Visual Evoked Cortical Potentials Research Articles

Relations between visual acuity, refraction and the pattern reversal visual-evoked cortical potential in aphakia.

The investigations included 20 aphakic patients. Relations were established between visual acuity, refraction and the pattern reversal visual-evoked cortical potentials (PRVECP). Close correlations were found between the three values. The optimum correction for obtaining best visual acuity, the skiascopic value, and the correction value for obtaining the largest PRVECP amplitude at minimum peak time differ by an average of 0.5 dptr.

Electrophysiologic Studies in Birdshot Chorioretinopathy

We investigated retinal function in 16 patients with birdshot chorioretinopathy. Consistent abnormalities of dark adaptation, color vision, visual field, electro-oculography, electroretinography, and visual-evoked cortical potentials were found. They included raised thresholds of dark adaptation, acquired dyschromatopsia, mainly of the blue-yellow type, an electroretinogram with reduced amplitude, increased latency of the b-wave and absent oscillatory potentials, an abnormal electro-oculogram, and in many a marked disturbance in the pattern reversal visual-evoked cortical potential. The a-wave of the electroretinogram, the fast oscillations of the standing potential, and the flash visual-evoked cortical potential were well preserved. The nature of the abnormalities suggests that dysfunction was caused by inner retinal disease. Little evidence indicated outer retinal dysfunction resulting from choroidal inflammation.

Electrophysiological analysis of factors involved in the primary demyelinating diseases: the rabbit eye model system

This study explores the longitudinal assessment of visual evoked potentials (VEPs) in the rabbit as a method for defining factors underlying functional and structural changes associated with optic neuritis and the inflammatory demyelinating diseases. In rabbits with experimental autoimmune encephalomyelitis (EAE) induced by sensitization with guinea pig spinal cord myelin, injection of lymphokines into the posterior chamber of one eye (monocular challenge) produces an early inflammatory response in the retina and optic nerve, and an alteration in the VEP, all limited to the injected eye and its projections. The earliest changes in the timing and distribution of the cortical VEP occur within hours of ocular challenge and precede histopathological evidence of structural demyelination at the light microscope level. Prechallenge assessment allows the induced monocular prechiasmal effects to be distinguished from the more diffuse electrophysiological findings associated with EAE (i.e. those due to sensitization alone). In sensitized/challenged animals there is a clear correspondence between electrophysiological and morphological measures of dysfunction at the time points sampled. These results suggest that this model system affords an excellent opportunity to examine the precise structural correlates of the early functional changes associated with the onset of inflammatory demyelination within the CNS. Furthermore, the stability of the system provides the capacity to monitor alterations over the complete course of inflammation, demyelination and remyelination, induced by experimental manipulations.

Effect of intravitreal liquid silicone on optic nerve function.

We recorded visual-evoked cortical potentials before and after pars plana vitrectomy and intravitreal liquid silicone filling in 30 patients (30 eyes) with complicated retinal detachments without vascular eye disease or glaucoma. The flash- and flicker-evoked cortical potentials increased in amplitude in all cases. Of 21 eyes followed up for more than 50 days, eight had a 30-Hz flicker response before and after surgery. Of 13 eyes with preoperatively reduced flicker-frequency responses, ten (77%) were improved after surgery. The visual-evoked cortical potential parameters did not deteriorate in any of the patients. We concluded that no toxic effect of intravitreal liquid silicone on the optic nerve could be shown by electrophysiologic methods.

Effect of Intravitreal Liquid Silicone on Optic Nerve Function

We recorded visual-evoked cortical potentials before and after pars plana vitrectomy and intravitreal liquid silicone filling in 30 patients (30 eyes) with complicated retinal detachments without vascular eye disease or glaucoma. The flash- and flicker-evoked cortical potentials increased in amplitude in all cases. Of 21 eyes followed up for more than 50 days, eight had a 30-Hz flicker response before and after surgery. Of 13 eyes with preoperatively reduced flicker-frequency responses, ten (77%) were improved after surgery. The visual-evoked cortical potential parameters did not deteriorate in any of the patients. We concluded that no toxic effect of intravitreal liquid silicone on the optic nerve could be shown by electrophysiologic methods.

Optic nerve involvement in patients with orbital phlebopathy: Pattern-reversal electroretinograms and visual evoked cortical potentials

Pattern-reversal electroretinograms (PERG) and visual evoked cortical potentials (VECP) were recorded from 24 patients with orbital phlebopathy, i.e., characteristic orbital pain and orbital phlebography changes, also occurring in painful ophthalmoplegia (Tolosa-Hunt syndrome). Twelve patients had no visual impairment and 12 had clinical signs of optic nerve involvement.Only two of the patients with optic nerve involvement had the marked VECP latency prolongation, typically seen in multiple sclerosis, on the orbital pain side. The mean amplitudes of the pattern-reversal ERG and VECP from the eyes on the orbital pain side were significantly reduced, when compared to the reference group. The mean VECP latency from these eyes was not significantly increased. These findings indicate that the optic neuropathy in orbital phlebopathy is characterized by axonal dysfunction rather than demyelination like in multiple sclerosis.

Visually evoked cortical potentials to pattern disappearance stimuli in multiple sclerosis

Visually evoked cortical potentials (VECPs) to pattern disappearance stimuli were studied in 32 patients with multiple sclerosis (MS). The mean peak latencies of the disappearance response were prolonged significantly in eyes with a history of optic neuritis compared with those obtained from normal subjects, whereas no significant delay of the response was found in eyes without such a history, with a history of ocular muscle paresis, or in unaffected eyes with a history of unilateral optic neuritis. In contrast to the pattern reversal response, the disappearance response did not show a delay in subclinical optic neuritis in MS. It was, thus, suggested that the natural characteristics of the two responses were different in the patients with multiple sclerosis.

Subnormal visual acuity in children: prognosis and visual evoked cortical potential findings.

Seventy-one children, age 4-12 years, with subnormal visual acuity (VA) in at least one eye (0.7 or less) were examined using visual evoked cortical potentials (VECPs) to pattern-reversal stimulation. Twenty-eight children with squint had mean VA 0.3 in squinting and 0.7 in non-squinting eyes. Thirty-one children had unexplained subnormal VA, mean 0.6. Twelve children with mild unclassifiable fundus abnormalities had mean VA 0.5. In the squinting eyes and the eyes with fundus abnormalities the mean latency of the VECP was significantly prolonged. In squinters the mean amplitude to stimulation of the squinting eyes and to binocular stimulation was significantly reduced. Statistically significant increase in the mean VA was observed in all groups except in the cases with visible fundus abnormalities. There was no statistically significant correlation between VECP parameters and final VA. In conclusion, VA prognosis could not be predicted from VECP data in individual cases.

Pattern electroretinogram and visual evoked cortical potential in ethambutol optic neuropathy.

Forty-one eyes in 21 cases of ethambutol optic neuropathy were investigated for the pattern visual evoked cortical potential (VECP) and the pattern electroretinogram (ERG). In 21 of the eyes the disappearance VECP responses were not detectable. In the other 20 eyes the peak latency and amplitude of the disappearance VECP were delayed and decreased significantly compared with normal eyes. The recovery of the peak latency of the disappearance VECP in ethambutol optic neuropathy was faster than that of the amplitude. Twelve eyes in six patients were studied by pattern reversal ERG. Though the mean peak latency of the pattern ERG was within normal limits, the mean amplitude was decreased significantly. Our investigations indicated that ethambutol optic neuropathy disturbed not only the optic nerve but also the retina.

Evidence of pericentral stereopsis in random dot VECP.

Dynamic random dot patterns generated on a TV screen by a special pattern generator are proven to be adequate stimuli for testing stereopsis. In our experimental set-up we use red-green coded striped or checkered patterns of various size and disparity as stimuli, which are viewed through red-green glasses (anaglyph method). The registration of transient visual evoked cortical potential (VECP) to these random dot stimuli offers objective proof of stereopsis. There is a typical amplitude behavior with maximum amplitudes at medium disparities. By recording the specific stereo VECP while masking the central retinal areas stepwise (artificial central scotoma) we can objectively show intact stereopsis of corresponding pericentral retinal areas. This peripheral stereopsis is demonstrable in the VECP by central scotomas up to eight degrees.

The electrical response of the human eye to patterned stimuli: clinical observations.

Following the first recording of electroretinographic responses in man to a barred pattern by Riggs and associates (1964) in normal and by Lawwill (1973, 1974) in clinical cases, the first striking observation of a complete loss of pattern electroretinogram (PERG) after injurious section of the optic nerve by Groneberg & Teping (1980) has led to the conclusion that the PERG originates from proximal retinal structures different from those responsible for the luminance electroretinogram (LERG). Typical changes of the PERG are seen during branch occlusion of the central retinal artery and vein. In ocular hypertension without visual field loss and glaucoma-related papillary changes the PERG is decreased at intraocular pressures above 26 mm Hg. In cases of primary glaucoma with regulated intraocular tension and without using miotics the amplitude of the PERG reflects the damage to the inner retinal layers. This favorably compares with the P100 latencies of the visual evoked cortical potential (VECP) which in primary glaucoma were partly within, partly outside the normal range. Other retinal diseases showing amplitude changes in the PERG are primary macular dystrophy, diabetic retinopathy, and the acute stage of optic neuritis. In all these cases the Ganzfeld LERG may be normal or nearly normal, whereas the PERG undergoes typical changes. On the contrary a highly preserved PERG can be recorded in cases of retinitis pigmentosa where the electrooculogram light rise and the LERG are already missing. In light of these findings the recording of PERG constitutes a new promising method of clinical electroretinography reflecting the activity of the hitherto omitted innermost retinal layers. It thereby contributes essentially to the location of disturbances within the visual system.

Contrast sensitivity and visual acuity of the pigmented rat determined electrophysiologically

The contrast sensitivity function of the rat was assessed by investigating the relationship between the amplitude of visually evoked cortical potentials (VECP) and the spatial frequency and contrast of grating stimuli. Pattern reversal VECPs were recorded in Area 17 in the region of representation of the central binocular visual field. Transient responses were obtained with a 1 Hz contrast reversal. The mean contralateral monocular CSF peaked around 0.1 c/deg, with a threshold sensitivity of 20–25, low frequency attenuation and a high frequency cut-off of 1.18 c/deg. The mean binocular CSF showed a cut-off of 1.20 c/deg, which matches several behavioural measurements of visual acuity. The greater binocular sensitivity in the low frequency range (0.04 c/deg) could be tentatively attributed to the greater influence of the population of large ganglion cells that reaches its maximal density in the ipsilateral projection

Isolation of short-wavelength-sensitive cone photoreceptors in 4–6-week-old human infants

Spectral sensitivity was measured for nine infants, 4–6 weeks of age, and three adults under conditions of chromatic adaptation chosen to reveal the presence of short-wavelength-sensitive cones. Monochromatic test stimuli (400–550 nm) were presented at 2 Hz superimposed on a broadband, yellow background. Following 4 min of adaptation to the background, test stimuli were presented while recording the steady-state, visually-evoked cortical potential (VECP). Response averages were obtained for several radiance levels at each test wavelength, and the amplitude of the fundamental frequency was extracted from the digitized response with a fast-Fourier transform. These data were used to construct response vs intensity functions for each wavelength. A fixed criterion response was chosen from the latter family of functions to generate individual spectral sensitivity curves. These VECP spectral sensitivity functions matched the psychophysically-determined functions of adults, measured by the method of adjustment and with the same stimulus configuration. Peak sensitivity for infants and adults under these conditions occurred at about 440 nm, and the main lobe of the curve (400–500 nm) was well fitted by the Vos-Walraven short-wavelength cone fundamental. The only major difference between the infant and adult data was in the relative sensitivity of the secondary mode of the curves (above 500 nm). These results demonstrate the presence of short-wavelength-sensitive cones and a functional pathway to the visual cortex by 4–6 weeks of age.

Visual resolution and sensitivity in a nocturnal primate (galago) measured with visual evoked potentials

Visual resolution and contrast sensitivity were examined in anesthetized, paralyzed galagos using visual evoked potentials (VEPs) resulting from stimulation with phase-reversed sinewave gratings. Spatial frequency vs contrast response functions were band-pass with peak sensitivity at 0.2–0.4 c/deg and a high frequency cut-off between 1.6 and 3 c/deg. Peak contrast sensitivities (estimated from extrapolation of contrast response functions) varied across animals from 10 to 170. Variation of the stimulus modulation rate showed that best responses occurred at 1 Hz with an upper limit of 6–16 Hz. As in other primates, an oblique effect was seen in 6 of 8 animals. The contrast sensitivity function (CSF) determined from cortical VEPs agrees well with the CSFs of cells in the lateral geniculate nucleus, but peak sensitivity and spatial frequency are slightly lower than found for the behavioral CSF. Overall visual performance resembled closely that of another nocturnal species, the cat.

Optic pathway conduction in insulin-dependent diabetics.

Abnormal latency delay of pattern-reversal visual evoked cortical potentials (VECPs) has been demonstrated in insulin-dependent diabetics without retinopathy as a sign of subclinical damage. Pattern-reversal VECPs and onset-offset (on-off) VECPs probably originated at different cortical levels. On-off latencies of a group of 50 insulin-dependent diabetics without retinopathy or neuropathy and with normal oscillatory potentials have been studied in relation to various clinical and metabolic parameters. The results of our study showed that on-off VECPs have in diabetes the same latency alterations as pattern-reversal VECPs, if to a lesser extent. This finding can be a useful index in the evaluation of patients at risk.

Visual evoked cortical potentials and pattern electroretinograms in Parkinson's disease and control subjects.

Parkinson's disease patients have been shown to have abnormal visually evoked cortical potentials (VEPs) to pattern stimulation. Whereas dopamine is not an important neurotransmitter in the central visual pathways, the retina is rich in dopamine and, together with previous animal and human studies, this suggests that the abnormal VEPs in Parkinson's disease patients may be due to a biochemical and electrophysiological disorder in the retina. This hypothesis has been examined by studying the VEPs and pattern electroretinogram (PERG) of Parkinson's disease patients and matched control subjects. The amplitudes of the cortical and retinal evoked potentials were significantly reduced in Parkinson's disease patients compared with the control subjects and this could not be attributed to any particular feature of the disease or its treatment. There was a significant relationship between the VEP P100 latency and the PERG amplitude. Moreover for those subjects in whom there was an interocular difference in both cortical and retinal evoked potentials, the abnormality was more commonly found in the potentials from the same eye. These findings suggest that the abnormality of the VEP in Parkinson's disease patients is, at least in part, secondary to an abnormality of the retina itself.

The relation between the after-negative potential of the pattern electroretinogram and the visually evoked cortical potential.

The relationship between the after-negative potential of the pattern electroretinogram (PERG) and the visually evoked cortical potential (VECP) was studied. The PERG was recorded through the use of Toray's high water content, soft contact lens electrode. The PERG consisted of an initial positive potential, a subsequent negative potential and then a slow positive potential. To reduce or avoid contamination of the VECP on the PERG, the most important factor was found to be the reference electrode position; special attention was paid in cases where the amplitude of the VECP was large. In the steady-state condition, the PERG was thought to be modulated by the VECP when the ear lobe was used as the reference electrode position; when the temple was used as the reference electrode position, the amplitude of the PERG was thought to represent that of the after-negative potential.

Evaluation of the central retina and optic nerve function in media opacities.

Conventional electroretinogram (ERG) and pattern VECP (or visual evoked cortical potential) are of limited value in estimating visual function in eyes with media opacities. We used a method consisting of flicker ERG and flicker VECP to successfully overcome this limitation. Three of 25 eyes with cataract had a reduced flicker VECP. These 3 patients also had a history of glaucomatous optic nerve damage. Normal flicker VECP was found in some patients with reduced flicker ERG or reduced scotopic and photopic a-wave. Analysis of the results showed that the flicker VECP is independent of the ERG and flicker ERG. Utilizing this method we could rule out maculopathy and optic nerve damage in patients with media opacities as well as recognize optic nerve damage in patients with coexisting maculopathy.

Visual acuity measurement using evoked potentials and fast Fourier transform.

Visual evoked cortical potentials (VECP) were recorded from 10 subjects with normal visual acuity (VA) 1.0. Reversing square-wave gratings of 16 different spatial frequencies were used as stimuli. In all 10 subjects significant increase in power at the stimulation frequency was observed in the Fourier spectrum. The VA, calculated from the Fourier spectra, ranged from 0.4 to 1.0. The described method for VA measurement is entirely objective, and the examination can be performed very rapidly and conveniently with the aid of a computer. However, the results indicate that the reliability of the measurement in individual cases may be doubtful.

Effects of ethyl alcohol on VECP.

Previous studies have demonstrated that ethyl alcohol ingestion affects the clinically recorded visually evoked cortical potential (VECP). However these studies have not related the possible relevance of such alcohol-induced VECP changes to visual performance. We studied the flash and pattern-reversal monopolar VECP recorded at the occiput before and after alcohol ingestion and compared the recordings with psychophysical parameters (e.g. contrast sensitivity) also measured before and after alcohol intake. Results are presented, and the potential usefulness of VECP alterations in predicting alcohol-induced effects on visual performance is evaluated. We found no clear, consistent effect of blood alcohol levels ranging from 0.05% to 0.15% on the parameters tested.