Executive attention deficits after traumatic brain injury reflect impaired recruitment of resources Academic Article uri icon


MeSH Major

  • Hypertrophy
  • Leukodystrophy, Globoid Cell
  • Optic Nerve Diseases


  • Deficits in attention are a common and devastating consequence of traumatic brain injury (TBI), leading to functional impairments, rehabilitation barriers, and long-term disability. While such deficits are well documented, little is known about their underlying pathophysiology hindering development of effective and targeted interventions. Here we evaluate the integrity of brain systems specific to attentional functions using quantitative assessments of electroencephalography recorded during performance of the Attention Network Test (ANT), a behavioral paradigm that separates alerting, orienting, and executive components of attention. We studied 13 patients, at least 6 months post-TBI with cognitive impairments, and 24 control subjects. Based on performance on the ANT, TBI subjects showed selective impairment in executive attention. In TBI subjects, principal component analysis combined with spectral analysis of the EEG after target appearance extracted a pattern of increased frontal midline theta power (2.5-7.5 Hz) and suppression of frontal beta power (12.5-22.5 Hz). Individual expression of this pattern correlated (r = - 0.67, p < 0.001) with executive attention impairment. The grading of this pattern of spatiotemporal dynamics with executive attention deficits reflects impaired recruitment of anterior forebrain resources following TBI; specifically, deafferentation and variable disfacilitation of medial frontal neuronal populations is proposed as the basis of our findings.

publication date

  • January 2017



  • Academic Article



  • eng

PubMed Central ID

  • PMC5288490

Digital Object Identifier (DOI)

  • 10.1016/j.nicl.2017.01.010

PubMed ID

  • 28180082

Additional Document Info

start page

  • 233

end page

  • 241


  • 14