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At least 937 records · Page 52Linked to original sources
PubMed1997

Cholinergic modulation, visual function and Alzheimer's dementia.

Electrophysiological evidence at a cellular level and in vivo macroelectrode recordings converge in indicating a degree of specificity of acetylcholine action in vision. Acetylcholine (ACh) function is also thought to play a significant role in memory, learning and other cognitive processes. In this respect, ACh action is suggested to serve in both sensory and cognitive processes. The pharmacological blocking of brain muscarinic transmission has been proposed as a model of geriatric memory impairment and Alzheimer's dementia. Visual electrophysiological testing is deemed of diagnostic specificity for this disease. ACh brain neurotransmission, however, mostly contributes to the modulation of nonspecific aspects of cognition, such as arousal or attention. Alzheimer's dementia results from complex neuron alterations [which also affect muscarinic receptors among other (sub)cellular structures] rather than simply reflecting ACh impoverishment. A substantial loss of retinal ganglion cells is documented in patients with Alzheimer's disease and is consistent with electrophysiological observations. However, it is unclear to what extent the dysfunction of the visual system observable in Alzheimer's dementia is qualitatively different from that occurring spontaneously during aging. The dissimilarities between the effect of acute muscarinic blocking (e.g. by scopolamine) and dementia outnumber the similarities. Accordingly, the conventional ACh agonist-antagonist model of dementia now appears questionable, and replacement treatment with compounds enhancing ACh function proved disappointing. It is suggested that (nonspecific) ACh action becomes function-specific, as determined by the architecture of local brain circuits in which it is involved.

Acetylcholine↗
PubMed1993

Corneal asphericity and visual function after radial keratotomy.

Corneal asphericity was measured before and after surgery in 81 radial keratotomy eyes. Asphericity was calculated between keratoscope rings 2 and 9, representing corneal diameters of 2.3 mm and 7.6 mm. Statistical methods were used to assess the relationship between postoperative asphericity and undilated, uncorrected visual acuity. Smaller radial keratotomy clear zones resulted in greater negative asphericity after surgery (R = 0.74, p < 0.0001). For eyes with smaller clear zones of < 4.0 mm, postoperative negative asphericity was high (mean -6.44). Eyes in this smaller clear zone range had better uncorrected visual acuity if they possessed higher levels of negative asphericity (Mann-Whitney U test, p < 0.0001). The study suggests that eyes with smaller clear zones gain a beneficial increase in depth of field as the degree of negative asphericity increases. The study offers this as one reason that radial keratotomy patients with residual refractive error often have better uncorrected visual acuity than expected.

Adult↗
PubMed1981

Visual function abnormalities in macular heterotopia caused by proliferative diabetic retinopathy.

In seven patients with displacement of the macula in one eye caused by vitreoretinal traction from proliferative diabetic retinopathy, the macula was displaced toward the optic disk in all but one eye. The eyes with macular heterotopia showed (1) reduced visual acuity (ranging from 6/6 (20/20) to 6/24 (20/80), (2) reduced static perimetry sensitivity (particularly in the temporal field) with displacement of the peak sensitivity toward the blind spot, (3) loss of hue discrimination, and (4) metamorphopsia. In two eyes with macular heterotopia, Stiles-Crawford data provided evidence for photoreceptor disorientation; one eye had mixed orientation, and the other a displaced peak suggesting regular photoreceptor tilting. The proposed mechanisms of visual loss in eyes with macular heterotopia secondary to traction from proliferative diabetic retinopathy include detachment of the macula, disorientation of photoreceptors in the macula, and disturbance of normal neural connections within the retina caused by stretching of the retina.

Adult↗
PubMed1985

Differentiation between recently resolved optic neuritis and central serous retinopathy. Use of tests of visual function.

A test battery was performed on 13 patients with resolved central serous retinopathy and on 13 patients with resolved optic neuritis to see whether the tests would help to distinguish between the two conditions. We found that the most useful discriminators were the relative afferent pupillary defect, followed by the visual evoked potential latency and the critical flicker frequency. The total error score on the Farnsworth-Munsell 100-Hue Test and the nature of the color vision defect were not helpful in separating the two diseases.

Adult↗
PubMed1998

[Changes in visual functions in myopia 6 months after photorefractive keratectomy].

I. 100 myopes (-0.25-(8.75) D) divided into 3 groups (I: < -3.0 D, II: -3.0-(-5.75) D, III: -6.0-(-8.75) D) were examined before and 1, 3, 6 months after photorefractive keratectomy (PRK). As a control group 20 emmetropes were examined. Best corrected visual acuity (BCVA) was tested using logMAR charts. Contrast sensitivity (CS) was measured using a computerized system. II. Preoperative BCVA in myopes of all three groups was significantly lower (p < 0.001) compared to the control group. A significant reduction of BCVA (p < 0.05 resp. p < 0.001) in all groups at all terms after PRK was noted. III. Significantly lower values of CS (p < 0.001) were found in myopes of all groups before PRK in comparison to the control group. One and 3 months after PRK only nonsignificant changes of the mean values of contrast sensitivity (MCK) were noted. After 6 months a significant improvement of MCK (p < 0.05) in myopes of I. and II. groups was observed.

Adolescent↗
PubMed2001

Nutritional factors and visual function in premature infants.

Approximately 5-7% of all infants are born prematurely, and birth before 37 weeks is the most common cause of neonatal mortality, morbidity and long-term disability. Premature infants are poorly equipped for life outside the womb, and oxidant stress has been implicated in the aetiology of visual impairment in these infants, who are often exposed to increased O2 concentrations and high light intensity in neonatal units. The carotenoids lutein and zeaxanthin, which give the macular area of the eye its yellow colour, are located in the retinal pigment epithelium of the eye, and are believed to play a role in protecting it against oxidative and light damage. The macular pigments are of dietary origin, and green leafy vegetables are the primary source of lutein and zeaxanthin. Lutein is one of the five most common carotenoids found in the diet. There is current interest in the macular pigment in relation to age-related macular degeneration, but these pigments may also have a protective role in the retinal pigment epithelium of the newborn infant. Little information is available on blood lutein and zeaxanthin levels in neonates. Levels of lutein in human milk are two to three times higher than those of beta-carotene, whereas their concentrations in the mothers' blood are approximately the same. Human milk is the main dietary source of lutein and zeaxanthin for infants until weaning occurs. The biochemical mechanisms which mediate the transport of the macular carotenoids into the eye are not known, but tubulin has been identified as the major carotenoid-binding protein, and may play a role in the physiology of the macula.

Antioxidants↗