The pathogenesis of complex visual hallucination in patients without visual lesions, appearing with eyes open and resolving with eyes closed, has been described to be associated with increased excitation at the lateral geniculate nucleus (LGN) and pulvinar of the thalamus (Winton-Brown, 2016). This reduces thefidelity of retinogeniculate transmissions and enhances aberrant projections to the visual cortex. Loss of the central sensory filtering function of the pulvinar increases “signal to noise ratio” in visual transmission. While visual hallucinations have been reported to disappear on eye closure (Manford, 1998), visual aberration with correction with refractionfollowed by focusing on actual visual images and visual hallucinations has not heretofore been reported. Such a case is presented.

Case study: This 28-year-old, myopic, right-handed man, at 5 years of age began hallucinating vivid images of people. The visual hallucinations were triggered only with his eye open. He was myopic and without visual correction, his visual sphere would be blurred. The visual hallucinations were also blurred without visual correction. With refraction, the hallucinations became clearly in focus. He would close his eyes and the visual hallucinations disappeared but would reappear in the same position upon opening his eyes. For over 20 years, he experienced about 100 hallucinations a day. Electroencephalography (EEG) revealed continuous spikes and slow waves in bilateral temporal lobes, consistent with temporal lobe status epilepticus. After treatment with diphenylhydantoin the frequency and duration of the hallucinations markedly decreased to a second epoch every other day. However, the characteristic of the hallucinations remained the same (people).

This phenomenon may involve epilepsy induced excitation of the thalamus. This then acts to reduce the fidelity of retinogeniculate transmission and increase “signal to noise ratio” in visual transmission. This may contribute to complex visual hallucinations with eyes open. The hallucinated figures becoming clearer with eyeglasses provides support that this complex hallucination arises in the pathway from retina-LGN-cortex, not from stored visual associated cortex of top-down cortical release.

Given the above, those with visual hallucinations should be queried as to the influence of refraction on the clarity of hallucination.

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