Friday, December 3, 2004

12 noon

Redwood Neuroscience Institute

 

Title " Human Prefrontal Cortex and Attention”

 

Robert T. Knight, M.D.

Helen Wills Neuroscience Institute and Department of Psychology

University of California, Berkeley

 

 

Abstract:

Humans fluidly move attention across the temporal domain rapidly shifting from the present state to past or future mental representations.  This capacity requires rapid engagement of parallel inhibitory and excitatory neural processes. Electrophysiological, fMRI and electrocorticographic evidence accrued from controls and neurological patients reveals that these processes aredependent on lateral prefrontal cortex (PFCx). PFCx patients fail to inhibit sensory input to primary sensory cortices in the first 25-50 msec of sensory processing resulting in a distractible PFCx  patient functioning in a noisy internal milieu. Deficits in inhibitory control extends to the cognitive domain in PFCx patients and is most readily observed as intrusions of previous information into current cognitive operations.  In addition to the critical role in inhibitory control of sensory flow and cognitive processing, PFCx exerts excitatory input in all sensory modalities which provides the critical substrate for voluntary attention. In the visual modality, PFCx controls three parallel top-down excitatory mechanisms to extrastriate processing during the initial 500 milliseconds of stimulus processing.  PFCx provides a tonic attention independent input to extrastriate cortex onsetting at 100 msec, a sustained attention dependent input from 150-400 msec and a third input engaged from 200-800 msec during detection of a target stimulus. Deficits in inhibitory and excitatory modulation of distributed neural networks after PFCx damage involving all sensory modalities  leads to a breakdown in voluntary attention and working memory. Automatic attention allocation as indexed by detection of novel environmental events is also dependent on a rapidly habituating prefrontal-hippocampal network.  PFCx initiates this novelty detection network within 150 msec of presentation of a novel event.  Direct cortical recording in neurosurgical patients reveals that ultra-high gamma bursting (60-160 Hz) is generated to automatically detected deviant sounds as well as other salient auditory events.  The capacity to detect novelty and produce novel behaviors is crucial for learning, creativity and mental flexibility which are all impaired after lateral PFCx damage. Thus, the devastating human prefrontal syndrome can be viewed as a failure in rapid PFCx control of multiple, parallel neural networks subserving both voluntary and automatic attention.