Electroretinogram Studies Research Articles

Alterations in center-surround contrast suppression in patients with major depressive disorder

Previous pattern electroretinogram studies indicate reduced retinal contrast gain in patients with a major depressive disorder (MDD) which may contribute to alterations in visual perception. In line, psychophysical investigations reported elevated contrast thresholds in MDD. This study aims to gain insights into higher-level processing of visual information in MDD by evaluating contrast suppression. We examined contrast suppression of 21 MDD patients and 23 healthy controls (HC) using four different stimulus conditions (spatial frequencies 6.3 and 12.6 cpd at 30% and 60% background contrast) in a psychophysical test. Participants were instructed to adjust perceived contrasts between two vertical target patches, embedded in a horizontally or vertically oriented grid background. With finer stimulus gratings, MDD patients exhibited less contrast suppression compared to HC, particularly when the stimulus contrast was high (p = 0.006; MDD vs. HC = − 45%). Contrast suppression in the HC group was significantly reduced for the coarse compared to the fine grating, while contrast suppression scores in MDD did not change with the spatial properties of the stimulus. The reduced contrast suppression in patients with MDD supports the hypothesis of altered dopaminergic neurotransmission and could be attributed to alterations in the retinal receptive fields or in dysfunctional adaptation mechanisms in depression.

Retinopathy in Mucopolysaccharidoses.

PurposeTo determine the pattern(s) of onset, variation, and progression of retinopathy in patients with Mucopolysaccharidosis (MPS). DesignProspective, longitudinal, observational study. ParticipantsBetween November 2015 and March 2023, individuals with MPS were recruited from Ophthalmology clinics at the Manchester Royal Eye Hospital, United Kingdom. MethodsParticipants underwent assessment of visual acuity, corneal clouding, intraocular pressure, along with fundoscopy, ultra-widefield (UWF) colour fundus photography, fundus autofluorescence (FAF) imaging, optical coherence tomography (OCT), and electroretinography (ERG), where feasible. Main Outcome MeasuresEvaluation of findings from clinical examination, retinal imaging, and electroretinogram studies, to ascertain the presence and patterns of retinopathy. ResultsData was collected for 75 patients, including 45 MPS I, 9 MPS II, 13 MPS IVA, and 8 MPS VI, aged 3-58 years. Fundus photography was conducted in 65 patients, FAF in 61, OCT in 58, and electrodiagnostic studies in 36 participants. Retinopathy was defined as signs of retinal disease evident through retinal examination or fundus photography such as depigmentation, bone-spicule pigmentation, vascular tortuosity, retinal pigment epithelium (RPE) mottling/other changes, macular atrophy/puckering/epiretinal membranes, FAF findings such as a central hyperautofluorescent dot, hyperautofluorescent parafoveal ring, hypoautofluorescent lesions around fovea (double bull’s eye), areas of hyper/hypoautofluorescence, and extrafoveal changes, OCT imaging features such as central external limiting membrane (ELM) thickening, RPE disturbance, photoreceptor layer loss, parafoveal retinal atrophy, and outer retinal/intrachoroidal cavities, or electroretinogram studies revealing rod-mediated retinopathy or rod-cone dystrophy. Retinopathy was confirmed in 32 patients, including 25 MPS I, 4 MPS II, 1 MPS IVA, and 2 MPS VI. Five participants were first diagnosed with retinopathy with clinical examination, while 31 participants were identified on UWF colour fundus photography supported by FAF and OCT. 21 patients exhibited ERG abnormalities consistent with retinopathy. Fifteen of the total 32 participants described symptoms of nyctalopia. The onset of retinopathy varied substantially, with initial detection between 2 and 53 years of age. ConclusionsMPS patients as young as 2 may develop retinopathy, diagnosed through fundus examination, ophthalmic imaging, or ERG. Emerging treatments, including gene therapy, may prevent or stabilise retinopathy. Phenotypic data and natural history of MPS-related retinopathy are thus of paramount importance.

Safety of intravitreally delivered AAV2 vector-mediated multi-characteristic opsin genetic construct in wild type beagle dogs.

A novel adeno-associated virus 2 (AAV2)-carried multi-characteristic opsin (MCO) (MCO-010) is undergoing several clinical trials as a novel therapeutic modality for the treatment of degenerative retinal diseases including retinitis pigmentosa and Stargardt disease. The present study aimed to determine the ocular and systemic safety of MCO-010 and the AAV2 vehicle in adult Beagle dogs following intravitreal (IVT) injection. The current safety/toxicology studies spanning 13 weeks described here utilized well-documented techniques to assess the effects of IVT injection of MCO-010 up to 2.2 × 1011 genome copies (gc) per eye, or the AAV2 capsid (vehicle control) on gross behavioral and immunogenic changes, alterations in body weights, blood biochemistry, hematology, blood coagulation, gross necropsy lesions, organ weight changes and histopathology in the dogs (n = 4 per group; two males and two females per group). Immunohistochemical and functional electroretinogram studies were also conducted to determine MCO expression in the retina and determine any retinal toxicity associated with MCO-010. There were no significant deleterious effects of the MCO-010 (or the AAV2 at the tested doses) on any of the examined parameters, including the absence of any severe ocular or systemic adverse events. However, as expected, inflammation after IVT delivery of AAV2 and MCO-010 was observed in the conjunctivae of all groups of animals, although this self-resolved within 1week post-injection. Quantitative immunohistochemical analyses of MCO-010-associated mCherry revealed successful delivery of the gene therapy within the inner retina. In summary, MCO-010 demonstrated a favorable safety profile when administered to the eyes of adult Beagle dogs of both sexes at dose levels up to 2.2 × 1011 gc per eye, with no adverse effects observed. This dose was identified as the No Observed Adverse Effect Level (i.e. NOAEL) and guided selection of safe doses for human clinical trials.

Differences in Multifocal Electroretinogram Study in Two Populations of Type 1 and Type 2 Diabetes Mellitus Patients without Diabetic Retinopathy.

(1) Background: Diabetic retinopathy (DR) is a diabetes mellitus (DM) complication where neurodegeneration plays a significant role. The aim of our study was to determine the differences between type 1 DM (T1DM) and 2 DM (T2DM) in the multifocal electroretinogram (mERG).; (2) Methods: A mERG study was performed in two groups, a T1DM group with 72 eyes of 36 patients compared with 72 eyes of 36 patients with T2DM, randomly selected from our DM databases, without DR. We studied how HbA1c and DM duration affects amplitude and implicit time of mERG; (3) Results: the study of DM duration shows patients with T1DM have lower amplitude values compared to T2DM patients, although implicit time increases in patients with T2DM. HbA1c over 7% only affects T1DM patients with an increase of implicit time; (4) Conclusions: the retinas of patients with T1DM seem more sensitive to changes in HbA1c levels than in patients with DMT2, although the duration of diabetes affects both types of DM patients.

Relationship between structural and functional changes in glaucomatous eyes: a multifocal electroretinogram study

BackgroundThe nasal to temporal amplitudes ratio (N/T) of multifocal electroretinography (mfERG) scans measured within 5° of the macula can be used to detect glaucomatous change. The photopic negative response (PhNR) of mfERG elicited by a circular stimulus centered on the fovea was significantly reduced in eyes with glaucoma. The PhNR to B-wave ratio (PhNR/B) is the optimal measure of the PhNR. However, clinical superiority for evaluating glaucoma patients has not been determined between N/T and PhNR/B yet.MethodsFor morphological assessments, ganglion cell complex (GCC) in six regions and the average were measured by optical coherence tomography (OCT). For functional assessment, Humphrey visual fields (VF) with mean sensitivities (MT) and mfERG scans with parameters of N/T and the multifocal photopic negative response to B-wave ratio (mfPhNR/B) were measured. Sixty-nine eyes of 44 glaucoma patients were included and correlations between mfERG parameters and OCT or VF parameters were evaluated.ResultsThe mean age of patients was 59.4 years. The mean deviation for all eyes obtained with the VF 30–2 and VF 10–2 was − 7.00 and − 6.31 dB, respectively. Significant correlations between GCC thickness or VF parameter and the N/T were found, especially in the inferior and inforotemporal retinal areas corresponding to superior and superonasal VF sectors (GCC vs N/T; coefficient = − 7.916 and − 7.857, and MT vs N/T; coefficient = − 4.302 and − 4.437, in the inferior and inforotemporal retinal areas, respectively, all p values < 0.05). However, similar associations were not obtained between mfPhNR/B and OCT or VF parameters. The mfPhNR/B only in the inferotemporal sector was significantly correlated with the average thickness of GCC (coefficient = 4.823, P = 0.012).ConclusionsThe N/T was correlated with GCC and VF in more numbers of measurement areas than the mfPhNR/B in the current study, however, a future study modifying the stimuli and amplitudes to obtain the spatial correspondence to OCT and VF measurement will be required to evaluate the value of mfERG.

The effect of ocular dominance on macular function: A pattern electroretinogram study.

To investigate the effect of ocular dominance on pattern electroretinogram (PERG) recordings in the participants who have no ophthalmic diseases. One hundred and twelve eyes of 56 participants (mean age 32.96 ± 10.82 years) were included in this prospective, cross-sectional study. After detailed ophthalmological examination and determination of the ocular dominance with hole-in-a-card test, the PERG was performed to determine implicit time and amplitudes of P50 and N95. There were no significant interocular differences in visual acuity, refractive error, or intraocular pressure (p > 0.05 for all). Thirty-six (64.3%) of the participants had ocular dominance in the right eye. The dominant eyes had significantly higher P50 amplitude than in the fellow nondominant eyes (6.90 µV in dominant vs 5.87 µV in nondominant; p = 0.015; 95% confidence interval). There was no significant difference in N95 amplitude, N95/P50 ratio, and implicit times of P50 and N95 between the dominant and nondominant eyes of the participants (p = 0.090, p = 0.124 p = 0.817, p = 0.668; respectively). The analysis revealed a significantly increased P50 amplitude of the PERG, which is known to be highly associated with macular function, in dominant eyes of the patients when compared to fellow nondominant eyes.

Pin1 Promotes Regulated Necrosis Induced by Glutamate in Rat Retinal Neurons via CAST/Calpain2 Pathway.

The purpose of the current study was to investigate whether peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (Pin1) can interact with calpastatin (CAST) and regulate CAST/calpain2, under excessive glutamate conditions, and subsequently regulate necrosis in rat retinal neurons. Glutamate triggered CAST/calpain2-mediated necrosis regulation in primary cultured retinal neurons, as demonstrated by propidium iodide-staining and lactate dehydrogenase assay. Co-IP results and a computer simulation suggested that Pin1 could bind to CAST. Western blot, real-time quantitative polymerase chain reaction, immunofluorescence, and phosphorylation analysis results demonstrated that CAST was regulated by Pin1, as proven by the application of juglone (i.e., a Pin1 specific inhibitor). The retinal ganglion cell 5 cell line, combined with siRNA approach and flow cytometry, was then used to verify the regulatory pathway of Pin1 in CAST/calpain2-modulated neuronal necrosis that was induced by glutamate. Finally, in vivo studies further confirmed the role of Pin1 in CAST/calpain2-modulated necrosis following glutamate excitation, in the rat retinal ganglion cell and inner nuclear layers. In addition, a flash electroretinogram study provided evidence for the recovery of impaired visual function, which was induced by glutamate, with juglone treatment. Our work aims to investigate the involvement of the Pin1-CAST/calpain2 pathway in glutamate-mediated excitotoxicity.

Early Retinal Neuronal Dysfunction in Diabetic Mice: Reduced Light-Evoked Inhibition Increases Rod Pathway Signaling.

PurposeRecent studies suggest that the neural retinal response to light is compromised in diabetes. Electroretinogram studies suggest that the dim light retinal rod pathway is especially susceptible to diabetic damage. The purpose of this study was to determine whether diabetes alters rod pathway signaling.MethodsDiabetes was induced in C57BL/6J mice by three intraperitoneal injections of streptozotocin (STZ; 75 mg/kg), and confirmed by blood glucose levels > 200 mg/dL. Six weeks after the first injection, whole-cell voltage clamp recordings of spontaneous and light-evoked inhibitory postsynaptic currents from rod bipolar cells were made in dark-adapted retinal slices. Light-evoked excitatory currents from rod bipolar and AII amacrine cells, and spontaneous excitatory currents from AII amacrine cells were also measured. Receptor inputs were pharmacologically isolated. Immunohistochemistry was performed on whole mounted retinas.ResultsRod bipolar cells had reduced light-evoked inhibitory input from amacrine cells but no change in excitatory input from rod photoreceptors. Reduced light-evoked inhibition, mediated by both GABAA and GABAC receptors, increased rod bipolar cell output onto AII amacrine cells. Spontaneous release of GABA onto rod bipolar cells was increased, which may limit GABA availability for light-evoked release. These physiological changes occurred in the absence of retinal cell loss or changes in GABAA receptor expression levels.ConclusionsOur results indicate that early diabetes causes deficits in the rod pathway leading to decreased light-evoked rod bipolar cell inhibition and increased rod pathway output that provide a basis for the development of early diabetic visual deficits.

An asymmetric outer retinal response to drifting sawtooth gratings.

Electroretinogram (ERG) studies have demonstrated that the retinal response to temporally modulated fast-ON and fast-OFF sawtooth flicker is asymmetric. The response to spatiotemporal sawtooth stimuli has not yet been investigated. Perceptually, such drifting gratings or diamond plaids shaded in a sawtooth pattern appear brighter when movement produces fast-OFF relative to fast-ON luminance profiles. The neural origins of this illusion remain unclear (although a retinal basis has been suggested). Thus we presented toad eyecups with sequential epochs of sawtooth, sine-wave, and square-wave gratings drifting horizontally across the retina at temporal frequencies of 2.5-20 Hz. All ERGs revealed a sustained direct-current (DC) transtissue potential during drift and a peak at drift offset. The amplitudes of both phenomena increased with temporal frequency. Consistent with the human perceptual experience of sawtooth gratings, the sustained DC potential effect was greater for fast-OFF cf. fast-ON sawtooth. Modeling suggested that the dependence of temporal luminance contrast on stimulus device frame rate contributed to the temporal frequency effects but could not explain the divergence in response amplitudes for the two sawtooth profiles. The difference between fast-ON and fast-OFF sawtooth profiles also remained following pharmacological suppression of postreceptoral activity with tetrodotoxin (TTX), 2-amino-4-phosphonobutric acid (APB), and 2,3 cis-piperidine dicarboxylic acid (PDA). Our results indicate that the DC potential difference originates from asymmetries in the photoreceptoral response to fast-ON and fast-OFF sawtooth profiles, thus pointing to an outer retinal origin for the motion-induced drifting sawtooth brightness illusion.

Crizotinib reduces the rate of dark adaptation in the rat retina independent of ALK inhibition.

Crizotinib (Xalkori) is a tyrosine kinase inhibitor of both anaplastic lymphoma kinase (ALK) and mesenchymal-epithelial transition factor (c-Met). Though not predicted from standard nonclinical toxicological evaluation, visual disturbance became a frequently observed adverse event in humans. To understand the possible mechanism of this vision effect, an in vivo electroretinogram (ERG) study was conducted to assess retinal functional changes following oral administration of crizotinib. Immunohistochemical (IHC) staining of ALK and c-Met in the neural retinas of human, non-human primate, dog, rat, and mouse was used to aid in the animal model selection. ALK IHC staining was identified predominantly in the ganglion cell and inner nuclear layers of most species evaluated, in the inner plexiform layer in human and rodent, and in the nerve fiber layer in human and rat only. There was no apparent staining of any layer of the neural retina for c-Met in any of the species evaluated. ERG measurements identified a significant reduction in b-wave amplitude during the initial phase of dark adaptation in the crizotinib-treated rats. ERGs were also taken following oral administration of PF-06463922 (an ALK-selective inhibitor), for an understanding of potential kinase involvement. ERG effects were not observed in PF-06463922-treated animals when comparable exposures in the vitreous humor were achieved. Collectively, our results suggest that the ERG b-wave amplitude decreases during dark adaption following crizotinib administration may be related to signaling changes within the retina in rats, likely independent of ALK inhibition.

Rod Photoreceptor Ribbon Synapses in DBA/2J Mice Show Progressive Age-Related Structural Changes

The DBA/2J mouse is a commonly used animal model in glaucoma research. The eyes of DBA/2J mice show severe age-related changes that finally lead to the degeneration of retinal ganglion cells and the optic nerve. Recent electroretinogram studies identified functional deficits, which suggest that also photoreceptor cells are involved in the pathological processes occurring in the DBA/2J mouse retina. In a comparative study, we examined anatomical and molecular changes in the retinae of DBA/2J and C57BL/6 control mice with light and electron microscopy and with PCR analyses. In the retina of the DBA/2J mouse, we found a thinning of the outer plexiform layer, the first synaptic layer in the transfer of visual signals, and age-dependent and progressive degenerative structural changes at rod photoreceptor ribbon synapses. The structural ribbon changes represent a photoreceptor synaptic phenotype that has not yet been described in this animal model of secondary angle-closure glaucoma. Furthermore, genes of the classical complement cascade were upregulated in the photoreceptor cells of aging DBA/2J mice, suggesting a putative link between ribbon synapse degradation and the innate immune system.

Structural and functional outcomes after treatment of uveitic macular oedema: an optical coherence tomography and multifocal electroretinogram study

Background: The aim was to evaluate the correlation between the anatomical and functional outcomes before and after treatment of uveitic macular oedema.Methods: Thirty‐three eyes of 33 patients with uveitic macular oedema were included in the present study. Visual acuity (VA), optical coherence tomography (OCT) and multifocal electroretinogram (mfERG) were measured before and after treatment of the macular oedema. Correlation analyses between VA, OCT and mfERG parameters were performed.Results: The VA and mfERG measurements showed statistically significant improvement after treatment of the macular oedema (p < 0.01) and OCT‐measured central foveal thickness decreased significantly from 434 ± 135 µm before treatment to 267 ± 92 µm after treatment (p < 0.001). Correlation analyses showed that uveitic central foveal thickness before treatment was correlated with mfERG N1 response amplitude of area 1 (Spearman's r = ‐0.62, p < 0.001). VA (logMAR) after treatment had a negative correlation with the mfERG N1 response amplitude of area 1 (Spearman's r = ‐0.56, p = 0.001). Also, there was no correlation between the final VA and pre‐treatment OCT and mfERG measurements.Conclusion: This study deals with cystoid macular oedema associated with recurrent uveitis. In cystoid macular oedema, the value of mfERG before treatment is related to the central foveal thickness and VA. In contrast, after treatment the decrease of macular thickness is not always followed by an improvement of mfERG and VA. This supports the view that in uveitic macular oedema, the decrease in macular thickness after treatment may not be used as a predictor of improvement of macular function.

Behavioral and Physiological Response ofMusca domesticato Colored Visual Targets

A better understanding of the visual attraction of house flies to colors and patterns is needed to improve fly trap performance. This study combined physiological responses measured with electroretinogram studies of the house fly's compound eyes and ocelli with behavioral attraction of flies to reflective colors and patterns in light tunnel assays. Compound eye and ocellar electroretinogram responses to reflected light were similar, with the largest responses to white and blue followed by yellow, red, green, and black. However, data from light tunnel behavioral assays showed that flies were attracted to white and blue light but were repelled by yellow. The addition of a black line pattern enhanced the attractiveness of blue visual targets, whereas yellow lines decreased attractiveness. Sensory input from the compound eye and the ocellus seems to be integrated to direct fly behavior. There is a direct correlation of house fly attractiveness to visual targets and the intensity of electrophysiological response, except for the yellow targets, which repel flies despite of intense electrophysiological response.

Myopia Progression in Children is Associated with Regional Changes in Retinal Function: A Multifocal Electroretinogram Study

Introduction:To determine if retinal function is associated with myopia progression in children over a one-year period.Methods:Twenty-two children (mean = 11±1 years) were recruited in this study. Refraction and global flash multifocal electroretinogram measurements were performed at 49% and 96% contrasts at the initial visit and after 1 year. The amplitudes and implicit times of direct (DC) and induced components (IC) of the mfERG responses were pooled into five concentric rings for analysis. Pearson's correlation (r) was performed to determine if myopia progression was correlated with the changes in these mfERG's parameters.Results:The mean myopia progression was −0.45±0.34D (range = plano∼−1.38). At 49% contrast, the IC implicit times from rings 2 to 5 (r = −0.57∼−0.65, p < 0.01), and the DC implicit time at ring 3 (r = 0.55, p < 0.01), were significantly delayed with myopia progression. At 96% contrast, only the IC implicit time within ring 1 was delayed (r = −0.60, p < 0.01). In contrast, neither DC nor IC amplitudes at both contrasts were affected (r = −0.11∼0.28, all p > 0.05).Conclusions:Myopia progression in children delayed IC implicit time at 49% contrast predominantly at the paracentral retina. These results support our previous findings (Ho et al., 2011) that the effect of myopia development on retinal function is regional dependent.

Optical coherence tomography and multifocal electroretinogram study in human immunodeficiency virus‐positive children without infectious retinitis

Background: The aim was to evaluate the macular structure and function in children with human immunodeficiency virus (HIV) disease without cytomegalovirus retinitis or visual symptoms.Methods: Thirty‐eight eyes of 19 HIV‐positive children (Group A) were examined. Group B included 20 (40 eyes) age‐ and sex‐matched control subjects. Each individual underwent a complete ophthalmic examination, optical coherence tomography (OCT) scan and multifocal electroretinogram (mfERG) recording.Results: In all patients, visual acuity and colour vision testing were normal. The mean foveal thickness in groups A and B was 190.28 ± 26.58 (SD) µm and 169.47 ± 10.17 µm, respectively (p = 0.0002). In Group A, the mean retinal response density of the fovea (area 1) was 19.87 ± 10.16-nV/deg2 and the latency was 38.56 ± 1.18-ms. In the parafoveal area (area 2), the mean retinal response density was 10.82 ± 2.34-nV/deg2 and the mean latency was 36.52 ± 1.73-ms. In the perifoveal area (area 3), the mean retinal response density was 10.83 ± 0.90-nV/deg2 and the mean latency was 36.36 ± 1.90-ms. In Group B, the mean retinal response density of area 1 was 22.02 ± 0.9-nV/deg2 and the mean latency was 32.56 ± 1.25-ms. In area 2, the mean retinal response density was 12.23 ± 0.55-nV/deg2 and the mean latency was 30.84 ±1.22-ms. Finally, in the perifoveal area (area 3), the mean retinal response density was 12.74 ± 0.44-nV/deg2 and the mean latency was 29.7 ± 11.09-ms. The differences in amplitude and latency were statistically significant.Conclusion: Increased foveal thickening and significant decrease of the electrical activity of areas 1, 2 and 3 were found in HIV‐positive children. These findings suggested some subclinical dysfunction of the photoreceptors and the inner retinal layers of the fovea in HIV‐positive children with normal vision and without ocular disease.

Nitric oxide amplifies the rat electroretinogram

It is well established that nitric oxide (NO) participates in retinal signal processing through stimulation of its receptor enzyme, soluble guanylyl cyclase (sGC). However, under pathological conditions such as uveoretinitis, diabetic or ischemic retinopathy, elevated NO concentrations may cause protein S-nitrosation and peroxynitrite formation in the retina, promoting cellular injury and apoptosis. Previous electroretinogram (ERG) studies demonstrated deleterious effects of NO on the retinal light response, but showed no evidence for a role in normal signal processing. To better understand the function of NO in ocular physiology, we investigated the effects of exogenous NO, produced by NO donors with different release kinetics, on the flash ERG of the rat. Within a limited concentration range, NO strongly amplified ERG a- and b-waves, oscillatory potentials, and the scotopic threshold response. Amplification exceeded 100% under dark adaptation, whereas the photopic ERG and the isolated cone response were increased by less than 50%. Blocking photoreceptor-bipolar cell synapses by AP-4 demonstrated a significant increase of the isolated a-wave by NO, and modeling the ERG generator PIII supported photoreceptors as primary NO targets. The sGC inhibitors ODQ and NS2028 did not reduce NO-dependent ERG amplification, ruling out an involvement of the classical NO effector cyclic GMP. Using immunohistochemistry, we show that illumination and exogenous NO altered the S-nitrosation level of the photoreceptor layer, suggesting that direct protein modifications caused by elevated levels of NO may be responsible for the observed phenomenon.

Functional involvement of cone photoreceptors in advanced glaucoma: a multifocal electroretinogram study

The purpose of the study is (1) to demonstrate the anatomical variation of cone photoreceptor density across normal retina as a sectoral amplitude asymmetry of photopic multifocal electroretinogram (mfERG) and (2) to study the potential presence of sequential or differential, functional cone photoreceptor damage in glaucoma using this amplitude asymmetry. A 37-Block scaled mfERG was recorded from 22 controls and 27 glaucoma subjects. The N1 and P1 amplitudes of averaged responses from corresponding zones nasal and temporal to fovea were analyzed for asymmetry in controls and glaucoma subjects. Amplitude asymmetry was demonstrable for both N1 (p < 0.001) and P1 (p < 0.001) parameters in control subjects. Although this amplitude asymmetry was preserved in glaucoma subjects with moderate field defects, it was not demonstrable in patients with advanced field defects. The anatomical variation in cone photoreceptor distribution across normal retina is demonstrated as an amplitude asymmetry in first order kernel responses of mfERG. The cone photoreceptors in the region nasal to fovea appear to be affected only in advanced glaucoma possibly suggesting that photoreceptors could follow a sequential damage like the overlying neuroretinal rim in glaucoma.

The effect of physical effort on retinal activity in the human eye: rod and cone flicker electroretinogram studies

The aim of our study was to assess the effect of physical exercise with increasing intensity on neuroretinal activity in healthy subjects (n = 30). We analysed the amplitude and implicit time of b-wave electroretinogram (ERG) responses in two experiments: (1) for a scotopic blue 10 Hz flicker stimulus (rod-mediated responses), and (2) for a photopic white 30 Hz flicker stimulus (cone-mediated responses). Using a cycloergometer, three 10-minute effort-tests with increasing intensity were performed. Each participant was assigned individual workload values (W) below the lactate threshold (40% VO(2)max), at the lactate threshold (60-65% VO(2)max) and above the lactate threshold (80% VO(2)max). Five ERG recordings were taken: (1) before, (2-4) immediately after the three subsequent efforts and (5) 1 hour after the completion of the last effort. The right eye was selected for monocular stimulation in both experiments. After the first effort (40% VO(2)max), we observed an increased amplitude (p < 0.001) and decreased implicit time of the b-wave (p < 0.01) in cone-mediated responses, and no significant effects in rod-mediated responses. Despite the increase in effort intensity, the cone b-wave amplitude remained unchanged, whereas the rod b-wave amplitude significantly decreased after the subsequent efforts (p < 0.001). Rod-mediated responses were more susceptible to effort-induced homeostasis disruptions than the cone-mediated responses. The application of ERGs may be used as neurophysiological criteria in defining the cardiovascular status of the physical performance.

Head-up tilt lowers IOP and improves RGC dysfunction in glaucomatous DBA/2J mice

The inbred DBA/2J (D2) mouse strain is a well established model of spontaneously elevated intraocular pressure (IOP), progressive glaucomatous loss of retinal ganglion cells (RGCs), and early damage of RGC axons at the level of optic nerve head. Pattern electroretinogram (PERG) studies have shown that surviving RGCs in mice 6–12-month-old may be dysfunctional. RGC dysfunction seems to be IOP-dependent, since it may be exacerbated by means of acute IOP elevation with head-down body tilt. Here we test the hypothesis that head-up body posture lowers IOP, resulting in improvement of PERG amplitude in aged D2 mice with glaucoma. We show that head-up body tilt induces age-independent IOP lowering whose magnitude increases with the angle of tilt. For a fixed angle (−60°) of head-up tilt, IOP progressively decreases with a time constant of about 5 min and stabilizes at a value lower by about 5–6 mm Hg compared to the baseline. Head-up tilt also results in an improvement of PERG amplitude in older D2 mice with glaucoma but not in younger D2 mice without glaucoma. Improvement of PERG amplitude in aged D2 mice upon head-up-induced IOP lowering is consistent with the idea that RGCs undergo a stage of IOP-dependent, reversible dysfunction before death. The head-up IOP/PERG protocol may represent a non-invasive way to probe the potential for recovery of RGC dysfunction in D2 mice.

The electroretinogram in children

The electroretinogram is an essential tool in the evaluation of the functional integrity of the retina, which may be especially useful in preverbal children. The present review describes the modifications needed for performing an electroretinogram in young children. Also, we present electroretinogram studies that have added to our understanding of the maturation of the visual system, the development of retinopathy of prematurity, and ametropia. The selected articles were grouped into four subjects: the technical modifications for performing a pediatric electroretinogram, including the possible need for sedation, the patient's position, and the recording electrodes; the maturation of the electroretinogram in preterm infants and in the first years of life; advancements in the understanding of retinopathy of prematurity; and understanding the development of ametropia based on the electroretinogram findings. Although the technique for performing an electroretinogram must be modified for young children, when needed, it can and should be performed early in life. This will yield an early diagnosis that may be useful for planning family and personal life.