Neural correlates of blink suppression and the buildup of a natural bodily urge

Abstract

Neuroimaging studies have elucidated some of the underlying physiology of spontaneous and voluntary eye blinking; however, the neural networks involved in eye blink suppression remain poorly understood. Here we investigated blink suppression by analyzing fMRI data in a block design and event-related manner, and employed a novel hypothetical time-varying neural response model to detect brain activations associated with the buildup of urge. Blinks were found to activate visual cortices while our block design analysis revealed activations limited to the middle occipital gyri and deactivations in medial occipital, posterior cingulate and precuneus areas. Our model for urge, however, revealed a widespread network of activations including right greater than left insular cortex, right ventrolateral prefrontal cortex, middle cingulate cortex, and bilateral temporo-parietal cortices, primary and secondary face motor regions, and visual cortices. Subsequent inspection of BOLD time-series in an extensive ROI analysis showed that activity in the bilateral insular cortex, right ventrolateral prefrontal cortex, and bilateral STG and MTG showed strong correlations with our hypothetical model for urge suggesting these areas play a prominent role in the buildup of urge. The involvement of the insular cortex in particular, along with its function in interoceptive processing, helps support a key role for this structure in the buildup of urge during blink suppression. The right ventrolateral prefrontal cortex findings in conjunction with its known involvement in inhibitory control suggest a role for this structure in maintaining volitional suppression of an increasing sense of urge. The consistency of our urge model findings with prior studies investigating the suppression of blinking and other bodily urges, thoughts, and behaviors suggests that a similar investigative approach may have utility in fMRI studies of disorders associated with abnormal urge suppression such as Tourette syndrome and obsessive-compulsive disorder.

Figure 1

(a) Surface EOG waveform showing two blinks recorded during a MRI scanning session after scanner artifact correction and band-pass filtering. Additional EOG post-processing included (b) importation of time series into Matlab, (c) rectification and down sampling of signal, and (d) isolation of blink events based on signal exceeding threshold of 0.25 of the standard deviation above the mean. Task paradigm timing in relation to EOG recording of blinks is superimposed for reference.

Figure 2

Hypothetical hemodynamic response model for task with linear buildup of urge to blink during 60 sec of suppression and 15 sec release of urge following end of blink suppression.

Figure 3

A priori ROIs derived from Talairach atlas used for ROI analysis (see text for details). ACC, anterior cingulate cortex; IC, insular cortex; IFG, inferior frontal gyrus; IPL, inferior parietal lobe; Lt, left; MeFG, medial frontal gyrus; MTG, middle temporal gyrus; PcG, precentral gyrus; Rt, right; SmG, supramarginal gyrus; STG, superior temporal gyrus.

Figure 4

Total number of detected blinks for all 18 scanning runs summed at each TR (1 sec). Each dot represents the total blink count at each time point, and the fit line was generated using a smoothing polynomial and averaging of the four nearest neighbors. Alternating 60 sec suppression blocks with 30 sec rest blocks are labeled and a dotted vertical line marks the middle of each rest block.

Figure 5

Axial brain slices with superimposed statistical parametric maps on the MNI Colin N27 brain showing significant activations (red) and deactivations (blue) identified using a standard block design analysis (BLOCK), an event-related analysis of blinks (EVENT), and a hypothetical hemodynamic response function for urge (URGE) during the blink suppression scanning runs. Parametric maps were all thresholded at t = 3.2 (p<0.005, corrected).

Figure 6

BOLD signal time courses from those ROIs that showed a strong correlation (R2 > 0.5) with our hypothetical URGE model (see text). IC, insular cortex; IFG, MTG, middle temporal gyrus; STG, superior temporal gyrus.

Figure 7

BOLD signal time courses from those ROIs that failed to show a strong correlation (R2 ≤ 0.5) with our hypothetical URGE model (see text). ACC, anterior cingulate cortex; IFG, inferior frontal gyrus; IPL, inferior parietal lobe; MeFG, medial frontal gyrus; PcG, precentral gyrus; SMG, supramarginal gyrus.