Unlabelled: Traumatic brain injury is (TBI) a leading cause of morbidity and mortality in children and adolescents in first-world nations. Research from our team investigating adult survivors of pediatric TBI indicate that survivors of severe TBI are particularly vulnerable to global impairments, including poorer school performance, greater employment difficulties, poor quality of life (QoL), and increased risk of mental health problems. Investigation into less observable consequences, including QoL, has emerged recently as an important outcome to assess in TBI populations. The status of QoL in pediatric TBI populations is mixed, likely a reflection of the varied methodological and theoretical perspectives on QoL.
Aim: This systematic study will clarify the nature of QoL in survivors of pediatric TBI, and identify predictors of QoL in this group. Of 419 articles identified, 11 studies met our inclusion criteria, and 9 were ultimately analyzed in this review. Four studies reported good QoL and 5 poor QoL. The difference between good and poor QoL was statistically significant due to TBI severity [chi-square(3)=77.38, p<0.001], timing of outcome assessment [chi-square(1)=565, p<0.001], and definition of QoL [chi-square(3)=34.73, p<0.001]. The odds of having a poor QoL increased 5.8 times (RR=1.21) when injuries were more severe. Good outcomes are contingent on milder injuries, proxy reporting, and early assessment, whereas poor outcomes reflect more severe injuries and later assessment (≤ 6 months versus ≥ 1 year post-trauma, respectively).
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http://dx.doi.org/10.1089/neu.2011.2157 | DOI Listing |
Clin Exp Emerg Med
January 2025
Department of Emergency Medicine, Chungbuk National University Hospital, 776, Sunhwan-ro, Seowon-gu, Cheongju, Republic of Korea.
Objective: The study aims to investigate the long-term impacts of traumatic brain injury (TBI) on neuroinflammation and neuronal apoptosis in pediatric and adult mice, specifically focusing on how age-at-injury influences these processes.
Methods: Controlled cortical impact (CCI) was used to induce TBI in pediatric (21-25 days old) and adult (8-12 weeks old) C57Bl/6 male mice. Neuroinflammation was evaluated through immunoreactivity for Iba-1 and GFAP, while apoptosis was assessed using markers such as Bax, Bcl- 2, and pro-caspase-3.
Crit Care Med
January 2025
Department of Surgery, University of Southern California, Los Angeles, CA.
Objectives: To explore practice variations in the rate and timing of tracheostomy and gastrostomy for adolescent with severe traumatic brain injury (TBI) across trauma center types.
Design: Retrospective cohort study.
Setting: Trauma centers participating in the American College of Surgeons Trauma Quality Improvement Program (2017-2021) included adult (ATC), mixed (MTC), and pediatric trauma centers (PTC).
PM R
January 2025
Division of Epidemiology, Department of Internal Medicine, University of Utah, Salt Lake City, Utah, USA.
Background: There are no evidence based guidelines for clinicians to follow in advising pediatric patients with traumatic brain injury (TBI) on return to play (RTP).
Objective: To understand practice patterns of experts in pediatric traumatic brain injury (TBI) in relation to how they assess severity of TBI and guide return to play (RTP) decisions with their patients who sustain complicated mild, moderate, or severe TBI.
Design: Cross-sectional web-based survey.
Indian J Crit Care Med
January 2025
Department of Pediatric Intensive Care Unit, St. John's Medical College Hospital, Bengaluru, Karnataka, India.
Background: Traumatic brain injury (TBI) in children can lead to grave consequences. The mechanism, mode, and management of pediatric neurotrauma are different from adult neurotrauma, and there is a growing demand to study the clinicoepidemiology of pediatric TBI.
Objective: To explore the clinicoepidemiological profile and outcome of pediatric neurotrauma.
Brain Res
January 2025
Department of Pediatrics, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address:
Traumatic brain injury (TBI) can lead to chronic neuroinflammation, and neurodegeneration associated with long-term cognitive deficits. Following TBI, the acute neuroinflammatory response involves microglial activation and the release of proinflammatory cytokines and chemokines which induce the recruitment of peripheral immune cells such as monocytes and ultimately T cells. Persistent innate and adaptive immune cells response can lead to chronic neurodegeneration and functional deficits.
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