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Bowren, M.

Publications and source records attributed to Bowren, M..

2 recordsLinked to original sources

Cognition Disconnected: The Influence of Domain-General Cognition (g) in Lesion-Deficit Mapping

Lesion-deficit mapping is a premier technique for dissociating neural correlates of cognitive functions. However, the contribution of domain-general cognition (g) to the performance of virtually all complex behavioral tasks may encumber such efforts. This possibility has been largely unexplored. Here, we examined the influence of g in lesion-deficit mapping using a combination of structural equation modeling, lesion-behavior mapping (LBM), and structural (sLNM) and functional (fLNM) lesion network mapping. We modeled latent variables for visuospatial ability, processing speed, language, and anterograde memory among 473 patients with focal brain damage (age range 20-93, 257 men, 216 women), both with and without g-associated variance embedded within each factor. Lesion-deficit maps for domain-specific cognitive abilities were statistically significantly less spatially inter-correlated after partitioning out g (p = 0.010 for LBM; p = 0.003 for sLNM; p = 0.003 for fLNM). Lesion-deficit maps also implicated the existence of distinct neuroanatomy for specific cognitive domains that was, in many cases, only apparent and clearly distinct from lesion-deficit maps of g after partitioning out the influence of g. Overall, our findings suggest that, if left unaccounted for, domain-general cognitive variance could tangibly affect conclusions about the extent to which different cognitive functions rely on distinct neuroanatomy.

neuroscience↗

Right inferior frontal cortex damage impairs the initiation of inhibitory control, but not its implementation

Inhibitory control is one of the most important control functions in the human brain. Much of our understanding of its neural basis comes from seminal work showing that lesions to the right inferior frontal cortex (rIFC) increase stop-signal reaction time (SSRT), a latent variable that expresses the speed of inhibitory control. However, recent work has identified substantial limitations of the SSRT method. Notably, SSRT is confounded by trigger failures: stop-signal trials in which inhibitory control was never initiated. Such trials inflate SSRT, but are typically indicative of attentional, rather than inhibitory deficits. Here, we used hierarchical Bayesian modeling to identify stop-signal trigger failures in human rIFC lesion patients, non-rIFC lesion patients, and healthy comparisons. Furthermore, we measured scalp-EEG to detect {beta}-bursts, a neurophysiological index of inhibitory control. rIFC lesion patients showed a more than five-fold increase in trigger failure trials and did not exhibit the typical increase of stop-related frontal {beta}- bursts. However, on trials in which such {beta}-bursts did occur, rIFC patients showed the typical subsequent upregulation of {beta} over sensorimotor areas, indicating that their ability to implement inhibitory control, once triggered, is intact. These findings suggest that the role of rIFC in inhibitory control has to be fundamentally reinterpreted.

neuroscience↗