[Effect of prolonged pain on the course of dark adaptation of the optic analyzer].
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The effects of light adaptation on the increment threshold, rhodopsin content, and dark adaptation have been studied in the rat eye over a wide range of intensities. The electroretinogram threshold was used as a measure of eye sensitivity. With adapting intensities greater than 1.5 log units above the absolute ERG threshold, the increment threshold rises linearly with increasing adapting intensity. With 5 minutes of light adaptation, the rhodopsin content of the eye is not measurably reduced until the adapting intensity is greater than 5 log units above the ERG threshold. Dark adaptation is rapid (i.e., completed in 5 to 10 minutes) until the eye is adapted to lights strong enough to bleach a measurable fraction of the rhodopsin. After brighter light adaptations, dark adaptation consists of two parts, an initial rapid phase followed by a slow component. The extent of slow adaptation depends on the fraction of rhodopsin bleached. If all the rhodopsin in the eye is bleached, the slow fall of threshold extends over 5 log units and takes 2 to 3 hours to complete. The fall of ERG threshold during the slow phase of adaptation occurs in parallel with the regeneration of rhodopsin. The slow component of dark adaptation is related to the bleaching and resynthesis of rhodopsin; the fast component of adaptation is considered to be neural adaptation.
The adaptive plasticity of the translational vestibulo-ocular reflex (VOR) was investigated in rhesus monkeys after 2-h exposure to either vertical or torsional optic flow stimulation accompanied by lateral translation stimuli (0.5 Hz). Because of the inherent ambiguity in the otolith system for the detection of gravitoinertial accelerations, we hypothesized that cross-axis adaptation of the translational VOR during lateral motion would be preferentially selective for a torsional optic flow stimulus that would mimic a roll tilt movement. However, we found that both vertical and torsional adaptation was possible. Furthermore, there was no significant preference for whether the torsional adaptation was in phase or out of phase with the apparent tilt induced by the motion stimulus. These results suggest that, at least at 0.5 Hz, there seems to be no preferential, visually induced adaptive capacity of the otolith system for tilt/translation reinterpretation during motion. Like the rotational VOR, translational VOR appears to exhibit a general form of cross-axis adaptation that operates for different directions of optic flow stimulation.
1. The vestibulo-ocular reflex, a sensorimotor process, operates in a similar manner for homeothermic (mammals) and poikilothermic (fish) animals. However, individual physiological, biochemical, and/or pharmacological thermolabile processes that underlie the operation of this reflex could alter the operation of this reflex in a poikilotherm. The object of this study was to determine what aspects of the vestibulo-ocular reflex are affected by temperature changes naturally experienced by a poikilothermic animal, the goldfish. 2. Experiments were conducted on the visuovestibulo-(Vis-VOR) and vestibulo-ocular reflex (VOR) during normal operation as well as during the acquisition (learning) and retention (memory) phases of adaptive gain change. These studies were carried out at temperatures to which goldfish had been acclimated over several weeks and after rapid (< 5 min) shifts from this acclimation temperature. 3. Normal sinusoidal Vis-VOR and VOR gains before adaptation were found to be independent of the acclimation temperature over a wide range. Acute temperature changes of up to 10 degrees C either above or below a 20 degrees C acclimation temperature (Ac degree C = 20 degrees C) did not significantly modify normal visual and/or vestibular oculomotor reflex gains. 4. Surprisingly, slight reductions in temperature, as small as 2.5 degrees C, noticeably reduced Vis-VOR and VOR gain adaptations. Both short (3 h) and intermediate (up to 48 h) term reflex modifications were affected. Loss of adaptation was observed 10 degrees C below the acclimation temperature (Ac - 10 degrees C); however, return to the original temperature immediately restored most (60-100%) of the previously acquired Vis-VOR and VOR gain changes. In contrast, elevation of temperature up to 10 degrees C above the acclimation temperature (Ac + 10 degrees C) did not alter either increases or decreases in the adapted Vis-VOR or VOR gain. 5. A decrease in temperature reduced the magnitude of an adapted VOR gain increase and elevated the magnitude of an adapted gain decrease, thus returning the VOR gain back toward its normal control gain before adaptation. Because both increases and decreases in VOR gain were affected by the same temperature reduction, the cold effect was not a generalized reflex suppression, but inactivation of a process responsible for maintaining VOR adaptation. 6. During the acquisition phase, the time course and magnitude of adaptive VOR gain increases at temperatures acutely set 8-10 degrees C below the acclimation temperature were similar to those obtained at the acclimation temperature. Because the same temperature decrease inactivated retention of adapted VOR gain changes, the neuronal processes underlying the acquisition and the retention phases of Vis-VOR or VOR adaptation are suggested to differ qualitatively. 7. With the use of velocity step stimuli, both the adapted dynamic (< 100 ms) and sustained (> 100 ms) components of VOR adaptation were reduced by cooling. This effect on the dynamic component demonstrates an alteration in the shortest latency pathway through the vestibular nucleus and indicates that one thermosensitive site resides in the brain stem. 8. These results also show that, over a wide range of temperatures (20 +/- 10 degrees C), the neuronal processing that is responsible for the normal operation of the visuovestibulo- and/or vestibulo-ocular reflex and for the retention of reflex adaptation functions by separate physiological processes within the same brain stem and cerebellar circuitry. 9. We conclude that temperature exhibits a unique, and unexpected, state-dependent effect on sensorimotor regulation and adaptation for periods up to 48 h. Temperature does not alter normal VOR or the acquisition phase of an adapted gain change. (ABSTRACT TRUNCATED)
Eye movement deficits caused by ocular muscle weakness vary according to the position of the eye in the orbit and the direction of eye movement. We studied the ability of both the saccadic and pursuit eye-movement systems to compensate for these anisotropic deficits in four patients with ocular muscle weakness. The eye-position dependence of each patient's motor deficit was characterized by plotting the position of the weak eye against that of the normal eye (in various orbital positions) when fusion was prevented, thus giving a static eye-position curve from which relative muscle strength could be inferred. Movements of the weak eye were smaller and slower than those made by the normal eye, so that the weak eye required more time to acquire a visual target. When patients were forced to view monocularly with their weak eye for several days, both the saccadic and pursuit systems showed changes in the movements of the normal eye consistent with an increased central innervation designed to decrease the time it takes to bring the target's image onto the fovea of the weak eye and to keep it there. These adaptive changes varied with eye position and movement direction and compensated for the weak muscle in both its agonistic and antagonistic actions. Saccadic adaptation consisted of a change in the relationship between saccadic amplitude and retinal error (distance between the target's image and the fovea) to compensate for hypometria (undershoot) and a readjustment of the ratio of the phasic (pulse) and tonic (step) components of the saccadic innervation to suppress postsaccadic ocular drift. Pursuit adaptation consisted of an increase in the relationship between eye acceleration and the rate of motion of the image of the target on the retina during the initial phase of tracking as well as an increase in the velocity during tracking of a target moving at a constant velocity. These changes reflect an increase in pursuit innervation that would cause the weak eye's velocity to approach target velocity sooner. The average acceleration of the normal eye during the initial period of tracking (130 ms) increased by as much as threefold. The corresponding maximum smooth eye velocity increased so that, for example, the pursuit response to a 15 degree/s target movement could be over 50 degree/s in the normal eye.
Before and after exposure to clockwise optical tilt, subjects' compensatory eye movements were recorded, as the head was oscillated around a vertical axis by the experimenter. An analysis of the horizontal and vertical components of eye movements showed a change in eye movement path in the clockwise direction. This corresponded to similar changes in visual spatial orientation judgments indicative of perceptual adaptation. It was suggested that long-term visual feedback serves to restore the compensatory nature of the eye movements which was altered by the introduction of the prism transformation.
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BACKGROUND: Fenretinide, a synthetic derivative of retinoic acid, is under study in clinical trials for the prevention of breast, skin basal cell, bladder, and oral cancer in patients at risk. Although fenretinide is well tolerated even after prolonged use, it does lower plasma retinol levels and thus may affect night vision. PURPOSE: The purpose of this study was to measure changes in dark adaptation resulting from fenretinide administration, to compare the measured results with the patient's subjective perception, to define the association with plasma retinol levels, to assess the reversibility of alterations in night vision, and to assess the effects of fenretinide on the surface of the eye. METHODS: The study involved 65 women who had been operated on for stage I breast cancer. Of the study group, 34 received 200 mg daily of fenretinide for a median of 32 months, while 31 control subjects did not. Dark adaptation was studied with the Goldmann-Weekers adaptometer and with a subjective questionnaire. Plasma retinol levels were measured at each test of dark adaptation. Effects of fenretinide on the ocular surface were evaluated through conjunctival impression cytology. RESULTS: Of the patients on fenretinide, eight (23.5%) showed mild and nine (26.5%) showed moderate alterations of measured dark adaptability, compared with just two controls (6.5%) with mild alterations (cumulative odds ratio = 15.4; P = .0008). A significant inverse correlation exists between the final sensitivity threshold of dark-adaptometry and plasma retinol levels, with mild alterations arising below 16 micrograms/dL and moderate alterations below 10 micrograms/dL. Abnormal rod function improved significantly after 7 days and normalized 1 month after use of fenretinide was stopped or vitamin A supplementation was begun, while the conventional 3-day drug suspension, or drug half dose, did not allow sufficient recovery. Alterations of conjunctival cytology were slightly higher in patients receiving fenretinide, but no clinical disorders of the ocular surface were observed. CONCLUSIONS: The women treated with 200 mg fenretinide daily showed a relatively high incidence of mild-to-moderate alterations of dark-adaptometry as measured with the Goldmann-Weekers adaptometer. However, the real-life implication of the measurements is an open question, for the questionnaire shows that 50% of the patients with altered dark adaptometry were asymptomatic.
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Adaptive modification of vestibuloocular reflex (VOR) direction was characterized in humans by recording vertical and horizontal VOR eye movements during horizontal rotations in darkness at frequencies of 0.05 to 1 Hz before and after exposure to a VOR direction adaptation procedure. This procedure paired yaw horizontal vestibular rotation at 0.25 Hz with synchronous pitch vertical optokinetic motion. Saccades were removed from eye position records and VOR gain and phase were recorded. With an onset time constant of 36 min, the VOR measured during horizontal rotation in complete darkness acquired a vertical component in phase with the optokinetic stimulus presented during adaptation. The amplitude of this newly acquired vertical VOR component was maximal during rotation at the frequency of adaptation; at other frequencies, the amplitude was lower, but still significant. Unlike VOR direction adaptation in cats, the phase of the adaptive VOR component in humans did not show significant leads or lags at test frequencies below or above the adaptation frequency. These data suggest that, like the cat, the human VOR can be directionally adapted, and the pathways involving the adaptive component of the VOR are frequency specific.
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