Abstracts fromThe 29th Annual National Neurotrauma SymposiumJuly 10–13, 2011Hollywood Beach, Florida

Thelin, Eric P.; Johannesson, Louise; Bellander, Bo‐Michael

doi:10.1089/neu.2011.9945

Cited by 3 publications

(4 citation statements)

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“…These groupings were as such to accommodate for the low prevalence (estimated 3.4%) of homozygous Met individuals amongst Caucasians (Pivac and others 2009). In regards to the longer term outcome, a preliminary study presented in abstract form also found the BDNF gene not to be associated with post-traumatic depression according to the Patient Health Questionnaire (PHQ-9) 6 and 12 months later in 78 patients with MTBI and sTBI (Carter and others 2011).…”

Section: Bdnfmentioning

confidence: 99%

“…Calcineurin is a calcium dependent protein phosphatase involved in cellular responses and calcium signal transduction, is composed of a regulatory and catalytic subunit, and has been implicated in neurologic diseases such as schizophrenia (Horiuchi and others 2007), although this is controversial (Xi and others 2007). In post-TBI animal models, calcineurin activity is up-regulated while its inhibition has been associated with improved recovery (Bales and others 2011).…”

Section: Ppp3ccmentioning

confidence: 99%

“…In a large initial study of 277 patients with TBI, a tagging SNP (rs2443504) in the PPP3CC gene was found to be a significant predictor of initial clinical severity (GCS) and recovery after TBI (GOS) (Bales and others 2011). This study was presented in abstract form, thus the patient characteristics were not included, however their risk genotype analysis revealed patients with “AA” in comparison to “GG” genotype had a 54.2% chance of initial GCS <6 (26.6% for “GG”).…”

Section: Ppp3ccmentioning

confidence: 99%

“…This study was presented in abstract form, thus the patient characteristics were not included, however their risk genotype analysis revealed patients with “AA” in comparison to “GG” genotype had a 54.2% chance of initial GCS <6 (26.6% for “GG”). Again “AA” and “GG” genotypes had chances of 3-, 6-, and 12-month severe GOS of 59.3%, 53.1%, 56.2%, respectively, and 31.3%, 32.4%, 33.3%, respectively (Bales and others 2011).…”

Section: Ppp3ccmentioning

confidence: 99%

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Post-Traumatic Brain Injury

2014

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It is estimated that 2% of the population from industrialized countries live with lifelong disabilities resulting from traumatic brain injury (TBI) and roughly one in four adults are unable to return to work 1 year after injury because of physical or mental disabilities. TBI is a significant public health issue that causes substantial physical and economical repercussions for the individual and society. Electronic databases (PubMed, Web of Science, Google Scholar) were searched with the keywords traumatic brain injury, TBI, genes and TBI, TBI outcome, head injury. Human studies on non-penetrating traumatic brain injuries reported in English were included. To provide health care workers with the basic information for clinical management we summarize and compare the data on post-TBI outcome with regard to the impact of genetic variation: apolipoprotein E (APOE), brain-derived neurotrophic factor (BDNF), calcium channel, voltage dependent P/Q type, catechol-O-methyltransferase (COMT), dopamine receptor D2 and ankyrin repeat and kinase domain containing 1 (DRD2 and ANKK1), interleukin-1 (IL-1), interleukin-6 (IL-6), kidney and brain expressed protein (KIBRA), neurofilament, heavy polypeptide (NEFH), endothelial nitric oxide synthase 3 (NOS3), poly (ADP-ribose) polymerase-1 (PARP-1), protein phosphatase 3, catalytic subunit, gamma isozyme (PPP3CC), the serotonin transporter (5-HTT) gene solute carrier family 6 member (SLC6A4) and tumor protein 53 (TP53). It is evident that contradicting results are attributable to the heterogeneity of studies, thus further researches are warranted to effectively assess a relation between genetic traits and clinical outcome following traumatic injuries.

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Section: Bdnfmentioning

confidence: 99%

Section: Ppp3ccmentioning

confidence: 99%

Section: Ppp3ccmentioning

confidence: 99%

Section: Ppp3ccmentioning

confidence: 99%

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Post-Traumatic Brain Injury

2014

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S100B, GFAP, UCH-L1 and NSE as predictors of abnormalities on CT imaging following mild traumatic brain injury: a systematic review and meta-analysis of diagnostic test accuracy

et al. 2021

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Biomarkers such as calcium channel binding protein S100 subunit beta (S100B), glial fibrillary acidic protein (GFAP), ubiquitin c-terminal hydrolase L1 (UCH-L1) and neuron-specific enolase (NSE) have been proposed to aid in screening patients presenting with mild traumatic brain injury (mTBI). As such, we aimed to characterise their accuracy at various thresholds. MEDLINE, SCOPUS and EMBASE were searched, and articles reporting the diagnostic performance of included biomarkers were eligible for inclusion. Risk of bias was assessed using the QUADAS-II criteria. A meta-analysis was performed to assess the predictive value of biomarkers for imaging abnormalities on CT. A total of 2939 citations were identified, and 38 studies were included. Thirty-two studies reported data for S100B. At its conventional threshold of 0.1 μg/L, S100B had a pooled sensitivity of 91% (95%CI 87-94) and a specificity of 30% (95%CI 26-34). The optimal threshold for S100B was 0.72 μg/L, with a sensitivity of 61% (95% CI 50-72) and a specificity of 69% (95% CI 64-74). Nine studies reported data for GFAP. The optimal threshold for GFAP was 626 pg/mL, at which the sensitivity was 71% (95%CI 41-91) and specificity was 71% (95%CI 43-90). Sensitivity of GFAP was maximised at a threshold of 22 pg/mL, which had a sensitivity of 93% (95%CI 73-99) and a specificity of 36% (95%CI 12-68%). Three studies reported data for NSE and two studies for UCH-L1, which precluded meta-analysis. There is evidence to support the use of S100B as a screening tool in mild TBI, and potential advantages to the use of GFAP, which requires further investigation.

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Medical Management of the Severe Traumatic Brain Injury Patient

et al. 2017

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Severe traumatic brain injury (sTBI) is a major contributor to long term disability and a leading cause of death worldwide. Medical management of the sTBI patient, beginning with pre-hospital triage, is aimed at preventing secondary brain injury. This review discusses prehospital and emergency department management of severe TBI, as well as aspects of TBI management in the intensive care unit where advances have been made in the past decade. Areas of emphasis include intracranial pressure management, neuromonitoring, management of paroxysmal sympathetic hyperactivity, neuroprotective strategies, prognostication, and communication with families about goals of care. Where appropriate, differences between the third and fourth editions of the Brain Trauma Foundation Guidelines for the Management of Severe Traumatic Brain Injury are highlighted.

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Abstracts fromThe 29^th Annual National Neurotrauma SymposiumJuly 10–13, 2011Hollywood Beach, Florida

Cited by 3 publications

References 1 publication

Post-Traumatic Brain Injury

Post-Traumatic Brain Injury

S100B, GFAP, UCH-L1 and NSE as predictors of abnormalities on CT imaging following mild traumatic brain injury: a systematic review and meta-analysis of diagnostic test accuracy

Medical Management of the Severe Traumatic Brain Injury Patient

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