Pattern Electroretinogram Changes Research Articles

Bilateral Pattern Electroretinogram Abnormalities in Patients with Herpes Zoster Keratitis and Conjunctivitis.

Herpes zoster ophthalmicus (HZO) results from the reactivation of varicella zoster virus (VZV) in the ophthalmic branch of the trigeminal nerve. The inflammation caused by VZV involves multiple tissues in the eyes. Our goal is to evaluate pattern electroretinogram (PERG) changes and their relationship with corneal sub-basal nerve changes in patients with HZO. Twenty-two patients with herpes zoster keratitis or conjunctivitis and 20 healthy volunteers were recruited for this cross-sectional study. A PERG test was performed on both eyes of HZO patients and one eye of the healthy controls. In vivo confocal microscopy (IVCM) was also performed on both eyes of the HZO patients to detect corneal nerve damage. Our results showed changes in the PERG parameters in both eyes of HZO patients compared to the healthy controls. Affected eyes showed delayed N95 peak time and decreased P50 and N95 amplitude compared to the unaffected eyes (p < 0.05, respectively). Both affected and unaffected eyes in HZO patients showed delayed P50 peak time and decreased N95 amplitude (p < 0.05, respectively) compared to controls. In HZO patients, no significant differences in each PERG parameter were found between eyes with and without corneal lesions or between eyes with and without increased Langham's cells in the corneal epithelial sub-basal layer. The IVCM images showed decreased total nerve length and number at the sub-basal layer of the epithelial cornea in affected eyes compared to unaffected eyes (p < 0.05). No significant correlation was found between total nerve length and PERG changes. Our results showed that VZV-affected eyes without central cornea involvement displayed reduced N95 amplitude and prolonged P50 peak time in bilateral eyes compared to the healthy controls. Larger studies are needed to further explore the effect of HZO on the electrophysiological response of the eye and the posterior segment.

Retinal Function in Long-Term Type 1 Diabetes without Retinopathy: Insights from Pattern Electroretinogram and Pattern Visual Evoked Potentials Assessments.

To evaluate changes in pattern electroretinogram (pERG) and pattern visual evoked potentials (pVEP) in patients with long-lasting type 1 diabetes without diabetic retinopathy (DR). Prospective study involving 92 eyes divided into two groups. The diabetic group included 46 eyes of 23 patients with type 1 diabetes (T1DM); the control group included 23 age-matched healthy subjects. pERG and pVEP were assessed using the RETI-port/scan21 recording software (version 1021.3.0.0). Mean age was 48 ± 9.77 years for the diabetic group and 51.7 ± 4.75 years for the control group. The mean duration of diabetes was 28.88 ± 8.04 years. The mean HbA1c value was 7.29 ± 0.89%. There were no differences in the age or sex distribution. Regarding the pERG, T1DM patients exhibited a significant decrease in the amplitude of the P50 and N95 waves compared to the control group (p = 0.018 and p = 0.035, respectively), with no differences in the peak time of each component. pVEP showed no significant changes in either peak time or amplitude of the different components. Long-term T1DM patients without DR showed changes in the amplitude of pERG waves with preserved peak times. We did not observe modifications in pVEP. pERG may serve as a subclinical marker of ganglion cell damage in long-term T1DM patients.

Pattern electroretinogram changes in patients with primary open-angle glaucoma in correlation with visual field and optical coherence tomography changes.

To study the pattern electroretinogram changes in primary open-angle glaucoma patients in correlation with visual field changes and optical coherence tomography measurements of retinal nerve fiber layer thickness in the peripapillary region in an attempt to evaluate the clinical value of pattern electroretinogram as an objective test of functional deficit in glaucoma. The study included 81 eyes of 81 participants: 50 primary open-angle glaucoma patients, 16 primary open-angle glaucoma suspects, and 15 controls. All subjects underwent visual field testing using 24-2 Humphrey standard automated perimetry, peripapillary retinal nerve fiber layer average thickness using the 3.4-mm circular scan of the Heidelberg OCT spectralis and pattern electroretinogram using CSO RetiMax device in accordance with the International Society for Clinical Electrophysiology of Vision guidelines. We had three main groups: normal, glaucoma suspect, and primary open-angle glaucoma patients, and the last group included three subgroups: mild, moderate, and severe. There was significant difference in the visual field mean deviation, peripapillary retinal nerve fiber layer average thickness, and most pattern electroretinogram measured parameters between the three main groups and in between primary open-angle glaucoma subgroups. There was significant positive correlation between visual field mean deviation and the peripapillary retinal nerve fiber layer average thickness, P50 amplitude, and P50-N95 amplitude (p < 0.001, p = 0.018, and p < 0.001, respectively). Significant negative correlation was also found between peripapillary retinal nerve fiber layer average thickness and N95 amplitude (p < 0.001). Significant positive correlation was found between retinal nerve fiber layer average thickness and P50-N95 amplitude (p = 0.001). Significant negative correlation was found between peripapillary retinal nerve fiber layer average thickness and N95 amplitude (p = 0.001) and significant positive correlation of retinal nerve fiber layer average thickness with P50-N95 amplitude (p = 0.017) in primary open-angle glaucoma patients. Peripapillary retinal nerve fiber layer average thickness shows significant negative correlation with pattern electroretinogram N95 amplitude and a significant positive correlation with P50-N95 amplitude. In combination with optical coherence tomography, pattern electroretinogram can be used to objectively assess functional loss in glaucoma.

Changes in pattern electroretinogram after application of 0.01% atropine eye drops

Changes in pattern electroretinogram after application of 0.01% atropine eye drops

Adaptation of the Steady-state PERG in Early Glaucoma

Previous studies have shown that the onset of high-contrast, fast reversing patterned stimuli induces rapid blood flow increase in retinal vessels in association with slow changes of the steady-state pattern electroretinogram (PERG) signal. We tested the hypothesis that adaptive PERG changes of normal controls differed from those of glaucoma suspects and patients with early manifest glaucoma. Subjects were 42 glaucoma suspects (Standard Automated Perimetry-MD -0.89±1.8 dB), 22 early manifest glaucoma (MD -2.12±2.4 dB) with visual acuity of ≥20/20 and 16 age-matched normal controls from a previous study. The PERG signal was sampled every ~15 seconds over 4 minutes in response to gratings (1.6 cyc/degree, 100% contrast) reversing 16.28 times/s. Amplitude/phase values of successive PERG samples were fitted with a nonparametric locally weighted polynomial regression smoothing function to retrieve the initial and final values and calculate their difference (δ) and the residual SD around the fitted function. The magnitude of PERG adaptive change compared to random variability was calculated as log10 of percentage coefficient of variation (CoV)=100×residual SDr÷δ. Grand-average PERGs were also obtained by averaging all samples of the same series. The grand-average PERG amplitude [analysis of variance (ANOVA), P=0.02], but not phase (ANOVA, P=0.63), decreased with increasing severity of disease. Adaptive changes [log10 (CoV)] of PERG amplitude were not significantly associated with disease severity (ANOVA, P=0.27) but adaptive changes [log10 (CoV)] of PERG phase were (ANOVA, P=0.037; linear trend, P=0.011). The steady-state PERG signal displayed slow adaptive changes over time that could be isolated from random variability. PERG adaptive changes differed from those of grand-average PERGs (corresponding the standard steady-state PERG), thus representing a new source of biological information about retinal ganglion cell function that may have potential in the study of glaucoma and optic nerve diseases.

Reduced habituation of the retinal ganglion cell response to sustained pattern stimulation in multiple sclerosis patients

ObjectiveSustained pattern stimulation in normal subjects induces adaptive changes in pattern electroretinogram (PERG), an effect that has been interpreted as a response of glial cells and retinal ganglion cells (RGC). The aim of this study was to compare the effect in normal subjects and in multiple sclerosis patients without previous optic neuritis. MethodsPERGs were elicited by a 7.5Hz pattern stimulus, presented continuously over 152s. Response cycles were averaged in 20 packets of 60 events each and amplitude and phase of the 2nd harmonic response was measured. Adaptive changes are expressed as amplitude reduction over the full examination time. ResultsIn normal subjects PERG amplitude declined progressively to a plateau (dA=−0.46μV, SE=0.09μV); in patients the effect size was severely reduced (dA=−0.20μV, SE=0.04μV). No significant difference was found in mean amplitude. ConclusionsThe results show reduced RGC habituation in patients, suggesting an abnormal gain and sensitivity control in the inner retina, even in absence of clinical optic neuritis. Recent findings in astrocyte biology and indications drawn from a mathematical model point to a key role of glial cells in this process. SignificanceThe proposed methodology may have implications in the assessment of MS patients and in understanding the pathophysiology of neurological and retinal disorders.

Retrograde signaling in the optic nerve is necessary for electrical responsiveness of retinal ganglion cells.

We investigated the role of retrograde signaling in the optic nerve on retinal ganglion cell (RGC) electrical responsiveness in the mouse model. Electrical response of RGC was measured by pattern electroretinogram (PERG) in 43 C57BL/6J mice 4 to 6 months old under ketamine/xylazine anesthesia. PERGs were recorded before and at different times after blockade of axon transport with lidocaine at either the retrobulbar level (2 μL, 40 μg/μL) or at level of the superior colliculus (SC, 1 μL, 40 μg/μL). PERGs also were recorded before and at different times after optic nerve crush 1.5 mm behind the eye, followed by TUJ1-positive RGC counts of excised retinas. As controls, PERGs also were recorded after either saline injections or sham optic nerve surgery. The photopic flash electroretinogram (FERG) and visual evoked potential (FVEP) also were recorded before lidocaine and at relevant times afterwards. Lidocaine injection caused rapid (retrobulbar ~10 minutes, SC 1 hour), reversible reduction of PERG amplitude (≥50%). Optic nerve crush caused rapid (10-20 minutes), irreversible reduction of PERG amplitude (70-75%), increase of PERG latency (>25%), as well as RGC loss (88%) 1 month after crush. FVEP was unaltered by lidocaine. For all procedures, the FERG was unaltered. As experimental interventions were made at postretinal level(s), PERG changes were likely associated with altered supply of retrogradely-delivered material from the SC. This implies that retrograde transport of target-derived molecules is necessary for normal RGC electrical responsiveness. The time course of early PERG changes is consistent with the speed of fast retrograde axon transport.

Pattern-reversal electroretinograms for the diagnosis and management of disorders of the anterior visual pathway

The pattern electroretinogram is an electrophysiological test that assesses the function of inner retinal layers, particularly the ganglion cells layer of retina, using a reversing checkerboard or grating pattern that produces no change in average luminance over time. The normal pattern electroretinogram is composed of a proeminent positive component (P50) and a large later negative component (N95). Since structural damage that compromises the retinal ganglion cell layer can lead to pattern electroretinogram changes, particularly in the N95 amplitude, the test can be useful in the treatment of a number of anterior visual pathway diseases. In this article, we review the methods for recording pattern electroretinogram and its usefulness in the diagnosis and management of diseases including inflammatory, hereditary, ischemic and compressive lesions of the anterior visual pathway.

IOP-Dependent Retinal Ganglion Cell Dysfunction in Glaucomatous DBA/2J Mice

To characterize the effect of postural IOP elevation and pharmacological IOP lowering on retinal ganglion cell (RGC) function in the DBA/2J mouse model of glaucoma. Four groups of DBA/2J mice (3 months old, n = 7; 5 months old, n = 7; 10 months old, n = 7; and 11 months old, n = 8) were anesthetized by intraperitoneal injection (0.6 mL/kg) of a mixture of ketamine (42.8 mg/mL), xylazine (8.5 mg/mL), and acepromazine (1.4 mg/mL). IOP and pattern electroretinogram (PERG) were sequentially measured with mice at 0 degrees (horizontal), 60 degrees head-down, and again at 0 degrees . IOP and PERG were also measured before and after intraperitoneal mannitol 25% (2.5 g/kg) administration with mice in a horizontal position. The head-down position induced reversible IOP elevations of 32% to 38% in all age groups (P < 0.01), and age-dependent reductions of PERG amplitude (3 months: +3%; 5 months: -47%, P < 0.01; and 10 months: -65%, P < 0.01). Administration of mannitol to 11-month-old mice resulted in a reduction in IOP of approximately 38% (P < 0.01) and a PERG amplitude improvement of approximately 83% (P < 0.001). IOP and PERG amplitude changes were inversely correlated (10 months head-down r(2) = 0.58, P < 0.001; 10-month-old mannitol r(2) = 0.41, P < 0.001). For all conditions, the light-adapted flash ERG was unaltered. In the DBA/2J mouse, RGC susceptibility to artificial IOP elevation increases with age. Abnormal RGC function in older mice may be improved with IOP lowering. Evaluation of PERG changes in response to artificial IOP modulation may represent a powerful tool to assess noninvasively RGCs' susceptibility to IOP insult in genetically distinct mouse models of glaucoma.

Habituation of Retinal Ganglion Cell Activity in Response to Steady State Pattern Visual Stimuli in Normal Subjects

To evaluate autoregulatory changes of retinal ganglion cell (RGC) activity, as measured by the pattern electroretinogram (PERG), when the eye is exposed to a steady state presentation of stimuli that maximize PERG amplitude and blood flow. The PERG was recorded from both eyes of 14 normal subjects in response to steady state presentation (4 minutes) of contrast-reversing (16.28/s) gratings (1.6 cyc/deg) with different contrast (12%-99%) and mean luminance (40-1.3 cd/m(2)). One temporal period of the stimulus (122.8 ms) was sampled and averaged in packets of 50 sweeps ( approximately 15 seconds each). PERG amplitude and phase were evaluated by Discrete Fourier Transform and displayed as a function of time. Data were fitted with an exponential decay function to evaluate PERG changes with time. For patterns of 99% contrast, the PERG amplitude progressively decreased with time until reaching a plateau approximately 30% lower than the initial amplitude after approximately 2 minutes (habituation). The ratio between initial and plateau amplitude did not change by reducing the stimulus luminance by 1 log unit. However, reducing contrast decreased amplitude habituation. The habituation was abolished at 25% contrast. Decrease of PERG amplitude with time is consistent with a slow adaptive change of RGC activity in response to high-contrast, steady state stimuli. The authors propose that the initial amplitude represents an index of RGC activity, and the plateau amplitude represents a dynamic equilibrium between RGC activity and the available energy supply. These results are relevant for a better understanding of glaucomatous optic neuropathy.

Restoration of retinal ganglion cell function in early glaucoma after intraocular pressure reduction: A pilot study

To investigate the changes of pattern electroretinogram (PERG) after intraocular pressure lowering in glaucoma patients and normal controls. Interventional retrospective cross-sectional study. Twenty-five patients (49 eyes) with ocular hypertension or glaucoma undergoing topical treatment to lower IOP served as a study group; 22 patients (44 eyes) with ocular hypertension or glaucoma observed without treatment served as a control group for treated glaucoma patients; 9 normal subjects (18 eyes) receiving a 250-mg acetazolamide tablet served as a second study group; and 17 normal subjects (34 eyes) from a previous study served as a second control group for treated normal subjects. Pattern electroretinograms were recorded simultaneously from both eyes using skin electrodes and automated analysis. Visual field (VF) analyses were performed with white-on-white standard automated perimetry (SAP). Intraocular pressure was measured with Goldmann applanation tonometry; central corneal thickness was measured with pachymetry. Pattern electroretinogram amplitude (microvolts), phase (pi rads), and test-retest variability (test 2-to-test 1 ratio, in decibels), SAP mean deviation (decibels), and IOP (millimeters of mercury). In 56% of right eyes and 21% of left eyes of the treated glaucoma subgroup, the PERG amplitude and/or phase improved beyond the 95% confidence intervals of the test-retest variability of the untreated glaucoma control group. Pattern electroretinogram improvement with IOP lowering occurred in both high- and low-tension glaucoma eyes. Eyes with severely impaired VFs showed little improvement in PERG; however, eyes of normal subjects treated with acetazolamide did not show significant PERG changes relative to the test-retest variability of normal controls. Retinal ganglion cell function can be at least partially restored after IOP reduction in glaucomatous eyes with early VF impairment.

The spatial distribution of ERG losses across the posterior pole of glaucomatous eyes in multifocal recordings.

Australian and New Zealand Journal of OphthalmologyVolume 24, Issue S2 p. 28-31 Free Access The spatial distribution of ERG losses across the posterior pole of glaucomatous eyes in multifocal recordings , Corresponding Author *The Eye and Vision Research Institute, Electrophysiology Department.Visiontest Australia, Suite 5, Level 5, 187 Macquarie Street, Sydney 2000, New South Wales.Search for more papers by this authorL. Buckland BSc, Corresponding Author L. Buckland BSc †Eye Clinic, Prince of Wales Hospital.Visiontest Australia, Suite 5, Level 5, 187 Macquarie Street, Sydney 2000, New South Wales.Search for more papers by this author , Corresponding Author *The Eye and Vision Research Institute, Electrophysiology Department.Visiontest Australia, Suite 5, Level 5, 187 Macquarie Street, Sydney 2000, New South Wales.Search for more papers by this authorL. Buckland BSc, Corresponding Author L. Buckland BSc †Eye Clinic, Prince of Wales Hospital.Visiontest Australia, Suite 5, Level 5, 187 Macquarie Street, Sydney 2000, New South Wales.Search for more papers by this author First published: May 1996 https://doi.org/10.1111/j.1442-9071.1996.tb00987.xCitations: 7AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References 1 Vaegan, Graham SL, Goldberg I., Millar TJ. Selective reduction of oscillatory potentials and patterr electroretinograms after retinal ganglion cell damage 05 disease in humans or by kainic acid toxicity in cat. Doc Ophthalmologica 1991; 77: 237– 53. 2 Vaegan, Graham SL, Goldberg I., Buckland L., Hollows FC Flash and pattern electroretinogram changes with optk atrophy and glaucoma. Exp Eye Res 1995; 60: 697– 706. 3 Yin ZQ, Vaegan, Millar TJ, Sarks J., Sarks SH. Choroida atrophy in chronic primary open angle glaucoma. [Abstrac 2714] Invest Ophthalmol Vis Sci 1994; 35(Suppl.): 1842. 4 Yin ZQ, Vaegan, Millar TJ, Sarks J., Sarks SH. The locui of choroidal blood vessel loss in chronic primary oper angle glaucoma. [Abstract 4446] Invest Ophthalmol Vi: Sci 1995; 36(Suppl.): S964. 5 Vaegan, Yin ZQ, Beaumont P. Delayed choroidal filling across the posterior pole of glaucomatous eyes shown by fluorescein angiography. [Abstract 4452] Inves Ophthalmol Vis Sci 1995; 36(Suppl.): S965. 6 Nork TM, Poulsen GL, Vaegan, Sarks SH. Photoreceptoi damage and loss in human eyes with primary open angl> glaucoma. [Abstract 1546] Invest Ophthalmol Vis Sc 1995; 36(Suppl.): S331. 7 Yin ZQ, Vaegan, Millar TJ, Beaumont P., Sarks J., Sarks SH. The locus of choroidal blood vessel loss in chronic primary open angle glaucoma. [Abstract 4446] Invest Ophthalmol Vis Sci 1995; 36(Suppl.): S964. 8 Sutter EE, Tran D. The field topography of ERG components in man | I. The photopic luminance response. Vision Res 1992; 32: 433– 46. 9 Sutter EE, Vaegan. Lateral interaction component and local luminance nonlinearities in the human pattern reversal ERG. Vision Res 1990; 30: 659– 71. 10 Vaegan, Sutter EE. Fundamental differences between the nonlinearities of pattern and focal electroretinograms. Doc Ophthalmologica 1990; 76: 13– 25. 11 Sutter EE, Bearse MA. Extraction of a ganglion cell component from the corneal response. Vision Science and its Applications. 1995 OSATechnical Digest Series, Vol 1. Optical Society of America, Washington DC. 1995; 310– 13. 12 Vaegan, Buckland L. Outer retinal changes in early glaucoma detected with the Sutter local luminance ERG field test. Proceedings of the 33rd ISCEV Symposium, Athens, Greece. 16–20 June 1995. 13 Hennessy MP, Vaegan. Amplitude scaling relationships of Burian-Allen, gold foil, and Dawson Trick and Iitzkow electrodes. Doc Ophthalmologica 1995; 89: 235– 48. 14 Vaegan, Buckland L. Relationship between means and variances of ERGs obtained with gold foil and DTL electrodes across the full range of recordable amplitudes. Proceedings of the 33rd ISCEV Symposium, Athens, Greece. 16–20 June 1995. 15 Holder GL. Pattern electroretinography in the evaluation of glaucoma and in optic nerve function. In JR Heckenlively, GB. Arden Principles and Practice Of Clinical Electrophysiology Of Vision. St Louis : Mosby Year Book, 1991; 549– 56. 16 James AC, Maddess T., Wine S., Goldberg I. A novel multiple region PERG for glaucoma. [Abstract 4317] Invest Ophthalmol Vis Sci 1994; 35(Suppl.): 2187. Citing Literature Volume24, IssueS2May 1996Pages 28-31 ReferencesRelatedInformation

Pattern electroretinogram in treated ocular hypertension: a cross-sectional study after timolol maleate therapy.

To investigate pattern electroretinogram changes in treated ocular hypertension, we evaluated pattern electroretinogram recordings of 48 hypertensive eyes following an 8-month timolol maleate therapy. During treatment, 27 of 48 eyes had normalized intraocular pressures (15-18 mm Hg), while 21 retained elevated values (21-25 mm Hg). Twenty-eight eyes with untreated hypertension (22-25 mm Hg) lasting at least 8 months, as well as 32 untreated, normotensive eyes served as controls. When compared to untreated normotensive controls, timolol-treated eyes with either elevated or normalized intraocular pressures showed reductions in the mean electroretinographic amplitudes. However, these amplitude reductions were substantially greater in treated eyes with elevated pressures as compared to those with normalized ones. Untreated hypertensive controls showed pattern electroretinogram reductions, with respect to normal values, that were comparable to those of treated hypertensive eyes, but larger than those of treated normotensive ones. These results indicate that, in treated ocular hypertension, pattern electroretinogram losses tend to be associated with moderately increased intraocular pressures in the range of 21-25 mm Hg. Electroretinographic abnormalities may be, at least in part, prevented only by lowering intraocular pressure into a normal range.