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.
Flicker light stimulation (FLS) induces hyperconnectivity between the lateral geniculate nucleus (LGN) and early visual areas, as well as proximal upstream areas of the ventral visual stream (e.g., hV4, VO1). An exploratory analysis indicates that higher-order thalamic nuclei, such as the anterior and mediodorsal nuclei, are strongly affected by FLS, with connectivity changes to upstream cortical visual areas directly reflecting a frequency-dependent increase in experienced visual phenomena. These findings help identify specific thalamocortical interactions involved in the emergence of visual hallucinations.