Putting 'CSF-Shift Edema' Hypothesis to Test: Comparing Cisternal and Parenchymal Pressures After Basal Cisternostomy for Head Injury.

BACKGROUND: Increased brain edema in head injury is due to shift of cerebrospinal fluid (CSF) from cisterns at high pressure to brain parenchyma at low pressure. By opening basal cisterns and decreasing the increased cisternal pressure, basal cisternostomy (BC) results in reversal of CSF shift from parenchyma to cisterns, leading to decreased brain edema. Though the CSF-shift edema hypothesis is based on pressure difference between cisterns and brain parenchyma, the relationship of these pressures has not been studied. METHODS: A prospective clinical study was conducted from November 2018 to March 2020 including adult patients with head injury who were candidates for standard decompressive hemicraniectomy (DHC). All patients had neurological assessment and head computed tomography preoperatively and postoperatively. All patients underwent BC with DHC. Postoperatively, parenchymal and cisternal pressures and neurological condition were monitored hourly for 72 hours. RESULTS: Nine (5 men, 4 women) patients with head injury (mean age, 45.7 years; range, 25-72 years) underwent DHC-BC. Median Glasgow Coma Scale score of patients at admission was 8 (range, 4-14), and median midline shift on computed tomography was 8 mm (range, 7-12 mm). There was a significant difference between opening (25.70 ± 10.48 mm Hg) and closing (11.30 ± 5.95 mm Hg) parenchymal pressures (t9 = 3.963, P = 0.003). Immediate postoperative cisternal pressure was 1-11 mm Hg and was lower than immediate postoperative parenchymal pressure in all except 1 patient. Postoperatively, if cisternal pressure remained low, parenchymal pressure also decreased, and patients showed clinical improvement. Patients showing increased cisternal pressure showed increased parenchymal pressure and clinical worsening. CONCLUSIONS: Our study supports the CSF-shift edema hypothesis. Following DHC-BC, cisternal pressure is lowered to near-atmospheric pressure, and its relationship to parenchymal pressure predicts the future course of patients by reversal or re-reversal of CSF shift.

Low Risk of Traumatic Intracranial Hematoma Expansion with Factor Xa Inhibitors without Andexanet Reversal.

BACKGROUND: Andexanet alfa, a novel anticoagulation reversal agent for factor Xa inhibitors, was recently approved. Traumatic intracranial hemorrhage presents a prime target for this drug. The Novel Antidote to the Anticoagulation Effects of Factor Xa Inhibitors study established the efficacy of andexanet alfa in reversing factor Xa inhibitors. However, the association between anticoagulation reversal and traumatic intracranial hemorrhage progression is not well understood. The objective of this study was to determine progression rates of patients with traumatic intracranial hemorrhage on factor Xa inhibitors prior to hospitalization who were managed without the use of andexanet alfa. METHODS: A retrospective cohort study was performed between 2016 and 2019 at a single institution. An institutional traumatic brain injury (TBI) registry was queried. Patients with recorded use of apixaban or rivaroxaban <18 hours before injury were included. The primary study outcome was <35% increase in hemorrhage volume or thickness on repeated head computed tomography (CT) scans. RESULTS: We identified 25 patients meeting the inclusion criteria. Two patients were excluded because of a lack of necessary CT data. Twelve patients (52%) were receiving apixaban, and 11 were (48%) on rivaroxaban. On admission CT scan, 14 patients had subdural hematoma, 6 had traumatic intraparenchymal hemorrhage, and 3 had subarachnoid hemorrhage. Anticoagulation reversal was attempted in 17 patients (74%), primarily using 4-factor prothrombin complex concentrate. Twenty patients (87%) were adjudicated as having excellent or good hemostasis on repeat imaging. CONCLUSIONS: Our results indicate that patients on factor Xa inhibitors with complicated mild TBI have a similar intracranial hemorrhage progression rate to patients who are not anticoagulated or anticoagulated with a reversible agent. The hemostatic outcomes in our cohort were similar to those reported after andexanet alfa administration.

Ratio of Optic Nerve Sheath Diameter to Eyeball Transverse Diameter by Ultrasound Can Predict Intracranial Hypertension in Traumatic Brain Injury Patients: A Prospective Study.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: The ratio of ONSD to ETD tested by ultrasound may be a reliable indicator for predicting intracranial hypertension in TBI patients.

Using components of the Glasgow coma scale and Rotterdam CT scores for mortality risk stratification in adult patients with traumatic brain injury: A preliminary study.

OBJECTIVE: 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. PATIENTS AND METHODS: 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. RESULTS: 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]. CONCLUSION: 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.

Early risk stratification of in hospital mortality following a ground level fall in geriatric patients with normal physiological parameters.

BACKGROUND: The purpose of this study was to identify risk factors of mortality for geriatric patients who fell from ground level at home and had a normal physiological examination at the scene. METHODS: Patients aged 65 and above, who sustained a ground level fall (GLF) with normal scene Glasgow Coma Scale (GCS) score 15, systolic blood pressure (SBP) > 90 and <160 mmHg, heart rate ≥ 60 and ≤100 beats per minute) from the 2012-2014 National Trauma Data Bank (NTDB) data sets were included in the study. Patients' characteristics, existing comorbidities [history of smoking, chronic kidney disease (CKD), cerebrovascular accident (CVA), diabetes mellitus (DM), and hypertension (HTN) requiring medication], injury severity scores (ISS), American College of Surgeons' (ACS) trauma center designation level, and outcomes were examined for each case. Risks factors of mortality were identified using bivariate analysis and logistic regression modeling. RESULTS: A total of 40,800 patients satisfied the study inclusion criteria. The findings of the logistic regression model for mortality using the covariates age, sex, race, SBP, ISS, ACS trauma level, smoking status, CKD, CVA, DM, and HTN were associated with a higher risk of mortality (p < .05). The fitted model had an Area under the Curve (AUC) measure of 0.75. CONCLUSION: Cases of geriatric patients who look normal after a fall from ground level at home can still be associated with higher risk of in-hospital death, particularly those who are older, male, have certain comorbidities. These higher-risk patients should be triaged to the hospital with proper evaluation and management.

Long-Term Outcomes after Severe Traumatic Brain Injury in Older Adults. A Registry-based Cohort Study.

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.

Neurostereologic Lesion Volumes and Spreading Depolarizations in Severe Traumatic Brain Injury Patients: A Pilot Study.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Is repeat head CT necessary in patients with mild traumatic intracranial hemorrhage.

BACKGROUND: Patients with traumatic intracranial hemorrhage (TIH) frequently receive repeat head CT scans (RHCT) to assess for progression of TIH. The utility of this practice has been brought into question, with some studies suggesting that in the absence of progressive neurologic symptoms, the RHCT does not lead to clinical interventions. METHODS: This was a retrospective review of consecutive patients with CT-documented TIH and GCS ≥ 13 presenting to an academic emergency department from 2009 to 2013. Demographic, historical, and physical exam variables, number of CT scans during admission were collected with primary outcomes of: neurological decline, worsening findings on repeat CT scan, and the need for neurosurgical intervention. RESULTS: Of these 1126 patients with mild traumatic intracranial hemorrhage, 975 had RHCT. Of these, 54 (5.5% (4.2-7.2 95 CI) had neurological decline, 73 (7.5% 5.9-9.3 95 CI) had hemorrhage progression on repeat CT scan, and 58 (5.9% 4.5-7.6 95 CI) required neurosurgical intervention. Only 3 patients (0.3% 0.1-0.9% 95 CI) underwent neurosurgical intervention due to hemorrhage progression on repeat CT scan without neurological decline. In this scenario, the number of RHCT scans needed to be performed to identify this one patient is 305. CONCLUSIONS: RHCT after initial findings of TIH and GCS ≥ 13 leading to a change to operative management in the absence of neurologic progression is a rare event. A protocol that includes selective RHCT including larger subdural hematomas or patients with coagulopathy (vitamin K inhibitors and anti-platelet agents) may be a topic for further study.

Low Glasgow Coma Score in Traumatic Intracranial Hemorrhage Predicts Development of Cerebral Vasospasm.

BACKGROUND: The exact mechanism, incidence, and risk factors for cerebral vasospasm after traumatic intracranial hemorrhage (ICH) continue to be poorly characterized. The incidence of post-traumatic vasospasm (PTV) varies depending on the detection modality. OBJECTIVE: We aimed to shed light on the predictors, associations, and true incidence of cerebral vasospasm after traumatic ICH using digital subtraction angiography (DSA) as the gold standard. METHODS: We examined a prospectively maintained database of traumatic brain injury (TBI) patients to identify patients with ICH secondary to TBI enrolled between 2002 and 2015 at our trauma center. Patients with TBI-associated ICH and evidence of elevated velocities on transcranial Doppler and computed tomography angiograms, confirmed with DSA were included. The diagnostic cerebral angiograms were evaluated by 2 blinded neurointerventionalists for cerebral vasospasm. Statistical analyses were conducted to determine predictors of PTV. RESULTS: Twenty patients with ICH secondary to TBI and evidence of vasospasm underwent DSAs. Seven patients (7/20; 35%) with traumatic ICH developed cerebral vasospasm and of those, 1 developed delayed cerebral ischemia (1/7; 14%). Of these 7 patients, 6 presented with subarachnoid hemorrhage (6/7; 85%). Vasospasm was substantially more common in patients with a Glasgow Coma Scale <9 (P = 0.017) than in all other groups. CONCLUSIONS: PTV as demonstrated by DCA may be more common than previously reported. Patients who exhibit PTV were more likely to have a Glasgow Coma Scale <9. This subgroup of patients may benefit from more systematic screening for the development of PTV, and earlier monitoring for signs of delayed cerebral ischemia.

Prospective Evaluation of Noninvasive HeadSense Intracranial Pressure Monitor in Traumatic Brain Injury Patients Undergoing Invasive Intracranial Pressure Monitoring.

BACKGROUND: Currently, intracranial pressure (ICP) is measured by invasive methods with a significant risk of infectious and hemorrhagic complications. Because of these high risks, there is a need for a noninvasive ICP (nICP) monitor with an accuracy similar to that of an invasive ICP (iICP) monitor. OBJECTIVE: We sought to assess prospectively the accuracy and precision of an nICP monitor compared with iICP measurement in severe traumatic brain injury (TBI) patients. METHODS: Participants were ICP-monitored patients who had sustained TBI. In parallel with the standard invasive ICP measurements, nICP was measured by the HeadSense HS-1000, which is based on sound propagation. The device generated an acoustic signal using a small transmitter, placed in the patient's ear, and picked up by an acoustic sensor placed in the other ear. The signal is then analyzed using proprietary algorithms, and the ICP value is calculated in millimeter of mercury (mm Hg). RESULTS: Analysis of 2911 paired iICP and nICP measurements from 14 severe TBI patients showed a good accuracy of the nICP monitor indicated by a mean difference of 0.5 mm Hg. The precision was also good with a standard deviation of 3.9 mm Hg. The Pearson r correlation was 0.604 (P < 0.001). CONCLUSIONS: The HeadSense HS-1000 nICP monitor seems sufficiently accurate to measure the ICP in severe TBI patients, is patient friendly, and has minimal risk of complications.

"Solid Red Line": An Observational Study on Death from Refractory Intracranial Hypertension.

The index of cerebrovascular pressure reactivity (PRx) correlates independently with outcome after traumatic brain injury (TBI). However, as an index plotted in the time domain, PRx is rather noisy. To "organise" PRx and make its interpretation easier, the colour coding of values, with green when PRx <0 and red when PRx> 0.3, has been introduced as a horizontal colour bar on the ICM+ screen. In rare cases of death from refractory intracranial hypertension, an increase in intracranial pressure (ICP) is commonly preceded by values of PRx >0.3, showing a "solid red line".Twenty patients after TBI and one after traumatic subarachnoid haemorrhage (SAH) from six centres in Europe and Australia have been studied. All of them died in a scenario of refractory intracranial hypertension. In the majority of cases the initial ICP was below 20 mmHg and finally increased to values well above 60 mmHg, resulting in cerebral perfusion pressure less than 20 mmHg. In three cases initial ICP was elevated at the start of monitoring. A solid red line was observed in all cases preceding an increase in ICP above 25 mmHg by minutes to hours and in two cases by 2 and 3 days, respectively. If a solid red line is observed over a prolonged period, it should be considered as an indicator of deep cerebrovascular deterioration.

Is Impaired Autoregulation Associated with Mortality in Patients with Severe Cerebral Diseases?

BACKGROUND: Cerebral autoregulation (CA) is a mechanism that compensates for variations in cerebral perfusion pressure (CPP) by changes in cerebral blood flow resistance to keep the cerebral blood flow constant. In this study, the relationship between lethal outcome during hospitalisation and the autoregulation-related indices PRx and Mx was investigated. MATERIALS AND METHODS: Thirty patients (aged 18-77 years, mean 53 ± 16 years) with severe cerebral diseases were studied. Cerebral blood flow velocity (CBFV), arterial blood pressure (ABP) and intracranial pressure (ICP) were repeatedly recorded. CA indices were calculated as the averaged correlation between CBFV and CPP (Mx) and between ABP and ICP (PRx). Positive index values indicated impairment of CA. RESULTS: Six patients died in hospital. In this group both PRx and Mx were significantly higher than in the group of survivors (PRx: 0.41 ± 0.33 vs 0.09 ± 0.25; Mx: 0.28 ± 0.40 vs 0.03 ± 0.21; p = 0.01 and 0.04, respectively). PRx and Mx correlated significantly with Glasgow Outcome Scale (GOS) score (PRx: R = -0.40, p < 0.05; Mx: R = -0.54, p < 0.005). PRx was the only significant risk factor for mortality (p < 0.05, logistic regression). CONCLUSION: Increased PRx and Mx were associated with risk of death in patients with severe cerebral diseases. The relationship with mortality was more pronounced in PRx, whereas Mx showed a better correlation with GOS score.

Impaired coagulation is a risk factor for clinical and radiologic deterioration in patients with traumatic brain injury and isolated traumatic subarachnoid hemorrhage.

BACKGROUND: Isolated traumatic subarachnoid hemorrhage (itSAH) is found in approximately 25% of all patients with mild traumatic brain injury (TBI). The aim of this study was to analyze the clinical course and identify risk factors for potential clinical and radiologic deterioration in consideration of impaired coagulation in patients with itSAH. METHODS: A retrospective analysis of 735 patients with TBI resulting in a pathologic computer-assisted tomography (CAT) was performed. Only those patients with itSAH and Glasgow Coma Scale (GCS) of greater than 8 points and follow-up CAT scan were included. Patients with hemorrhage in any other brain compartment (subdural, epidural, and intracerebral) were excluded. Impaired coagulation was operationally defined. RESULTS: Of the 735 patients, 89 met the inclusion criteria. The majority of these patients experienced mild TBI. The rate of radiologic expansion or conversion of the SAH was 28.1%. The rate of clinical deterioration was 6.7%. Neither the initial pattern of itSAH on different intracranial localizations nor the number of sulci involved in the itSAH was associated with clinical worsening. The rate of patients with impaired coagulation was 38%; 17.9% of all patients showed elevated international normalized ratio (INR). Radiologic and clinical deterioration was significantly associated with elevated INR. INR was shown to be independent of age in a logistic regression analysis. CONCLUSION: TBI patients with itSAH and impaired coagulation especially those who showed elevated INR are at risk of clinical and radiologic deterioration. Despite coagulation status, routine repetition of cranial CAT scan is advised in patients with itSAH to detect potential radiologic worsening, which if occurring should result in close clinical monitoring. LEVEL OF EVIDENCE: Therapeutic study, level IV; prognostic study, level III.

Traumatic brain injuries: the influence of the direction of impact.

BACKGROUND: Head impact direction has been identified as an influential risk factor in the risk of traumatic brain injury (TBI) from animal and anatomic research; however, to date, there has been little investigation into this relationship in human subjects. If a susceptibility to certain types of TBI based on impact direction was found to exist in humans, it would aid in clinical diagnoses as well as prevention methods for these types of injuries. OBJECTIVE: To examine the influence of impact direction on the presence of TBI lesions, specifically, subdural hematomas, subarachnoid hemorrhage, and parenchymal contusions. METHODS: Twenty reconstructions of falls that resulted in a TBI were conducted in a laboratory based on eyewitness, interview, and medical reports. The reconstructions involved impacts to a Hybrid III anthropometric dummy and finite element modeling of the human head to evaluate the brain stresses and strains for each TBI event. RESULTS: The results showed that it is likely that increased risk of incurring a subdural hematoma exists from impacts to the frontal or occipital regions, and parenchymal contusions from impacts to the side of the head. There was no definitive link between impact direction and subarachnoid hemorrhage. In addition, the results indicate that there is a continuum of stresses and strain magnitudes between lesion types when impact location is isolated, with subdural hematoma occurring at lower magnitudes for frontal and occipital region impacts, and contusions lower for impacts to the side. CONCLUSION: This hospital data set suggests that there is an effect that impact direction has on TBI depending on the anatomy involved for each particular lesion.

Does isolated traumatic subarachnoid hemorrhage affect outcome in patients with mild traumatic brain injury?

BACKGROUND: The importance of isolated traumatic subarachnoid hemorrhage (SAH) in relation to functional outcome in patients with mild traumatic brain injury (TBI) has not been frequently studied. The aim of this study was to compare the impact of isolated SAH with normal computed tomographic (CT) scan on outcome of patients with mild TBI. METHODS: This is a retrospective study of clinical records and CT scans of all patients with mild TBI (Glasgow Coma Scale score ≥13) evaluated from January 1, 2010, to March 15, 2010, at our institution. The patients were divided into 2 groups: isolated SAH and normal CT scan. The telephonic Glasgow Outcome Scale-Extended, Rivermead Post-Concussion Symptoms Questionnaire (RPCSQ), and Rivermead Head Injury Follow-up Questionnaire (RHFUQ) scores were used to assess outcome after 1 year of injury. Independent sample t test in SPSS was used to assess difference in outcome. RESULTS: A total of 1149 patients with mild TBI were evaluated during study period. Among them, 34 (2.9%) patients had isolated SAH. Twenty-eight patients were male and 6 were female, with a mean age of 36.5 years. Subarachnoid hemorrhage was cortical in 19 (55.9%) patients, interhemispheric in 3 (8.8%) patients, Sylvian fissure in 2 (5.9%) patients, and basal cisternal in 1 (2.9%) patient. Nine (26.5%) patients had SAH at multiple locations. The mean RPCSQ and RHFUQ scores for patients with isolated SAH were 1.38 ± 2.40 and 1.11 ±3.305, respectively. The mean RPCSQ and RHFUQ scores for patients with normal CT scans were 0.40 ± 1.549 and 0.533 ± 1.59, respectively. There was no significant difference in the outcome scores between the SAH and the normal CT scan groups (RHFUQ, P = .45; RPCSQ, P = .248). CONCLUSION: In our study sample of patients with mild TBI, there is no difference in outcome of patients with isolated SAH compared with those with normal CT scans 1 year after injury.

Delayed post-traumatic pseudoaneurysmal formation of the intracranial ophthalmic artery after closed head injury. Case report.

A 42-year-old male presented with a rare case of delayed aneurysmal formation of the intracranial ophthalmic artery after closed head injury manifesting as subarachnoid hemorrhage. Initial magnetic resonance angiography revealed no aneurysmal formation, but angiography 7 days after the injury demonstrated an intracranial ophthalmic artery aneurysm. Follow-up computed tomography angiography demonstrated enlargement of the aneurysm. The aneurysm was successfully treated by surgical resection. Histological examination revealed that the aneurysm was a pseudoaneurysm. Traumatic intracranial aneurysm (TICA) is rare and usually occurs in the peripheral arteries of the cerebral circulation or the basal portion of the internal carotid artery. The present case shows that failure to demonstrate an aneurysm on the initial angiography in the acute stage does not exclude the presence of traumatic aneurysm. This case clearly shows the time course of development of a TICA of the ophthalmic artery after closed head injury.

Role of autophagy in early brain injury after experimental subarachnoid hemorrhage.

Autophagy is a self-degradative process and it plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, and eliminating intracellular pathogens. Previous studies have demonstrated that autophagy pathway was activated in brain after experimental subarachnoid hemorrhage (SAH); however, the role of autophagy in the pathogenesis of early brain injury (EBI) following SAH remains unknown. Experiment 1 aimed to investigate the time-course of the autophagy in the cortex following SAH. In experiment 2, we chose the maximum time point of autophagy activation and assessed the effects of rapamycin (RAP, autophagy activator) and 3-methyladenine (3-MA, autophagy inhibitor) on regulation of EBI. All SAH animals were subjected to injection of 0.3 ml fresh arterial, nonheparinized blood into prechiasmatic cistern in 20 s. As a result, microtubule-associated protein light chain-3 (LC3), a biomarker of autophagosome, and beclin-1, a Bcl-2-interacting protein required for autophagy, were significantly increased at the early stage of SAH and their expressions peaked at 24 h after SAH. In RAP-treated group, the early brain damage such as brain edema, blood-brain barrier (BBB) impairment, cortical apoptosis, and clinical behavior scale was significantly ameliorated in comparison with vehicle-treated SAH rats. Conversely, 3-MA decreased expression of LC3 and beclin-1, increased the average value of brain edema and BBB disfunction, and aggravated neurological deficits. Our results suggest that autophagy pathway is activated in the brain after SAH and may play a beneficial role to EBI development.

Alcoholism and traumatic subarachnoid hemorrhage: an experimental study on vascular morphology and biomechanics.

BACKGROUND: Traumatic subarachnoid hemorrhage (TSAH) related to alcohol abuse is a notable risk factor. Here, we investigated the vascular morphology and biomechanics of TSAH in rat models of acute alcoholic intoxication and chronic alcoholism rats to explore the possible mechanisms of TSAH. METHODS: Sixty male Sprague-Dawley rats were divided into acute alcoholic intoxication and chronic alcoholism groups. Edible spirituous liquor (56% vol/vol) was intragastrically given (15 mL/kg) once to the rats in the acute group, and given twice daily (8 mL/kg for 2 weeks and 12 mL/kg for another 2 weeks) to rats in the chronic group. A self-made instrument was used to inflict head injury. Whole brain, arterial blood, and thoracic aorta of rats were sampled for morphologic and biomechanical examination. RESULTS: Compared with the acute alcoholic rats, the chronic alcoholic rats showed significant morphologic and biomechanical changes: (1) decreased body weight (p<0.05), (2) higher morbidity and mortality from TSAH (p<0.01), (3) greater mean thickness of vascular wall of subarachnoid small arteries and each layer thickness of thoracic aorta (p<0.05), (4) decreased failure load and corresponding extensibility (60 kPa and limit load) of thoracic aorta, and (5) increased elastic modulus (30 kPa, range in physiologic stress) (p<0.05). CONCLUSIONS: Chronic alcoholism can induce the morphologic and biomechanical changes in cerebral vessels and thoracic aorta. The synergistic effect of alcohol abuse and minor blow may be one of the mechanisms of TSAH. High blood pressure from long-term alcohol abuse is also a notable factor.