Thalamocortical interactions reflecting the intensity of flicker light-induced visual hallucinatory phenomena.

Rhythmic flicker light stimulation at 10 Hz reliably induces transient visual hallucinations in healthy people, while arrhythmic flicker does so less. Using fMRI, rhythmic flicker produced stronger activation in higher order visual cortices and selectively increased connectivity between ventroanterior thalamic nuclei and those cortices, compared to arrhythmic control. The strength of this connectivity correlated positively with the subjective intensity of hallucinations. Because the ventroanterior thalamus and higher order visual areas do not receive primary visual inputs, the findings suggest the thalamus coordinates cortical activity to generate hallucinatory experiences, offering insight into pathological hallucinations.

Study at a glance

Abstract

Aberrant thalamocortical connectivity occurs together with visual hallucinations in various pathologies and drug-induced states, highlighting the need to better understand how thalamocortical interactions may contribute to hallucinatory phenomena. Flicker light stimulation (FLS) at 10-Hz reliably and selectively induces transient visual hallucinations in healthy participants. Arrhythmic flicker elicits fewer hallucinatory effects while delivering equal amounts of visual stimulation, together facilitating a well-controlled experimental setup to investigate the neural correlates of visual hallucinations driven by flicker rhythmicity. Using rhythmic and arrhythmic FLS during fMRI scanning, we found that rhythmic FLS elicited stronger activation in higher order visual cortices compared with arrhythmic control. Consistently, we found that rhythmic flicker selectively increased connectivity between ventroanterior thalamic nuclei and higher order visual cortices, which was also positively associated with the subjective intensity of visual hallucinatory effects. As these thalamic and cortical areas do not receive primary visual inputs, it suggests that the thalamocortical connectivity changes relate to a higher order function of the thalamus, such as in the coordination of cortical activity. In sum, we present novel evidence for the role of specific thalamocortical interactions with ventroanterior nuclei within visual hallucinatory experiences. Importantly, this can inform future clinical research into the mechanistic underpinnings of pathologic hallucinations.