Isolated traumatic subarachnoid hemorrhage (tSAH) after traumatic brain injury (TBI) on head computed tomography (CT) scan is often regarded as a \"mild\" injury, with reduced need for additional workup. However, tSAH is also a predictor of incomplete recovery and unfavorable outcome. This study aimed to evaluate the characteristics of CT-occult intracranial injuries on brain magnetic resonance imaging (MRI) scan in TBI patients with emergency department (ED) arrival Glasgow Coma Scale (GCS) score 13-15 and isolated tSAH on CT. The prospective, 18-center Transforming Research and Clinical Knowledge in Traumatic Brain Injury Study (TRACK-TBI; enrollment years 2014-2019) enrolled participants who presented to the ED and received a clinically-indicated head CT within 24 h of TBI. A subset of TRACK-TBI participants underwent venipuncture within 24 h for plasma glial fibrillary acidic protein (GFAP) analysis, and research MRI at 2-weeks post-injury. In the current study, TRACK-TBI participants age ≥17 years with ED arrival GCS 13-15, isolated tSAH on initial head CT, plasma GFAP level, and 2-week MRI data were analyzed. In 57 participants, median age was 46.0 years [quartile 1 to 3 (Q1-Q3): 34-57] and 52.6% were male. At ED disposition, 12.3% were discharged home, 61.4% were admitted to hospital ward, and 26.3% to intensive care unit. MRI identified CT-occult traumatic intracranial lesions in 45.6% (26 of 57 participants; one additional lesion type: 31.6%; 2 additional lesion types: 14.0%); of these 26 participants with CT-occult intracranial lesions, 65.4% had axonal injury, 42.3% had subdural hematoma, and 23.1% had intracerebral contusion. GFAP levels were higher in participants with CT-occult MRI lesions compared with without (median: 630.6 pg/mL, Q1-Q3: [172.4-941.2] vs. 226.4 [105.8-436.1], p = 0.049), and were associated with axonal injury (no: median 226.7 pg/mL [109.6-435.1], yes: 828.6 pg/mL [204.0-1194.3], p = 0.009). Our results indicate that isolated tSAH on head CT is often not the sole intracranial traumatic injury in GCS 13-15 TBI. Forty-six percent of patients in our cohort (26 of 57 participants) had additional CT-occult traumatic lesions on MRI. Plasma GFAP may be an important biomarker for the identification of additional CT-occult injuries, including axonal injury. These findings should be interpreted cautiously given our small sample size and await validation from larger studies.

We investigated the characteristics of midbrain injuries in patients with spontaneous subarachnoid hemorrhage (SAH) by using diffusion tensor imaging (DTI). Twenty-seven patients with SAH and 25 healthy control subjects were recruited for this study. Fractional anisotropy (FA) and mean diffusivity (MD) data were obtained for four regions of the midbrain (the anterior ventral midbrain, posterior ventral midbrain, tegmentum area, and tectum) in 27 hemispheres that did not show any pathology other than SAH. The mean FA and MD values of the four regions of the midbrain (anterior ventral midbrain, posterior ventral midbrain, tegmentum, and tectum) of the patient group were significantly lower and higher than those of the control group, respectively (p < 0.05). The mean FA values of the patient group were significantly different among the anterior ventral midbrain, posterior ventral midbrain, tegmentum, and tectum regions (ANOVA; F = 3.22, p < 0.05). Post hoc testing showed that the mean FA value of the anterior ventral midbrain was significantly lower than those of the posterior ventral midbrain, tegmentum, and tectum (p < 0.05); in contrast, there were no differences in mean FA values of the posterior ventral midbrain, tegmentum, and tectum (p > 0.05). However, differences were not observed among four regions of the midbrain (anterior ventral midbrain, posterior ventral midbrain, tegmentum, and tectum) in the mean MD values. We detected evidence of neural injury in all four regions of the midbrain of patients with SAH, and the anterior ventral midbrain was the most severely injured among four regions of the midbrain. Our results suggest that a pathophysiological mechanism of these neural injuries might be related to the occurrence of a subarachnoid hematoma.

BACKGROUND The pathophysiology of traumatic subarachnoid hemorrhage and brain injury has not been fully elucidated. In this study, we examined abnormalities of white matter in isolated traumatic subarachnoid hemorrhage patients by applying tract-based spatial statistics. MATERIAL AND METHODS For this study, 10 isolated traumatic subarachnoid hemorrhage patients and 10 age- and sex-matched healthy control subjects were recruited. Fractional anisotropy data voxel-wise statistical analyses were conducted through the tract-based spatial statistics as implemented in the FMRIB Software Library. Depending on the intersection between the fractional anisotropy skeleton and the probabilistic white matter atlases of Johns Hopkins University, we calculated mean fractional anisotropy values within the entire tract skeleton and 48 regions of interest. RESULTS The fractional anisotropy values for 19 of 48 regions of interest showed significant divergences (P<0.05) between the patient group and control group. The regions showing significant differences included the corpus callosum and its adjacent neural structures, the brainstem and its adjacent neural structures, and the subcortical white matter that passes the long neural tract. CONCLUSIONS The results demonstrated abnormalities of white matter in traumatic subarachnoid hemorrhage patients, and the abnormality locations are compatible with areas that are vulnerable to diffuse axonal injury. Based on these results, traumatic subarachnoid hemorrhage patients also exhibit diffuse axonal injuries; thus, traumatic subarachnoid hemorrhage could be an indicator of the presence of severe brain injuries associated with acute or excessive mechanical forces.

Traumatic brain injury (TBI) with isolated subarachnoid hemorrhage (iSAH) is a common finding in the emergency department. In many centers, a repeat CT scan is routinely performed 24 to72 h following the trauma to rule out further radiological progression. The aim of this study is to assess the clinical utility of the repeat CT scan in clinical practice.
We reviewed the medical charts of all patients who presented to our institution with mild TBI (mTBI) and isolated SAH between January 2015 and October 2017. CT scan at admission and control after 24 to 72 h were examined for each patient in order to detect any possible change. Neurological deterioration, antiplatelet/anticoagulant therapy, coagulopathy, SAH location, associated injuries, and length of stay in hospital were analyzed.
Of the 649 TBI patients, 106 patients met the inclusion criteria. Fifty-four patients were females and 52 were males with a mean age of 68.2 years. Radiological iSAH progression was found in 2 of 106 (1.89) patients, and one of them was under antiplatelet therapy. No neurological deterioration was observed. Ten of 106 (9.4%) patients were under anticoagulation therapy, and 28 of 106 (26.4%) were under antiplatelet therapy.
ISAH in mTBI seems to be a radiological stable entity over 72 h with no neurological deterioration. The clinical utility of a repeat head CT in such patients is questionable, considering its radiation exposure and cost. Regardless of anticoagulation/antiplatelet therapy, neurologic observation and symptomatic treatment solely could be a reasonable alternative.

Some previously reported cases of brain evisceration in catastrophic craniocerebral injuries showed the presence of brain swelling. The aim of this study was to observe the occurrence of focal or diffuse brain swelling in such cases in order to explain the underlying mechanism. An observational autopsy study included 23 adults, 18 males and 5 females, whose average age was 48 ± 22 years (range: 19-89 years) and who died as the result of catastrophic craniocerebral injury with brain evisceration. In all the examined cases, either focal (12 cases) or diffuse (11 cases) brain swelling was present. Grossly visible brain contusions (either cortical or deep) were rarely present - only in 6 out of 23 cases, while microscopic brain contusions were observed in 22 out of 23 cases, with 1 remaining case of microscopic subarachnoid bleeding. Blood aspiration in the lungs, as a vital reaction, was noted in 20 out of 23 cases. Microscopic examination showed absence of edema in 20 cases and mild edema in only 3 cases, while microscopic signs of moderate or severe edema were absent. Brain swelling in cases of brain evisceration likely represents a biomechanical reaction (i.e. decompression) due to a sudden decrease in intracranial pressure. The rapidity of death, together with marked absence of microscopic signs of edema, suggests that this is not a form of biological response to injury, but rather a pure physical phenomenon, strictly in a living person. In such cases, the occurrence of brain swelling and parenchymal microbleeding should be considered vital reactions.

Traumatic subarachnoid hemorrhage (SAH) is the second most frequent intracranial hemorrhage and a common radiologic finding in computed tomography. This study aimed to estimate the risk of mortality in adult trauma patients with traumatic SAH concurrent with other types of intracranial hemorrhage, such as subdural hematoma (SDH), epidural hematoma (EDH), and intracerebral hemorrhage (ICH), compared to the risk in patients with isolated traumatic SAH. We searched our hospital\'s trauma database from 1 January, 2009 to 31 December, 2018 to identify hospitalized adult patients ≥20 years old who presented with a trauma abbreviated injury scale (AIS) of ≥3 in the head region. Polytrauma patients with an AIS of ≥3 in any other region of the body were excluded. A total of 1856 patients who had SAH were allocated into four exclusive groups: (Group I) isolated traumatic SAH, n = 788; (Group II) SAH and one diagnosis, n = 509; (Group III) SAH and two diagnoses, n = 493; and (Group IV) SAH and three diagnoses, n = 66. One, two, and three diagnoses indicated occurrences of one, two, or three other types of intracranial hemorrhage (SDH, EDH, or ICH). The adjusted odds ratio with a 95% confidence interval (CI) of the level of mortality was calculated with logistic regression, controlling for sex, age, and pre-existing comorbidities. Patients with isolated traumatic SAH had a lower rate of mortality (1.8%) compared to the other three groups (Group II: 7.9%, Group III: 12.4%, and Group IV: 27.3%, all p < 0.001). When controlling for sex, age, and pre-existing comorbidities, we found that Group II, Group III, and Group IV patients had a 4.0 (95% CI 2.4-6.5), 8.9 (95% CI 4.8-16.5), and 21.1 (95% CI 9.4-47.7) times higher adjusted odds ratio for mortality, respectively, than the patients with isolated traumatic SAH. In this study, we demonstrated that compared to patients with isolated traumatic SAH, traumatic SAH patients with concurrent types of intracranial hemorrhage have a higher adjusted odds ratio for mortality.

The Glasgow Coma Scale (GCS) and Rotterdam Computed Tomography Score (RCTS) are widely used to predict outcomes after traumatic brain injury (TBI). The objective of this study was to determine whether the GCS and RCTS components can be used to predict outcomes in patients with traumatic intracranial hemorrhage (IH) after TBI.
Between May 2009 and July 2017, 773 patients with IH after TBI were retrospectively reviewed. Data on initial GCS, RCTS according to initial brain CT, and status at hospital discharge and last follow-up were collected. Logistic regression analysis was performed to evaluate the relationship between GCS and RCTS components with outcomes after TBI.
Among the 773 patients, the overall in-hospital mortality rate was 14.0%. Variables independently associated with outcomes were the verbal (V-GCS) and motor components of GCS (M-GCS), epidural mass lesion (E-RCTS) and intraventricular or subarachnoid hemorrhage components of RCTS (H-RCTS) (p < 0.0001). The new TBI score was obtained with the following calculation: [V-GCS + M-GCS] - [E-RCTS + H-RCTS].
The new TBI score includes both clinical status and radiologic findings from patients with IH after TBI. The new TBI score is a useful tool for assessing TBI patients with IH in that it combines the GCS and RCTS components that increases area under the curve for predicting in-hospital mortality and unfavorable outcomes and eliminates the paradoxical relationship with outcomes which was observed in GCS score. It allows a practical method to stratify the risk of outcomes after TBI.

Rationale: Older adults (≥65 yr old) account for an increasing proportion of patients with severe traumatic brain injury (TBI), yet clinical trials and outcome studies contain relatively few of these patients.Objectives: To determine functional status 6 months after severe TBI in older adults, changes in this status over 2 years, and outcome covariates.Methods: This was a registry-based cohort study of older adults who were admitted to hospitals in Victoria, Australia, between 2007 and 2016 with severe TBI. Functional status was assessed with Glasgow Outcome Scale Extended (GOSE) 6, 12, and 24 months after injury. Cohort subgroups were defined by admission to an ICU. Features associated with functional outcome were assessed from the ICU subgroup.Measurements and Main Results: The study included 540 older adults who had been hospitalized with severe TBI over the 10-year period; 428 (79%) patients died in hospital, and 456 (84%) died 6 months after injury. There were 277 patients who had not been admitted to an ICU; at 6 months, 268 (97%) had died, 8 (3%) were dependent (GOSE 2-4), and 1 (0.4%) was functionally independent (GOSE 5-8). There were 263 patients who had been admitted to an ICU; at 6 months, 188 (73%) had died, 39 (15%) were dependent, and 32 (12%) were functionally independent. These proportions did not change over longer follow-up. The only clinical features associated with a lower rate of functional independence were Injury Severity Score ≥25 (adjusted odds ratio, 0.24 [95% confidence interval, 0.09-0.67]; P = 0.007) and older age groups (P = 0.017).Conclusions: Severe TBI in older adults is a condition with very high mortality, and few recover to functional independence.

Measuring optic nerve sheath diameter (ONSD), an indicator to predict intracranial hypertension, is noninvasive and convenient, but the reliability of ONSD needs to be improved. Instead of using ONSD alone, this study aimed to evaluate the reliability of the ratio of ONSD to eyeball transverse diameter (ONSD/ETD) in predicting intracranial hypertension in traumatic brain injury (TBI) patients.
We performed a prospective study on patients admitted to the Surgery Intensive Care Unit. The included 52 adults underwent craniotomy for TBI between March 2017 and September 2018. The ONSD and ETD of each eyeball were measured by ultrasound and computed tomography (CT) scan within 24 h after a fiber optic probe was placed into lateral ventricle. Intracranial pressure (ICP) > 20 mmHg was regarded as intracranial hypertension. The correlations between invasive ICP and ultrasound-ONSD/ETD ratio, ultrasound-ONSD, CT-ONSD/ETD ratio, and CT-ONSD were each analyzed separately.
Ultrasound measurement was successfully performed in 94% (n = 49) of cases, and ultrasound and CT measurement were performed in 48% (n = 25) of cases. The correlation efficiencies between ultrasound-ONSD/ETD ratio, ultrasound-ONSD, CT-ONSD/ETD ratio, and ICP were 0.613, 0.498, and 0.688, respectively (P < 0.05). The area under the curve (AUC) values of the receiver operating characteristic (ROC) curve for the ultrasound-ONSD/ETD ratio and CT-ONSD/ETD ratio were 0.920 (95% CI 0.877-0.964) and 0.896 (95% CI 0.856-0.931), respectively. The corresponding threshold values were 0.25 (sensitivity of 90%, specificity of 82.3%) and 0.25 (sensitivity of 85.7%, specificity of 83.3%), respectively.
The ratio of ONSD to ETD tested by ultrasound may be a reliable indicator for predicting intracranial hypertension in TBI patients.

Spreading depolarizations (SDs) occur in 50-60% of patients after surgical treatment of severe traumatic brain injury (TBI) and are independently associated with unfavorable outcomes. Here we performed a pilot study to examine the relationship between SDs and various types of intracranial lesions, progression of parenchymal damage, and outcomes.
In a multicenter study, fifty patients (76% male; median age 40) were monitored for SD by continuous electrocorticography (ECoG; median duration 79 h) following surgical treatment of severe TBI. Volumes of hemorrhage and parenchymal damage were estimated using unbiased stereologic assessment of preoperative, postoperative, and post-ECoG serial computed tomography (CT) studies. Neurologic outcomes were assessed at 6 months by the Glasgow Outcome Scale-Extended.
Preoperative volumes of subdural and subarachnoid hemorrhage, but not parenchymal damage, were significantly associated with the occurrence of SDs (P\'s < 0.05). Parenchymal damage increased significantly (median 34 ml [Interquartile range (IQR) - 2, 74]) over 7 (5, 8) days from preoperative to post-ECoG CT studies. Patients with and without SDs did not differ in extent of parenchymal damage increase [47 ml (3, 101) vs. 30 ml (- 2, 50), P = 0.27], but those exhibiting the isoelectric subtype of SDs had greater initial parenchymal damage and greater increases than other patients (P\'s < 0.05). Patients with temporal clusters of SDs (≥ 3 in 2 h; n = 10 patients), which included those with isoelectric SDs, had worse outcomes than those without clusters (P = 0.03), and parenchymal damage expansion also correlated with worse outcomes (P = 0.01). In multivariate regression with imputation, both clusters and lesion expansion were significant outcome predictors.
These results suggest that subarachnoid and subdural blood are important primary injury factors in provoking SDs and that clustered SDs and parenchymal lesion expansion contribute independently to worse patient outcomes. These results warrant future prospective studies using detailed quantification of TBI lesion types to better understand the relationship between anatomic and physiologic measures of secondary injury.