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Effect of the cholinesterase inhibiting substance galanthamine on human EEG and visual evoked potentials.

The action of galanthamine (GAL), a cholinesterase inhibiting substance, on resting EEG and on flash visual evoked potentials (VEPs) was tested in 9 healthy subjects. Alpha power was increased significantly in 4 of 8 subjects after the infusion of 10 mg, which provided a median inhibition of 47% of acetylcholinesterase in erythrocytes. Mean alpha frequency and peak alpha frequency decreased significantly in 5 of the 8 subjects by 0.22-0.98 Hz. Alpha power increase and alpha frequency decrease were not accompanied by changes in theta power. The amplitudes of the late components of the flash VEP were increased in 8 of 9 subjects receiving doses of 10-35 mg of GAL, while the early components remained unaffected. Increase of late VEP components was significantly correlated with the strength of cholinesterase inhibition. The synchronizing effect of GAL in these healthy volunteers obviously contrasts with the known desynchronizing effect of physostigmine in animal experiments.

Adult↗

Spatial frequency tuning in the visual evoked potential elicited by sine-wave gratings.

This investigation examined the onset response of the transient visually evoked potential elicited by the appearance-disappearance of sine-wave gratings at various levels of spatial frequency, suprathreshold contrast, and stimulus duration. The response was most easily characterized by two negative-positive complexes that were differentially tuned to spatial frequency. The earlier complex peaked at high spatial frequencies while the later complex peaked at low spatial frequencies. For both complexes, amplitude showed only slight variations across three-octave ranges of contrast and duration. Latency was curvilinearly related to spatial frequency, decreased with increasing contrast, and showed no apparent change as a function of duration.

Adult↗

Source derivation: application to topographic mapping of visual evoked potentials.

The application of a source derivation technique to topographic mapping of the pattern-reversal visual evoked potential is described. Comparisons were made with non-cephalic and common average reference recordings. Source derivation yielded wave forms which were less influenced by activity of reference origin. Source derivation wave forms were similar to those obtained with common average referencing but contour plots showed less spread of regions of maximal activity in the case of source derivation. It is suggested that source derivation may be useful in further studies of the topography and sources of cerebral evoked potentials.

Adult↗

Effects of iloprost on visual evoked potentials and brain tissue oxidative stress after bilateral common carotid artery occlusion.

Effects of iloprost on visual evoked potentials and oxidant/antioxidant status were evaluated after bilateral carotid artery occlusion. There were three experimental groups; Sham (S) group (n=10), bilateral common carotid artery occluded (BCCAO) group (n=10) and after bilateral common carotid artery occlusion, iloprost-treated (BCCAOI) group (n=10). Iloprost was administered (0.5ng/kg/day) for 10 days by intraperitoneal injection. N(2) and P(2) latencies (millisecond) and N(2)-P(2) (microV) amplitudes were recorded 10 days after operation for evaluating VEPs. The rats were sacrificed by decapitation immediately after recording of VEPs. Malondialdehyte (MDA), glutathione (GSH), Cu-Zn superoxide dysmutase (SOD) were studied spectrophotometricly. After BCCAO, MDA levels were increased, GSH and Cu-Zn SOD levels were decreased significantly, and abnormal VEPs parameters were observed. Iloprost treatment after BCCAO decreased MDA and increased GSH levels significantly. Low Cu-Zn SOD levels and impaired VEPs remained after iloprost treatment. Iloprost treatment may protect the brain tissue from oxidative damage during cerebral hypoperfusion.

Animals↗

Visual evoked potentials in children with occipital epilepsies.

The objectives of this study are to see if any visual evoked potential (VEP) differences are present in two forms of occipital epilepsy, childhood epilepsy with occipital paroxysms (CEOP) and symptomatic occipital epilepsy (SOE) with respect to etiology, as CEOP is a benign age- and localization-related idiopathic epilepsy while SOE is a symptomatic form. Nineteen patients with CEOP and 13 patients with SOE were included in the study and P100 potential latency and amplitude values obtained from these patients were compared with the values recorded from normal controls. The amplitude values recorded from the patients with CEOP were significantly high (P=0.033). P100 potential latency values recorded in patients with SOE were significantly long (P=0.028). High amplitude VEP responses were mostly attributed to hyperexcitability of the occipital cortical structures whereas prolonged latency P100 responses were attributed to occipital structural changes.

Child↗

Visual evoked potentials in elderly patients with primary or multi-infarct dementia.

Flash and pattern-reversal visual evoked potentials (VEP) were recorded in 35 elderly patients with dementia, and 19 controls of equivalent age. Dementia produced a slowing of the major positive (P2) component of the flash VEP but did not affect the latency of the flash P1 component or the P100 pattern-reversal component. This unusual type of abnormality was found in both primary and multi-infarct types of dementia, and has previously been found in primary presenile dementia. The results show that the VEP can be used for the diagnosis of multi-infarct, and primary presenile and senile dementias.

Aged↗

Intensity-dependent changes of visually evoked potential components in the superior colliculus of freely moving rats.

Amplitudes and peak times of averaged visually evoked potentials (VEP) recorded in the superficial layers of the anterior medial superior colliculus were measured in 7 freely moving rats. The amplitudes of P21-N29 decreased significantly to 47% (p = 0.01), the amplitudes of components N41-P54 and P54-N64 to 29 and 32% (p = 0.01) when the flash intensity was lowered six times, whereas components N29-P36 and P74-N85 showed no significant decrease. During exploratory behaviour all the components were significantly lower than during relaxed wakefulness, except N29-P36 and P74-N85. The course of their intensity-dependent decrease was different. Peak times of both early negative components N29 and N41 increased exponentially with decreasing flash intensity during relaxed wakefulness. The peak times of later negative components N64 and N85 increased only with the lowest intensity. During exploratory behaviour peak time changes were evidently smaller. The data suggest that the different changes of components reflect the activity of different neuron types.

Animals↗

Improving the ensemble average of visual evoked potentials. I. Theory of correction by spectral phase difference methods.

The considered causes of variability of visual evoked potentials (VEPs) are additive noise and time variability. The time variability can be modelled in three different ways: 1. time invariant VEP waveform and delay-time "jitter"; 2. time variant VEP waveform, due to 2a. jitter of individual components or 2b. constant VEP waveform and "wow", i.e. expansion or compression of the time scale. The wow model has not been considered so far in the literature. Correction of jitter and/or wow is based on a frequency domain method: the "spectral phase difference" method (SPD). When jitter is present the SPD method is applied in the frequency domain on the single responses, or on a subensemble of a small number of responses. For the wow a new method is proposed where the time scale is logarithmically compressed prior to the calculation of the spectrum. It is shown that the SPD method can also be applied then to estimate the compression factor yielding the wow. The single responses, or the averaged sub-ensembles, can subsequently be corrected by this factor and finally be averaged. Improvement of the precision and accuracy of estimates of both the peak latencies and the peak amplitudes, as well as a comparison between the results of the jitter and wow models, have been reported in a companion paper.

Computer Simulation↗

Developmental changes in human infant visual-evoked potentials to patterned stimuli recorded at different scalp locations.

Visual-evoked potentials (VEPs) to patterned stimuli were recorded from 4 different scalp locations in 2 groups of infant subjects (ages 6 weeks and 10 weeks). Seven VEP components were identified that changed in amplitude as a function of changes in the amount of contour in the stimuli presented. Developmental shifts in these effects were interpreted to indicate a change in the physiological locus of control of infant visual preferences from a subcortical to a cortical locus over the age range examined.

Age Factors↗

[The dynamics of somatosensory and visual evoked potentials as a correlate of reversible states of altered consciousness].

Somatosensory and visual evoked potentials (EPs) of the brain of 17 sensitive subjects (extrasenses) and 12 ordinary healthy subjects were studied. It was found that during extrasensory activity (direct impact, meditation) in comparison to rest values, the amplitude of intermediate and late components of visual and somatosensory EPs of both hemispheres and early components of somatosensory EPs of ipsilateral in relation to stimulation hemisphere diminished 2-4--fold. There was a recovery of these components after discontinuation of extrasensory activity. It is shown that ordinary subjects could not change their EPs when they tried their best to decrease EPs. It is shown that ordinary subjects could not change their EPs when they tried their best to decrease EPs. It is suggested that the ability of extrasenses for reversible changes of their mind by direct adjustment of the activity of the ascending nonspecific systems of the brain and by alterations of interhemispheric relations forms the basis of extrasensory activity.

Adult↗

Prolonged follow-up of abnormal visual evoked potentials in multiple sclerosis: evidence for delayed recovery.

A case is described in which the latency of the P100 component of the pattern evoked visual response (VEP) was shown in serial recordings to have remained greatly prolonged for three years after an attack of optic neuritis, but had returned to normal after a further three and a half years. A similar pattern was found in one of a group of 21 patients re-examined between 6 and 8 years after abnormal VEP had been recorded. The pathophysiological implications are briefly discussed.

Adult↗

Visual evoked potentials of the blue-sensitive pathway under cold provocation in normals and glaucomas.

BACKGROUND: Vascular dysregulation in open-angle glaucomas can be identified by measuring the blood circulation during exposure to cold water. Aim of this study was to find out whether the same cold stimulus would lead to functional changes in the visual evoked potentials (VEP) of the short-sensitive pathway in normals and glaucoma patients. PATIENTS AND METHODS: Blue-on-yellow pattern-visual evoked potentials were studied in 22 healthy control persons and 47 patients with primary open-angle glaucoma (25 high-pressure glaucomas, 22 normal pressure glaucomas with clinical signs of vasospastic hyperreactivity). A blue stripe pattern, presented in onset-offset mode on a yellow adaptation light served as the stimulus. Cold provocation was initiated by dipping one hand of the patient into cold water of 3 degrees C to 5 degrees C. The onset amplitudes and peak times were measured without cold exposition as well as two and four minutes after the cold exposition began. RESULTS: In the group of vasospastic glaucoma patients a significant reduction of visual evoked potential-amplitudes was observed during cold provocation (amplitude before ice exposition: 4.17 microV, amplitude following two minutes of ice exposition: 3.52 microV; paired test: P < 0.01). Other subject groups showed no significant amplitude reductions after cold provocation. Peak times of both open-angle glaucoma groups (132.3 +/- 18.7 milliseconds in high pressure, 132.7 +/- 14.5 milliseconds in normal pressure) were significantly increased in comparison to normals (117.4 +/- 8.0 milliseconds). However, no significant influence of the cold provocation on peak times could be found in all groups. CONCLUSION: Peak times of the blue-on-yellow visual evoked potentials are significantly prolonged in patients with primary open-angle glaucomas. Cold provocation causes a significant amplitude reduction of the blue-on-yellow visual evoked potential in the present normal-pressure glaucoma patients and reflects vascular dysregulation in patients with vasospastic hyperreactivity.

Blood Pressure↗

Training induced alterations of visual evoked potentials are not related to body temperature.

The purpose of this study was to investigate the effect of mild chronic exercise on visual evoked potentials (VEPs). Twenty male Wistar rats were randomly divided into two groups: Control (C) and Exercise (E) groups. Exercise was performed on a motor-driven treadmill for 8 weeks. After 5 min of exercise, plasma lactic acid levels were determined. At the end of the experimental period, VEPs were recorded from E group twice: Five min (E-5 min) and 24 h (E-24 h) after the last bout of exercise. During visual evoked potential (VEP) recordings body temperature of the animals was kept constant to eliminate the effect of temperature changes. No difference was found between the lactic acid levels of two groups. The mean latencies of VEPs from E-5 min were shortened compared with the control group. The mean latencies of VEP components in E-24 h were observed to have returned to the control levels. Peak to peak amplitudes of VEPs were found to be unaltered among all measurements. We concluded that immediately after exercise, VEPs latencies were shortened independently from body temperature via unknown mechanisms. The latencies of VEPs were returned to control values after 24 h.

Analysis of Variance↗

Further investigation of visual evoked potentials elicited by lateralized stimuli: effects of stimulus eccentricity and reference site.

Visual evoked potentials (VEPs) to small lateralized flashes were recorded from the parietal midline, homotopic lateral central and occipital electrodes, and from left and right mastoid processes, all referred to a balanced non-cephalic reference. Two stimulus eccentricities, 4 degrees and 10 degrees, were employed, and a comparison made between the non-cephalic and linked mastoid references. P120 (measured at lateral occipital sites only) peaked earlier and was of smaller amplitude at the electrode contralateral to the visual field of stimulus exposure. N160 peaked earlier at central than occipital sites, was larger from electrodes over the contralateral hemisphere, and at the occipital sites only, peaked earlier in the electrode contralateral to the visual field of stimulus exposure. These effects were virtually unaffected by the eccentricity manipulation and it is concluded that light scatter across the visual midline is unlikely to be responsible for the observed pattern of ipsilateral-contralateral VEP asymmetries. The mastoids were found to detect significant stimulus-locked activity in the same latency range as the occipital N160 component. However, comparison of the non-cephalic and linked mastoid references revealed only non-specific effects, and no sign of any change in the pattern of ipsilateral-contralateral VEP asymmetries, or the magnitude of the associated latency differences. It is concluded that these effects may be of value in the study of callosal transfer.

Adult↗

Visual-evoked potentials and electroretinograms in ruminants with thiamine-responsive polioencephalomalacia or suspected listeriosis.

Electrodiagnostic visual testing (electroretinogram [ERG] and visual-evoked potential [VEP]) was performed on 5 ruminants (3 lambs, 1 kid, and 1 steer) with thiamine-responsive polioencephalomalacia (PEM) and on 2 sheep with listeriosis. The lambs and kid had typical clinical signs of PEM, especially blindness. In these animals, the ERG was normal but the VEP was abnormal. Follow-up recordings in the kid and 1 lamb indicated an improvement in VEP recordings accompanying a gradual return of vision after thiamine treatment. Possible subtle changes in VEP peak latencies could not be assessed because of lack of normative VEP data for sheep and goats. All animals had complete return of vision (owner-assessed). The steer did not have signs of blindness, and the ERG and VEP were normal. Changes in VEP accompanying permanent PEM blindness are not known. One sheep with suspected listeriosis had lack of menace response and palpebral and corneal reflexes, but had intact vision. The ERG and VEP were normal. The second sheep with suspected listeriosis had intact menace response and vision, but became acutely blind and died; the ERG was normal, but VEP amplitudes were depressed.

Animals↗

[Comparison of electrically evoked response (EER) and visual evoked potential (VEP) by topography and dipole-tracing].

To study the possibility of the clinical application of the electrically evoked response (EER) of the visual system, we analyzed P2 of EER as well as P100 of flash VEP by means of topography and dipole-tracing. By applying a constant electric current of 1.0 mA (duration 5 msec, frequency 1.39 Hz) and a strobo flash light of 0.6 Joules (frequency 1.39 Hz) to each eye, P2 and P100 were recorded respectively. It was found that the source generators of P2 and P100 showed the same localization and dipole vector. The results indicated flat the significance of P2 in applying EER clinically was comparable to the P100 of VEP.

Adult↗

An electroretinal and visual evoked potential study in Friedreich's ataxia.

We made an electroretinographic (ERG) and visual evoked potential (VEP) study of 12 patients with Friedreich's ataxia whose diagnosis was established using the Quebec diagnostic criteria. ERGs and VEPs were elicited to the same stimulating conditions. Flash evoked luminance changes and pattern-specific evoked potentials to check and diamond stimuli were used. Statistical analysis of the data was made using independent sample t-tests. Significant VEP delays were present under all test conditions. The presence of significant interocular and interhemispheric delays as well as evidence of abnormal temporal dispersion of the VEP response suggest there to be both diffuse anterior visual system disease and retrochiasmal involvement in Friedreich's ataxia. The implicit times of the ERG b-waves were statistically within normal limits but the waveforms were of low amplitude and deformed and there were significant interocular implicit time differences. These ERG results suggest there are retinal conduction abnormalities in Friedreich's ataxia which possibly play a role in the genesis of the abnormal VEPs.

Adolescent↗