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An experimental study on the early diagnosis of traumatic brain injury in rabbits based on a noncontact and portable system.

ABSTRACT: Closed cerebral hemorrhage (CCH) is a common symptom in traumatic brain injury (TBI) patients who suffer intracranial hemorrhage with the dura mater remaining intact. The diagnosis of CCH patients prior to hospitalization and in the early stage of the disease can help patients get earlier treatments that improve outcomes. In this study, a noncontact, portable system for early TBI-induced CCH detection was constructed that measures the magnetic induction phase shift (MIPS), which is associated with the mean brain conductivity caused by the ratio between the liquid (blood/CSF and the intracranial tissues) change. To evaluate the performance of this system, a rabbit CCH model with two severity levels was established based on the horizontal biological impactor BIM-II, whose feasibility was verified by computed tomography images of three sections and three serial slices. There were two groups involved in the experiments (group 1 with 10 TBI rabbits were simulated by hammer hit with air pressure of 600 kPa by BIM-II and group 2 with 10 TBI rabbits were simulated with 650 kPa). The MIPS values of the two groups were obtained within 30 min before and after injury. In group 1, the MIPS values showed a constant downward trend with a minimum value of -11.17 ± 2.91° at the 30th min after 600 kPa impact by BIM-II. After the 650 kPa impact, the MIPS values in group 2 showed a constant downward trend until the 25th min, with a minimum value of -16.81 ± 2.10°. Unlike group 1, the MIPS values showed an upward trend after that point. Before the injury, the MIPS values in both group 1 and group 2 did not obviously change within the 30 min measurement. Using a support vector machine at the same time point after injury, the classification accuracy of the two types of severity was shown to be beyond 90%. Combined with CCH pathological mechanisms, this system can not only achieve the detection of early functional changes in CCH but can also distinguish different severities of CCH.

SUBMITTER: Yang J

PROVIDER: S-EPMC6463870 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectiveTo investigate possible electroencephalography (EEG) correlates of epileptogenesis after traumatic brain injury (TBI) using the fluid percussion model.MethodsExperiments were conducted on adult 2- to 4-month-old male Sprague-Dawley rats. Two groups of animals were studied: (1) the TBI group with depth and screw electrodes implanted immediately after the fluid percussion injury (FPI) procedure, and (2) a naive age-matched control group with the same electrode implantation montage. Pairs of tungsten microelectrodes (50 μm outer diameter) and screw electrodes were implanted in neocortex inside the TBI core, areas adjacent to TBI, and remote areas. EEG activity, recorded on the day of FPI, and continuously for 2 weeks, was analyzed for possible electrographic biomarkers of epileptogenesis. Video-EEG monitoring was also performed continuously in the TBI group to capture electrographic and behavioral seizures until the caps came off (28-189 days), and for 1 week, at 2, 3, and 6 months of age, in the control group.ResultsPathologic high-frequency oscillations (pHFOs) with a central frequency between 100 and 600 Hz, were recorded from microelectrodes, beginning during the first two post-FPI weeks, in 7 of 12 animals in the TBI group (58%) and never in the controls. pHFOs only occurred in cortical areas within or adjacent to the TBI core. These were associated with synchronous multiunit discharges and popSpikes, duration 15-40 msec. Repetitive pHFOs and EEG spikes (rHFOSs) formed paroxysmal activity, with a unique arcuate pattern, in the frequency band 10-16 Hz in the same areas as isolated pHFOs, and these events were also recorded by screw electrodes. Although loss of caps prevented long-term recordings from all rats, pHFOs and rHFOSs occurred during the first 2 weeks in all four animals that later developed seizures, and none of the rats without these events developed late seizures.SignificancepHFOs, similar to those associated with epileptogenesis in the status rat model of epilepsy, may also reflect epileptogenesis after FPI. rHFOSs could be noninvasive biomarkers of epileptogenesis.

Project description:Traumatic brain injuries (TBI) are an important public health challenge. In addition, subsequent events at TBI can compromise the quality of life of these patients. In fact, TBI is associated with several complications for both long and short term, some evidence shows how TBI is associated with a decline in cognitive functions such as the risk of developing dementia, cerebral atrophy, and Parkinson disease. After the direct damage from TBI, a key role in TBI injury is played by the inflammatory response and oxidative stress, that contributes to tissue damage and to neurodegenerative processes, typical of secondary injury, after TBI. Given the complex series of events that are involved after TBI injury, a multitarget pharmacological approach is needed. Artesunate is a more stable derivative of its precursor artemisin, a sesquiterpene lactone obtained from a Chinese plant Artemisia annua, a plant used for centuries in traditional Chinese medicine. artesunate has been shown to be a pluripotent agent with different pharmacological actions. therefore, in this experimental model of TBI we evaluated whether the treatment with artesunate at the dose of 30 mg\Kg, had an efficacy in reducing the neuroinflammatory process after TBI injury, and in inhibiting the NLRP3 inflammasome pathway, which plays a key role in the inflammatory process. We also assessed whether treatment with artesunate was able to exert a neuroprotective action by modulating the release of neurotrophic factors. our results show that artesunate was able to reduce the TBI-induced lesion, it also showed an anti-inflammatory action through the inhibition of Nf-kb, release of proinflammatory cytokines IL-1β and TNF-α and through the inhibition NLRP3 inflammasome complex, furthermore was able to reduce the activation of astrocytes and microglia (GFAP, Iba-1). Finally, our results show that the protective effects of artesunate also occur through the modulation of neurotrophic factors (BDNF, GDNF, NT-3) that play a key role in neuronal survival.

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An experimental study on the early diagnosis of traumatic brain injury in rabbits based on a noncontact and portable system.

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