[10][11] Experiments in neurophysiology from different laboratories showed that fixational eye movements, particularly microsaccades, strongly modulate the activity of neurons in the visual areas of the macaque brain.
In the lateral geniculate nucleus (LGN) and the primary visual cortex (V1), microsaccades can move a stationary stimulus in and out of a neuron's receptive field, thereby producing transient neural responses.
[19] Neural circuits within the superior colliculus integrate sensory inputs and motor commands, resulting in the precise, coordinated movements of microsaccades.
Inputs from cortical areas such as the frontal eye fields and parietal cortex modulate these interactions, influencing microsaccade frequency and direction.
[21] Experiments in primates have shown that electrically stimulating specific regions of the superior colliculus can evoke microsaccade-like movements, highlighting its role in their generation.
[24] Microsaccades are disrupted in several ophthalmologic disorders, including amblyopia, strabismus, myopia, and macular disease, reflecting the impact of visual impairment on eye movement control.
In amblyopia, monocular fixation with the amblyopic eye leads to increased drift and frequent saccadic intrusions, especially in cases involving strabismus.
Along with this, macular disease results in increased drift and larger microsaccadic amplitudes, which correlate with visual acuity loss and serve as signs of fixation instability.