[Relation of visual evoked potentials to the clinical state in patients with chronic renal insufficiency].
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Biomedical subjects
Publications and source records attributed to M Kuba.
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Differences in visual evoked responses (VER) to three types of stimuli were studied in 70 volunteers, using checkerboard pattern reversal stimulation--a circular target in the central part of the visual field (VF) and stimuli composed of either the upper or the lower half of the circle. The responses to semicircular stimulation displayed great variability (latency shifts, reverse polarity, absence of a response), particularly to the upper half of the circle, where the amplitude of the responses was significantly smaller and their latency longer than in lower semicircle and whole circle stimulation.
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Chronic glaucoma has been shown preferentially to damage larger retinal cells and optic nerve fibres that provide the input to the magnocellular visual pathway. We compared the motion-onset visual evoked potentials (primarily the magnocellular system) with those to standard pattern reversal in 20 patients with bilateral chronic glaucoma. For motion-onset visual evoked potentials, the pattern (isolated 40' checks of 10% contrast) moved in four cardinal directions (varied randomly from trial to trial) at a velocity of 10 deg/s for 20 ms, with an interstimulus interval of 1 s. In pattern-reversal stimulation, the checkerboard reversed at a rate of 2 reversals per second. In 60% of the eyes investigated, the results of both types of visual evoked potentials correlated, showing either normal (27.5%) or increased (32.5%) latencies. In the remaining 40% of the eyes, the normal pattern-reversal visual evoked potential latencies were accompanied by prolonged motion-onset visual evoked potentials. The high occurrence of delayed motion-onset visual evoked potentials in our patients confirms the primary magnocellular loss in chronic glaucoma and suggests that the motion-onset VEPs are suitable for detection of glaucomatous changes.
Two cases of necrotizing myelopathy, one with lung carcinoma and the other with adult T cell leukemia (ATL), displayed flaccid paraplegia and sphincter dysfunction. Both cases did not show any direct neoplastic cell invasion of the spinal cord. Pathologically, diffuse and random necrosis was found in the spinal cord in both cases. In the case of ATL, small numbers of inclusion bodies in the nerve cell nuclei were demonstrated. Using polyclonal and also monoclonal antibodies, herpes simplex virus type 2 (HSV-2) was clearly demonstrated in the spinal cord in both cases. By electron microscopy, numerous herpes virus particles were observed in the spinal cord in both cases. The usefulness of electrophysiological studies should be emphasized in the differentiation of these cases from others which might also display flaccid paraplegia. The possibility of necrotizing myelopathy caused by HSV-2 should always be considered in the differential diagnosis of spinal cord diseases displaying flaccid paraplegia.