Enhanced retinal responses without signs of optic nerve involvement

Abstract

Seven patients with low visual acuity displaying enhanced positive waves in retinal responses of normal shape and reduced or extinct visual evoked potentials were presented. None of these cases exhibited any sign of optic nerve affection and visual field defects nor any localizing neurological deficits. Conclusions drawn in an earlier report from similar electrophysiological findings but obtained in cases with optic nerve atrophy were applied here. On the basis of these findings, it is hypothesized that the enhanced ERG represents the result of an abolition of a physiological rivalry between the increasing retinal sensitivity in the dark and an inhibitory cerebral influence upon retinal activity exerted via efferent fibers in the optic nerve. The possible origins of this assumed negative feedback mechanism are discussed, though neither experimental facts nor speculation did provide a reasonable clue. An answer may be given by observing the patients during the following years and possibly by animal experiments.

Outer Retinal Dysfunction in the Absence of Structural Abnormalities in Multiple Sclerosis

“…With regard to response amplitudes, previous results are mixed, with studies showing normal, [28][29][30] reduced, 31,32 or increased 13 ERG amplitudes in MS patients relative to control subjects; none of these studies also analyzed peak time. In this context, our results showing mostly normal amplitudes (with increased or decreased amplitudes for some conditions) are not contrary to previous studies.…”

“…Previous work examining the ERG in MS patients has produced apparently contradictory findings, with some authors reporting normal ERG results [28][29][30] and others a range of abnormalities. [11][12][13][31][32][33][34] Significantly, those studies that reported normal ERG findings in MS patients analyzed only response amplitudes, with no peak time values presented. [28][29][30] Previous studies showing changes to the peak time of the cone 12,34 or mixed rod/cone 11,34 ERG responses are unanimous in recording delayed responses relative to normative values, as described here.…”

“…9 It has also been proposed that an atypical subset of MS patients may exhibit thinning of the INL and outer nuclear layer (ONL) without corresponding inner retinal changes. 10 The functional correlates of these proposed structural changes remain unknown; although electroretinographic studies of MS patients have been previously published, [11][12][13] results vary considerably between studies, and to date no published work has examined the relationships between OCT-derived outer retinal structure and function in MS.…”

Electroretinogram findings in unilateral optic neuritis

“…No such changes were observed in the present study population. Auerbach and colleagues [8,9,17] used a b-wave cut-off value of 600 lV to define a ''supernormal ERG'' when they reported supernormal ERGs in optic nerve disease. Notwithstanding the need for each laboratory to establish its own normal ranges, that series was ascertained prior to the introduction of ISCEV Standard ERGs making direct comparison with more modern data even more difficult.…”

Effects of high peak power microwaves on the retina of the Rhesus monkey

“…Agents known to cause transient enhancement of ERG amplitude are sodium azide, trichloroethylene, sodium pentobarbital [Noell, 1958], hyperbaric oxygen [Ray and Hawgood, 1977], ische- mia [Brunette et al, 1986], sodium iodate [Adachi-Usame et al, 1992;Hosoda et al, 1993;Sugimoto et al, 1996], and in siderosis caused by intraocular metal particles [Knave, 1969]. Because of the correlation between enhanced ERG amplitude and the presence of reduced or extinct visual evoked potentials, ERG amplitude enhancement was hypothesized to result from abolition of a physiologic rivalry between photoreceptor's increasing sensitivity in the dark and inhibitory cerebral in¯uence upon retinal activity exerted via efferent ®bers in the optic nerve [Feinsod et al, 1971a;1971b]. Enhanced ERG amplitudes in isolated retina in vitro could be achieved pharmacologically by dopaminergic antagonists (haloperidol and chlorpromazine), anticholinergic drug (atropine), and monoamine uptake inhibitor (amitriptyline) [Nakagawa et al, 1988] or in vivo in rabbits after dopamine depletion by intravitreal injection of 6hydroxydopamine [Olivier et al, 1987].…”