Visual evoked potential and

Seppalainen AM, Raitta C, Huuskonen MS. 1979. -Hexane-induced changes in visual evoked potentials and electroretinograms of industrial workers. Electroencephal Clin Neurophysiol 47 492-498. 

Carbamazepine can cause altered visual evoked potentials and brainstem evoked potentials (20). In 100 epileptic patients aged 8-18 years taking carbamazepine in a modified-release formulation, interpeak latencies of I-III and III-V of brainstem evoked potentials were significantly delayed and N75/P100 and P100/N145 amplitudes in the visual evoked potentials were reduced. 

Valproate can cause altered visual evoked potentials and brainstem evoked potentials (14). In 100 epileptic... 

Other antiepileptic drugs can also alter visual evoked potentials and brainstem evoked potentials. Visual field defects associated with various antiepileptic drugs (carba-mazepine, diazepam, gabapentin, phenytoin, tiagabine, and vigabatrin) have been reviewed (37). 

Harding GF, WUd JM, Robertson KA, Lawden MC, Betts TA, Barber C, Barnes PM. Electro-oculography, electroretinography, visual evoked potentials, and multifocal electroretinography in patients with vigabatrin-attributed visual field constriction. Epilepsia 2000 41(11) 1420-31. 

Term infants fed breast milk for the first 4 mo of life increase visual acuity, measured by the Teller Acuity Card, more rapidly compared to formula-fed infants (Jorgensen et al., 1996). Carlson et al. (1996) have reported that term infants fed formula with 2% 18 3n-3 and 0.1% 22 6n-3 show better 2-mo visual acuity than infants fed formula. Makrides et al. (1995) also have found that visual evoked potential and visual acuity of breast-fed neonates and infants fed a formula supplemented with 22 6n-3 are better than those of placebo-formula-fed infants at 16 and 30 wk of age. Although these results show an effect of diet on the development of the visual function in different groups of infants, other studies have provided comparable results (Jorgensen et al., 1998). 

Sikora A, Lanuauer-Lewowicka H, Kazibutowska Z. 1990. Visually evoked potentials and simple reaction times to visual stimuli in chronic disulphide intoxication. Pol J Occup Med 3(3) 293-299. 

In contrast to the Hake and Stewart (1977) study, Altmaim et al. (1990) found a statistically significant (p<0.05) increase in latency of pattern reversal visual-evoked potentials in 10 male volunteers exposed to tetrachloroethylene at 50 ppm for 4 hours/day for 4 days, relative to 12 subjects exposed at 10 ppm. No effects on brainstem auditory-evoked potentials were noted. Tests of visual contrast measured in a few individuals showed a tendency for loss of contrast in the low and intermediate spatial frequencies at 50 ppm. In this study, measurements were also completed the day before exposure so each individual served as his own control. The 10-ppm group was considered the control group, and this concentration was used because it is well above the odor threshold of tetrachloroethylene so that there was at least an attempt to blind the subjects to the exposure concentrations. Blood tetrachloroethylene concentrations were measured before, in the middle, and at the end of each day s exposure, and an association between the effect on pattern reversal visual-evoked potentials and blood tetrachloroethylene concentrations was observed (p<0.03). The lack of effect on flash visual-evoked potentials in the Hake and Stewart (1977) study at concentrations up to 100 ppm compared to an effect on pattern reversal visual-evoked potentials at 50 ppm in the Altmann et al. (1990) study may reflect the greater inter- and intrasubject variability of waveforms for flash visual-evoked potentials (Otto et al. 1988). 

Dyer, R.S. and Howell, W.E. 1982a. Acute triethyltin exposure effects on the visual evoked potential and hippocampal afterdischarge. Neurobehav. Toxicol. Teratol. 4 259-266. 

Lihenthal, G.H., Lenaerts, C., Winneke, G, and Hennekes, R., 1988, Alteration of the visual evoked potential and the electroretinogram in lead-treated monkeys, Newotoxicol. Teratol 10 417. 

The experiments reported here deal with three different topics (1) the search for brain structures primarily involved in lead-induced neurobehavioural dysfunction, (2) the influence of the time span between indirect maternal exposure and age at behavioural testing in the rat, and (3) the role of lead in central and peripheral visual processes in monkeys. The results indicate that there are differences in the effects of lead exposure and hippocampal lesions, that permanent post-weaning lead exposure does not add to the neurobehavioural deficit due to indirect maternal exposure, and that in monkeys parameters of the visual evoked potentials and electroretinograms are altered by lead. 

An increased level of exploratory activity immediately after exposure, attributed to reduced anxiety on the part of the rats, was also observed in this study. Decreased avoidance was observed in rats exposed to 125 ppm trichloroethylene 4 hours per day, 5 days per week for 30 days (Goldberg et al. 1964a). Changes in visually evoked potentials (Blain et al. 1992) and electroretinal responses to flash stimulation (Blain et al. 1994) were seen in rabbits exposed to 350 ppm trichloroethylene for 12 weeks (4 days/week, 4 hours/day). The study authors suggested that binding of trichloroethanol to blood proteins may enable it to reach the visual cortex. 

Dissemination in space by MRI evidence of nine or more T2-weighted brain lesions, or two or more cord lesions, or four to eight brain and one cord lesion, or positive visual evoked potentials with four to eight MRI lesions, or positive visual evoked potentials with less than four brain lesions plus one cord lesion. 

Zeneroli ML, Ventura E, Baraldi M, Penne A, Messori E, Zieve L Visual evoked potentials in encephalopathy induced by galactosamine, ammonia, dimethyldisulfide and octanoic acid. Hepatology 1982 2 532-538. 

P. A. Bhaskar, S. Vanchilingam, E. A. Bhaskar, A. Devaprabhu, and R. A. Ganesan. Effect of L-dopa on visual evoked potential in patients with Parkinson s disease. Neurology 36 1119-1121 (1986). 

Reeves RR, Struve FA, Patrick G. (1999). The effects of caffeine withdrawal on cognitive P300 auditory and visual evoked potentials. Clin Electroencephalogr. 30(1) 24-27. 

Figure 3.5 Classification of the components of visually evoked potentials (VEPs). The two negative peaks I and III and the positive peak II were termed the primary response by Ciganek (1961), peaks IV-VII (negative peaks = upwards pointing peaks) being termed the secondary response. The amplitude of these peaks lies in the region of 10-30/iV. In addition to amplitudes (e.g. between peaks I and II), latencies are determined, i.e. the time in milliseconds between the stimulus and the appearance of a peak, e.g. peak IV...

Lanting, P. et al., The cause of increased pupillary light reflex latencies in diabetic patients the relationship between pupillary light reflex and visual evoked potential latencies, EEG Clin. Neurophysiol., 78, 111, 1991. 

McKeeffy DJ, Russell MH, Murray IJ, Kulikowski JJ. 1996. Amplitude and phase variations of harmonic components in human achromatic and chromatic visual evoked potentials. Vis Neurosci 13 639-653. 

Schechter I, Butler PD, Zemon VM, et al. 2005. Impairments in generation of early-stage transient visual evoked potentials to magno- and parvocellular-selective stimuli in schizophrenia. Clin Neurophysiol 116 2204-2215. 

NMDA receptor antagonists induce schizophrenia-like deficits in early sensory information processing, such as abnormal mismatch negativity, abnormal visual Pl-evoked potentials and deficits in continuous performance tasks (Javitt et al., 2008). 

Antal A, Keri S, Bodis-Wollner I (1997) Dopamine D2 receptor blockade tilters the primary and cognitive components of visual evoked potentials in the monkey, Macaca fascicularis. Neurosci Lett 232 179-181... 

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