Flash Visual Evoked Potentials Research Articles

Establishment of animal model of traumatic optic neuropathy and its function evaluation by F-VEP

Background Visual electrophysiology is a sensitive index for the evaluation of visual function.It has an important value in the assessment of traumatic optic neuropathy.Rabbit is an ideal animal model of traumatic optic neuropathy,and it is simple for the record of flash visual evoked potential(F-VEP)in rabbits.ObjectiveThe present study is to establish the animal model of traumatic optic neuropathy with or without lens injury and observe the repairing procedure using F-VEP. MethodsModels of traumatic optic neuropathy associated with lens injury were established in the right eyes and only traumatic optic neuropathy were created in the left eyes of 64 healthy SPF Chinese white rabbits using fluid percussion brain injury device(FPI).F-VEP was recorded based on the Proposal of International Visual Electrophysiology on 1,2,4,7,10,14,21,28 days after injury of optic nerves.Experimental animals were sacrificed in above time points for the histopathological examination.Macrophages were labeled by ED-1 antibody and survival retinal ganglion cells (RGCs)were stained by Nissl method.Results At the first day after injury,the latencies of P_(100) in both group were longer,and the amplitudes of P_(100) in both group were lower than before injury,showing statistically significant differences among different time points(P 0.05).The duration of latency in traumatic optic neuropathy associated with lens injury group was shorter than that in only traumatic optic neuropathy group(P<0.05).The restore of latency in traumatic optic neuropathy associated with lens injury group was much faster than that in only traumatic optic neuropathy group(P<0.05).The numbers of macrophages were significantly increased and numbers of survival RGCs were considerably decreased with lapse of injury time (P<0.05).The abnormalities of VEP P_(100) and RGCs were obviously improved in 28 days after injury in both groups. ConclusionThis animal model can be established successfully by FPI.The result of retinal histopathological examination confirms F-VEP findings in this model. Key words: optic nerve injury; retina; lens; visual evoked potential; visual function

Clinical electrophysiology and visual outcome in optic nerve hypoplasia

AimsIn optic nerve hypoplasia (ONH), the extent of functional loss of retinal ganglion cells cannot be determined by ophthalmoscopic examination. The prognostic value of visual electrodiagnostic tests in infants and...

Cortical Visual Impairment

1. Luis H. Ospina, MD* 1. *Assistant Professor, Pediatric Ophthalmology and Neuro-ophthalmology, Ste-Justine Hospital, University de Montreal, Montreal, Quebec, Canada After completing this article, readers should be able to: 1. Recognize cortical visual impairment (CVI) as an important cause of pediatric visual loss. 2. Identify the most frequent causes of pediatric CVI and, more specifically, understand the role of hypoxia as a cause of central visual damage. 3. Describe the different patterns and implications for future vision of hypoxic central visual damage occurring in preterm compared with term babies. 4. Know the clinical signs suggestive of CVI in children. 5. Discuss the involvement of visual functions other than visual acuity (ie, cognitive visual aspects) in CVI and correlate them with the likely affected neuroanatomic substrates. 6. Explain the value of using a multidisciplinary approach in rehabilitating children who have CVI early in their development. Vision loss caused by central nervous system damage often is referred to as CVI but also may be referred to as cerebral visual impairment or neurologic visual impairment. These terms refer to the fact that the primary defect may not necessarily be limited to the striate (primary visual) cortex and may affect other areas subserving vision, such as the visual associative cortex, optic radiations, and visual attention pathways. Although it is not yet certain which of these three terms best describes the visual deficit, it is clear that use of the label cortical blindness must be abandoned. That term not only evokes negative connotations for the child and the family but is inaccurate because in almost every instance, some degree of residual vision remains, and visual improvement can occur. CVI has become the greatest cause of pediatric visual impairment in developed countries (1)(2)(3)(4)(5) and is becoming increasingly prevalent in developing nations. CVI is a problem of increasing frequency for two primary reasons. First, the progress in neonatal care has resulted in improved survival of …

ISCEV standard for clinical visual evoked potentials (2009 update)

Visual evoked potentials (VEPs) can provide important diagnostic information regarding the functional integrity of the visual system. This document updates the ISCEV standard for clinical VEP testing and supersedes the 2004 standard. The major change in this revision is that test parameters have been made more precise to achieve better consistency of results within and between test centers. The ISCEV standard VEP protocols are defined for a single recording channel with a midline occipital active electrode. These protocols are intended for assessment of prechiasmal function; additional electrode sites are recommended for evaluation of chiasmal and postchiasmal function. ISCEV has selected a subset of stimulus and recording conditions that provide core clinical information and can be performed by most clinical electrophysiology laboratories throughout the world. These are: 1. Pattern-reversal VEPs elicited by checkerboard stimuli with large 1 degrees (i.e., 60 min of arc; min) and small 0.25 degrees (15 min) checks. 2. Pattern onset/offset VEPs elicited by checkerboard stimuli with large 1 degrees (60 min) and small 0.25 degrees (15 min) checks. 3. Flash VEP elicited by a brief luminance increment, a flash, which subtends a visual field of at least 20 degrees.

Frequency-Band Coupling in Surface EEG Reflects Spiking Activity in Monkey Visual Cortex

Although the electroencephalogram (EEG) is widely used in research and clinical settings, its link to the underlying neural activity during sensory processing remains poorly understood. To investigate this, we made simultaneous recordings of surface EEG, intracortical local field potential, and multiunit activity (MUA) in the alert monkey visual cortex during presentation of natural movies. Using a general linear model, we show that in single trials, EEG power in the gamma band (30-100 Hz) and phase in delta band (2-4 Hz) are significant predictors of the MUA response. Specifically, we found that the MUA response was strongest only when increases in EEG gamma power occurred during the negative-going phase of the delta wave, thus revealing a frequency-band coupling mechanism that can be exploited to infer population spiking activity. This finding may open up a new dimension in the use and interpretation of EEG in normal and pathological conditions.

Studying electrophysiological characteristics in children with congenital sensory nystagmus‐ case presentations

Abstract Purpose In classification of sensory congenital nystagmus (CN) is important to recognize the underlying retinal or visual pathway dysfunction. The aim was to distinguish ERGs and VEPs charcteristics which may identify among variety of disorders associated with sensory CN. Methods In infants and small children that were ophthalmologically classified as sensory CN were ERGs and VEPs recorded simultaneously in the same session. ERGs were detected without dilated pupils and with skin electrodes. Under darkened laboratory conditions were ERGs recorded to white (cone/rod mediated response) and dim blue (rod mediated response) flash and under lighten room were ERGs recorded to white, red and 30 Hz flicker flash (cone mediated responses). VEPs were recorded from three occipital electrodes to flash and onset stimulation. Results Cases with abnormal ERGs showed: in Leber’s congenital amaurosis were undetectable both rod and cone mediated responses from early infancy; in cone‐rod retinal dystrophy abnormal cone and rod mediated responses progressed in time; in achromatopsia abnormal cone mediated responses did not progress in time; in congenital stationary night blindness a negative ERG did not progress in time. Cases with abnormal VEPs showed: in ocular albinism VEP contralateral asymmetry; in achiasmia VEP ipsilateral asymmetry; in severe optic nerve hypoplasia flash VEP was non‐recordable, while in moderate optic nerve hypoplasia flash and pattern onset VEP findings might not correlate with clinic findings. Conclusion Sensory CN is associated with a variety of disorders affecting the retina, optic nerve, chiasm and electrophysiology may characterize retinal or postretinal pathway dysfunction and therefore help in early diagnosis.

Optic nerve injury model in rats set up by fluid percussion brain injury device

Objective To observe whether the animal model of optic nerve injury in rats can be set up by fluid percussion brain injury device (FPI) or not.Methods Seventy-one healthy female Wister rats were randomly divided into 2 groups,inlcuding model group with 66 rats and control group with 5 rats.The rats in model group were randomly divided into 3 groups.Eight rats in group 1 were examined by flash-visual evoked potential (F-VEP) and magnetic resonance imaging (MRI) examines before and 1,3 days,1,2,4,6,and 8 weeks after injury;56 rats in group 2 were randomly divided into 7 subgroups with 8 rats in each subgroup,and were detected by histopathologieal and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) apoptosis examines 1,3 days,1,2,4,6,8 weeks after injury;2 rats in group 3 were examined by electron microscopy 4 and 8 weeks aher injury.According to the degree of injury,the injured eyes were divided into 2 groups including severe injury group with the beat pressure of (699.14±60.79) kPa and mild injury group with the beat pressure of (243.18±20.26) kPa.The right and left eyes in rats in each group were in severe and mild injury group,respectively.Results One day after injury,the latency duration of F-VEP prolonged in severe injury group,wich differed much form which in the normal control group (P 0.05).The latency duration prolonged in mild injury group,and its difference with the normal control group was statistically significant (P 0.05).The abnormal high signal could be seen on optic nerve 1 day after injury,and was still obvious 8 weeks later.The results of histopathological examination showed ruptured capillary in ganglion cell layer 1 day after injury;retinal ganglion ceils without nucleus could be seen 4 weeks after injury.The apoptosis of positive cells was found in each layer of the retina 3 days after injury.TUNEL results indicated that the number of apoptotic positive cells increased significantly 1-2 weeks after injury.Conclusion An animal model of optic nerve injury can be successfully set up using FPI in rats. Key words: Craniocerebral trauma/complications; Optic nerve injuries/surgery; Models,animal

The clinical significance of flash visual evoked potential detection in very low birth weight infants

Objective To study the clinical significance of flash visual evoked potential(FVEP)detection in very low birth weight infants.Methods FVEP was performed in group of 43 very low birth weight infants with Medelecsynergy evoked potential instrument(Oxford Company,UK) comparing with the group of 56 term infants.Results The mean latency periods of N1,P1 and N2 waves in very low birth weight infant group were(181.43±26.73) ms,(217.27±26.54) ms,(249.21±26.49) ms respectively,while in term infant group were(159.51±18.27) ms,(200.26±13.94) ms,(231.56±15.72) ms.There were significant differences between two groups(P＜0.05,P＜0,001).The abnormal rates of main wave P1 were 75.6% and 0 respectively in very low birth weight infant group and term infant group.Furthermore,the major effect model for related influencing factors in very low birth weight infants with abnormal main wave was 3.898-2.861 intracranial lesion.Intracranial lesion was the independent risk factor for abnormal FVEP (0R=0.057,95% CI 0.006～0.579,P=0.015).Conclusion The abnormal rate of FVEP is higher in the very low birth weight infants,which is closely related to the intraeranial lesion.It is recomraended that FVEP is detected at least twice in the first month after birth or achieving the corrected gestational age of 42 weeks for dynamic observation. Key words: Visual evoked potential; Very low birth weight infants

Effect of iron deficiency anemia on visual evoked potential of growing children

Iron deficiency anemia is one of the most prevalent yet neglected nutritional deficiencies in the world. Iron is an essential micronutrient and it is ubiquitous in distribution in body. Iron deficiency leads to anemia, hampered physical growth and capacity, and decreased immunoprotective mechanisms. Impairments in cognitive and motor development in children are also seen in iron deficiency. There is increasing number of evidence to support that iron plays important role in central nervous system functions that include synthesis of neurotransmitters and myelination of the nerve. The objective of our study was to observe the effect of iron deficiency anemia on visual evoked potential (VEP) in children between 6 and 24 months of age. The subjects were categorized on the basis of hematological parameters in two groups: iron replete children in the control group ( n = 25) and iron deplete children in the anemic group ( n = 25). Iron status of the children was also assessed. Due care was taken to exclude all conditions known to adversely affect the visual evoked potential or the iron status of the children. Flash VEP was studied in all children from each eye individually. In both eyes each of the three waves (N1, P1 and N2) of the flash VEP showed longer latencies ( p < 0.05) in the anemic group compared with the control group. A negative correlation was found between the severity of iron deficiency anemia and latencies of waves of VEP. Hence, there is a need for prevention and early detection of iron deficiency anemia in growing infants.

Pathologic changes in chronic intraorbital optic nerve damage in rabbits

To construct a chronic intraorbital optic nerve compression damage model in rabbits and investigate pathologic changes of the retina and optic nerve. A balloon was implanted into the orbit of rabbits, in which contrast medium was filled at designated time points to simulate chronic tumor compression on the intraorbital optic nerve. Funduscopy, visual electrophysiology, histopathology, immunohistochemistry, apoptosis and gene assays were used to examine the changes of retinal ganglion cells (RGCs) and neuroglial cells, as well as the expression of ciliary neurotrophic factor (CNTF) and growth associated protein 43 (GAP-43) in each phase of the chronic intraorbital optic nerve damage (2, 4 and 8 weeks after modeling). Funduscopic examination showed that there was no significant change in the optic disk in non-compression group; the optic disk was congested and edematous in 2 w-compression group, but with no significant change in color; in 4 w-compression group, edema was lessened but color became lighter; in 8 w-compression group, no edema was found but the color was pale. Flash visual evoked potential (FVEP) suggested that the change of FVEP wave forms was more obvious as the compression extended, especially the low, flat, wide and irregular wave forms; the latent period of P(1), N(1) and P(2) was prolonged and the amplitude became lower. Compared with the wave form in non-compression group, there was no significant difference in 2 w-compression group (P>0.05), but the differences were prominent in 4 w- and 8 w-compression groups (P<0.01). Histopathology checks indicated no changes in the retina and optic nerve in non-compression group; in 2 w-compression group, there were also no significant changes, but the cell number of optic nerve decreased, the fibers were deranged, and the bundle membrane was damaged; in 4 w-compression group, nuclei in the RGC layer became sparse, the cell number of optic nerve increased significantly, the optic nerve bundles were deranged; in 8 w-compression group, nuclei in the RGC layer remained sparse and disordered, in the optic nerve there were a large number of disordered and deranged cells, the structure of fiber bundles was not clear, the bundle membrane was incomplete. Immunohistochemistry results showed there was no obvious change in the content of glial fibrillary acidic protein (GFAP) in the optic nerve in non-compression group; its expression began increasing in 2 w-compression group and remained high level in 8 w-compression group. With the compression extending, the number of apoptotic cells in RGCs layer increased gradually, and it was positive correlation with the compression time. CNTF and GAP-43 expressions were low in blank control and non-compression groups, and were up-regulated in 2 w-compression group (P<0.01); with the compression extending, the expressions of two genes increased gradually (P<0.01). A chronic intraorbital optic nerve compression damage model was constructed successfully, and in that way we found that with the compression extending, more RGCs were lost; the structure of optic nerve fibers was damaged; the number of neuroglial cells tended to decreased at the beginning and then increased; and the CNTF and GAP-43 expressions increased gradually 2 weeks after damage.

A Case of Complete Visual Recovery From No Light Perception After Resection of Pituitary Adenoma

Purpose: We report a case of a patient with no preoperative light perception who achieved complete visual recovery after transsphenoidal resection of a pituitary adenoma. Case summary: A 53-year-old man with a history of pituitary adenomectomy visited our clinic complaining of decreased vision of 7 weeks ducation. His best-corrected visual acuity was 1.2 in his right eye, and he had no light perception (NLP) in his left eye. Light reflex was absent in the left eye, and no consistent wave was detected in the left eye on flash visual evoked potential (FVEP). A pituitary adenoma 33.5 cm in diameter was found following magnetic resonance imaging (MRI), and was removed using a transsphenoidal approach and gamma knife radiosurgery. Six weeks postoperatively, his best corrected visual acuity improved to 1.0 in the left eye. Conclusions: Prompt management should be initiated in patients with no light perception vision, due to compressive optic neuropathy.

Research on Influences of Transient High IOP during LASIK on Retinal Functions and Ultrastructure

Objectives. To study the influences of transient high intraocular pressure(IOP) during LASIK on retinal functions and ultrastructure. Methods. Thirty-two New Zealand white rabbits were randomly divided into normal control, experimental control, negative suction 20 s and negative suction 3 min groups. The experimental control group was treated only by laser. Rabbit eyes received suction for different periods of time (20 s, 3 min) by negative pressure generator in different groups. The changes of neuro-optic and retinal ultrastructure were observed under electron and light microscopes; retinal neurofunctional changes were observed with flash-visual evoked potential (F-VEP) and flash-electroreinogram (F-ERG). Results. There was no obvious change in optic nerve, retina, ERG a-wave and b-wave in normal control and experimental control groups. There were slight changes in tissues of optic nerve and retina at various times of suction 20 s compared with control group, and a sharp change in suction 3 min group within 14d after operation, but these changes recovered at 28d . Amplitude of ERG b-wave observed at different time will decrease with suction periods prolonged. It can recover to normal level with the prolonged recovery periods. Amplitude and incubation period of ERG a-wave and VEP-P did not change significantly after different duration of suction. Conclusions. The transient high IOP during LASIK might have influence on retinal function and ultrastructure, but these changes were reversible.

P-VEP as Predictor of Occlusion Therapy

Dear Editor, We read the article Pattern Visual Evoked Potential as a Predictor of Occlusion Therapy for Amblyopia by Chung et al in December issue with keen interest. Amblyopia represents a major public health problem, the prevalence of which is usually underestimated, often because of lack of awareness. Strabismus develops in approximately 5% to 8% of the general population.1 The authors deserve to be congratulated for highlighting the role of pattern-shift VEP's in predicting the course of improvement. Based on our little experience in the ever evolving world of Evoked Potential studies, we supplement a few points in this regard. The use of pattern visual evoked potential (P-VEP) has been the primary technique for electrophysiologically detecting amblyopia in patients unable to undergo conventional testing. Amblyopia affects the broad spectrum of visual subsystems that constitute vision, including contrast and color, motion, and vernier discriminations. P-VEP studies show that the pursuit of high-contrast acuity does not ensure optimum performance at lower contrasts. Rather than relying on just one measure to monitor amblyopia therapy (e.g., high-contrast recognition acuity), it is likely that a battery of specific stimuli may provide an enhanced profile of amblyopia against which the results of occlusion can be better monitored.2 It is pertinent to mention here another pioneer Korean study reporting fMRI as a useful tool for the study of amblyopia in humans. Choi et al found calcarine activation from amblyopic eyes in anisometropic amblyopes was more suppressed at higher spatial frequencies, while that from amblyopic eyes in strabismic amblyopes was more suppressed at lower spatial frequencies.3 An important but unanswered question concerns the quality of vision that amblyopics have on binocular viewing. When visual performance is measured with a P-VEP, the amplitude of VEP responses is enhanced on binocular compared with that on monocular viewing by 30 to 40%. Holmes et al., compared monocular and binocular flash VEP amplitude with abnormal retinal correspondence (ARC) in strabismic and normal subjects.4 A recent study was performed to evaluate the effectiveness of P-VEP parameters in amblyopic patients under monocular and binocular conditions.5 In binocular viewing, the amount of VEP amplitude was greater in normal subjects than that in both amblyopic groups. The mean binocular amplitude was significantly greater in the anisometropic group than in the strabismic group. Listing above mentioned studies would have made the study even more interesting. It is also of interest to note multifocal-VEP difference between early- and late-onset strabismus amblyopia. A study found no significant difference in latency or amplitude between amblyopic and fellow eyes for the early-onset amblyopic group, whereas in the late-onset amblyopic group, latencies were significantly prolonged and amplitudes were attenuated in the central region of visual field in the amblyopic eye.6 Endorsed by authors, we conclude by emphasizing usefulness of P-VEP as a reliable and reproducible indicator of occlusion therapy for amblyopia.

Ophthalmic Features of Joubert Syndrome

Joubert syndrome (Online Mendelian Inheritance in Man 213300) is a rare autosomal recessive congenital malformation of the brainstem and cerebellar vermis. Diagnosis is based on characteristic clinical features (e.g., hypotonia, episodic hyperpnea, developmental delay, progressive ataxia) and is confirmed by distinctive neuroradiologic findings (e.g., the "molar tooth" sign). Variable ophthalmic features have been mentioned in prior reports; however, most do not detail eye findings and the few that do were before the publication of suggested diagnostic criteria. The objective of the current study is to describe the ophthalmic phenotype in a cohort of patients with Joubert syndrome for whom the diagnosis was made using current diagnostic criteria. Prospective case series. Eight children diagnosed clinically with radiologic confirmation. Ophthalmic examination and visual electrophysiology. Ocular and oculomotor examination (as allowed by patient cooperation), electroretinography, flash visual-evoked potential (fVEP). Patients' ages ranged from 7 months to 10 years. Saccadic dysfunction was observed in all cooperative patients (6/6); compensatory head thrusts or turns were present in all except the youngest patient (7 months of age). Most patients (5/8) had primary-position nystagmus (see-saw in 3/5). Abnormal pursuit (3/7) and a dystrophic retinal appearance (3/8) were also seen. One patient had bilateral asymmetric ptosis with unilateral lid elevation during ipsilateral abduction. Electroretinography findings were normal for all 8 patients. Seven patients underwent fVEP; 6 were abnormal (asymmetric) and one was not interpretable because of study artifact. Ophthalmologists should be aware that saccadic dysfunction (typically with head thrusts) and primary position nystagmus (typically see-saw) in a developmentally delayed child suggest the diagnosis of Joubert syndrome, especially if a dystrophic retinal appearance is also present. Our findings of asymmetric fVEPs and see-saw nystagmus suggest an abnormality in optic nerve decussation, consistent with the concept that impaired axonal guidance occurs in patients with Joubert syndrome. The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Sudden unilateral visual loss after autologous fat injection into the nasolabial fold

A 27-year-old female presented with sudden visual loss of her right eye after receiving an autologous fat injection into the right nasolabial fold. Fundus examination of the right eye showed multiple whitish patchy lesions with macular edema. Fluorescein angiogram showed deterioration of choroidal circulation with patchy choroidal filling and arm-to-retina circulation time and retinal arteriovenous passage time were delayed to 30 seconds and 20 seconds, respectively. There was no response in flash visual evoked potential (VEP). High dose steroid therapy (methylprednisolone 1 g/day/i.v.) was done and about 2 weeks later, the disc edema subsided and retinal arteriovenous passage time of fluorescein angiogram was normalized but there was no improvement in visual acuity. Absence of a cherry red spot, deterioration of choroidal circulation with patchy choroidal fillings seen in fluorescein angiogram, and no response in flash VEP suggests multiple choroidal infarction due to perfusion defect of the short posterior ciliary artery. The autologous fat injected is thought to have entered the dorsal nasal artery and the retrograde migration of the emboli to the ophthalmic artery might have caused the multiple occlusions of the short posterior ciliary artery.

Maturation of steady-state flicker VEPs in infants: fundamental and harmonic temporal response frequencies

Transient flash VEPs allow objective assessment of visual function and are easily recorded in young infants. However, due to their high variability, they are an insensitive surrogate marker of visual development. The aim of our study was to investigate the early maturation of temporal characteristics of steady-state flicker VEPs. Data from 53 VEP sessions were analyzed in term-born infants between birth and 20 months of age. The stimulus was a square-wave modulated luminance flicker with 80% modulation depth at temporal frequencies of 4.7, 7.5, 12.5, and 19 Hz. A total of 18 healthy adults aged between 21 and 54 years served as controls. Contingent on the stimulus frequency, we found pronounced changes of the flicker VEP with age. Regression lines fit to the first harmonic VEP magnitude as a function of age between 3 and 88 weeks of age indicated increases at 7.5 (P = 0.004), 12.5 (P < 0.001), and 19 Hz (P = 0.07) and a non-significant decrease at 4.7 Hz (P = 0.3). The magnitude of the second harmonic increased for all frequencies (4.7 (P = 0.05), 7.5 (P = 0.01), 12.5 (P = 0.13), and 19 Hz (P = 0.18)). Over the whole infant age range, the flicker VEP was dominated by the first harmonic, in contrast to adults, where the response was typically shifted to a higher harmonic at low stimulus frequencies. The optimal stimulus frequency, defined as the frequency eliciting the highest magnitude for F1, shifted to higher rates with age. Due to the difference from adult responses, further developmental changes of the temporal properties must be assumed to occur after the age of 20 months. Changes in temporal characteristics of the flicker VEP with age may be useful as an indicator of visual system maturation and a useful tool to detect visual delay.

F‐Visual evoked potentials (f VEPs), nystagmus vs. motor &amp; neurological disorders in quadriplegia

Abstract Purpose To correlate flash VEPs and nystagmus with the severity of the motor and brain disorder in spastic quadriplegic children. Methods 52 quadriplegic children (2‐9 years of age) participated in this study. Flash VEPs (ICEVE), and brain MRI were performed, also nystagmus (clinical evaluation) and gross motor function (GMFCS) were evaluated. Results 29 children were premature and 23 were full terms. 15 out of 52 (28.84%) had normal f VEPs and 37(71.15%) had abnormal. epilepsy, 13 (25%) had nystagmus (horizontal). 73.07% of the children had moderate to very severe motor disorders. 32 children (61.53%) had periventricular leukomalacia and 20 (38.47%) had various brain damages. Conclusion Affected flash VEPs and nystagmus are common in quadriplegic children. There is a statistically significant relationship between VEPs, nystagmus and neurological and brain damage.

Pattern electroretinography and imaging of the macula

Abstract Purpose Pattern electroretinogram (PERG) is retinal response to contrast stimulation that originates from inner retina, mostly from ganglion cells. PERG may help to answer frequent diagnostic ambiguities between macular and optic nerve diseases and can serve as a link between flash and multifocal ERG and VEP. Methods Current trends with emphasis on PERG recording in relation to mfERG, flash ERG and VEP, perimetry, microperimetry and scanning laser ophthalmoscope imaging including autofluorescence of the RPE and OCT will be reviewed in representative clinical cases. Results Global retinal function is well assessed by flash evoked ERGs, but these may be normal in macular disease. PERG and multifocal ERG in combination with autofluorescence imaging and OCT may delineate macular diseases in very early stages. OCT may reveal transversal loss of photoreceptors which correlates well with PERG amplitude. In differential diagnosis, optic nerve diseases usually do not affect multifocal ERG but can affect PERG, especially its N95 component. Combination of reduced N95 component and delay in VEP is strongly suggestive for optic nerve or ganglion cell disease in which autofluorescence imaging would usually be normal. Conclusion By judging the cause of visual loss, PERG in combination with mfERG and morphological features by RPE autofluorescence and OCT with psychophysical methods usually leads to correct diagnosis.

Electroencephalogram and Flash Visual Evoked Potentials for Detecting Periventricular Leukomalacia

The aim of this study was to evaluate the usefulness of a combination of electroencephalogram (EEG) and flash visual evoked potentials (FVEPs) for predicting periventricular leukomalacia (PVL) in the early days of life. Eighty-six of 108 infants admitted to Anjo Kosei Hospital during 1998 through 2000 were enrolled in this study. All subjects underwent EEG and FVEP during the early neonatal period and were followed-up until 18 months of corrected age. EEG was performed once within 72 h after birth, every 1-2 weeks during the first month and every 2-4 weeks during the second month. FVEPs were recorded at least twice, at the first and the second week of life. Of the 86 infants, 13 were diagnosed as having PVL. Among them, EEG abnormalities were observed in 11 infants and FVEP abnormalities in 10. The sensitivity and specificity of EEG were 0.85 and 0.95, respectively. The sensitivity and specificity of FVEPs were 0.77 and 0.96, respectively. All except one (92%) infant with PVL had EEG and/or FVEP abnormalities. The combination of EEG and FVEPs can increase the sensitivity, but reduces the specificity to identify infants with PVL. The combination can makes up for the shortcomings of each method.

Neuroprotective effects of recombinant human granulocyte colony-stimulating factor (G-CSF) in neurodegeneration after optic nerve crush in rats

The purpose of the present study was to investigate the effects of granulocyte colony-stimulating factor (G-CSF) on neurodegeneration of optic nerve (ON) and retinal ganglion cells (RGCs) in a rat model of ON crush. The ONs of adult male Wistar rats (150–180 g) were crushed by a standardized method. The control eyes received a sham operation. G-CSF (100 μg/kg/day in 0.2 ml phosphate-buffered saline) or phosphate-buffered saline (PBS control) was immediately administered after ON crush for 5 days by subcutaneous injection. Rats were euthanized at 1 or 2 weeks after the crush injury. RGC density was counted by retrograde labeling with FluoroGold application to the superior colliculus, and visual function was assessed by flash visual evoked potentials (FVEP). TUNEL assay, Western blot analysis and immunohistochemistry of p-AKT in the retina and ED1 (marker of macrophage/microglia) in the ON were conducted. 2 weeks after the insult, the RGC densities in the central and mid-peripheral retinas in ON-crushed, G-CSF-treated rats were significantly higher than that of the corresponding ON-crushed, PBS-treated rats (survival rate was 60% vs. 19.6% in the central retina; 46.5% vs. 23.9% in mid-peripheral retina, respectively; p < 0.001). FVEP measurements showed a significantly better preserved latency of the p1 wave in the ON-crushed, G-CSF-treated rats than the ON-crushed, PBS-treated rats (78 ± 9 ms in the sham operation group, 98 ± 16 ms in the G-CSF-treated group, and 174 ± 16 ms in the PBS-treated group; p < 0.001). TUNEL assays showed fewer apoptotic cells in the retinal sections in the ON-crushed, G-CSF-treated rats. p-AKT immunoreactivity was up-regulated in the retinas of the ON-crushed, G-CSF-treated rats at 1 and 2 weeks. In addition, the number of ED1-positive cells was attenuated at the lesion site of the optic nerve in the ON-crushed, G-CSF-treated group. From these results, we gather that administration of G-CSF is neuroprotective in the rat model of optic nerve crush, as demonstrated both structurally by RGC density and functionally by FVEP. G-CSF may work by being anti-apoptotic involving the p-AKT signaling pathway as well as by attenuation of the inflammatory responses at the injury site, as evidenced by less ED1-positive cell infiltration in the optic nerve.