Local Immediate versus Long-Range Delayed Changes in Functional Connectivity Following rTMS on the Visual Attention Network.

Abstract

The interhemispheric competition hypothesis attributes the distribution of selective attention to a balance of mutual inhibition between homotopic, interhemispheric connections in parietal cortex (Kinsbourne 1977; Battelli etal., 2009). In support of this hypothesis, repetitive inhibitory TMS over right parietal cortex in healthy individuals rapidly induces interhemispheric imbalance in cortical activity that spreads beyond the site of stimulation (Plow etal., 2014). Behaviorally, the impacts of inhibitory rTMS may be long delayed from the onset of stimulation, as much as 30 minutes (Agosta etal., 2014; Hubl etal., 2008). In this study, we examine the temporal dynamics of inhibitory rTMS on cortical network integrity that supports sustained visual attention. Healthy individuals received 15 min of 1 Hz offline, inhibitory rTMS (or sham) over left parietal cortex, and then immediately engaged in a bilateral visual tracking task while we recorded brain activity with fMRI. We computed functional connectivity (FC) between three nodes of the attention network engaged by visual tracking: the intraparietal sulcus (IPS), frontal eye fields (FEF) and human MT+ (hMT+). FC immediately and significantly decreased between the stimulation site (left IPS) and all other regions, then recovered to normal levels within 30 minutes. rTMS increased FC between left and right FEF at approximately 36 min following stimulation, and between sites in the unstimulated hemisphere approximately 48 min after stimulation. These findings demonstrate large-scale changes in cortical organization following inhibitory rTMS. The immediate impact of rTMS on connectivity to the stimulation site dovetails with the putative role of interhemispheric balance for bilateral visual sustained attention. The delayed, compensatory increases in functional connectivity have implications for models of dynamic reorganization in networks supporting spatial and nonspatial selective attention, and compensatory mechanisms within these networks that may be stabilized in chronic stroke.