Journal of neurotrauma
-
Journal of neurotrauma · Jul 2016
Novel rat model of weight drop-induced closed diffuse traumatic brain injury compatible with electrophysiological recordings of vigilance states.
Traumatic brain injury (TBI) is a major cause of persistent disabilities such as sleep-wake disorders (SWD). Rodent studies of SWD after TBI are scarce, however, because of lack of appropriate TBI models reproducing acceleration-deceleration forces and compatible with electroencephalography/myography (EEG/EMG)-based recordings of vigilance states. We therefore adapted the Marmarou impact acceleration model to allow for compatibility with EEG-headset implantation. ⋯ EEG implants were stable for at least 1 month and enabled qualitative and quantitative sleep analyses. Histological assessments revealed no major bleedings or necrosis but intense diffuse axonal damage after TBI. This approach fulfills major pre-conditions for experimental TBI models and offers a possibility to electrophysiologically study behavioral states before and after trauma.
-
Journal of neurotrauma · Jul 2016
The Default Mode Network connectivity predicts cognitive recovery in severe acquired brain injured patients: a longitudinal study.
To study the functional connectivity in patients with severe acquired brain injury is very challenging for their high level of disability because of a prolonged period of coma, extended lesions, and several cognitive and behavioral disorders. In this article, we investigated in these patients the default mode network and somatomotor connectivity changes at rest longitudinally, in the subacute and late phase after brain injury. ⋯ Notably, strongest changes in functional connectivity significantly correlated to consistent clinical and cognitive recovery. This evidence seems to indicate that the reorganization of the Default Mode Network may represent a valid biomarker for the cognitive recovery in patients with severe acquired brain injury.
-
Journal of neurotrauma · Jul 2016
Time Course and Size of Blood-Brain Barrier Opening in a Mouse Model of Blast-Induced Traumatic Brain Injury.
An increasing number of studies have reported blood-brain barrier (BBB) dysfunction after blast-induced traumatic brain injury (bTBI). Despite this evidence, there is limited quantitative understanding of the extent of BBB opening and the time course of damage after blast injury. In addition, many studies do not report kinematic parameters of head motion, making it difficult to separate contributions of primary and tertiary blast-loading. ⋯ Exposure to blast with 272 ± 6 kPa peak overpressure, 0.69 ± 0.01 ms duration, and 65 ± 1 kPa*ms impulse resulted in significant acute extravasation of NaFl, 3 kDa dextran, and EB. However, there was no significant acute extravasation of 70 kDa or 500 kDa dextrans, and minimal to no extravasation of NaFl, dextrans, or EB 1 day after exposure. This study presents a detailed analysis of the time course and pore size of BBB opening after bTBI, supported by a characterization of kinematic parameters associated with blast-induced head motion.