Multifocal visual evoked potentials in amblyopia due to anisometropia.

PURPOSE: To investigate multifocal visual evoked potentials (mfVEP) of the amblyopic and fellow eye in amblyopia due to anisometropia. METHODS: We recorded mfVEP in both eyes of 15 anisometropic amblyopic patients and 15 normal control subjects. The responses from the central 7.0 degrees arc of the visual field were measured, and changes in latency and amplitude were compared between the amblyopic, fellow, and normal control eyes. RESULTS: There was a significant difference in the latency and amplitude of mfVEP between the amblyopic and fellow eyes. The responses in the central region of the visual field (rings 1 and 2) had a longer latency and smaller amplitude in the amblyopic eye. In contrast, there was no difference in mfVEP latency or amplitude between the fellow eye and normal control eyes. CONCLUSION: These results suggest that mfVEP may be used as an alternative objective method for diagnosis and monitoring of anisometropic amblyopia.

L-carnitine improvement of cardiac function is associated with a stimulation in glucose but not fatty acid metabolism in carnitine-deficient hearts.

OBJECTIVES: Increasing myocardial carnitine content can improve heart function in patients with carnitine deficiency. We were interested in determining the effects of L-carnitine on cardiac function and substrate metabolism in a rat model of carnitine deficiency. METHODS: Carnitine deficiency was induced in male Sprague-Dawley rats by supplementing the drinking water with 20 mM sodium pivalate. Control animals received an equimolar concentration of sodium bicarbonate. Following treatment, cardiac function and myocardial substrate utilization were determined in isolated working hearts perfused with glucose and relevant levels of fatty acids. To increase tissue levels of carnitine, hearts were perfused with 5 mM L-carnitine for a period of 60 min. RESULTS: Hearts from sodium pivalate-treated animals demonstrated a 60% reduction in total heart carnitine content, depressions in cardiac function and rates of palmitate oxidation, and elevated rates of glycolysis compared to control hearts. Treatment with L-carnitine increased total carnitine content and reversed the depression in cardiac function seen in carnitine-deficient hearts. However, this was not associated with any improvement in palmitate oxidation. Rates of glycolysis and glucose oxidation, on the other hand, were increased with L-carnitine. CONCLUSIONS: Our findings indicate that acute L-carnitine treatment is of benefit to cardiac function in this model of secondary carnitine deficiency by increasing overall glucose utilization rather than normalizing fatty acid metabolism.