemic disorders.  Latency of VEP : Time from stimulus onset to peak of the response. Pred ominantly affected in demyelinating disorders.
  72. 72. APPLICATIONS OF VEP  Recording visual acuity in nonverbal patients.  Macular function test.  Screening and early diagnosis of Multiple Sclerosis.  To identify optic nerve diseases, visual pathway abnormalities.  Amblyopia : latency relatively spared, so VEP can be used to monitor response to occlusion therapy.  Detection of a malingerer.  To detect color blindness : Using chromatic patterned light stimuli
  73. 73. DIABETIC RETINOPATHY :  In DR there is reduction in amplitude & delay of peak implicit times.  These changes are directly proportional to severity of retinopathy.  Amplitude of oscillatory potentials (OP) is a good predictor of progression of retinopathy from NPDR to PDR.  Abnormal amplitude of OP indicate high risk of developing PDR.
  74. 74. RETINAL DETACHMENT (RD) & CENTR AL SEROUS RETINOPATHY (CSR) :  In RD & CSR there is significant reduction in ERG amplitude.  However there is no significant change seen in waveforms of ERG.
  75. 75. RETINOSCHISIS :  ERG in retinoschisis is typically characterized by marked decrease amplitude or absence of b wave.
  76. 76. RETINITIS PIGMENTOSA : Retinitis Pigmentosa  A full field ERG in RP shows marked reduction in both rod & cone signals although loss of rod signals is predominant  There is significant reduction in amplitude of both a & b waves of ERG.
  77. 77. CRAO :  In vascular occlusions like CRAO, ERG t ypically shows shows absent b wave.  Ophthalmic artery occlusions usually re sults in unrecordable ERG
  78. 78. CONE DYSTROPHY :  ERG in cone dystrophy shows good rod b-waves that are just slower.  The early cone response of the scotop ic red flash ERG is missing.  The scotopic bright white ERG is fairly normal in appearance but with slow implicit times.  The 30 Hz flicker & photopic white ER Gs which are dependent upon cones are very poor.
  79. 79. RETAINED IOFB :  A retained metallic FB like iron & cop per shows changes in ERG early as we ll as late stages.  A characteristic change is b-wave am plitude is reduced by 50% or more a s compared with normal eye.  No intervention finally results into an unrecordable ERG (Zero ERG)
  80. 80. A small piece of stainless steel or plastic outside the macula may have a minor aff ect on the retina. A piece of copper or iron have deleterious affects within a few weeks In general if b-wave amplitudes are reduced 50% or greater compared to the fellow eye, it is unlikely that the retinal physiology will recover unless the fore ign body is removed.
  81. 81. BEST’S DISEASE Vitelliform lesions represent the accumulation of lipofuscin in the macular area. Further effects of retinal pigment epithelium (RPE) dysfunction incl ude accumulation of degenerated photoreceptor outer segments in the subretinal space. Normal ERG, Abnormal EOG : Clinical utility : Carriers ; end stage disease
  82. 82. MULTIPLE SCLEROSIS :  Abnormalities in VEP are bilateral & seen 90 % of cases irrespective of visual symptoms.  In MS, increase in latency period is more predominant than decrease in P100 amplitude.
  83. 83. TOXIC & COMPRESSIVE OPTIC NEUROPATHY :  Following 2 changes are seen :  Decreased amplitude of P100 wave.  Increase in latency period.  Decreased amplitude of P100 is more predominant than increased latency period.
  84. 84. OPTIC NEURITIS :  In optic neuritis, VEP shows increased latency period &/or decreased amplit ude as compared to normal eye.  These findings develop even before o ccurrence of visual symptoms & color defects.  In recovery stage, amplitude may retur n to normal but latency period continu es to be decreased.
  85. 85. Stationary rod dystrophies Congenital stationary night blindness (CSNB) is found in several forms. Two types. Type 1 have an abnormal dim scotopic ERGs b ut the bright flash ERG maintains oscillatory po tentials on the ascending limb of the b-wave. Type 2 has a very abnormal dim scotopic ERG and the bright flash scotopic ERG has a large a -wave and no b-wave. Oscillatory potentials are also missing
  86. 86. Drug toxicities Several drugs taken in high doses or for l ong periods of time can cause retinal deg eneration with pigmentary changes. The effects of toxic medications can be detected and quantified using ERGs. The effects of toxic medications can be detected and quantified using ERGs. Chloroquine retinopathy appears as a characteristic “bullseye” maculopathy
  87. 87. The better substitute for chloroquine, Pla quenil, can also have macular effects noti ceable by multifocal electroretinograms. Hydroxychloroquine (Plaquenil) is usually l ess disruptive to the retina than chloroqui ne, but ERG changes can still occur. Vigabatrin, a pediatric seizure medication, can be toxic to the retina. Attenuation of full-field ERG b-wave amp litudes can detect toxicity. Often the first indication of toxicity is red uced amplitude to 30 Hz flicker Cis-platinum used to treat brain tumors s ometimes reaches ophthalmic vascularizat ion and causes a reduction in ERG wavef orm in the affected eye (OD in this case)
  88. 88. Steroid Retinopathy The fundus photo shows a cherry red spot in th e macula. The ERG response was diminished in size particularly following dim scotopic flashes
  89. 89. Talc retinopathy Seen in iv drug abusers Global ERG is attenuated
  90. 90. OGUCHI DISEASE Absent rod ERG Normal cone ERG Negative configuration of combined response; normal OP Photopic hill phenomenon Improvement after prolonged dark adaptation
  91. 91. FUNDUS ALBIPUNCTATUS Rod ERG absent after 30 min dark ad aptation Normal after 3 hour dark adaptation Combined response : negative after 3 0 min, normal after 3 hours
  92. 92. REFERENCES 1.The electroretinogram and the electro oculogram : Clinical applications By Donnell J. Creel 2.Neuro- Ophthalmology Clinical signs and symptoms By Thomas J Walsh 3.Electrodiagnosis of Retinal Diseases By Y. Miyake 4.Diagnostic Procedures in Ophthalmology BY HV Nema 5.Anatomy and Physiology of the eye by A.K. khurana 6.Clinical Neurophthalmology by Ulrich Schiefer 7.Clinical Anatomy and Physiology of the visual system by Lee Ann Remington
  93. 93. THANK YOU ALLPPT.com _ Free PowerPoint Templates, Diagrams and Charts

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