Colored floaters as a manifestation of digoxin toxicity.

PURPOSE: Since its report in one patient more than 70 years ago, digitalis-induced colored muscae volitantes have not surfaced again in the literature. We report here a case of digoxin induced colored floaters. OBSERVATIONS: An 89-year-old man on 0.25 mg digoxin daily developed visual hallucinations and colored floaters. He had floaters in the past but now they were in various colors including yellow, green, blue and red, though predominantly in yellow. These "weirdly" shaped little particles wiggled around as if in a viscous solution and casted shadows in his vision. He also saw geometric shapes, spirals, and cross hatch patterns of various colors that moved and undulated, especially on wallpaper. Ophthalmic examination revealed reduced visual acuity, poor color vision especially in his left eye, along with central depression on Amsler grid and Humphrey visual field in his left eye. Discontinuation of digoxin resulted in complete resolution of his visual symptoms. On subsequent ophthalmic examination, the patient's visual acuity, field testing and color vision improved and he had normal Amsler grid test results. CONCLUSIONS AND IMPORTANCE: Colored floaters may occur in patients taking cardiac glycosides but this association has not been explored. Unlike optical illusions and visual hallucinations, floaters are entoptic phenomena casting a physical shadow upon the retina and their coloring likely arise from retinal dysfunction. Colored floaters may be a more common visual phenomenon than realized.

Corollary Discharge and Oculomotor Proprioception: Cortical Mechanisms for Spatially Accurate Vision.

A classic problem in psychology is understanding how the brain creates a stable and accurate representation of space for perception and action despite a constantly moving eye. Two mechanisms have been proposed to solve this problem: Herman von Helmholtz's idea that the brain uses a corollary discharge of the motor command that moves the eye to adjust the visual representation, and Sir Charles Sherrington's idea that the brain measures eye position to calculate a spatial representation. Here, we discuss the cognitive, neuropsychological, and physiological mechanisms that support each of these ideas. We propose that both are correct: A rapid corollary discharge signal remaps the visual representation before an impending saccade, computing accurate movement vectors; and an oculomotor proprioceptive signal enables the brain to construct a more accurate craniotopic representation of space that develops slowly after the saccade.

Hippocampal CA3 NMDA receptors are crucial for memory acquisition of one-time experience.

Lesion and pharmacological intervention studies have suggested that in both human patients and animals the hippocampus plays a crucial role in the rapid acquisition and storage of information from a novel one-time experience. However, how the hippocampus plays this role is poorly known. Here, we show that mice with NMDA receptor (NR) deletion restricted to CA3 pyramidal cells in adulthood are impaired in rapidly acquiring the memory of novel hidden platform locations in a delayed matching-to-place version of the Morris water maze task but are normal when tested with previously experienced platform locations. CA1 place cells in the mutant animals had place field sizes that were significantly larger in novel environments, but normal in familiar environments relative to those of control mice. These results suggest that CA3 NRs play a crucial role in rapid hippocampal encoding of novel information for fast learning of one-time experience.

Requirement for hippocampal CA3 NMDA receptors in associative memory recall.

Pattern completion, the ability to retrieve complete memories on the basis of incomplete sets of cues, is a crucial function of biological memory systems. The extensive recurrent connectivity of the CA3 area of hippocampus has led to suggestions that it might provide this function. We have tested this hypothesis by generating and analyzing a genetically engineered mouse strain in which the N-methyl-D-asparate (NMDA) receptor gene is ablated specifically in the CA3 pyramidal cells of adult mice. The mutant mice normally acquired and retrieved spatial reference memory in the Morris water maze, but they were impaired in retrieving this memory when presented with a fraction of the original cues. Similarly, hippocampal CA1 pyramidal cells in mutant mice displayed normal place-related activity in a full-cue environment but showed a reduction in activity upon partial cue removal. These results provide direct evidence for CA3 NMDA receptor involvement in associative memory recall.