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

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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