Visual Evoked Potentials Latency Research Articles

Evaluation of visual function and retinal structure in adult amblyopes.

To evaluate visual function and its relationship to structure in adult amblyopic subjects. This observational, cross-sectional study included 24 adult amblyopes and 19 healthy subjects. The amblyopes were separated into three groups: anisometropic amblyopes (n = 15), strabismic amblyopes (n = 5), and strabismic amblyopes with anisometropia (n = 4). The relationships of the multifocal visual evoked potential (VEP) results with the clinical findings and psychophysical (Humphrey visual field) and structural (spectral domain optical coherence tomography) diagnostic test data were then investigated. Significant differences in the multifocal VEP amplitude responses (abnormal cluster defects), combining the interocular and monocular probability analysis, were observed between the anisometropic amblyopic (80%) and nonamblyopic eyes (13.3%) (p < 0.001), whereas in strabismic amblyopia, such defects were found in 100% of the amblyopic and nonamblyopic eyes. Delayed multifocal VEP interocular and monocular latencies were seen in 66.6 and 26.6% of the anisometropic amblyopic and nonamblyopic eyes, with no significant differences between eyes (p = 0.065). Likewise, latency delays were found in 40% of both strabismic amblyopic and nonamblyopic eyes. Multifocal VEP latency showed significant differences between anisometropic and strabismic amblyopic eyes (p = 0.036). Significant agreement was found between the Humphrey visual field and the multifocal VEP visual field defects in the central area of the visual field (p = 0.033). The average retinal nerve fiber layer thickness, foveal and macular thickness, and macular volume, as measured by spectral domain optical coherence tomography, did not show any significant differences between the amblyopic and nonamblyopic eyes and the control group. Multifocal VEP amplitudes and latencies were significantly affected in amblyopic eyes and, to a lesser extent, in nonamblyopic eyes. Multifocal VEP response latencies were more delayed in anisometropic eyes than in strabismic eyes, suggesting that anisometropic and strabismic amblyopia may represent different neural abnormalities.

Acute optic neuritis: a clinical paradigm for evaluation of neuroprotective and restorative strategies?

What makes the acute optic neuritis model unique in an era of trials for neuroprotective and myelin repair agents? Acute optic neuritis (AON) is a common, and often the earliest manifestation of central nervous system (CNS) inflammatory demyelinating disorders like multiple sclerosis (MS) and neuromyelitis optica (NMO). It affects at least half the patients with MS and is the presenting feature in 15–20% of patients. Vision loss in AON secondary to NMO tends to be more severe with less potential for recovery and greater axonal degeneration, as measured by optical coherence tomography (OCT) (Bennett et al., 2014). Several unique features of the afferent visual pathway (AVP) make the AON model an ideal system to study disease pathogenesis and evaluate potential neuroprotective and myelin repair strategies.

Impact of Length of Visual Pathway on VEP Latency

Impact of Length of Visual Pathway on VEP Latency

Evaluation of optic and vestibulocochlear nerve involvement in type 2 diabetes mellitus patients by using evoked potential

Background and Objectives: Cranial neuropathy is one of the common late complications of Diabetes Mellitus(DM), including distal symmetric sensory polyneuropathy and peripheral neuropathy(PN). Though many studies support the involvement of Cranial nerves III, VI and VII in diabetic patients, little was known about the involvement of II & VIII nerve. The goal of this study was to evaluate the involvement of optic nerve and vestibulocochlear nerve using Visual Evoked potential (VEP) and Brainstem Auditary Evoked Potential (BAEP). Methods: Forty patients with 8 to 12 years duration of type 2 DM in 40 to 60 years age group (Group1) were selected from diabetic outpatient department in Thanjavur medical college hospital and compared with control group (Group 2) who were normal subjects and was age and sex matched. Physical examination and laboratory investigations including fasting glucose, renal functions were done in addition to VEP & BAEP for all groups. P100 latency using VEP and bilateral inter-peak latency IPL I-III, IPL III-V & IPL I-V using BAEP was evaluated and and analyzed for the study group and control group. Result: VEP P100 latency and BAEP bilateral inter-peak latency IPL I-III, IPL III-V & IPL I-V were prolonged in the study group compared to control group. Conclusion: This study concluded the involvement of optic and vestibulocochlear nerve in type 2 DM as the latency was prolonged.

Enhanced Retinal Ganglion Cell Survival in Glaucoma by Hypoxic Postconditioning After Disease Onset.

The neuroprotective efficacy of adaptive epigenetics, wherein beneficial gene expression changes are induced by nonharmful "conditioning" stimuli, is now well established in several acute, preclinical central nervous system injury models. Recently, in a mouse model of glaucoma, we demonstrated retinal ganglion cell (RGC) protection by repetitively "preconditioning" with hypoxia prior to disease onset, indicating an epigenetic approach may also yield benefits in chronic neurodegenerative disease. Herein, we determined whether presenting the repetitive hypoxic stimulus after disease initiation [repetitive hypoxic "postconditioning" (RH-Post)] could afford similar functional and morphologic protection against glaucomatous RGC injury. Chronic elevations in intraocular pressure (IOP) were induced unilaterally in adult male C57BL/6 mice by episcleral vein ligation. Mice were randomized to an RH-Post [1 h of systemic hypoxia (11% oxygen) every other day, starting 4 days after IOP elevation] or an untreated control group. After 3 weeks of experimental glaucoma, the 21-27% reduction and 5-25% prolongation in flash visual-evoked potential amplitudes and latencies, respectively, and the 30% impairment in visual acuity were robustly improved in RH-Post-treated mice, as was the 17% loss in RGC soma number and 20% reduction in axon integrity. These protective effects were observed without RH-Post affecting IOP. The present findings demonstrate that functional and morphologic protection of RGCs can be realized by stimulating epigenetic responses during the early stages of disease, and thus constitute a new conceptual approach to glaucoma therapeutics.

33. Optical coherence tomography and visual evoked potentials combined use as monitoring tools in Multiple Sclerosis patients

In Multiple Sclerosis-MS, optical coherence tomography-OCT is used to measure retinal nerve fiber layer-RNFL thickness as a marker of axonal loss and visual evoked potentials-VEPs as an indicator of demyelination. However, no clear indications are available on their combined use in MS monitoring. 80 MS patients underwent neurological and neurophysiological evaluation with OCT and VEPs, with routine clinical and MRI monitoring for a mean period of 1 year. Additional OCT-VEPs follow-up was obtained in 50 patients. Comparing eyes with and without previous ON, VEP latency and RNFL thickness were respectively significantly higher (131.2 ms Vs 118.8 ms, p = 0.008) and lower (78,15 μm Vs 90,00 μm, p < 0.001) in the first subgroup. No significant differences were found between the two subgroups when analyzing VEP latency and RNFL thickness evolution during the follow-up period. However, eyes with baseline recent ON had significant reduction in VEP latency (−15,3 ms) and RNFL thickness (−7,7 μm) at follow-up. No significant correlation was found between OCT-VEPs parameters and disease activity. Similar results were found when considering only RR and CIS patients. The main role for OCT and VEPs in short-to-medium term follow-up programs would consist in monitoring neural damage after acute ON.

Relationship of high blood lactate levels with latency of visual-evoked potentials.

We studied, in healthy adult subjects, the association of high blood lactate levels, induced with an exhaustive exercise (12 subjects) or an intravenous infusion (four subjects) of a lactate solution (3 mg/kg in 1 min), with amplitude and latency of visual-evoked potentials. Amplitude of N75, P100, and N145 components did not show significant changes, whereas latency of P100 was reduced at exercise's end and that of N145 increased 10 min after the conclusion. Therefore, an increase of blood lactate induced by an exhaustive exercise or an intravenous infusion appears to induce an improvement in the conduction time between eye and striate cortex, while it seems to evoke a worsening of intracortical communication between striate and extrastriate areas.

Association between Visual Evoked Potential and Disease Severity, Disease Duration and Visual Hallucination in Patients with Idiopathic Parkinsonism

Background: Parkinson's disease (PD) is a neurodegenerative disorder impairing motor, verbal and other abilities. Visual evoked potential (VEP) assessment is a useful method for analysis of visual system and its function. The present study was designed in order to evaluate whether VEP changes are associated with PD. Materials and Methods: In the present study, 100 subjects encompassing 40 patients with Idiopathic Parkinson’s Disease (Idiopathic PD) and 60 aged-matched controls were selected and assigned into case and control groups, respectively. VEP analysis was conducted in either group and the results were compared. Results: In the present study, 16 patients (40%) showed prolonged P100 latency. P100 latency in the case group was significantly longer than in controls. P100 Amplitude was significantly higher in case group than control. There were no significant association between prolonged VEP and sex and diseases duration, in the participants. Also from our participants who suffer from visual hallucination, P100 latency was significantly longer than in the controls. There was a significant association between prolonged P100 latency and severity of disease in the case group. Conclusion: We suggest that prolonged VEP latencies and amplitude are associated with PD and might be associated with a predisposition for visual hallucinations.

Diagnostic value of visual evoked potentials for clinical diagnosis of multiple sclerosis.

Prolonged latency of visual evoked potentials (VEP) has been used to identify clinically silent lesions in multiple sclerosis (MS) suspects. The objective of this study was to determine the reliability of VEP to predict the development of MS in MS suspects. Retrospective hospital records of MS suspects were evaluated. VEP was analyzed together with subsequent diagnostic confirmation of MS by McDonald diagnostic criteria for MS-2005. MS developed in 12 of 35 patients (34 %) and 23 (66 %) failed to exhibit diagnostic characteristics. P100 latencies and interocular latency differences were longer in clinically definite multiple sclerosis (CDMS) than non-CDMS patients (p = 0.002, 0.001, respectively). All patients in the subsequent MS group had P100 latencies longer than102 ms, a mean of our MS-free subjects thus providing 100 % of sensitivity. No patient developed MS with a P100 latency <102 ms. Brain MRI lesions associated significantly with developing CDMS (p = 0.001). Predictability of developing CDMS was highest when criteria for P100 latency, interocular latency difference, and brain MRI lesions were combined. MS suspects with a P100 latency longer than mean of MS-free subjects are more likely to develop MS than those with lower values. VEP latency combined with MRI could improve the accuracy of MS prediction.

The relationship between oxidative stress markers and visual evoked potentials in different hypertension models.

We aimed to define the influence of different hypertension models on lipid peroxidation markers [conjugated dienes (CD) and thiobarbituric acid-reactive substances (TBARS)], antioxidant protection [paraoxonase-1 (PON1) activity] and visual evoked potential (VEP) changes in rats. The study was designed as four different hypertension models. Rats (n=84) were divided equally into six groups: Control group (C), Sham operated (Sham), Two kidney-one clip (2K-1C), One kidney-one clip (1K-1C), Deoxycorticosterone acetate (DOCA) and N-omega-nitro-L-arginine-methyl ester (L-NAME). Brain TBARS, serum lipids (total and lipoprotein bound cholesterols and triglycerides) CD and TBARS levels and PON1 activity were assayed. Comparisons were performed using ANOVA or Wilcoxon/Kruskal-Wallis tests. Pearson correlation and linear regression analysis were used to evaluate associations of independent predictors with hypertension. Mean arterial pressure, brain and serum lipid peroxidation markers, VEP latencies were significantly higher in four hypertensive groups compared with control and sham groups (p<0.05). Compared with controls, PON1 activity was decreased in DOCA, 1K1C and L-NAME groups (p<0.05). Serum PON1 activity was negatively correlated with lipid peroxidation markers and VEPs. In terms of VEP's records linear regression analysis showed that changes in N2 (B=1.51±0.34; p<0.001), P1 (B=-1.71±0.28; p<0.001), P3 (B=0.54±0.14; p<0.001), serum TBARS levels (B=0.94±0.24; p<0.001) and PON1 activity (B=0.05±0.02; p<0.01) were independently associated with elevated blood pressure. Lipid peroxidation measured in serum and brain was associated with increased electrophysiological alterations recorded as VEPs. This study might suggest that serum PON1 activity may be protective against brain and serum lipid peroxidation as well as electrophysiological alterations in the brain in different hypertension models.

The best corrected visual acuity and retinal thickness are associated with improved cortical visual processing in treated wet‐AMD patients

AbstractPurpose Age‐related macular degeneration is the most common cause of blindness in the western world among elderly people. In response to anti‐VEGF treatment for wet‐AMD retinal anatomy and visual acuity is often remedied. In our previous study, we showed that also visual evoked potentials (VEP) improve following successful anti‐VEGF treatment. The aim of the present study was to investigate, if visual acuity and retinal thickness changes are associated with VEP parameters.Methods Fifteen patients enrolled this study. Patients received three bevacizumab intravitreal injections. At the beginning of the study and 4‐6 weeks after the last injection, the best corrected visual acuity (BCVA) test, full biomicroscope examination, OCT analysis and VEP were performed.Results In treated eyes, logMAR visual acuity decreased on average 0.2±0.3 units, OCT retinal thickness decreased 170±200 micrometers and VEP amplitude increased 1.0±1.4 microvolts. All changes were significant at p&lt;0.05. The relative changes of VEP amplitude and retinal thickness correlated significantly r=‐0.630 (p&lt;0.05), as well visual acuity (logMAR) and retinal thickness r=0.576 (p&lt;0.05). VEP latency did not correlate with retinal thickness or visual acuity.Conclusion We showed that both the increase in VEP amplitude and the improvement in visual acuity are correlated with the decrease in retinal thickness in treated wet‐AMD patients indicating that successful intravitreal anti‐VEGF treatment initiates significant changes in upstream visual processing in the brain.

Optic radiation damage in multiple sclerosis is associated with visual dysfunction and retinal thinning--an ultrahigh-field MR pilot study.

To investigate posterior visual pathway damage in multiple sclerosis using ultrahigh-field magnetic resonance imaging (MRI) at 7 Tesla (7 T), and to determine its correlation with visual disability and retinal fibre layer (RNFL) damage detectable by optic coherence tomography (OCT). We studied 7 T MRI, OCT, functional acuity contrast testing (FACT), and visually evoked potentials (VEP, n = 16) in 30 patients (including 26 relapsing-remitting MS and four clinically isolated syndrome patients) and 12 healthy controls to quantify RNFL thickness, optic radiation lesion volume, and optic radiation thickness. Optic radiation lesion volume was associated with thinning of the optic radiation (p < 0.001), delayed VEP (p = 0.031), and visual disability indicated by FACT (p = 0.020). Furthermore, we observed an inverse correlation between optic radiation lesion volume and RNFL thickness (p < 0.001), including patients without previous optic neuritis (p < 0.001). Anterior visual pathway damage, but also (subclinical) optic radiation integrity loss detectable by 7 T MRI are common findings in MS that are mutually affected. Given the association between optic radiation damage, visual impairment, and increased VEP latency in this exploratory study of a limited sample size, clinicians should be aware of acute lesions within the optic radiation in patients with (bilateral) visual disturbances. • Focal destruction of the optic radiation is detectable by 7 T MRI. • Focal optic radiation damage is common in MS. • Optic radiation damage is associated with RNFL thinning, detectable by OCT. • Optic radiation damage is associated with delayed VEP and visual dysfunction. • RNFL thickness in non-optic neuritis eyes correlates with optic radiation demyelination.

The pathogenesis of optic neuritis caused by Angiostrongylus cantonensis in BALB/c mice.

BackgroundOne of the most common causes of meningitis in South East Asia is angiostrongyliasis or infection by the parasitic nematode Angiostrongyliasis cantonensis. Although this nematode usually resides in the pulmonary arteries of rats, its incidental occurence in other hosts such as humans can cause optic neuritis and lead to serious vision sequelae. Nevertheless, there are currently no systematic studies conducted in this area.MethodsIn order to study the pathogenesis of optic neuritis, mice were tried as a new animal model to study and challenge with A. cantonensis on 7d, 14d and 21d, respectively. Electroretinogram (ERG), visual evoked potential (VEP), ophthalmoscopy and histology were examined on day 7d, 14d and 21d and tribendimidine (TBD) was later used to treat optic neuritis on day 14d for a week to evaluate its therapeutic effects.ResultsInfection of A. cantonensis caused obvious inflammatory cell infiltration in the retina and optic nerve adventitia in day 14d and 21d followed by optic nerve fiber demyelination and retinal ganglion swelling at day 21d in the challenged mice. Prolonged VEP latency and decreased ERG amplitude were also observed on day 21. After treatment of TBD in the infected mice, retinal and optic nerve inflammation were alleviated, but VEP latency and ERG amplitude did not improve on day 21d and 28d.ConclusionsThe current study provides evidence that A. cantonensis can cause optic neuritis along with optic nerve demyelination and retinal ganglion cell damage in a mouse model. TBD alone treatment can improve the symptoms of optic neuritis, but does not aid in vision recovery, suggesting that both neuroprotective agents and Dexamethasone should be administered, along with treatment for the infection, to protect the optic nerve and ganglion cells. Furthermore, as the symptoms of optic neuritis caused by A. cantonensis in mice are similar to the optic neuritis in multiple sclerosis (MS) human patients, we suggest that the BALB/c mouse model provided in this study may be useful to explore therapies of optic neuritis in MS patients.

Transorbital sonography in acute optic neuritis: a case-control study.

Acute unilateral optic neuritis is associated with a thickening of the retrobulbar portion of the optic nerve as revealed by transorbital sonography, but no comparison has been made between nerve sheath diameter and optic nerve diameter in patients with acute optic neuritis versus healthy controls. We evaluated optic nerve sheath diameter and optic nerve diameter in patients with acute optic neuritis and healthy controls and compared optic nerve sheath diameter and optic nerve diameter with visual-evoked potentials in patients. A case-control study was performed in 2 centers. Twenty-one consecutive patients with onset of visual loss during the prior 10 days and established acute noncompressive unilateral optic neuritis were compared with 21 healthy controls, matched for sex and age (±5 years). Two experienced vascular sonographers performed the study by using B-mode transorbital sonography. Visual-evoked potentials were performed on the same day as the transorbital sonography and were evaluated by an expert neurophysiologist. Sonographers and the neurophysiologist were blinded to the status of the patient or control and to clinical information, including the side of the affected eye. The median optic nerve sheath diameter was thicker on the affected side (6.3 mm; interquartile range, 5.9-7.2 mm) compared with the nonaffected side (5.5 mm; interquartile range, 5.1-6.2 mm; P < .0001) and controls (5.2 mm; interquartile range, 4.8-5.5 mm; P < .0001). The median optic nerve diameter was 3.0 mm (range, 2.8-3.1 mm) on the affected side and 2.9 mm (range, 2.8-3.1 mm) on the nonaffected side (P = not significant.). Both sides were thicker than those in controls (2.7 mm; interquartile range, 2.5-2.8 mm; P = .001 and .009). No correlation was found between optic nerve sheath diameter and optic nerve diameter and amplitude and latency of visual-evoked potentials in patients with optic neuritis. Transorbital sonography is a promising tool to support the clinical diagnosis of acute optic neuritis. Further studies are needed to define its specific role in the diagnosis and follow-up of optic neuritis.

Whole-brain diffusion tensor imaging in correlation to visual-evoked potentials in multiple sclerosis: a tract-based spatial statistics analysis.

Functional correlates of microstructural damage of the brain affected by MS are incompletely understood. The purpose of this study was to evaluate correlations of visual-evoked potentials with microstructural brain changes as determined by DTI in patients with demyelinating central nervous disease. Sixty-one patients with clinically isolated syndrome or MS were prospectively recruited. The mean P100 visual-evoked potential latencies of the right and left eyes of each patient were calculated and used for the analysis. For DTI acquisition, a single-shot echo-planar imaging pulse sequence with 80 diffusion directions was performed at 3T. Fractional anisotropy, radial diffusivity, and axial diffusivity were calculated and correlated with mean P100 visual-evoked potentials by tract-based spatial statistics. Significant negative correlations between mean P100 visual-evoked potentials and fractional anisotropy and significant positive correlations between mean P100 visual-evoked potentials and radial diffusivity were found widespread over the whole brain. The highest significance was found in the optic radiation, frontoparietal white matter, and corpus callosum. Significant positive correlations between mean P100 visual-evoked potentials and axial diffusivity were less widespread, notably sparing the optic radiation. Microstructural changes of the whole brain correlated significantly with mean P100 visual-evoked potentials. The distribution of the correlations showed clear differences among axial diffusivity, fractional anisotropy, and radial diffusivity, notably in the optic radiation. This finding suggests a stronger correlation of mean P100 visual-evoked potentials to demyelination than to axonal damage.

Visual-evoked potentials in patients with brain circulatory problems

Purpose: The aim of this study was to find out if local brain circulatory problems may influence visual-evoked potentials (VEP). Patients and methods: Thirty-eight patients were divided into the following groups: (I) those with hemianopsia or quadrantanopsia and hemiparesis after brain stroke; (II) those with hemianopsia or quadrantanopsia without paresis after brain stroke; and (III) those with amaurosis fugax. The control group consisted of 38 patients. The VEP pattern (PVEP) and flash VEP (FVEP) were examined monocularly using two electrodes placed at O1 and O2. Latency and amplitude of the N75, P100 and N2, P2 waves were measured. The Newman–Keuls test was used for statistical analysis. Results: In PVEP, no differences between the groups were observed. In FVEP, the mean P2 latency was significantly longer in group I than in group III, and the P2 amplitude was significantly lower in all examined groups when compared with the control group. PVEP and FVEP revealed differences in P latency over 3 ms between brain hemispheres and differences in P amplitude over 30% in all examined groups. In the control group, there were no differences in latency between brain hemispheres and only a small difference in amplitude. Conclusion: Local brain circulatory problems that may lead to brain ischemia cause differences in VEP amplitude and latency between brain hemispheres. Changes in VEPs observed in patients with amaurosis fugax may be considered the result of recurrent brain ischemia.

The spatiotemporal frequency tuning of pattern visual evoked potentials in rats

To observe the spatiotemporal frequency tuning of pattern visual evoked potentials in Wistar rats. Experimental study. 15 Wistar rats of 8 weeks old were used in this study. Recording electrodes were chronically inserted into the skull without piercing the dura at the corresponding sites to the primary visual cortex under anesthesia. Reference electrodes were inserted into the nose bone in the same way. Pattern visual evoked potentials were recorded on the 3(rd), 5(th), 7(th) and 9(th) postoperation days. The visual stimuli were chessboard patterns with spatial frequency of 0.01, 0.02, 0.04 or 0.08 cpd, and temporal frequency of 1, 2, 4 or 6 Hz, respectively. Data were processed and statistically analyzed with Matlab and SPSS. The amplitudes and latencies of pattern visual evoked potentials under different spatial and temporal frequencies, the inter-individual variations and the repeated measurement variations were compared. With the increase of spatial frequencies, the P100 amplitudes of PVEPs were gradually reduced, which were (29.87 ± 10.37) µV (0.01 cpd), (31.92 ± 10.98) µV (0.02 cpd), (28.46 ± 6.18) µV (0.04 cpd) and (20.71 ± 6.54) µV(0.08 cpd), respectively, with significant difference among groups (F = 3.725, P = 0.018), and the P100 latencies of PVEPs were gradually elongated, which were (96.25 ± 12.12) ms (0.01 cpd), (95.73 ± 15.13) ms (0.02 cpd), (101.75 ± 8.11) ms (0.04 cpd) and (125.58 ± 18.32) ms (0.08 cpd), respectively, with significant difference among groups (F = 12.187, P = 0.000) . With the increase of temporal frequencies, the P100 amplitudes of PVEPs were gradually reduced, which were (30.71 ± 8.25) µV (1 Hz), (29.75 ± 4.76) µV (2 Hz), (25.79 ± 8.51) µV (4 Hz) and (19.63 ± 6.00) µV (6 Hz), with significant difference among groups (F = 6.115, P = 0.001), and there was no change of P100 latencies, which were (102.58 ± 16.09) ms (1 Hz), (101.75 ± 10.32) ms (2 Hz), (104.25 ± 12.51) ms (4 Hz) and (102.67 ± 13.59) ms (6 Hz), respectively, with no significant difference among groups (F = 0.074, P = 0.974). The inter-individual variation was the smallest under the spatial frequency of 0.04 cpd and temporal frequency of 2 Hz. The repeated measurement variations showed no significant change under tested conditions. Under appropriate stimuli and recording conditions, PVEP can be reliably recorded in Wistar rats. The spatiotemporal frequency tuning of P100 amplitudes of Wistar rats exhibit low-pass selectivity. The spatial frequency affects the P100 latency in Wistar rat, but not so does the temporal frequency.

Amiodarone neurotoxicity: the other side of the medal

Abstract The efficacy of amiodarone is tempered by its toxicity, with 50% of long-term users discontinuing the drug. The non-cardiac side effects of amiodarone may involve central and peripheral nervous system. We studied two patients treated with amiodarone for 46 and 15 months respectively. Both patients exhibited progressive distal extremity weakness, impaired perception, loss of deep reflexes. Electrophysiology identified a widespread, sensorimotor polyneuropathy with features of axonal loss and demyelination. Visual evoked potentials (VEPs) showed prolonged P100 latency bilaterally in absence of visual symptoms or brain magnetic resonance imaging (MRI) abnormalities. Extensive laboratory examinations excluded known causes of peripheral neuropathies. At 21 months after amiodarone withdrawal, P100 latency of case 1 VEPs returned to normal, whereas polyneuropathy continued to progress. In the second patient neuropathy has worsened similarly over 2 years whereas P100 latency of VEPs recovered to normal within 7 months after withdrawal of amiodarone. These findings may suggest different mechanisms of toxicity, which could be due to amiodarone pharmacokinetic and its metabolite effects on the peripheral nerves, as opposed to the optic nerve. We emphasize that use of amiodarone needs monitoring of patients at risk of development side effects.

Interleukin-8 is associated with acute and persistent dysfunction after optic neuritis

Background: Acute optic neuritis is often in association with multiple sclerosis (MS). Proinflammatory cytokines trigger neuronal damage in neuroinflammatory disorders but their role in optic neuritis is poorly investigated. Objective: The objective of this work is to investigate the associations of intrathecal contents of proinflammatory cytokines with transient and persistent dysfunctions after optic neuritis. Methods: In 50 MS patients followed for up to six months, cerebrospinal fluid (CSF) levels of IL-1β, TNF and IL-8 were determined, along with clinical, neurophysiological and morphological measures of optic neuritis severity. Results: Visual impairment, measured by high- and low-contrast visual acuity, and delayed visual-evoked potential (VEP) latencies were significantly correlated to IL-8 levels during optic neuritis. IL-8 at the time of optic neuritis was also associated with persistent demyelination and final axonal loss, inferred by VEP and optical coherence tomography measures, respectively. Contents of IL-8 were correlated to functional visual outcomes, being higher among patients with incomplete recovery. Multivariate analysis confirmed that IL-8 significantly predicted final visual acuity, at equal values of demographics and baseline visual scores. Conclusion: Our study points to IL-8 as the main inflammatory cytokine associated with demyelination and secondary neurodegeneration in the optic nerve after optic neuritis.

The role of nitric oxide on visual-evoked potentials in MPTP-induced Parkinsonism in mice

The present study aimed to elucidate visual evoked potentials (VEP) changes in MPTP induced Parkinson’s disease (PD) and investigate the possible benefical effects of neuronal (n) and inducible (i) nitric oxide synthase (NOS) inhibitors on altered VEPs, lipid peroxidation and apoptosis. 3months old C57BL/6 mice were randomly divided into 6 groups which included control (C), 7-nitra indazole treated (7-NI), S-methylisothiourea (SMT) treated, 1,2,3,6-tetrahydropyridine (MPTP) treated, 7-NI+MPTP treated and SMT+MPTP treated. Motor activity of mice was evaluated via the pole test. At the end of the experimental period VEPs were recorded, brain and retina tissues were removed for biochemical analysis. Dopaminergic neuron death at substantia nigra (SN) was determined by immunohistochemical analysis of tyrosine hydroxylase (TH). Immunohistochemical staining was also performed to determine iNOS and nNOS in all tissue sections. Mice with experimental PD exhibited decreased motor activity. Dopaminergic cell death at pars compacta of SN (SNpc) was significantly increased in MPTP treated group compared to control. Diminished Parkinsonism symptoms were observed in 7-NI+MPTP and SMT+MPTP groups. Treatment with 7-NI and SMT decreased dopaminergic cell death in MPTP treated mice. Caspase-3 activity, nitrite/nitrate and 4-hydroxynonenal (4-HNE) levels were significantly increased in SN of MPTP treated mice compared to control. Treatment with 7-NI and SMT significantly decreased elevated caspase-3 activity, nitrite/nitrate and 4-HNE levels in SN of MPTP treated mice. No significant difference in above parameters were observed in the retina. VEP latencies were significantly prolonged in MPTP group compared to control group. 7-NI and SMT treatment caused a significant decrease in VEP latencies in MPTP treated mice compared to none treated MPTP group. This data shows that 7-NI and SMT improves prolonged VEP latencies. The protective effects of 7-NI and SMT on VEP alterations can be related to decreased dopaminergic cell death and reduced lipid peroxidation.