Abstract
Traumatic brain injury (TBI) is the leading cause of death in young individuals, and is a major health concern that often leads to long-lasting complications. However, the electrophysiological events that occur immediately after traumatic brain injury, and may underlie impact outcomes, have not been fully elucidated. To investigate the electrophysiological events that immediately follow traumatic brain injury, a weight-drop model of traumatic brain injury was used in rats pre-implanted with epidural and intracerebral electrodes. Electrophysiological (near-direct current) recordings and simultaneous alternating current recordings of brain activity were started within seconds following impact. Cortical spreading depolarization (SD) and SD-induced spreading depression occurred in approximately 50% of mild and severe impacts. SD was recorded within three minutes after injury in either one or both brain hemispheres. Electrographic seizures were rare. While both TBI- and electrically induced SDs resulted in elevated oxidative stress, TBI-exposed brains showed a reduced antioxidant defense. In severe TBI, brainstem SD could be recorded in addition to cortical SD, but this did not lead to the death of the animals. Severe impact, however, led to immediate death in 24% of animals, and was electrocorticographically characterized by non-spreading depression (NSD) of activity followed by terminal SD in both cortex and brainstem.
Highlights
Traumatic brain injury (TBI) is a major global health burden that has been estimated to affect over 40 million people annually [1,2,3]
Following TBI (Figure 1a), the near-direct current recordings showed the characteristic large slow potential change of spreading depolarization (SD) [45], whereas alternating current (AC) recordings showed the rapidly evolving reduction in amplitudes of spontaneous activity that spread along with SD between adjacent recording sites, which is characteristic of spreading depression of activity (Figure 1b–d) [25,34,43,46]
Our findings using near-direct current recordings, alternating current recording and analysis of intrinsic optical signaling (IOS) show that SD and SD-induced spreading depression are common i both mild and severe TBI, and are initiated within minutes after impact
Summary
Traumatic brain injury (TBI) is a major global health burden that has been estimated to affect over 40 million people annually [1,2,3]. The two main neural network functional disturbances linked with acute brain dysfunction after TBI are epileptic seizures [16,17] and spreading depolarization (SD) [18,19,20]. While both phenomena relate to a sustained depolarization in a large set of neuronal populations, and both potentially propagate along the injured cortex, there are critical differences between the two. During epileptic seizures, sustained depolarization is associated with repetitive firing of action potentials, the transmembrane ion concentration gradients are largely preserved, and the recorded negative direct current (DC) shift is relatively small [21].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
