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A. M. Hanneken, N. Babai, W. B. Thoreson; Visual Hallucinations in Age-Related Macular Degeneration Patients Are Induced or Exacerbated by Proton Pump Inhibitors: Clinical and Electrophysiological Studies. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3276.
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Visual hallucinations are enigmatic visual phenomenon which are poorly understood from a mechanistic perspective. We report a series of patients with advanced age-related macular degeneration who described the onset or exacerbation of visual hallucinations following the use of prevacid, prilosec or protonix, proton pump inhibitors that are widely used to treat heartburn. We explored the mechanism underlying this effect.
A complete retinal evaluation was obtained on four macular degeneration patients who reported the onset of visual hallucinations with PPIs. Ophthalmodynamometry was performed to assess whether changes in retinal circulation modified the perception of the hallucinations. Simultaneous whole-cell recordings from horizontal cells (HCs) and cones were performed in salamander retinas to assess the effect of prevacid and prilosec on feedback from horizontal cells to photoreceptors.
Clinical examinations confirmed that all patients had advanced age-related macular degeneration in at least one eye. In all cases the visual hallucinations were associated temporally either with the initiation of PPI intake or a change from one PPI to another. External pressure to the globe with ophthalmodynamometry led to the complete cessation of the hallucinations, which then recurred within one minute when the retinal circulation was restored. Whole cell recordings in salamander retinas demonstrated that prevacid and prilosec inhibited proton-dependent feedback mechanisms by which HCs regulate calcium currents in cones.
We conclude that proton pump inhibitors can induce or exacerabate visual hallucinations in macular degeneration patients. These hallucinations decrease in response to external pressure to the globe, suggesting that the neuronal impulses involved in these perceptual abnormalities are dependent on retinal perfusion. The mechanism of action is consistent with the interruption of HC to cone feedback by inhibition of proton pumps in HCs. HC to cone feedback contributes to the formation of central surround receptive fields and is essential for normal chromatic and spatial perception. These results raise the interesting possibility of whether visual hallucinations in the setting of macular degeneration are retinal in origin.
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