Dual-Energy CT in Hemorrhagic Progression of Cerebral Contusion: Overestimation of Hematoma Volumes on Standard 120-kV Images and Rectification with Virtual High-Energy Monochromatic Images after Contrast-Enhanced Whole-Body Imaging.

BACKGROUND AND PURPOSE: In patients with hemorrhagic contusions, hematoma volumes are overestimated on follow-up standard 120-kV images obtained after contrast-enhanced whole-body CT. We aimed to retrospectively determine hemorrhagic progression of contusion rates on 120-kV and 190-keV images derived from dual-energy CT and the magnitude of hematoma volume overestimation. MATERIALS AND METHODS: We retrospectively analyzed admission and follow-up CT studies in 40 patients with hemorrhagic contusions. After annotating the contusions, we measured volumes from admission and follow-up 120-kV and 190-keV images using semiautomated 3D segmentation. Bland-Altman analysis was used for hematoma volume comparison. RESULTS: On 120-kV images, hemorrhagic progression of contusions was detected in 24 of the 40 patients, while only 17 patients had hemorrhagic progression of contusions on 190-keV images (P = .008). Hematoma volumes were systematically overestimated on follow-up 120-kV images (9.68 versus 8 mm3; mean difference, 1.68 mm3; standard error, 0.37; P < .001) compared with 190-keV images. There was no significant difference in volumes between admission 120-kV and 190-keV images. Mean and median percentages of overestimation were 29% (95% CI, 18-39) and 22% (quartile 3 - quartile 1 = 36.8), respectively. CONCLUSIONS: The 120-kV images, which are comparable with single-energy CT images, significantly overestimated the hematoma volumes, hence the rate of hemorrhagic progression of contusions, after contrast-enhanced whole-body CT. Hence, follow-up of hemorrhagic contusions should be performed on dual-energy CT, and 190-keV images should be used for the assessment of hematoma volumes.

The Role of Forensic Botany in Solving a Case: Scientific Evidence on the Falsification of a Crime Scene.

Forensic botany can provide useful information for pathologists, particularly on crime scene investigation. We report the case of a man who arrived at the hospital and died shortly afterward. The body showed widespread electrical lesions. The statements of his brother and wife about the incident aroused a large amount of suspicion in the investigators. A crime scene investigation was carried out, along with a botanical morphological survey on small vegetations found on the corpse. An autopsy was also performed. Botanical analysis showed some samples of Xanthium spinosum, thus leading to the discovery of the falsification of the crime scene although the location of the true crime scene remained a mystery. The botanical analysis, along with circumstantial data and autopsy findings, led to the discovery of the real crime scene and became crucial as part of the legal evidence regarding the falsity of the statements made to investigators.

Transient receptor potential channel 1/4 reduces subarachnoid hemorrhage-induced early brain injury in rats via calcineurin-mediated NMDAR and NFAT dephosphorylation.

Transient receptor potential channel 1/4 (TRPC1/4) are considered to be related to subarachnoid hemorrhage (SAH)-induced cerebral vasospasm. In this study, a SAH rat model was employed to study the roles of TRPC1/4 in the early brain injury (EBI) after SAH. Primary cultured hippocampal neurons were exposed to oxyhemoglobin to mimic SAH in vitro. The protein levels of TRPC1/4 increased and peaked at 5 days after SAH in rats. Inhibition of TRPC1/4 by SKF96365 aggravated SAH-induced EBI, such as cortical cell death (by TUNEL staining) and degenerating (by FJB staining). In addition, TRPC1/4 overexpression could increase calcineurin activity, while increased calcineurin activity could promote the dephosphorylation of N-methyl-D-aspartate receptor (NMDAR). Calcineurin antagonist FK506 could weaken the neuroprotection and the dephosphorylation of NMDAR induced by TRPC1/4 overexpression. Contrarily, calcineurin agonist chlorogenic acid inhibited SAH-induced EBI, even when siRNA intervention of TRPC1/4 was performed. Moreover, calcineurin also could lead to the nuclear transfer of nuclear factor of activated T cells (NFAT), which is a transcription factor promoting the expressions of TRPC1/4. TRPC1/4 could inhibit SAH-induced EBI by supressing the phosphorylation of NMDAR via calcineurin. TRPC1/4-induced calcineurin activation also could promote the nuclear transfer of NFAT, suggesting a positive feedback regulation of TRPC1/4 expressions.

Microbleeds may expand acutely after traumatic brain injury.

BACKGROUND AND PURPOSE: Susceptibility weighted imaging (SWI) is a very sensitive tool for the detection of microbleeds in traumatic brain injury (TBI). The number and extent of such traumatic microbleeds (TMBs) have been shown to correlate with the severity of the injury and the clinical outcome. However, the acute dynamics of TMBs have not been revealed so far. Since TBI is known to constitute dynamic pathological processes, we hypothesized that TMBs are not constant in their appearance, but may progress acutely after injury. MATERIALS AND METHODS: We present here five closed moderate/severe (Glasgow coma scale≤13) TBI patients who underwent SWI very early (average=23.4 h), and once again a week (average=185.8 h) after the injury. The TMBs were mapped at both time points by a conventional radiological approach and their numbers and volumes were measured with manual tracing tools by two observers. TMB counts and extents were compared between time points. RESULTS: TMBs were detected in four patients, three of them displaying an apparent TMB change. In these patients, TMB confluence and apparent growth were detected in the corpus callosum, coronal radiation or subcortical white matter, while unchanged TMBs were also present. These changes caused a decrease in the TMB count associated with an increase in the overall TMB volume over time. CONCLUSION: We have found a compelling evidence that diffuse axonal injury-related microbleed development is not limited strictly to the moment of injury: the TMBs might expand in the acute phase of TBI. The timing of SWI acquisition may be relevant for optimizing the prognostic utility of this imaging biomarker.

[CRANIO­CEREBRAL TRAUMA WITH ESTIMATED SEVERITY OF 13­15 POINTS IN ACCORDANCE TO GLASGOW SCALE ­ A LIGHT TRAUMA].

Retrospective analysis of cranio­cerebral trauma (CCT) in 141 injured persons, ageing (38.3 ± 14.3) yrs at average, severity of which in accordance to Glasgow scale was estimated in 13 ­ 15 points, was performed. The injured persons were managed in accordance to actual recommendations of Ministry of Health of Ukraine. In accordance to CT data, the brain commotion was noted in 40 patients, the brain contusion type І ­ in 25, the brain contusion type ІІ with the skull fornix fracture ­ in 30, with linear fracture of the skull bones and traumatic hematomas into the brain­tunics ­ in 30, with fracture of the temporal bone pyramid ­ in 16. In indices 14 points and less (in accordance to Glasgow scale) in terms up to 24 h after CCT and absence of alcohol intoxication in 76.9% injured persons in accordance to CT data the intracranial traumatic affections were revealed. In indices of 15 points in 21% of injured persons false­negative results were determined, witnessing disparity of CCT signs with a CT data.

Melatonin attenuated early brain injury induced by subarachnoid hemorrhage via regulating NLRP3 inflammasome and apoptosis signaling.

Subarachnoid hemorrhage (SAH) is a devastating condition with high morbidity and mortality rates due to the lack of effective therapy. Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation associated with the upregulation of apoptotic signaling pathway has been implicated in various inflammatory diseases including hemorrhagic insults. Melatonin is reported to possess substantial anti-inflammatory properties, which is beneficial for early brain injury (EBI) after SAH. However, the molecular mechanisms have not been clearly identified. This study was designed to investigate the protective effects of melatonin against EBI induced by SAH and to elucidate the potential mechanisms. The adult mice were subjected to SAH. Melatonin or vehicle was injected intraperitoneally 2 hr after SAH. Melatonin was neuroprotective, as shown by increased survival rate, as well as elevated neurological score, greater survival of neurons, preserved brain glutathione levels, and reduced brain edema, malondialdehyde concentrations, apoptotic ratio, and blood-brain barrier (BBB) disruption. Melatonin also attenuated the expressions of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), cleaved caspase-1, interleukin-1ß (IL-1ß), and interleukin-6 (IL-6); these changes were also associated with an increase in the anti-apoptotic factor (Bcl2) and reduction in the pro-apoptotic factor (Bim). In summary, our results demonstrate that melatonin treatment attenuates the EBI following SAH by inhibiting NLRP3 inflammasome-associated apoptosis.

Traumatic brain injury presenting with bilateral basal ganglia hemorrhage.

CONTEXT: Traumatic basal ganglia hemorrhage (TBGH) is a rare presentation of traumatic brain injury. Bilateral lesions are even rarer. Only twelve similar cases were previously published. CASE REPORT: We report the case of a patient with bilateral TBGH. He was managed conservatively. Long-term follow-up disclosed a cognitive dysfunctions attributed to associated diffuse axonal injury. Acceleration and deceleration forces may have torn pallidum arterial branches determining hemorrhage. CONCLUSION: Bilateral TBGH is an uncommon presentation of traumatic brain injury. Associated diffuse axonal injury worsens the outcome.

Predictors of Hypopituitarism in Patients with Traumatic Brain Injury.

Hypopituitarism may often occur in association with traumatic brain injury (TBI). Identification of reliable predictors of pituitary dysfunction is of importance in order to establish a rational testing approach. We searched the records of patients with TBI, who underwent neuroendocrine evaluation in our institution between 2007 and 2013. One hundred sixty-six adults (70% men) with TBI (median age: 41.6 years; range: 18-76) were evaluated at a median interval of 40.4 months (0.2-430.4).Of these, 31% had ≥1 pituitary deficiency, including 29% of patients with mild TBI and 35% with moderate/severe TBI. Growth hormone deficiency was the most common deficiency (21%); when body mass index (BMI)-dependent cutpoints were used, this was reduced to 15%. Central hypoadrenalism occurred in10%, who were more likely to have suffered a motor vehicle accident (MVA, p = 0.04), experienced post-traumatic seizures (p = 0.04), demonstrated any intracranial hemorrhage (p = 0.05), petechial brain hemorrhages (p = 0.017), or focal cortical parenchymal contusions (p = 0.02). Central hypothyroidism occurred in 8% and central hypogonadism in 12%; the latter subgroup had higher BMI (p = 0.03), were less likely to be working after TBI (p = 0.002), and had lower Global Assessment of Functioning (GAF) scores (p = 0.03). Central diabetes insipidus (DI) occurred in 6%, who were more likely to have experienced MVA (p < 0.001) or sustained moderate/severe TBI (p < 0.001). Patients with MVA and those with post-traumatic seizures, intracranial hemorrhage, petechial brain hemorrhages, and/or focal cortical contusions are at particular risk for serious pituitary dysfunction, including adrenal insufficiency and DI, and should be referred for neuroendocrine testing. However, a substantial proportion of patients without these risk factors also developed hypopituitarism.

Pre-Clinical Traumatic Brain Injury Common Data Elements: Toward a Common Language Across Laboratories.

Traumatic brain injury (TBI) is a major public health issue exacting a substantial personal and economic burden globally. With the advent of "big data" approaches to understanding complex systems, there is the potential to greatly accelerate knowledge about mechanisms of injury and how to detect and modify them to improve patient outcomes. High quality, well-defined data are critical to the success of bioinformatics platforms, and a data dictionary of "common data elements" (CDEs), as well as "unique data elements" has been created for clinical TBI research. There is no data dictionary, however, for preclinical TBI research despite similar opportunities to accelerate knowledge. To address this gap, a committee of experts was tasked with creating a defined set of data elements to further collaboration across laboratories and enable the merging of data for meta-analysis. The CDEs were subdivided into a Core module for data elements relevant to most, if not all, studies, and Injury-Model-Specific modules for non-generalizable data elements. The purpose of this article is to provide both an overview of TBI models and the CDEs pertinent to these models to facilitate a common language for preclinical TBI research.

Susceptibility-weighted MRI in mild traumatic brain injury.

OBJECTIVE: To compare the frequency of microbleeds identified by susceptibility-weighted MRI (SWMRI) in patients with mild traumatic brain injury (mTBI) and normal controls, and correlate these findings with neuropsychological tests. METHODS: Research ethics committee approval and patient written informed consents were obtained. One hundred eleven patients with mTBI without parenchymal hemorrhage on CT and conventional MRI received SWMRI as well as a digit span and continuous performance test. One hundred eleven healthy volunteers without history of traumatic brain injury were enrolled as the control group and received conventional MRI with additional SWMRI study. We analyzed the number and location of microbleeds in both groups. RESULTS: Twenty-six patients with mTBI and 12 control subjects presented microbleeds on SWMRI (p = 0.0197). Sixty microbleeds were found in 26 patients with mTBI and 15 microbleeds in 12 control subjects. The mTBI group showed notably more microbleeds in the cortex/subcortical region (52 microbleeds, 86.7%, vs 3 microbleeds, 20%; p < 0.0001). Conversely, the control group showed more microbleeds in the central brain (9 microbleeds, 60%, vs 3 microbleeds, 5%; p < 0.0001). There was no statistical difference in number of microbleeds in the cerebellum and brainstem (p = 0.2598 and p = 0.4932, respectively). Patients with mTBI who had detected microbleeds had lower digit span scores than the patients with negative SWMRI findings (p = 0.017). CONCLUSION: Presence of mTBI-related microbleeds showed a neuropsychological defect on short-term memory function, indicating that the presence of microbleeds could be a possible severity biomarker for mTBI. Addition of the SWMRI technique to the MRI protocol for patients with mTBI is recommended.

Pharmacological induction of the 70-kDa heat shock protein protects against brain injury.

The 70-kDa heat shock protein (HSP70) is known to protect the brain from injury through multiple mechanisms. We investigated the effect of pharmacological HSP70 induction in experimental traumatic brain injury (TBI). 3-month-old male C57/B6 mice were given 17-N-allylamino-17-demethoxygeldanamycin (17-AAG) intraperitoneally (IP, 2 mg/kg) or intracerebroventricularly (ICV, 1 µg/kg) to determine whether HSP70 could be induced in the brain. Mice were subjected to TBI via cortical controlled impact, and were treated with 17-AAG (or vehicle) IP according to one of two treatment regimens: (1) 2 mg/kg at the time of injury, (2) a total of three doses (4 mg/kg) at 2 and 1d prior to TBI and again at the time of injury. Brains were assessed for HSP70 induction, hemorrhage volume at 3 d, and lesion size at 14 d post-injury. Immunohistochemistry showed that both IP and ICV administration of 17-AAG increased HSP70 expression primarily in microglia and in a few neurons by 24 h but not in astrocytes. 17-AAG induced HSP70 in injured brain tissue as early as 6 h, peaking at 48 h and largely subsiding by 72 h after IP injection. Both treatment groups showed decreased hemorrhage volume relative to untreated mice as well as improved neurobehavioral outcomes. These observations indicate that pharmacologic HSP70 induction may prove to be a promising treatment for TBI.

Association between peripheral oxidative stress and white matter damage in acute traumatic brain injury.

The oxidative stress is believed to be one of the mechanisms involved in the neuronal damage after acute traumatic brain injury (TBI). However, the disease severity correlation between oxidative stress biomarker level and deep brain microstructural changes in acute TBI remains unknown. In present study, twenty-four patients with acute TBI and 24 healthy volunteers underwent DTI. The peripheral blood oxidative biomarkers, like serum thiol and thiobarbituric acid-reactive substances (TBARS) concentrations, were also obtained. The DTI metrics of the deep brain regions, as well as the fractional anisotropy (FA) and apparent diffusion coefficient, were measured and correlated with disease severity, serum thiol, and TBARS levels. We found that patients with TBI displayed lower FAs in deep brain regions with abundant WMs and further correlated with increased serum TBARS level. Our study has shown a level of anatomic detail to the relationship between white matter (WM) damage and increased systemic oxidative stress in TBI which suggests common inflammatory processes that covary in both the peripheral and central reactions after TBI.

CD36-mediated hematoma absorption following intracerebral hemorrhage: negative regulation by TLR4 signaling.

Promoting hematoma absorption is a novel therapeutic strategy for intracerebral hemorrhage (ICH); however, the mechanism of hematoma absorption is unclear. The present study explored the function and potential mechanism of CD36 in hematoma absorption using in vitro and in vivo ICH models. Hematoma absorption in CD36-deficient ICH patients was examined. Compared with patients with normal CD36 expression, CD36-deficient ICH patients had slower hematoma adsorption and aggravated neurologic deficits. CD36 expression in perihematomal tissues in wild-type mice following ICH was increased, whereas the hematoma absorption in CD36(-/-) mice was decreased. CD36(-/-) mice also showed aggravated neurologic deficits and increased TNF-α and IL-1ß expression levels. The phagocytic capacity of CD36(-/-) microglia for RBCs was also decreased. Additionally, the CD36 expression in the perihematoma area after ICH in TLR4(-/-) and MyD88(-/-) mice was significantly increased, and hematoma absorption was significantly promoted, which was significantly inhibited by an anti-CD36 Ab. In vitro, TNF-α and IL-1ß significantly inhibited the microglia expression of CD36 and reduced the microglia phagocytosis of RBCs. Finally, the TLR4 inhibitor TAK-242 upregulated CD36 expression in microglia, promoted hematoma absorption, increased catalase expression, and decreased the H2O2 content. These results suggested that CD36 mediated hematoma absorption after ICH, and TLR4 signaling inhibited CD36 expression to slow hematoma absorption. TLR4 inhibition could promote hematoma absorption and significantly improve neurologic deficits following ICH.

The effect of hemorrhage on the development of the postnatal mouse cerebellum.

Recent studies have shown that hemorrhagic injury in the preterm cerebellum leads to long-term neurological sequelae, such as motor, affective, and cognitive dysfunction. How cerebellar hemorrhage (CBH) affects the development and function of the cerebellum is largely unknown. Our study focuses on developing a mouse model of CBH to determine the anatomical, behavioral, and molecular phenotypes resulting from a hemorrhagic insult to the developing cerebellum. To induce CBH in the postnatal mouse cerebellum, we injected bacterial collagenase, which breaks down surrounding blood vessel walls, into the fourth ventricle at postnatal day two. We found a reduction in cerebellar size during postnatal growth, a decrease in granule cells, and persistent neurobehavioural abnormalities similar to abnormalities reported in preterm infants with CBH. We further investigated the molecular pathways that may be perturbed due to postnatal CBH and found a significant upregulation of genes in the inflammatory and sonic hedgehog pathway. These results point to an activation of endogenous mechanisms of injury and neuroprotection in response to postnatal CBH. Our study provides a preclinical model of CBH that may be used to understand the pathophysiology of preterm CBH and for potential development of preventive therapies and treatments.

Correlation of diffusion MRI findings with lesion progression in patients with traumatic intracerebral hemorrhage : diffusion MRI in traumatic intracerebral hemorrhages with progression.

PURPOSE: The aim of this study is to evaluate the association between lesion progression and the ischemic or edematous area that can develop around the hemorrhage in intraparenchymal hemorrhagic lesions originating after head trauma. METHODS: Thirty patients with intracerebral hemorrhage due to head trauma of a mild or intermediate degree were evaluated in this study. Brain diffusion MRI examinations were performed in the first 6 h after trauma in all patients. In addition, a computerized cranial tomography (CCT) was performed upon admission (in the first hour), and at 24 and 48 h after admission. Patients with or without progression of the lesion were compared. RESULTS: The increase in the risk of progression of the lesion in patients with an ischemia/hemorrhage rate > 2 identified in the diffusion MRIs by evaluation of the hemorrhagic and the surrounding ischemic area, obtained in the first 6 h after trauma was found to be statistically significant. The possibility of progression was found to be very low when this rate was less than two. CONCLUSIONS: As a result of the study, the ischemic area was found to be proportionally larger in patients with progression compared to nonprogressing patients with traumatic intracerebral hemorrhage. The ischemia/hemorrhage rate in the diffusion MRI is thought to be an important parameter, beneficial to identify the risk of lesion progression.

Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury.

BACKGROUND: Blast-related traumatic brain injury (TBI) has been a significant cause of injury in the military operations of Iraq and Afghanistan, affecting as many as 10-20% of returning veterans. However, how blast waves affect the brain is poorly understood. To understand their effects, we analyzed the brains of rats exposed to single or multiple (three) 74.5 kPa blast exposures, conditions that mimic a mild TBI. RESULTS: Rats were sacrificed 24 hours or between 4 and 10 months after exposure. Intraventricular hemorrhages were commonly observed after 24 hrs. A screen for neuropathology did not reveal any generalized histopathology. However, focal lesions resembling rips or tears in the tissue were found in many brains. These lesions disrupted cortical organization resulting in some cases in unusual tissue realignments. The lesions frequently appeared to follow the lines of penetrating cortical vessels and microhemorrhages were found within some but not most acute lesions. CONCLUSIONS: These lesions likely represent a type of shear injury that is unique to blast trauma. The observation that lesions often appeared to follow penetrating cortical vessels suggests a vascular mechanism of injury and that blood vessels may represent the fault lines along which the most damaging effect of the blast pressure is transmitted.

Perioperative complications of superficial temporal artery to middle cerebral artery bypass for the treatment of complex middle cerebral artery aneurysms.

OBJECT: Only a few studies have reported the risk of ischemic complications occurring when superficial temporal artery (STA) to middle cerebral artery (MCA) anastomosis is performed during surgery for complex MCA aneurysms. SUBJECTS AND METHODS: This is a retrospective study of 10 patients (age 52-73) with MCA aneurysms treated with revascularization surgery. The aneurysms were 10-50mm in size (mean: 21mm). We studied the causes and frequency of ischemic complications by analyzing postoperative magnetic resonance imaging. RESULTS: Postoperative diffusion-imaging confirmed ischemic complications in six of the 10 patients (in two of the five ruptured aneurysms and in four of the five unruptured). The ischemic complications that observed were infarction of the lenticulostriate artery territory in three cases, cortical infarction in two cases, and cerebral infarction that was likely to be due to cerebral vasospasm in one case. In one case, both cortical infarction and infarction of the lenticulostriate artery territory were observed. The Glasgow Outcome Scale (GOS) scores at the time of discharge indicated good recovery (GR) and moderate disability (MD) in seven cases, severe disability (SD) in two cases, and death (D) in one case. CONCLUSIONS: The present study suggests the possibility that STA-MCA anastamosis in surgeries for MCA aneurysms can be performed with comparatively better safety. However, the temporary occlusion time with this surgery is longer than that with a temporary clipping for aneurysmal surgery; thus, we believe that adequate countermeasures are required to prevent ischemic complications.

Mouse brain PSA-NCAM levels are altered by graded-controlled cortical impact injury.

Traumatic brain injury (TBI) is a worldwide endemic that results in unacceptably high morbidity and mortality. Secondary injury processes following primary injury are composed of intricate interactions between assorted molecules that ultimately dictate the degree of longer-term neurological deficits. One comparatively unexplored molecule that may contribute to exacerbation of injury or enhancement of recovery is the posttranslationally modified polysialic acid form of neural cell adhesion molecule, PSA-NCAM. This molecule is a critical modulator of central nervous system plasticity and reorganization after injury. In this study, we used controlled cortical impact (CCI) to produce moderate or severe TBI in the mouse. Immunoblotting and immunohistochemical analysis were used to track the early (2, 24, and 48 hour) and late (1 and 3 week) time course and location of changes in the levels of PSA-NCAM after TBI. Variable and heterogeneous short- and long-term increases or decreases in expression were found. In general, alterations in PSA-NCAM levels were seen in the cerebral cortex immediately after injury, and these reductions persisted in brain regions distal to the primary injury site, especially after severe injury. This information provides a starting point to dissect the role of PSA-NCAM in TBI-related pathology and recovery.

Predicting progressive hemorrhagic injury after traumatic brain injury: derivation and validation of a risk score based on admission characteristics.

Previous studies have demonstrated that patients with traumatic brain injury (TBI) who also have progressive hemorrhagic injury (PHI), have a higher risk of clinical deterioration and worse outcomes than do TBI patients without PHI. Therefore, the early prediction of PHI occurrence is useful to evaluate the status of patients with TBI and to improve outcomes. The objective of this study was to develop and validate a prognostic model that uses information available at admission to determine the likelihood of PHI after TBI. Retrospectively collected data were used to develop a PHI prognostic model with a logistic regression analysis. The prediction model was validated in 114 patients from a separate hospital. Eight independent prognostic factors were identified: age ≥ 57 years (5 points), intra-axial bleeding/brain contusion (4 points), midline shift ≥ 5 mm (6 points), platelet (PLT) count<100×109/L (10 points), PLT count ≥ 100 but <150×109/L (4 points), prothrombin time>14 sec (7 points), D-dimer ≥ 5 mg/L (12 points), and glucose ≥ 10 mmol/L (10 points). Each patient was assigned a number of points proportional to the regression coefficient. We calculated risk scores for each patient and defined three risk groups: low risk (0-13 points), intermediate risk (14-22 points), and high risk (23-54 points). In the development cohort, the PHI rates after TBI for these three groups were 10.3%, 47.3%, and 85.2%, respectively. In the validation cohort, the corresponding PHI rates were 10.9%, 47.3%, and 86.9%. The C-statistic for the point system was 0.864 (p=0.509 by the Hosmer-Lemeshow test) in the development cohort, and 0.862 (p=0.589 by the Hosmer-Lemeshow test) in the validation cohort. In conclusion, a relatively simple risk score using admission predictors accurately predicted the risk for PHI after TBI.

Fibrillary structure is key for hemostasis: a similar effect of collagen fleece and oxidized cellulose on experimental hemorrhagic brain injury.

BACKGROUND: The choice of the ideal hemostatic agent for intraoperative cerebral bleeding is under continuous debate. Our aim was to assess the influence of such materials on bleeding time in hemorrhagic cerebral contusions. We compared oxidized regenerated cellulose in fibrillar form (ORC) to microfibrillar collagen fleece (CF) in an experimental study. METHODS: N=50 Sprague Dawley rats underwent a bilateral craniectomy. 3 separate standardized superficial cortical impacts were inflicted using a high-speed drill. Immediately after lesion placement, each of the 3 lesions was covered with (a) nothing (control), (b) ORC, or (c) CF. We observed the 3 lesions with a surgical microscope. The bleeding times were recorded for each cerebral lesion and compared using ANOVA test. RESULTS: All traumatic lesions produced significant bleeding. The statistical analysis showed a clear reduction in bleeding time for groups treated with either ORC or CF compared to the control group. Lesions covered with ORC and CF showed no significant difference with regard to bleeding time. CONCLUSIONS: ORC and CF significantly reduce blood loss from hemorrhagic contusions. Our data suggest that they effectively reduce bleeding time. We advocate the use of hemostatic material for limiting bleeding from superficial cortical lesions.