Multiscale alterations of intrinsic neural timescales in anterior ischemic optic neuropathy

Anterior ischemic optic neuropathy (AION) is primarily an optic nerve disorder, but loss of visual afferent input may also be associated with cortical reorganization. Intrinsic neural timescale (INT), derived from resting-state fMRI, indexes the temporal persistence of BOLD activity. We examined whether AION is associated with altered cortical INT and whether the spatial pattern of these alterations aligns with normative molecular and neurochemical architecture.

Resting-state fMRI data were analyzed from 30 patients with AION and 25 healthy controls. Voxel-wise INT was estimated from the autocorrelation of BOLD signals, and group differences were tested using Gaussian random field correction. Exploratory network-level comparisons were performed without multiple-comparison correction. Spatial associations with Allen Human Brain Atlas gene expression and PET-derived neurotransmitter maps were assessed using partial least squares regression and spatial permutation tests, respectively.

Compared with healthy controls, patients with AION showed lower INT in the bilateral calcarine cortex, with no regions showing higher INT. Exploratory uncorrected network comparisons yielded lower estimates in the auditory and anterior attention networks. The regional INT contrast aligned with normative transcriptional gradients enriched for synaptic and neuronal processes and with the spatial distributions of several neurotransmitter receptor systems.

AION was associated with a focal reduction in calcarine INT under the primary operational definition used in this study. Normative transcriptomic and receptor maps provided biological context for the spatial pattern but did not establish patient-specific molecular changes or causal mechanisms.