mild tbi
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2022 ◽  
Author(s):  
Daniel R. Griffiths ◽  
L. Matthew Law ◽  
Conor Young ◽  
Alberto Fuentes ◽  
Seth Truran ◽  
...  

Severe traumatic brain injury results in cognitive dysfunction in part due to vascular perturbations. In contrast, the long-term vasculo-cognitive pathophysiology of mild TBI (mTBI) remains unknown. We evaluated mTBI effects on chronic cognitive and cerebrovascular function and assessed their interrelationships. Sprague-Dawley rats received midline fluid percussion injury (N=20) or sham (N=21). Cognitive function was assessed (3- and 6-month novel object recognition (NOR), novel object location (NOL) and temporal order object recognition (TOR)). 6-month cerebral blood flow (CBF) and blood volume (CBV) using contrast MRI and ex vivo pial artery endothelial and smooth muscle-dependent function were measured. mTBI rats showed impaired NOR, with similar (non-significant) trends in NOL/TOR. Regional CBF and CBV were similar in sham and mTBI. NOR correlated with CBF in lateral hippocampus, medial hippocampus and primary somatosensory barrel cortex while inversely correlating with arterial smooth muscle-dependent dilation. 6-month baseline endothelial and smooth muscle-dependent arterial function were similar among mTBI and sham, but post-angiotensin II stimulation, mTBI showed no change in smooth muscle-dependent dilation from baseline response, unlike the reduction in sham. mTBI led to chronic cognitive dysfunction and altered angiotensin II-stimulated smooth muscle-dependent vasoreactivity, a paradigm that could advance understanding of the long-term sequelae of human mild TBI.


2021 ◽  
Author(s):  
Jack Williams ◽  
Katharine Ker ◽  
Ian Roberts ◽  
Haleema Shakur-Still ◽  
Alec Miners

Abstract Background Tranexamic acid reduces head injury deaths in patients with CT scan evidence of intracranial bleeding after mild traumatic brain injury (TBI). However, the cost-effectiveness of tranexamic acid for people with mild TBI in the pre-hospital setting, prior to CT scanning, is uncertain. A large randomised controlled trial (CRASH-4) is planned to address this issue, but the economic justification for it has not been established. The aim of the analysis was to estimate the likelihood of tranexamic acid being cost-effective given current evidence, the treatment effects required for cost-effectiveness, and the expected value of performing further research. Methods An early economic decision model compared usual care for mild TBI with and without tranexamic acid, for adults aged 70 and above. The evaluation was performed from a UK healthcare perspective over a lifetime time horizon, with costs reported in 2020 pounds (GBP) and outcomes reported as quality adjusted life years (QALYs). All analyses used a £20,000 per QALY cost-effectiveness threshold. Results In the base case analysis, tranexamic acid was associated with an incremental cost-effectiveness ratio of £4,994 per QALY gained, and was 85% likely to be cost-effective in the base case probabilistic sensitivity analysis. The value of perfect information was £13.2 million, and the value of perfect information for parameters that could be collected in a trial was £12.4 million. The all-cause mortality risk ratio for tranexamic acid and the functional outcomes following TBI had the most impact on cost-effectiveness. Conclusions Tranexamic acid can be cost-effective at a very modest treatment effect, and there is a high value of performing future research in the UK. The value in a global context is likely to be far higher.


Author(s):  
Sebastian Vestlund ◽  
Sebastian Tryggmo ◽  
Tomas Vedin ◽  
Per-Anders Larsson ◽  
Marcus Edelhamre

Abstract Purpose To determine and compare the sensitivity, specificity, and proportion of patients eligible for discharge by the Brain Injury Guidelines and the Mild TBI Risk Score in patients with mild traumatic brain injury and concomitant intracranial injury. Methods Retrospective review of the medical records of adult patients with traumatic intracranial injuries and an initial Glasgow Coma Scale score of 14–15, who sought care at Helsingborg Hospital between 2014/01/01 and 2019/12/31. Both guidelines were theoretically applied. The sensitivity, specificity, and percentage of the cohort that theoretically could have been discharged by either guideline were calculated. The outcome was defined as death, in-hospital intervention, admission to the intensive care unit, requiring emergency intubation due to intracranial injury, decreased consciousness, or seizure within 30 days of presentation. Results Of the 538 patients included, 8 (1.5%) and 10 (1.9%) were eligible for discharge according to the Brain Injury Guidelines and the Mild TBI Risk Score, respectively. Both guidelines had a sensitivity of 100%. The Brain Injury Guidelines had a specificity of 2.3% and the Mild TBI Risk Score had a specificity of 2.9%. Conclusion There was no difference between the two guidelines in sensitivity, specificity, or proportion of the cohort eligible for discharge. Specificity and proportion of cohort eligible for discharge were lower than each guideline’s original study. At present, neither guideline can be recommended for implementation in the current or similar settings.


2021 ◽  
Vol 10 (23) ◽  
pp. 5695
Author(s):  
Jun T. Park ◽  
Sarah J. DeLozier ◽  
Harry T. Chugani

Rationale: Posttraumatic epilepsy (PTE) is a common cause of morbidity in children after a traumatic brain injury (TBI), occurring in 10–20% of children following severe TBI. PTE is diagnosed after two or more unprovoked seizures occurring 1-week post TBI. More often, studies have focused on children with epilepsy due to severe TBI. We aim to understand the utility of head computed tomography (HCT), EEG, and the risk of developing drug-resistant epilepsy in children after mild TBI. Method: We retrospectively studied 321 children with TBI at a tertiary pediatric referral center during a 10-year period. Mild TBI was defined as loss of consciousness (LOC) or amnesia < 30 min, moderate TBI as LOC or amnesia between 30 min and 1 day, and severe TBI as LOC or amnesia > 1 day, subdural hemorrhage, or contusion. Multiple clinical variables were reviewed, including past and present antiepileptic drug(s), seizure control, and mode of injury. First and subsequent post-TBI EEGs/prolonged video-EEGs were obtained acutely, subacutely, and/or chronically (range, day 1–3 years, median 1 month). Descriptive analyses were conducted using medians and ranges for continuous data. Categorical data were reported using frequencies and percentages, while comparisons between groups were made using Fisher’s exact test for small sample sizes. Results: Forty-seven children were diagnosed with posttraumatic epilepsy: eight children (17%) due to mild TBI, 39 children (83%) due to severe TBI. For the eight children with mild TBI whom all had an accidental trauma (non-inflicted), the median follow-up time was 25 months (range 1.5 months–84 months). The median age was 10 years (range 4–18 years), and the median age at the time of injury was seven years (range: 23 months–13 years). No relevant previous medical history was present for six patients (80%), and two patients’ (20%) relevant previous medical histories were unknown. Seven patients (88%) had no history of seizures, and patient #6 (12%) had unknown seizure history. Six patients (75%) had normal routine EEG(s). Patient #6 (13%) had an abnormal VEEG 3 months after the initial normal routine EEG, while patient #1 (13%) had an initial prolonged EEG 8 months after TBI. Compared to the 39 patients with severe TBI, 31 (79%) of whom had abnormal EEGs (routine and/or prolonged with video), mild TBI patients were more likely to have normal EEGs, p = 0.005. Head CT scans were obtained acutely for seven patients (90%), all of which were normal. One patient only had brain magnetic resonance imaging (MRI) 8 months after the injury. Compared to the 39 patients with severe TBI, all of whom had abnormal HCTs, mild TBI patients were less likely to have abnormal HCTs, p < 0.0001. In patients with mild TBI, no patient had both abnormal EEG/VEEG and HCT, and no one was on more than one Antiepileptic drug (AED), p < 0.005. Six patients (75%) had MRIs, of which five (63%) were normal. Two patients (#1, 7) did not have MRIs, while one patient’s (#4) MRI was unavailable. Five patients (63%) had a seizure <24 h post TBI, while the rest had seizures after the first week of injury. Conclusion: Children with epilepsy due to mild TBI, loss of consciousness, or amnesia < 30 min are more likely to have normal HCT and EEG and to be on 0–1 AED. Limitations of our study include the small sample size and retrospective design. The current findings add to the paucity of data in children who suffer from epilepsy due to mild TBI.


Author(s):  
Carly A. Cermak ◽  
Shannon E. Scratch ◽  
Nick P. Reed ◽  
Lisa Kakonge ◽  
Deryk S. Beal

Abstract Objectives: To examine the effects of pediatric traumatic brain injury (TBI) on verbal IQ by severity and over time. Methods: A systematic review and subsequent meta-analysis of verbal IQ by TBI severity were conducted using a random effects model. Subgroup analysis included two epochs of time (e.g., <12 months postinjury and ≥12 months postinjury). Results: Nineteen articles met inclusion criteria after an extensive literature search in MEDLINE, PsycInfo, Embase, and CINAHL. Meta-analysis revealed negative effects of injury across severities for verbal IQ and at both time epochs except for mild TBI < 12 months postinjury. Statistical heterogeneity (i.e., between-study variability) stemmed from studies with inconsistent classification of mild TBI, small sample sizes, and in studies of mixed TBI severities, although not significant. Risk of bias on estimated effects was generally low (k = 15) except for studies with confounding bias (e.g., lack of group matching by socio-demographics; k = 2) and measurement bias (e.g., outdated measure at time of original study, translated measure; k = 2). Conclusions: Children with TBI demonstrate long-term impairment in verbal IQ, regardless of severity. Future studies are encouraged to include scores from subtests within verbal IQ (e.g., vocabulary, similarities, comprehension) in addition to functional language measures (e.g., narrative discourse, reading comprehension, verbal reasoning) to elucidate higher-level language difficulties experienced in this population.


Diagnostics ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 2070
Author(s):  
Sung-Ho Jang ◽  
Chang-Hoon Bae ◽  
Jae-Woon Kim ◽  
Hyeok-Gyu Kwon

Some studies have reported that a core vestibular projection (CVP) injury is associated with dizziness following a brain injury using diffusion tensor tractography (DTT). On the other hand, there has been no DTT study on dizziness caused by a CVP injury in patients with mild traumatic brain injury (TBI). In this study, DTT was used to examine the relationship between dizziness and CVP injury in patients with mild TBI. Forty-three patients with mild TBI and twenty-nine normal subjects were recruited. The patients were classified into two groups based on the dizziness score: group A, patients with a dizziness score less than 2 on the sub-item score for dizziness in the Rivermead Post-concussion Symptoms Questionnaire; group B, patients with a dizziness score above 2. The tract volume (TV) in group B was significantly lower than group A and the control group (p < 0.05). By contrast, the TV in group A was similar to the control group (p > 0.05). Regarding the correlation, the dizziness score of all patients showed a strong negative correlation with the TV of the CVP (r = −0.711, p < 0.05). DTT revealed the CVP injury in patients with dizziness after mild TBI. In addition, the severity of dizziness of these patients was closely related to the injury severity of the CVP.


2021 ◽  
pp. 000313482110508
Author(s):  
Olivia A. Keane ◽  
Mauricio A. Escobar ◽  
Lucas P. Neff ◽  
Ian C. Mitchell ◽  
Joshua J. Chern ◽  
...  

Background Pediatric traumatic brain injury (TBI) affects about 475,000 children in the United States annually. Studies from the 1990s showed worse mortality in pediatric TBI patients not transferred to a pediatric trauma center (PTC), but did not examine mild pediatric TBI. Evidence-based guidelines used to identify children with clinically insignificant TBI who do not require head CT were developed by the Pediatric Emergency Care Applied Research Network (PECARN). However, which patients can be safely observed at a non-PTC is not directly addressed. Methods A systematic review of the literature was conducted, focusing on management of pediatric TBI and transfer decisions from 1990 to 2020. Results Pediatric TBI patients make up a great majority of preventable transfers and admissions, and comprise a significant portion of avoidable costs to the health care system. Majority of mild TBI patients admitted to a PTC following transfer do not require ICU care, surgical intervention, or additional imaging. Studies have shown that as high as 83% of mild pediatric TBI patients are discharged within 24 hrs. Conclusions An evidence-based clinical practice algorithm was derived through synthesis of the data reviewed to guide transfer decision. The papers discussed in our systematic review largely concluded that transfer and admission was unnecessary and costly in pediatric patients with mild TBI who met the following criteria: blunt, no concern for NAT, low risk on PECARN assessment, or intermediate risk on PECARN with negative imaging or imaging with either isolated, nondisplaced skull fractures without ICH and/or EDH, or SDH <0.3 cm with no midline shift.


2021 ◽  
Vol 22 (16) ◽  
pp. 9005
Author(s):  
Sathiya Sekar ◽  
Raja Solomon Viswas ◽  
Hajar Miranzadeh Mahabadi ◽  
Elahe Alizadeh ◽  
Humphrey Fonge ◽  
...  

Brain injury/concussion is a growing epidemic throughout the world. Although evidence supports association between traumatic brain injury (TBI) and disturbance in brain glucose metabolism, the underlying molecular mechanisms are not well established. Previously, we reported the release of cellular prion protein (PrPc) from the brain to circulation following TBI. The PrPc level was also found to be decreased in insulin-resistant rat brains. In the present study, we investigated the molecular link between PrPc and brain insulin resistance in a single and repeated mild TBI-induced mouse model. Mild TBI was induced in mice by dropping a weight (~95 g at 1 m high) on the right side of the head. The procedure was performed once and thrice (once daily) for single (SI) and repeated induction (RI), respectively. Micro PET/CT imaging revealed that RI mice showed significant reduction in cortical, hippocampal and cerebellum glucose uptake compared to SI and control. Mice that received RI also showed significant motor and cognitive deficits. In co-immunoprecipitation, the interaction between PrPc, flotillin and Cbl-associated protein (CAP) observed in the control mice brains was disrupted by RI. Lipid raft isolation showed decreased levels of PrPc, flotillin and CAP in the RI mice brains. Based on observation, it is clear that PrPc has an interaction with CAP and the dislodgment of PrPc from cell membranes may lead to brain insulin resistance in a mild TBI mouse model. The present study generated a new insight into the pathogenesis of brain injury, which may result in the development of novel therapy.


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