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An Explicit Model of Executive Control and Deficits.

 Thad A. Polk, Richard L. Lewis and J. Paul Hamilton
  
 

Abstract:
Damage to prefrontal cortex (PFC) can lead to a variety of dissociable cognitive deficits (e.g., perseveration, distractibility, disinhibition, working memory impairments, etc.). Although these deficits are quite diverse, they share a family resemblance and are often classified together as executive deficits or as a dysexecutive syndrome. A central challenge is to provide an explicit model of executive control and show how it can unify these seemingly disparate cognitive deficits. We present a simple and computationally explicit model of executive control that provides a unified account of a range of executive deficits. The model assumes massive, bidirectional connectivity, continuous-valued units, and Hebbian learning. Together these assumptions give rise to continuous attractor nets that settle into stored patterns of distributed activity, but that can be modulated (enhanced and maintained, or inhibited) by external input. The PFC module of the model represents control signals (excite/inhibit) rather than task content and serves to modulate activity in posterior attractor nets. We present neural network models based on this attractor modulation theory for three quite different tasks: delayed response (a working memory task), letter fluency (a verbal association task), and Stroop (a selective attention task). We show that damage to the PFC component of the models simulates the major executive deficits of patients with prefrontal damage.

 
 


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