Hyperactive neurones conjure up hallucinations
An Australian professor has put forward a hypothesis for the origin of hallucinations which, if correct, would help their diagnosis and possible treatment. His thinking stems from personal experience of simple Charles Bonnet hallucinations.
These were brought about by the development of a macular hole <400 μm in the left eye four years after one >400 μm in the right. Hallucinations started 11 weeks afterwards, when acuity in the left eye was 6/12–6/18. They were simple black and white, non-evoked, geometric arrays. The first looked like “brickwork” (fig A:a-c) within an area <10. Later came arrays of arches angled at 450. Then after seven days groups of dark spots appeared (fig B:a, b) and then lozenges angled at 450 (fig C). Finally, all but the arches and previously seen “flashes” faded about 10–12 days after the hallucinations first began. Faint hallucinations returned about 38 days later and lasted 10 days or so. Brickwork reappeared briefly during an episode of macular cystoid oedema in the left eye.
Professor Burke extends current thinking that links particular hallucinations with particular areas of the brain, deducing that they result from “deafferentation” of visual structures in the brain or silencing of the principal afferents to them. This induces changes leading to increased excitability of affected neurones and spontaneous activity—perceived as hallucinations. As the neurones gradually become reactivated the hallucinations fade and vanish.
Charles Bonnet hallucinations occur after injury to the brain or other parts of the visual system, most commonly after age related macular degeneration.
Sketched parts of Charles Bonnet hallucinations seen by the author. Scale bar applies to all sketches.
