Deficits in Functional Connectivity of Hippocampal and Frontal Lobe Circuits After Traumatic Axonal Injury

Abstract

Traumatic brain injury (TBI) is a major public health problem in modern societies, with an incidence in the United States estimated between 92 and 250 per 100 000 persons annually; approximately 50 000 individuals each year are left with long-term physical and psychological limitations that limit their independence and ability to work.^1,2 Diffuse axonal injury, more recently referred to as traumatic axonal injury (TAI), is a common subtype of TBI occurring in most motor vehicle collisions in which deceleration and rotational forces cause shearing of the brain's white matter.³ Computed tomography is insensitive to white matter lesions resulting from TAI,^4,5 but more novel neuroimaging modalities have shown sensitivity toward white matter injury.^6-9