Flash Visual Evoked Potentials Research Articles

The Effect of Magnesium on Visual Evoked Potentials in L-NAME-Induced Hypertensive Rats.

In the literature, although there are many studies regarding complications of hypertension, information concerning its influence on visual evoked potentials (VEPs) is limited. This study aims to clarify the possible therapeutic effects of the preferential magnesium (Mg) treatment on VEPs in an experimental hypertension model. Rats were divided into four groups as follows: control, Mg treated (Mg), N(omega)-nitro-L-arginine methyl ester (L-NAME) hypertension, and L-NAME hypertension + Mg treated (L-NAME + Mg). Hypertension was induced by L-NAME which was given to rats orally over 6weeks (25mg/kg/day in drinking water). A magnesium-enriched diet (0.8g/kg) was given to treatment groups for 6weeks. Systolic blood pressure (SBP) was determined by using the tail-cuff method. Flash VEPs were recorded. Our results revealed that the SBP was significantly increased in the L-NAME group compared to control. Magnesium treatment significantly attenuated SBP in the hypertensive rats compared to the L-NAME group. The mean latencies of P1, N1, P2, N2, and P3 components were significantly prolonged in hypertensive rats compared to control. Treatment with Mg provided a significant decrease in the latencies of P1, N1, P2, N2, and P3 potentials in the L-NAME + Mg group compared to the L-NAME group. Plasma Mg levels were increased in the L-NAME + Mg group compared to the L-NAME group. No change was detected in the Mg levels of the brains in all experimental groups. Magnesium treatment had no effect on the brain nitrate/nitrite and thiobarbituric acid-reactive substances (TBARS) levels in hypertensive rats compared to non-treated rats. There was a positive correlation between the brain TBARS levels and SBP of the rats. The present study suggests that Mg supplementation has the potential to prevent VEP changes in the L-NAME-induced hypertension model.

Low-dose carbon monoxide inhalation protects neuronal cells from apoptosis after optic nerve crush

Glaucomatous optic neuropathy, including axonal degeneration and apoptotic death of retinal ganglion cells (RGCs), eventually leads to irreversible visual impairment. Carbon monoxide (CO) acts as a therapeutic agent against neural injury via its anti-apoptotic effect. Here we hypothesized that low-dose CO inhalation can protect RGCs in a rat model of optic nerve crush (ONC). ONC was performed on adult male Sprague Dawley rats to imitate glaucomatous optic damage. Low-dose CO (250 ppm) or air was inhaled for 1 h immediately after ONC, and all the tests were carried out 2 weeks later. Flash visual evoked potentials (FVEP) and pupil light relax (PLR) were recorded for the assessment of visual function. RGC density was evaluated by hematoxylin and eosin staining and Fluorogold labeling. Retinal apoptotic process was assessed by TUNEL staining and caspase-3 activity measurement. Low-dose CO treatment significantly ameliorated the abnormalities of FVEP and PLR induced by ONC. As expected, the RGC density was increased remarkably by CO inhalation after the glaucomatous optic nerve insult. Moreover, CO treatment after ONC significantly decreased the number of TUNEL-positive cells in ganglion cell layer and attenuated the retinal caspase-3 activity. Low-dose CO inhalation protects RGCs from optic nerve injury via inhibiting caspase-3 dependent apoptosis.

Postconditioning with inhaled hydrogen promotes survival of retinal ganglion cells in a rat model of retinal ischemia/reperfusion injury

Retinal ischemia/reperfusion (I/R) injury plays a crucial role in the pathophysiology of various ocular diseases. Intraperitoneal injection or ocular instillation with hydrogen (H2)-rich saline was recently shown to be neuroprotective in the retina due to its anti-oxidative and anti-inflammatory effects. Our study aims to explore whether postconditioning with inhaled H2 can protect retinal ganglion cells (RGCs) in a rat model of retinal I/R injury. Retinal I/R injury was performed on the right eyes of rats and was followed by inhalation of 67% H2 mixed with 33% oxygen immediately after ischemia for 1h daily for one week. RGC density was counted using haematoxylin and eosin (HE) staining and retrograde labeling with cholera toxin beta (CTB). Visual function was assessed using flash visual evoked potentials (FVEP) and pupillary light reflex (PLR). Potential biomarkers of retinal oxidative stress and inflammatory responses were measured, including the expression of 4-Hydroxynonenalv (4-HNE), interleukin-1 beta (IL1-β) and tumor necrosis factor alpha (TNF-α). HE and CTB tracing showed that the survival rate of RGCs in the H2-treated group was significantly higher than the rate in the I/R group. Rats with H2 inhalation showed better visual function in assessments of FVEP and PLR. Moreover, H2 treatment significantly decreased the number of 4-HNE-stained cells in the ganglion cell layer and inhibited the retinal overexpression of IL1-β and TNF-α that was induced by retinal I/R injury. Our results demonstrate that postconditioning with inhaled high-dose H2 appears to confer neuroprotection against retinal I/R injury via anti-oxidative, anti-inflammatory and anti-apoptosis pathways.

May clinical neurophysiology help to predict the recovery of neurological early rehabilitation patients?

BackgroundSo far, the role of clinical neurophysiology in the prediction of outcome from neurological and neurosurgical early rehabilitation is unclear.MethodsClinical and neurophysiological data of a large sample of 803 early rehabilitation cases of the BDH-Clinic Hessisch Oldendorf in Northern Germany have been carefully reviewed. Most patients (43.5 %) were transferred to rehabilitation after stroke, mean age was 66.6 (15.5) years. Median somatosensory (SEP), auditory (AEP) and visual evoked potentials (VEP) along with EEG recordings took place within the first two weeks after admission. Length of stay (LOS) in early rehabilitation was 38.3 (37.2) days.ResultsAbsence of SEP on one or both sides was associated with poor outcome, χ2 = 12.98 (p = 0.005); only 12.5 % had a good outcome (defined as Barthel index, BI ≥50) when SEP were missing on both sides. In AEP, significantly longer bilateral latencies III were observed in the poor outcome group (p < 0.05). Flash VEP showed that patients in the poor outcome group had a significantly longer latency III on both sides (p < 0.05). The longer latency III, the smaller BI changes (BI discharge minus admission) were observed (latency III right r = −0.145, p < 0.01; left r = −0.206, p < 0.001). While about half of the patients with alpha EEG activity belonged to the good outcome group (80/159, 50.3 %), only 39/125 (31.2 %) with theta and 5/41 (12.2 %) with delta rhythm had a favourable outcome, χ2 = 24.2, p < 0.001.ConclusionsResults from this study suggest that loss of median SEP, prolongation of wave III in AEP and flash-VEP as well as theta or delta rhythms in EEG are associated with poor outcome from neurological early rehabilitation. Further studies on this topic are strongly encouraged.

Normative data of Visual Evoked Potential in children and correlation with age

Background: Visual Evoked Potential is the assessment of the visual pathway and the visual cortex. The present study was descriptive analysis of normal VEP between the age of 6 months to 4 years of age and the determination of the neuronal development among healthy children of above age group.Materials and Methods: The study was conducted in neurological lab of BPKIHS on healthy children (n=36) of well-baby clinic between the age of 0.5 to ≤4 years (yr). Subjects were divided into subgroup 1(0.5 to ≤2 yr), subgroup 2(2 to ≤3 yr) and subgroup 3(3 to ≤4 yr). Visual stimulator provided with flash light emitting diode (LED) goggle was used to stimulate the retina and VEP recording was done. Flash VEP parameters: latencies (N90, P120) and amplitude (N90-P120) were recorded. Post hoc (Bonferroni) analysis was done for comparing VEP variables. Pearson correlation and scatter plot with trend line analysis were done for VEP with respect to ageResults: VEP latencies of children, age-group 3 to Μ4 yr showed significantly less N90 latency on right eye stimulation comparing age-group 0.5 to Μ2 yr (103.75±22.54 vs. 79.09±17.77ms, p=0.012). P120 latency was significantly less on right eye stimulation (148.5±15.38 vs. 116.67±13.65ms p=0.001) and on left eye stimulation (145.91±18.11 vs. 116.67±13.65 ms, p=0.001) in age-group 3 to Μ4 yr children as compared to age-group 0.5 to Μ2 yr.Conclusion: Significant decrement of VEP latencies as age advances which explains the maturation of central nervous system and functionally approaching to adult value at around 3 to 4 yr.Asian Journal of Medical Sciences Vol.7(2) 2015 39-43

Neuroprotective effect of 4-(Phenylsulfanyl)butan-2-one on optic nerve crush model in rats

This study is to investigate the effect of coral-related compound, 4-(phenylsulfanyl)butan-2-one (4-PSB-2) on optic nerves (ON) and retinal ganglion cells (RGC) in a rat model subjected to ON crush. The ONs of adult male Wistar rat (150–180 g) were crushed by a standardized method. The control eyes received a sham operation. 4-PSB-2 (5 mg/kg in 0.2 mL phosphate-buffered saline) or phosphate-buffered saline (PBS control) was immediately administered after ON crush once by subcutaneous injection. Rats were euthanized at 2 weeks after the crush injury. RGC density was counted by retrograde labeling with FluoroGold (FG) application to the superior colliculus, and visual function was assessed by flash visual evoked potentials (FVEP). TUNEL assay, immunoblotting analysis of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX2) in the retinas, and immunohistochemistry of ED1 in the ON were evaluated. Two weeks after the insult, the RGC densities in the central and mid-peripheral retinas in ON-crushed, 4-PSB-2-treated rats were significantly higher than that of the corresponding ON-crushed, PBS-treated rats FVEP measurements showed a significantly better preserved latency of the P1 wave in the ON-crushed, 4-PSB-2-treated rats than the ON-crushed, PBS treated rats. TUNEL assays showed fewer TUNEL positive cells in the ON-crushed, 4-PSB-2-treated rats. The number of ED1 positive cells was reduced at the lesion site of the optic nerve in the ON-crushed, 4-PSB-2-treated group. Furthermore, administration of 4-PSB-2 significantly attenuated ON crush insult-stimulated iNOS and COX2 expression in the retinas. These results demonstrated that 4-PSB-2 protects RGCs and helps preserve the visual function in the rat model of optic nerve crush. 4-PSB-2 may work by being anti-apoptotic and by attenuation of the inflammatory responses involving less ED1 positive cells infiltration in ON as well as suppression of iNOS/COX-2 signaling pathway in the retinas to rescue RGCs after ON crush injury.

Clinical value of electrophysiology in determining the diagnosis of visual dysfunction in neuro-ophthalmology patients.

To assess clinical value of visual electrophysiology in identifying causes of visual dysfunction in patients referred from neuro-ophthalmology clinics. A review of 410 subjects (aged 0.3-88 years) referred for visual electrophysiology from neuro-ophthalmologists between 2009 and 2013 was performed. Subjects were divided into those with unexplained poor vision, visual field defects, visual symptoms or other reasons (e.g. monitoring for drug toxicity or known conditions). Subjects underwent pattern, full-field and multifocal electroretinography (ERG) and pattern visual evoked potential (VEP) tests. Flash and multifocal VEP were included where indicated. Most subjects referred for poor vision (n = 158) had electrophysiology findings suggestive of retinopathy (37 %) or post-retinal pathology (34 %). Those with poorer vision (worse than 6/24) were more likely to have abnormal recordings (86 vs. 62 %, p = 0.002). Among subjects with unexplained visual field defects (n = 102), findings of retinopathy, post-retinal pathology and normal recordings were noted in 31, 24 and 28 %, respectively. Most subjects with other visual symptoms (n = 97) had normal findings (69 %). The multifocal ERG was most sensitive for detecting retinopathy (96 %) and maculopathy (95 %), while pattern VEP was most sensitive for post-retinal pathology (94 %). An indeterminate result was noted in 9 %. Electrophysiology was effective in differentiating between retinopathy, post-retinal pathology and normality in 91 % of subjects. Pre-testing provisional diagnoses of retinopathy and post-retinal pathology were revised in 30 and 42 %, respectively, after electrophysiology. Appreciation of characteristics of each test, correlation with the clinical picture and interpretation of results in totality are required to localize the site of pathology.

Roles of Treg/Th17 Cell Imbalance and Neuronal Damage in the Visual Dysfunction Observed in Experimental Autoimmune Optic Neuritis Chronologically.

Optic neuritis associated with multiple sclerosis and its animal model, experimental autoimmune optic neuritis (EAON), is characterized by inflammation, T cell activation, demyelination, and neuronal damage, which might induce permanent vision loss. Elucidating the chronological relationship among the features is critical for treatment of demyelinating optic neuritis. EAON was induced in C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein subcutaneously, and visual function was assessed by flash-visual evoked potential (F-VEP) at days 7, 11, 14, 19, 23, 28 post-immunization. Retinal ganglion cell (RGC) apoptosis was measured by terminal-deoxynucleotidyl transferase-mediated nick-end labeling. Demyelination and axonal damage were verified with myelin basic protein (MBP) and β-amyloid precursor protein staining, respectively. Real-time polymerase chain reaction quantified IL-17, IL-1β, TGF-β, FoxP3, IL-6, and IL-10 mRNA expression in the optic nerve, as well as FoxP3 and IL-17 staining. Systemic changes of Th17 and Treg cells were tested by flow cytometry in spleen. F-VEP latency was prolonged at 11 days and peaked at 23 days commensurate with demyelination. However, F-VEP amplitude was reduced at 11 days, preceding axon damage, and was exacerbated at 23 days when a peak in RGC apoptosis was detected. Th17 cells up-regulated as early as 7 days and peaked at 11 days, while Treg cells down-regulated inversely compared to Th17 cells change as verified by IL-17 and FoxP3 expression; spleen cell samples were slightly different, demonstrating marked changed at 14 days. Treg/Th17 cell imbalance in the optic nerve precedes and may initiate neuronal damage of axons and RGCs. These changes are commensurate with the appearances of visual dysfunction reflected in F-VEP and hence may offer a novel therapeutic avenue for vision preservation.

Delayed visual evoked potentials in children with Plasmodium falciparum malaria and reduced consciousness

We aimed to investigate the visual evoked potential (VEP) in children unconscious with Plasmodium falciparum malaria, a common cause of death in Africa. Flash VEPs were carried out in Malawi during one peak malaria season. Children were included in the study if they had P. falciparum malaria and reduced consciousness – Blantyre Coma Score (BCS) 4 or less out of 5. Initial VEPs were performed after stabilising the patient and commencing treatment. To investigate optimal VEP protocols, varying stimulus parameters were tested. Where possible, VEPs were repeated daily until the child recovered full consciousness (BCS 5). The initial traces of 40 children were included in the study and serial traces were obtained in 30 of these. Mean VEP latency was greater on admission than either on day 1 or at BCS 5 (paired t-test, P P P. falciparum malaria have delayed VEP responses and recovery occurs in parallel with return to normal consciousness. VEP recordings are quick and reproducible and may find a place in assessing levels of coma and cerebral function in severe malaria.

Neuregulin-1 protects against acute optic nerve injury in rat model

ObjectivesIn this study, we employed a rat model and examined the expression pattern of neuregulin-1 (NRG-1) in optic nerve and retinal ganglion cells (RGCs) in response to optic nerve injury to understand the role of NRG-1 in conferring protection against acute optic nerve injury. MethodForty-eight male rats were randomly divided into two groups, the sham-operation group (n=24) and optic nerve injury group (n=24). Flash visual evoked potentials (FVEP) and fundography images were acquired at different time points following optic nerve injury (2h, 1d, 2d, 7d, 14d and 28d). Semi-quantitative analysis of NGR-1 expression pattern was performed by immunohistochemistry (IHC) staining. In a related experiment, 100 male rats were randomly divided into NGR-1 treatment group (n=60) (treated with increasing dose of NGR-1 at 0.5μg, 1μg and 3μg), normal saline (NS) group (n=20) and negative control group (n=20). Optic nerve injury was induced in all the animals and in situ cell death was measured by detecting the apoptosis rates using TUNEL assay. ResultsFundus photography results revealed no detectable differences between the sham-operation group and optic nerve injury group at 2h, 1d, 2d and 7d. However at 2weeks, the optic discs turned pale in all animals in the optic nerve injury group. NRG-1 expression increased significantly at all time points in the optic nerve injury group (P<0.05), compared to the sham-operation group, with NRG-1 expression peaking at 14d and gradually declining by 28d. Statistically significant differences in amplitude and latency of P100 wave were also detected between the optic nerve injury and sham-operation group (P<0.05). In related experiment, compared to NS group, treatment with 1μg and 3μg of recombinant human NRG-1 resulted in statistically significant FVEP-P100 amplitude values (all P<0.05). Further, compared to the NS group, ganglion cell apoptosis was dramatically reduced in the NRG-1 group at all time points and the reduction was statistically significant in 3μg NRG-1 treatment group at 7d, 14d and 28d (all P<0.05). ConclusionOur results strongly suggest that NRG-1 is highly effective in preserving normal optic nerve function and is essential for tissue repair following optic nerve injury. Thus, NRG-1 expression confers protection against acute optic nerve injury in a dose-dependent manner.

Outcome and prognosis of hypoxic brain damage patients undergoing neurological early rehabilitation.

BackgroundThe prevalence of patients suffering from hypoxic brain damage is increasing. Long-term outcome data and prognostic factors for either poor or good outcome are lacking.MethodsThis retrospective study included 93 patients with hypoxic brain damage undergoing neurological early rehabilitation [length of stay: 108.5 (81.9) days]. Clinical data, validated outcome scales (e.g. Barthel Index—BI, Early Rehabilitation Index—ERI, Glasgow Coma Scale—GCS, Coma Remission Scale—CRS), neuroimaging data, electroencephalography (EEG) and evoked potentials were analyzed.Results75.3% had a poor outcome (defined as BI <50). 38 (40.9%) patients were discharged to a nursing care facility, 21 (22.6%) to subsequent rehabilitation, 17 (18.3%) returned home, 9 (9.7%) needed further acute-care hospital treatment and 8 (8.6%) died. Barthel Index on admission as well as coma length were strong predictors of outcome from hypoxic brain damage. In addition, duration of vegetative instability, prolongation of wave III in visual evoked potentials (flash VEP), theta and delta rhythm in EEG, ERI, GCS and CRS on admission were related to poor outcome. All patients with bilateral hypodensities of the basal ganglia belonged to the poor outcome group. Age had no independent influence on functional status at discharge.ConclusionsAs with other studies on neurological rehabilitation, functional status on admission turned out to be a strong predictor of outcome from hypoxic brain damage.

Visual Evoked potential signal processing and analysis for normal and galucomic eyes

Visual evoked potentials (VEPS) are obtained from optic tract by recording the evoked potentials generated by retinal stimulation. The flash VEP (FVEP) is used less frequently than pattern reversal VEP (PRVEP) because; it shows great variation in both latency and amplitude. The present study was undertaken to evaluate the effect of change of wavelength of flash and change of check size on the parameters of visual evoked potential (amplitude and latency) in normal individuals and glaucoma patients. The group of healthy subjects in the age of 20-45 years while the group of glaucoma subjects where  in the age of 25-50 years.  The two groups were exposed to flash VEP with white light and blue color and they also were exposed to checks subtending a visual angles of 15, 30,60 and 120 minutes of arc. The measured data were statistically analyzed and summarized by histograms. The interindividual and intraindividual in latencies and amplitudes for FVEP were assessed using  the coefficient of variation (COV). In conclusion, monochromatic flash VEP was preferred than white as there were minimal inter and intra individual variation of latencies and amplitudes. The most preferred check size in PRVEP was 120' for  the two groups. Â

Efficacy of Intravitreal Injections of Antivascular Endothelial Growth Factor Agents in a Rat Model of Anterior Ischemic Optic Neuropathy

We investigated the efficacy of intravitreal injections of anti-VEGF agents in a rat model of anterior ischemic optic neuropathy. We applied laser-induced photoactivation on the optic nerve head after intravenously administered rose bengal (RB). The rats immediately received an intravitreal injection of either ranibizumab or PBS. The density of retinal ganglion cells (RGCs) was calculated using retrograde FluoroGold labeling. Visual function was assessed by flash visual-evoked potentials (FVEP). We investigated TUNEL assays of the retinal sections and ED1 staining of the optic nerve. After treatment, the RGC densities in the anti-VEGF-treated rats were not statistically significant different from those of the PBS-treated rats (57.0% vs. 40.0% in the central retinas; 39.8% vs. 33.6% in midperipheral retinas, both P > 0.05). Measurements of FVEP showed no statistically significant differences in preserved latency or amplitude of the P1 wave between anti-VEGF and PBS groups (latency 131 ± 15 ms versus 142 ± 14 ms, P = 0.157; amplitude 34 ± 12 μv versus 41 ± 13 μv, P = 0.423). Assays of TUNEL showed that there was no statistical difference in the number of apoptotic cells in the RGC layers between anti-VEGF and PBS groups (7.0 ± 0.8 cells/high-power field [HPF] versus 7.8 ± 1.3 cells/HPF; P = 0.275). In the optic nerves, we did not observe statistically significant differences in ED1-positive cells/HPF between anti-VEGF and PBS groups (P = 0.675). Intravitreal injections of anti-VEGF did not have a protective effect in the rat model of anterior ischemic optic neuropathy.

Visual evoked potentials show strong positive association with intracranial pressure in patients with cryptococcal meningitis.

To verify the relationship between intracranial pressure and flash visual evoked potentials (F-VEP) in patients with cryptococcal meningitis. Method The sample included adults diagnosed with cryptococcal meningitis admitted at a reference hospital for infectious diseases. The patients were subjected to F-VEP tests shortly before lumbar puncture. The Pearson’s linear correlation coefficient was calculated and the linear regression analysis was performed. Eighteen individuals were subjected to a total of 69 lumbar punctures preceded by F-VEP tests. At the first lumbar puncture performed in each patient, N2 latency exhibited a strong positive correlation with intracranial pressure (r = 0.83; CI = 0.60 - 0.94; p < 0.0001). The direction of this relationship was maintained in subsequent punctures. The intracranial pressure measured by spinal tap manometry showed strong positive association with the N2 latency F-VEP in patients with cryptococcal meningitis.

Electrophysiolocal findings in Mohr-Tranebjærg syndrome

Mohr-Tranebjaerg syndrome (MTS) is an X-liked recessive rare syndrome also known as deafness-dystonia syndrome. The severity of the symptoms may vary, but they progress usually to severe deafness and dystonia and sometimes they are accompanied by cortical deterioration of vision and mental deterioration. The purpose of this paper is to illustrate a very interesting case of Mohr-Tranebjaerg syndrome. A 24-year-old italian man with Mohr-Tranebjaerg syndrome underwent full field electroretinography (ERG) and visual evoked potentials (VEPs). Fundus examination showed apparently normal retina with pallor of the optic disc. Pattern reversal VEP and flash VEP responses were non-recordable. ERG showed amplitude reduction of the fotopic, scotopic and 30 Hz flicker responses revealing generalized retinal dysfunction with reduction of cone and rod responses. The progressive neurodegeneration in Mohr-Tranebjaerg syndrome can be also associated with a retinal degeneration.

Protective effects of systemic treatment with methylprednisolone in a rodent model of non-arteritic anterior ischemic optic neuropathy (rAION)

This study investigated the protective effects of the administration of steroids on optic nerves (ON) and retinal ganglion cells (RGCs) in a rodent model of non-arteritic anterior ischemic optic neuropathy (rAION). We induced rAION using rose bengal and argon laser irradiation in a photodynamic procedure on the optic discs of rats. The treated groups received methylprednisolone (MP) via peritoneal injection for 2 weeks. The control group received intraperitoneal injections of phosphate-buffered saline (PBS) post-rAION. At the 4th week post-infarct, MP treatments significantly rescued the RGCs (mm2) in the central retinas (1920 ± 210, p < 0.001) and mid-peripheral retinas (950 ± 240, respectively, p = 0.018) compared with those of the PBS-treated rats (central: 900 ± 210 and mid-peripheral: 440 ± 180). Functional assessment with flash visual-evoked potentials demonstrated that P1 latency (ms) was shortened in the MP group compared to the PBS group (108 ± 14 and 147 ± 9, respectively, p < 0.001). In addition, the P1 amplitude (uV) was enhanced in the MP group compared to the PBS group (55 ± 12 and 41 ± 13, respectively, p < 0.05). TUNEL assays showed a decrease in the number of apoptotic cells in the RGC layers of MP-treated retinas compared to the PBS-treated group (p < 0.05). ED1 positive cells (/HPF) were significantly decreased in the ONs of the MP group compared to the PBS group (p < 0.001). In conclusion, systemic administration of MP had neuroprotective effects on RGC survival and ON function in the rAION animal model.

34. Flash visual evoked potentials in infant with congenital microphthalmia

Congenital microphthalmia (CM) is a rare developmental defect of the primary optic vesicle. The estimated incidence is around 1.5–19/10 000 births and it may be unilateral or bilateral, usually associated with other ocular anomalies. The morphogenetic defect can be due to external gestational factors (infection or drugs), or to a primary genetic abnormality, occurring as an isolated finding or as a part of a generalized syndrome. Flash visual evoked potentials (FVEPs) can be useful in assessing acuity and detect any optic nerve dysfunction in patients with CM at an early age. Here we describe the FVEPs findings of five infants of age ranged between birth and 6 months with unilateral CM. The FVEPs were recorded according to ISCEV standard 2010; the amplitude and peak latency of the main P2 wave were matched for postconceptional age and other ocular or systemic morphogenetic defects associated. An isolated microphthalmia was assessed in four patients, while in one case it occurred as a part of Microphthalmia and Skin Linear defect (MSL) Syndrome. Left eye was involved in 4/5 patients (M/F ratio 1/1). All our patients presented asymmetric FVEPs traces with an increased latency of P-2 wave (equivalent to P100) in the affected eye. Binocular stimulation patterns and measurements of peak amplitude of main waves were normal except for two patients, respectively carriers of MSL syndrome and opacities of dioptric media, whose traces revealed a decreased waves’ amplitude. According to our experience, FVEPs can help in distinguishing isolated CM idiopathic cases from those with widespread ocular and/or neurological abnormalities and can provide a reasonable prediction of visual outcome to parents as soon as possible, allowing an appropriate management.

35. Visual evoked potentials and MRI in monitoring optic nerve involvement in a relapsing remitting model of EAE

Experimental Autoimmune Encephalomyelitis (EAE) is a pre-clinical disease model of Multiple Sclerosis (MS), traditionally induced by injecting Myelin Oligodendrocyte Glycoprotein(MOG). Optic nerve involvement and VEP diagnostic reliability have been already shown in MOG induced EAE rat. In the present study we used spinal cord homogenate (SCH) to induce disease in Dark-Agouti (DA) rats, proposing to show optic nerve involvement and assess VEP usefulness as neurophysiological biomarker also in this model. Nineteen DA rats were used in the experiment: 7 immunized by SCH (EAE) and 12 healthy (H) controls. Flash VEPs from both eyes were recorded with epidural electrodes under sevoflurane volatile anesthesia once a week for 6 weeks (one day before immunization, days 6, 13, 20, 27, 34 post) with measurement P1 latency from N1-P1-N2 complex. Values exceeding 2.5 SD from control mean were considered abnormal. MRI analyses on both Optic Nerves were also performed using a 7 Tesla technology. After the last VEP session, 7 EAE and 3 H animals underwent histological analysis on a transverse section of both optic nerves. P1 latency in EAE group was significantly increased at days 13–20-27 post immunization and was abnormal in 10/14 eyes in EAE rats (p

The effect of ingested sulfite on visual evoked potentials, lipid peroxidation, and antioxidant status of brain in normal and sulfite oxidase-deficient aged rats.

Sulfite, commonly used as a preservative in foods, beverages, and pharmaceuticals, is a very reactive and potentially toxic molecule which is detoxified by sulfite oxidase (SOX). Changes induced by aging may be exacerbated by exogenous chemicals like sulfite. The aim of this study was to investigate the effects of ingested sulfite on visual evoked potentials (VEPs) and brain antioxidant statuses by measuring superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities. Brain lipid oxidation status was also determined via thiobarbituric acid reactive substances (TBARS) in normal- and SOX-deficient aged rats. Rats do not mimic the sulfite responses seen in humans because of their relatively high SOX activity level. Therefore this study used SOX-deficient rats since they are more appropriate models for studying sulfite toxicity. Forty male Wistar rats aged 24 months were randomly assigned to four groups: control (C), sulfite (S), SOX-deficient (D) and SOX-deficient + sulfite (DS). SOX deficiency was established by feeding rats with low molybdenum (Mo) diet and adding 200 ppm tungsten (W) to their drinking water. Sulfite in the form of sodium metabisulfite (25 mg kg(-1) day(-1)) was given by gavage. Treatment continued for 6 weeks. At the end of the experimental period, flash VEPs were recorded. Hepatic SOX activity was measured to confirm SOX deficiency. SOX-deficient rats had an approximately 10-fold decrease in hepatic SOX activity compared with the normal rats. The activity of SOX in deficient rats was thus in the range of humans. There was no significant difference between control and treated groups in either latence or amplitude of VEP components. Brain SOD, CAT, and GPx activities and brain TBARS levels were similar in all experimental groups compared with the control group. Our results indicate that exogenous administration of sulfite does not affect VEP components and the antioxidant/oxidant status of aged rat brains.

Visual processing during recovery from vegetative state to consciousness: Comparing behavioral indices to brain responses

Auditory stimulation is often used to evoke responses in unresponsive patients who have suffered severe brain injury. In order to investigate visual responses, we examined visual evoked potentials (VEPs) and behavioral responses to visual stimuli in vegetative patients during recovery to consciousness. Behavioral responses to visual stimuli (visual localization, comprehension of written commands, and object manipulation) and flash VEPs were repeatedly examined in eleven vegetative patients every two weeks for an average period of 2.6months, and patients' VEPs were compared to a healthy control group. Long-term outcome of the patients was assessed 2-3years later. Visual response scores increased during recovery to consciousness for all scales: visual localization, comprehension of written commands, and object manipulation. VEP amplitudes were smaller, and latencies were longer in the patient group relative to the controls. VEPs characteristics at first measurement were related to long-term outcome up to three years after injury. Our findings show the improvement of visual responding with recovery from the vegetative state to consciousness. Elementary visual processing is present, yet according to VEP responses, poorer in vegetative and minimally conscious state than in healthy controls, and remains poorer when patients recovered to consciousness. However, initial VEPs are related to long-term outcome.