Visual function and academic performance.
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The multifocal m-sequence technique is a versatile set of tools for visual electrophysiology designed to provide access to the complex dynamic interplay of converging signals in the central nervous system. Here, a number of uses for the technique are demonstrated, with examples from human electroretinography. A simple relationship between the binary kernels extracted from a single experiment permits us to distinguish local from lateral interactions in the retina. Transformation of the series of binary kernels into response sequences provides new insight into unexpected fast dynamic properties of retinal responses and facilitates future modeling of the signals as well as identification of the signal sources.
In seeing rats light flashes inhibit acoustic startle reflexes at short lead times. In contrast, visually impaired (light-blinded) rats show an early phase of exaggerated reflex expression, revealing the presence of pathological visual processing, and then an aberrant late phase of delayed inhibition. Grafting fetal retinal cells into the damaged retina entirely removed reflex facilitation and restored a modest degree of properly timed and statistically significant reflex inhibition. This restoration of visually-mediated behaviour, observed in two independent groups, reveals that intraretinal grafts provide useful information to blinded hosts.
This chapter describes the utility of event-related potential recordings in the assessment of auditory and visual system integrity in the newborn infant. A battery of electrophysiologic tests is described that permits the evaluation of sequential levels of processing within these sensory system.
Monocular and binocular reading curves of 20 patients (4 with cataract, 5 with glaucoma, 11 with maculopathy) were recorded by infrared oculography. Reading speed was found to be directly proportional to the visual acuity of the eye tested. However, the same visual acuity in both eyes does not always mean that the subject reads at the same speed with both eyes. For example, paracentral visual field defects impair reading ability and eyes which appear to have good vision may easily become tired. Twelve of 16 examined eyes with maculopathy showed a significant decrease in reading speed during a reading test lasting no more than 2 minutes. In tests of the same duration cataract patients did not tire; their reading speed increased. Binocular vision helps improve reading speed in cases of maculopathy, and even more so in cases of glaucoma with visual field defects. Attention is drawn to Mackensen's suggestion that measurement of reading speed is a valuable function test, and to the fact that in certain cases fatigue of an eye during reading is a new and measurable criterion of the degree of visual impairment.
Current diabetes research is directed at preventing secondary complications such as diabetic retinopathy (DR) that can have devastating effects on vision. Diagnosis of DR is traditionally dependent on visible alterations of retinal vasculature. However, the detection of functional disorders, likely occurring before observable changes in structure, may provide advanced warning of impending DR. We examined the neural function of the retina by electroretinograms (ERG's) and the macular-cortical pathways by visual evoked potentials (VEP's) in 30 insulin-controlled juvenile diabetics and an age-and sex-matched group of nondiabetics. The average duration of diabetes in the test group with normal retinal vasculature was 5.6 +/- 4.6 years. Results showed small but measurable differences in the amplitude and timing characteristics of retinal and cortical potentials for the test and control groups. The most surprising findings related to shorter response times for the "b" wave of the photopic ERG, larger amplitude oscillatory potentials, and larger steady-state VEP's. These may be the earliest signs of increased segmental blood flow by vascular autoregulatory mechanisms to compensate for generalized hypoxia. Longitudinal studies are required to determine the physiological significance of our findings and the prognostic value of evoked potentials in diabetes.
Age-related macular degeneration (AMD) is the leading cause of blindness in developed countries. With an ageing population, the prevalence of such a condition has resulted in a large proportion of the population relying on peripheral vision to undertake activities of daily living. Peripheral vision is not a scaled-down version of the fovea, simply requiring larger print or increased contrast for detection of objects or reading text. Even when print size is scaled and eye movements are minimised, the peripheral retina cannot perform at the level of the foveal region. Understanding how and why reading performance is limited as a function of eccentricity has important implications for how we approach rehabilitation of patients with central visual loss. This brief review of the extensive literature on reading with peripheral vision and the research aimed at better reading rehabilitation for low vision patients focuses on why many of the problems associated with the reduced reading capability of peripheral vision cannot be completely solved with magnification, reducing eye movements or modifying print.
Careful clinical correlation of the appearance of the optic nerve and retinal nerve fiber layer with measurements of the visual field is an important aspect of the evaluation of patients with glaucoma. The anatomy of the nerve fiber layer and its retinotopic projections to the optic nerve head form the basis of the spatial relationships between structure and function in glaucoma. Clinical experience with the temporal correlations of structure and function indicates that visible alterations of the optic nerve and surrounding nerve fiber layer may occur before scotomas in the visual field can be detected. Quantitative clinical studies of the optic nerve and visual field support this concept, and provide additional clues regarding the pathogenesis of glaucomatous optic nerve damage.
The purpose of this review is to: (1) compare and contrast the relative contributions that the four principle regions in cat extrastriate parietal cortex make to a battery of visual tasks which require motion, spatial, or attentional processing; and (2) examine the laminar parcellation of visual behaviors within one of these parietal regions which mediates multiple visual behaviors. We examined a battery of visual tasks presumed to be mediated by parietal cortex, including direction of motion, differential motion, and landmark discriminations, and visual orienting to moving stimuli. As a control, we also examined performance on form (pattern and object) recognition tasks mediated by the temporal processing stream. The four regions of parietal cortex we examined included the: middle suprasylvian (MS) gyrus (area 7), anterior middle suprasylvian (aMS) sulcus (AMLS, ALLS), posterior middle suprasylvian (pMS) sulcus (PMLS, PLLS), and the dorsal posterior suprasylvian (dPS) gyrus (area 21a). The contributions made to each of the six different behavioral tasks was examined before, during, and after reversible cooling deactivation of each cortical area. Deactivation of pMS sulcal cortex resulted in deficits on all four tasks that required motion, spatial or attentional processing. Deactivation of aMS sulcal cortex resulted in deficits on only tasks that required motion processing. Deactivation of neither aMS nor pMS sulcal cortex yielded any deficits on the form recognition tasks. In contrast, deactivation of dPS cortex only produced deficits on the form recognition tasks. This finding confirmed our early hypothesis that dPS cortex is a key component of the temporal, and not the parietal, processing stream. Regardless of the task, no deficits were identified on any of the six tasks during deactivation of the MS gyrus. We then more closely examined pMS sulcal cortex to determine if its multiple functions could be dissociated on a laminar level. We found that cooling deactivation of the superficial layers (I-III) of pMS sulcal cortex selectively and completely impaired performance on the direction of motion discrimination task, while leaving visual attention unimpaired. Additional deactivation of the deeper layers (IV-VI) resulted in impaired visual attention as assessed with visual orienting. These results show a functional bipartite division of labor between upper and lower cortical layers of pMS sulcal cortex. Therefore, spatial, motion and attentional functions can be localized within visuoparietal cortex on both an areal and laminar level.
Disturbance of vision commonly accompanies hypoglycaemia. This study was designed to investigate the nature of the visual disturbance, the blood glucose threshold at which the disturbance occurred and the physiological basis. Measurements were made of the corrected visual acuity, colour vision (100 Hue test), visual evoked potentials (VEP), electroencephalography (EEG) frequency analysis and psychometry (digit recall) during stepwise induction of controlled hypoglycaemia produced by an intravenous insulin infusion. Six male volunteers and five insulin-dependent diabetic subjects were studied. During hypoglycaemia corrected visual acuity was unchanged. Colour vision was significantly impaired. Baseline VEP were normal in both groups but significantly prolonged during hypoglycaemia (mean increment 10.8 ms) and increased by greater than 5 ms in nine out of 11 subjects. Quantitative EEG analysis demonstrated slowing with a power density spectral shift from fast alpha to slow alpha, theta and delta which correlated with VEP latency and amplitude changes. The findings have clinical implications. A deterioration in colour vision is likely to impair the ability to read reagent strips by eye. VEP measurements in diabetic patients are likely to be misleading if hypoglycaemia is present; EEG changes are a sensitive index of cortical dysfunction during hypoglycaemia and provide a theoretical basis for developing a portable device to detect early hypoglycaemia.
BACKGROUND AND METHODS: It is well known that deferoxamine (DFO) treatment in thalassemia major can produce ocular toxicity. In one experience, Visual evoked potentials (VEPS) to pattern reversal were formed to be altered in 4 out of 10 patients under conventional treatment with DFO, before supplementary high-dose i.v. deferoxamine. In all 4 cases the alterations consisted of bilaterally delayed P100 latency, always obtained by stimulation with high spatial frequency (15' checks) and associated in three cases with low spatial frequency (55'). Computerized EEG (cEEG) studies showed a generalized increase of slowing activity. All patients underwent high-dose DFO treatment. RESULTS: At the control performed at the end of treatment in all 4 cases with previous VEP alterations, a further delay in P100 latency was observed bilaterally while two of the six patients, without previous involvement, showed delayed responses when using checks of 15'. The EEG slowing activity was not modified. Three weeks after terminating i.v. DFO therapy, the patients were still under subcutaneous treatment (50 mg/kg/day); a more evident VEP recovery towards the initial values was observed in those patients without initial alterations. No significant changes were found between electrophysiological parameters and serum ferritin levels. CONCLUSIONS: Our results indicate that high-dose DFO therapy in patients with iron overload induces reversible visual impairment without significant changes in brain electrical activity. The employment of VEP in intensive chelation programs in thalassemia major is discussed.
In the past few years, there have been significant advances in the understanding of how the so-called higher cortical functions are organized and mapped into various anatomic brain regions. There has been considerable refinement in lesion localization provided by magnetic resonance imaging (MRI), so the precise regions that are damaged in patients with particular types of visual perceptual problems can be demonstrated. In addition, functional MRI has provided insight into neural networks serving higher cortical functions in normal human subjects as they perform perceptual and cognitive tasks.
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Perinatal macular haemorrhage has been suggested as being a cause of amblyopia and strabismus. 39 of 48 children with macular haemorrhage after birth were examined at the age of 5 years. The study comprised visual acuity with E-test types and cycloplegic refraction. Binocular function was evaluated by cover test, and 4d-prism test. Fixation was studied by an ophthalmoscope with a central dark star. Sensory function was estimated by Schober test and Worth 4-dot-test. The observations gave no support to the existence of organic amblyopia or strabismus following perinatal macular haemmorrhage.