In conclusion, our results suggest that VSS is characterised by a complex disturbance in the interaction of multiple brain systems. This dysfunction particularly involves the pre-cortical and cortical visual pathway, the visual motion network, the attentional networks and finally the salience network; further, it does not depend on the activity state of the brain. What we observed suggests that there is a disruption in the filtering and integration of incoming sensory visual stimuli, versus the modulation of internally generated visual information. Future studies will help determine if this fingerprint of altered network dysfunction, indeed represents the main pathophysiological mechanism underlying the symptoms of this complex and disabling condition. In particular, it will be important to distinguish the impact of concomitant migraine, photophobia and aura on these findings, especially with regard to changes in connectivity affecting the visual system.
Given that no widely applicable treatment seems to fully suppress the symptoms of VSS, achieving an improved understanding of its underlying neurobiology is important, as it aids clinicians in explaining the condition to affected patients and also directs future research to more targeted approaches. In particular, the finding that diffuse brain networks are implicated in the genesis of VSS, could have the clinical implication of redirecting treatment from generic pharmacological interventions to a more focused modulation of brain function, possibly through techniques such as neuromodulation or neurofeedback.