scholarly journals Increased Sample Entropy in EEGs During the Functional Rehabilitation of an Injured Brain

Entropy ◽  
2019 ◽  
Vol 21 (7) ◽  
pp. 698 ◽  
Author(s):  
Qiqi Cheng ◽  
Wenwei Yang ◽  
Kezhou Liu ◽  
Weijie Zhao ◽  
Li Wu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Sham Group ◽  
Brain Area ◽  
Recovery Process ◽  
Sample Entropy ◽  
Control Group ◽  
Functional Rehabilitation ◽  
Injured Brain ◽  
Injury Group ◽  
Neural Remodeling

Complex nerve remodeling occurs in the injured brain area during functional rehabilitation after a brain injury; however, its mechanism has not been thoroughly elucidated. Neural remodeling can lead to changes in the electrophysiological activity, which can be detected in an electroencephalogram (EEG). In this paper, we used EEG band energy, approximate entropy (ApEn), sample entropy (SampEn), and Lempel–Ziv complexity (LZC) features to characterize the intrinsic rehabilitation dynamics of the injured brain area, thus providing a means of detecting and exploring the mechanism of neurological remodeling during the recovery process after brain injury. The rats in the injury group (n = 12) and sham group (n = 12) were used to record the bilateral symmetrical EEG on days 1, 4, and 7 after a unilateral brain injury in awake model rats. The open field test (OFT) experiments were performed in the following three groups: an injury group, a sham group, and a control group (n = 10). An analysis of the EEG data using the energy, ApEn, SampEn, and LZC features demonstrated that the increase in SampEn was associated with the functional recovery. After the brain injury, the energy values of the delta1 bands on day 4; the delta2 bands on days 4 and 7; the theta, alpha, and beta bands and the values of ApEn, SampEn, and LZC of the cortical EEG signal on days 1, 4 and 7 were significantly lower in the injured brain area than in the non-injured area. During the process of recovery for the injured brain area, the values of the beta bands, ApEn, and SampEn of the injury group increased significantly, and gradually became equal to the value of the sham group. The improvement in the motor function of the model rats significantly correlated with the increase in SampEn. This study provides a method based on EEG nonlinear features for measuring neural remodeling in injured brain areas during brain function recovery. The results may aid in the study of neural remodeling mechanisms.

scholarly journals Aspirin Exerts Neuroprotective Effects by Reversing Lipopolysaccharide-Induced Secondary Brain Injury and Inhibiting Matrix Metalloproteinase-3 Gene Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Depeng Feng ◽  
Dezhe Chen ◽  
Tuanzhi Chen ◽  
Xiaoqian Sun
Keyword(s):  
Matrix Metalloproteinase ◽  
Test Scores ◽  
Neuroprotective Effect ◽  
Brain Area ◽  
Cerebral Injury ◽  
Control Group ◽  
Secondary Brain Injury ◽  
Walking Test ◽  
Matrix Metalloproteinase 3 ◽  
Injured Brain

Objective. This study is aimed at exploring the possible neuroprotective mechanism of aspirin and the effect of bacterial endotoxin lipopolysaccharide (LPS) during cerebral ischaemia-reperfusion (CIRP) injury. Methods. We established three animal models: the CIRP, LPS, and CIRP+LPS models. Mortality, the injured brain area, and the beam walking test were used to estimate the degree of cerebral injury among the rats. Immunohistochemistry and immunofluorescence were used to detect activated microglia, matrix metalloproteinase-3 (MMP-3), and osteopontin (OPN). Results. The injured brain area and mortality were dramatically reduced ( p < 0.01 ), and the beam walking test scores were elevated ( p < 0.01 ) in the acetylsalicylic acid (ASA) group compared to the control group. The number of microglia-, MMP-3-, and OPN-positive cells also increased. Furthermore, the number of GSI-B4, OPN, and MMP-3 cells decreased in the ASA group compared to the control group. After LPS stimulation, the number of microglia reached a peak at 24 h; at 7 d, these cells disappeared. In the ASA group, the number of microglia was significantly smaller ( p < 0.05 ), especially at 24 h ( p < 0.01 ), compared to the LPS group. Moreover, the injured brain area and the mortality were dramatically increased and the beam walking test scores were reduced ( p < 0.01 ) after LPS simulation following CIRP. The degree of injury in the ASA group resembled that in the control group. However, the number of MMP-3-immunoreactive neurons or microglia was significantly larger than that of the control group ( p < 0.05 ). In the ASA group, the MMP-3 expression was also considerably decreased ( p < 0.05 ). Conclusions. After CIRP, microglia were rapidly activated and the expression of MMP-3 and OPN significantly increased. For rats injected with LPS at reperfusion, the injured brain area and mortality also dramatically increased and the neurologic impairment worsened. However, ASA exhibited a neuroprotective effect during CIRP injury. Furthermore, ASA can reverse LPS-induced cerebral injury and inhibit the inflammatory reaction after CIRP injury.

scholarly journals The effect of perinatal brain injury on dopaminergic function and hippocampal volume in adult life

2017 ◽  
Author(s):  
Sean Froudist-Walsh ◽  
Michael A.P. Bloomfield ◽  
Mattia Veronese ◽  
Jasmin Kroll ◽  
Vyacheslav Karolis ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Brain Injury ◽  
Hippocampal Volume ◽  
Dopamine Synthesis ◽  
Control Group ◽  
Perinatal Brain Injury ◽  
Very Preterm ◽  
Very Preterm Birth ◽  
Injury Group ◽  
Increased Risk

AbstractBackgroundVery preterm birth (<32 weeks of gestation) is associated with long-lasting brain alterations and an increased risk of psychiatric disorders associated with dopaminergic abnormalities. Preclinical studies have shown perinatal brain injuries, including hippocampal lesions, cause lasting changes in dopamine function, but it is not known if this occurs in humans. The purpose of this study was to determine whether very preterm birth and perinatal brain injury were associated with altered dopamine synthesis and reduced hippocampal volume in humans in adulthood.MethodsWe compared adults who were born very preterm with associated perinatal brain injury to adults born very preterm without perinatal brain injury, and age-matched controls born at full term using [18F]-DOPA PET and structural MRI imaging.ResultsDopamine synthesis capacity was significantly reduced in the perinatal brain injury group relative to both the group born very preterm without brain injury (Cohen’s d=1.36, p=0.02) and the control group (Cohen’s d=1.07, p=0.01). Hippocampal volume was reduced in the perinatal brain injury group relative to controls (Cohen’s d = 1.17, p = 0.01). There was a significant correlation between hippocampal volume and striatal dopamine synthesis capacity (r = 0.344, p= 0.03).ConclusionsPerinatal brain injury, but not very preterm birth without macroscopic brain injury, is associated with persistent alterations in dopaminergic function and reductions in hippocampal volume. This is the first evidence in humans linking neonatal hippocampal injury to adult dopamine dysfunction, and has implications for understanding the mechanism underlying cognitive impairments and neuropsychiatric disorders following very preterm birth.

scholarly journals Reducing the Amount of M1 Microglia by Inhibiting CXCR4 and iNOS Exerts Neuroprotection in a Rat Model of Subarachnoid Hemorrhage

2021 ◽  
Author(s):  
Wenhao Qu ◽  
Ying Cheng ◽  
Wei Peng ◽  
Tongyu Rui ◽  
Chengliang Luo ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Brain Area ◽  
Early Brain Injury ◽  
Inflammatory Factors ◽  
Potential Therapeutic Target ◽  
Injured Brain ◽  
Related Proteins ◽  
Anti Inflammation

Abstract Early inflammation is a significant factor in acute pathophysiological events of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Although there have been numerous studies of neuroinflammation and SAH, the effect of M1 microglia on the progressions of neuroinflammation in SAH remains non-elucidated. CXCR4 is thought to be the critical regulator of the migration and recruitment of microglia, and early studies found that iNOS/NO• does represent an effective ferroptosis regulator and leads to the M1 microglia more resistant to the initiator of ferroptosis. Thus, we investigated the effect of AMD3100 (a highly selective antagonist of CXCR4) and L-NIL (an inhibitor of iNOS) on neuroinflammation in a rat SAH model. We found AMD3100 could suppress the migration of M1 microglia through the CXCL12/CXCR4 pathway. Treatment of AMD3100 could decrease the level of related inflammation factors and improved the prognosis within 24 h after SAH. Moreover, L-NIL could inhibit the expression of (i)NOS and promote the expression of ferroptosis-related proteins and the degree of lipid peroxidation. Importantly, the combination of AMD3100 and L-NIL could reduce the quantity of M1 microglia in the injured brain area and reduce the secretion of related inflammatory factors to improve the prognosis. To sum up, these data indicate that inhibiting CXCR4 and iNOS following SAH produces cerebral protection, and its anti-inflammation provides a potential therapeutic target for treating SAH.

scholarly journals Oral Doxycycline on the Level of Matrix Metalloproteinase 9 in Rat Models Experiencing Traumatic Brain Injury

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Faruk M ◽  
Daud K.R. ◽  
Islam A.A. ◽  
Ihwan A. ◽  
Alfian Zainuddin A.A
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Matrix Metalloproteinase ◽  
Cerebral Edema ◽  
Wistar Rats ◽  
Matrix Metalloproteinase 9 ◽  
Control Group ◽  
Oral Doxycycline ◽  
Injury Group ◽  
Metalloproteinase 9

  INTRODUCTION: Cerebral edema in traumatic brain injury (TBI) results from hyperpermeability of the bloodbrain barrier (BBB). One of the causes in BBB permeability disorders is the activation of matrix metalloproteinase 9 (MMP-9) which can be inhibited by the administration of doxycycline. Knowing the role of oral doxycycline administration as an inhibitor of MMP-9 activation on the level of MMP-9 in cerebral edema in traumatic brain injury. MATERIALS AND METHODS: This study was an experimental study in Wistar rats with a post-test control design consisting of one control group, one group with provoked brain injury, and one group with provoked brain injury followed by oral doxycycline administration. RESULT: There were significant differences in the level of MMP -9 between the control group, the provoked brain injury group and the provoked brain injury group followed by oral doxycycline administration with p-value = 0.01 (p<0.05). CONCLUSION: Oral doxycycline administration can inhibit the increase of MMP-9 levels in cerebral edema in traumatic brain injury in Wistar rats.

scholarly journals The effect of perinatal brain injury on dopaminergic function and hippocampal volume in adult life

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Sean Froudist-Walsh ◽  
Michael AP Bloomfield ◽  
Mattia Veronese ◽  
Jasmin Kroll ◽  
Vyacheslav R Karolis ◽  
...  
Keyword(s):  
Brain Injury ◽  
Adult Life ◽  
Hippocampal Volume ◽  
Dopamine Synthesis ◽  
Control Group ◽  
Perinatal Brain Injury ◽  
Very Preterm ◽  
Cohen’S D ◽  
Injury Group ◽  
Cohen's D

Perinatal brain injuries, including hippocampal lesions, cause lasting changes in dopamine function in rodents, but it is not known if this occurs in humans. We compared adults who were born very preterm with perinatal brain injury to those born very preterm without perinatal brain injury, and age-matched controls born at full term using [18F]-DOPA PET and structural MRI. Dopamine synthesis capacity was reduced in the perinatal brain injury group relative to those without brain injury (Cohen’s d = 1.36, p=0.02) and the control group (Cohen’s d = 1.07, p=0.01). Hippocampal volume was reduced in the perinatal brain injury group relative to controls (Cohen’s d = 1.17, p=0.01) and was positively correlated with striatal dopamine synthesis capacity (r = 0.344, p=0.03). This is the first evidence in humans linking neonatal hippocampal injury to adult dopamine dysfunction, and provides a potential mechanism linking early life risk factors to adult mental illness.

Traumatic Brain Injury: A Trauma Surgeon's Perspective

2012 ◽  
Vol 22 (3) ◽  
pp. 82-89
Author(s):  
Oscar D. Guillamondegui
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Multidisciplinary Approach ◽  
Trauma Team ◽  
The United States ◽  
Long Term Outcomes ◽  
Term Care ◽  
Injured Brain ◽  
The Moment

Traumatic brain injury (TBI) is a serious epidemic in the United States. It affects patients of all ages, race, and socioeconomic status (SES). The current care of these patients typically manifests after sequelae have been identified after discharge from the hospital, long after the inciting event. The purpose of this article is to introduce the concept of identification and management of the TBI patient from the moment of injury through long-term care as a multidisciplinary approach. By promoting an awareness of the issues that develop around the acutely injured brain and linking them to long-term outcomes, the trauma team can initiate care early to alter the effect on the patient, family, and community. Hopefully, by describing the care afforded at a trauma center and by a multidisciplinary team, we can bring a better understanding to the armamentarium of methods utilized to treat the difficult population of TBI patients.

scholarly journals Remotely delivered environmental enrichment intervention for traumatic brain injury: Study protocol for a randomised controlled trial

BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e039767
Author(s):  
Zorry Belchev ◽  
Mary Ellene Boulos ◽  
Julia Rybkina ◽  
Kadeen Johns ◽  
Eliyas Jeffay ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Active Control ◽  
Environmental Enrichment ◽  
Spatial Navigation ◽  
Controlled Trial ◽  
Control Group ◽  
Hippocampal Atrophy ◽  
Active Control Group ◽  
Navigation Group

IntroductionIndividuals with moderate-severe traumatic brain injury (m-sTBI) experience progressive brain and behavioural declines in the chronic stages of injury. Longitudinal studies found that a majority of patients with m-sTBI exhibit significant hippocampal atrophy from 5 to 12 months post-injury, associated with decreased cognitive environmental enrichment (EE). Encouragingly, engaging in EE has been shown to lead to neural improvements, suggesting it is a promising avenue for offsetting hippocampal neurodegeneration in m-sTBI. Allocentric spatial navigation (ie, flexible, bird’s eye view approach), is a good candidate for EE in m-sTBI because it is associated with hippocampal activation and reduced ageing-related volume loss. Efficacy of EE requires intensive daily training, prohibitive within most current health delivery systems. The present protocol is a novel, remotely delivered and self-administered intervention designed to harness principles from EE and allocentric spatial navigation to offset hippocampal atrophy and potentially improve hippocampal functions such as navigation and memory for patients with m-sTBI.Methods and analysisEighty-four participants with chronic m-sTBI are being recruited from an urban rehabilitation hospital and randomised into a 16-week intervention (5 hours/week; total: 80 hours) of either targeted spatial navigation or an active control group. The spatial navigation group engages in structured exploration of different cities using Google Street View that includes daily navigation challenges. The active control group watches and answers subjective questions about educational videos. Following a brief orientation, participants remotely self-administer the intervention on their home computer. In addition to feasibility and compliance measures, clinical and experimental cognitive measures as well as MRI scan data are collected pre-intervention and post-intervention to determine behavioural and neural efficacy.Ethics and disseminationEthics approval has been obtained from ethics boards at the University Health Network and University of Toronto. Findings will be presented at academic conferences and submitted to peer-reviewed journals.Trial registration numberVersion 3, ClinicalTrials.gov Registry (NCT04331392).

scholarly journals Physical Activity and Sport for Acquired Brain Injury (PASABI): A Non-Randomized Controlled Trial

Medicina ◽  
2021 ◽  
Vol 57 (2) ◽  
pp. 122
Author(s):  
Marta Pérez-Rodríguez ◽  
Saleky García-Gómez ◽  
Javier Coterón ◽  
Juan José García-Hernández ◽  
Javier Pérez-Tejero
Keyword(s):  
Quality Of Life ◽  
Physical Activity ◽  
Brain Injury ◽  
Functional Capacity ◽  
Intervention Group ◽  
Chronic Phase ◽  
Acquired Brain Injury ◽  
Control Group ◽  
Wide Range

Background and objectives: Acquired brain injury (ABI) is the first cause of disability and physical activity (PA) is a key element in functional recovery and health-related quality of life (HRQoL) during the subacute and chronic phases. However, it is necessary to develop PA programs that respond to the heterogeneity and needs of this population. The aim of this study was to assess the effectiveness of a PA program on the HRQoL in this population. Materials and Methods: With regard to recruitment, after baseline evaluations, participants were assigned to either the intervention group (IG, n = 38) or the control group (CG, n = 35). Functional capacity, mood, quality of life and depression were measured pre- and post-intervention. The IG underwent the “Physical Activity and Sport for Acquired Brain Injury” (PASABI) program, which was designed to improve HRQoL (1-h sessions, two to four sessions/week for 18 weeks). The CG underwent a standard rehabilitation program without PA. Results: Results for the IG indicated significant differences and large effect sizes for the physical and mental dimensions of quality of life, as well as mood and functional capacity, indicating an increase in HRQoL. No significant differences were found for the CG across any variables. Conclusions: The PASABI program was feasible and beneficial for improving physiological and functionality variables in the IG. The wide range of the activities of the PASABI program allow its application to a large number of people with ABI, promoting health through PA, especially in the chronic phase.

scholarly journals Action of vanillin (Vanilla planifolia) on the morphology of tibialis anterior and soleus muscles after nerve injury

2017 ◽  
Vol 15 (2) ◽  
pp. 186-191 ◽  
Author(s):  
Ana Luiza Peretti ◽  
Juliana Sobral Antunes ◽  
Keli Lovison ◽  
Regina Inês Kunz ◽  
Lidyane Regina Gomes Castor ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Tibialis Anterior ◽  
Morphological Analysis ◽  
Morphological Changes ◽  
Control Group ◽  
Vanilla Planifolia ◽  
Morphological Alterations ◽  
Injury Group ◽  
Fiber Atrophy ◽  
Oral Doses

ABSTRACT Objective To evaluate the action of vanillin (Vanilla planifolia) on the morphology of tibialis anterior and soleus muscles after peripheral nerve injury. Methods Wistar rats were divided into four groups, with seven animals each: Control Group, Vanillin Group, Injury Group, and Injury + Vanillin Group. The Injury Group and the Injury + Vanillin Group animals were submitted to nerve injury by compression of the sciatic nerve; the Vanillin Group and Injury + Vanillin Group, were treated daily with oral doses of vanillin (150mg/kg) from the 3rd to the 21st day after induction of nerve injury. At the end of the experiment, the tibialis anterior and soleus muscles were dissected and processed for light microscopy and submitted to morphological analysis. Results The nerve compression promoted morphological changes, typical of denervation, and the treatment with vanillin was responsible for different responses in the studied muscles. For the tibialis anterior, there was an increase in the number of satellite cells, central nuclei and fiber atrophy, as well as fascicular disorganization. In the soleus, only increased vascularization was observed, with no exacerbation of the morphological alterations in the fibers. Conclusion The treatment with vanillin promoted increase in intramuscular vascularization for the muscles studied, with pro-inflammatory potential for tibialis anterior, but not for soleus muscle.

Extracellular fluid S100B in the injured brain: a future surrogate marker of acute brain injury?

2005 ◽  
Vol 147 (8) ◽  
pp. 897-900 ◽  
Author(s):  
J. Sen ◽  
A. Belli ◽  
A. Petzold ◽  
S. Russo ◽  
G. Keir ◽  
...  
Keyword(s):  
Brain Injury ◽  
Surrogate Marker ◽  
Extracellular Fluid ◽  
Acute Brain Injury ◽  
Injured Brain
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