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Neurorehabil Neural Repair. 2012 Sep;26(7):870-80. doi: 10.1177/1545968311434553. Epub 2012 Feb 22.

A perfusion fMRI study of the neural correlates of sustained-attention and working-memory deficits in chronic traumatic brain injury.

Author information

  • 1Moss Rehabilitation Research Institute, Albert Einstein Healthcare Network, Elkins Park, PA 19027, USA. kimj@einstein.edu

Abstract

BACKGROUND:

Given that traumatic brain injury (TBI) results in chronic alteration of baseline cerebral perfusion, a perfusion functional MRI (fMRI) method that dissociates resting- and task-related cerebral blood flow (CBF) changes can be useful in noninvasively investigating the neural correlates of cognitive dysfunction and recovery in TBI.

OBJECTIVE:

The authors used continuous arterial spin-labeled (ASL) perfusion fMRI to characterize CBF at rest and during sustained-attention and working-memory tasks.

METHODS:

A total of 18 to 21 individuals with moderate to severe TBI and 14 to 18 demographically matched healthy controls completed 3 continuous 6-minute perfusion fMRI scans (resting, visual sustained attention, and 2-back working memory).

RESULTS:

For both tasks, TBI participants showed worse behavioral performance than controls. Voxelwise neuroimaging analysis of the 2-back task found that group differences in task-induced CBF changes were localized to bilateral superior occipital cortices and the left superior temporal cortex. Whereas controls deactivated these areas during task performance, TBI participants tended to activate these same areas. These regions were among those found to be disproportionately hypoperfused at rest after TBI. For both tasks, the control and TBI groups showed different patterns of correlation between performance and task-related CBF changes.

CONCLUSIONS:

ASL perfusion fMRI demonstrated differences between individuals with TBI and healthy controls in resting perfusion and in task-evoked CBF changes as well as different patterns of performance-activation correlation. These results are consistent with the notion that sensory/attentional modulation deficits contribute to higher cognitive dysfunction in TBI.

PMID:
22357634
[PubMed - indexed for MEDLINE]
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