The Effect of Targeted Hyperoxemia on Brain Immunohistochemistry after Long-Term, Resuscitated Porcine Acute Subdural Hematoma and Hemorrhagic Shock.

Epidemiological data suggest that moderate hyperoxemia may be associated with an improved outcome after traumatic brain injury. In a prospective, randomized investigation of long-term, resuscitated acute subdural hematoma plus hemorrhagic shock (ASDH + HS) in 14 adult, human-sized pigs, targeted hyperoxemia (200 < PaO2 < 250 mmHg vs. normoxemia 80 < PaO2 < 120 mmHg) coincided with improved neurological function. Since brain perfusion, oxygenation and metabolism did not differ, this post hoc study analyzed the available material for the effects of targeted hyperoxemia on cerebral tissue markers of oxidative/nitrosative stress (nitrotyrosine expression), blood-brain barrier integrity (extravascular albumin accumulation) and fluid homeostasis (oxytocin, its receptor and the H2S-producing enzymes cystathionine-ß-synthase and cystathionine-γ-lyase). After 2 h of ASDH + HS (0.1 mL/kgBW autologous blood injected into the subdural space and passive removal of 30% of the blood volume), animals were resuscitated for up to 53 h by re-transfusion of shed blood, noradrenaline infusion to maintain cerebral perfusion pressure at baseline levels and hyper-/normoxemia during the first 24 h. Immediate postmortem, bi-hemispheric (i.e., blood-injected and contra-lateral) prefrontal cortex specimens from the base of the sulci underwent immunohistochemistry (% positive tissue staining) analysis of oxidative/nitrosative stress, blood-brain barrier integrity and fluid homeostasis. None of these tissue markers explained any differences in hyperoxemia-related neurological function. Likewise, hyperoxemia exerted no deleterious effects.

Predictors of subacute hematoma expansion requiring surgical evacuation after initial conservative treatment in patients with acute subdural hematoma.

BACKGROUND: The aim of this study was to clarify the factors associated with requiring subacute surgery in patients with acute subdural hematoma (ASDH) treated conservatively at admission. METHODS: Among the patients with ASDH admitted to our hospital from 2007 to 2018, we retrospectively reviewed data for 200 patients initially treated conservatively. We compared patients' characteristics, medical history, radiological findings, and clinical outcomes and differences between patients undergoing subacute surgery or no surgery. RESULTS: Of the 200 patients treated conservatively, 17 (8.5%) patients underwent subacute surgery due to deterioration of their clinical and/or computed tomography (CT) findings, while 183 (91.5%) patients did not undergo subacute surgery. There were significant differences in the presence of focal neurological deficits, modified Rankin Scale scores, degree of midline shift, hematoma thickness, hematoma volume, cella media index, Sylvian fissure ratio, and hematoma density between the two groups. CONCLUSIONS: Large hematoma, brain atrophy, and hematoma density may be useful predictors for the need for subacute surgery in patients with ASDH treated conservatively at admission. Intensive investigation of clinical findings or CT images is warranted in patients with adverse prognostic factors, even if their initial symptoms are mild.

Leakage sign for acute subdural hematoma in clinical treatment.

BACKGROUND: Acute subdural hematoma (ASDH) is a serious traumatic disease, and predictive methods for hematoma growth are necessary to decide whether emergent operation is necessary. This study aimed to evaluate the incidence of "leakage" using computed tomography angiography (CTA) in patients with ASDH and to identify its prognostic value. METHODS: Sixty-seven patients with ASDH were examined using CTA (mean age 64.1 ± 20.6 years; 24 men) by analyzing two serial scans (CTA phase and delayed phase). We defined a positive leakage sign as a > 10% increase in Hounsfield units (HU) in the region of interest. Hematoma expansion was determined using plain CT after 24 h in patients who did not undergo emergent surgery. RESULTS: Of the 67 patients, conservative therapy was administered to 35 patients; of these patients, 9 showed hematoma expansion, and 8 of these 9 patients (88.9%) showed positive leakage signs. The sensitivity and specificity of leakage signs to hematoma expansion in the no-surgery group were 88.8% and 76.1%, respectively. All positive leakage signs were found within 4.5 h of injury; patients showing negative leakage signs showed a decreased tendency towards hematoma 24 h after injury. Patients presenting with positive leakage signs had poor outcomes. CONCLUSIONS: The results indicated that the leakage sign is a sensitive predictor of hematoma expansion and poor outcomes in ASDH. If the hematoma is small but leakage sign-positive, strict observation is necessary and aggressive surgery may improve outcomes.

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.

Thrombin contributes to the injury development and neurological deficit after acute subdural hemorrhage in rats only in collaboration with additional blood-derived factors.

BACKGROUND: Acute subdural hemorrhage (ASDH) is a severe consequence of traumatic brain injury. The occurrence of subdural blood increases the lethality of these patients independent of the amount of blood or elevated intracranial pressure. Thrombin is one of the potential harmful blood components. Possible harmful effects of thrombin are mediated via the Protease-activated-receptor-1 (PAR1) and thus, translating the acute Thrombin release after ASDH into cell loss. The objectives of the present study were twofold, namely to examine (1) the impact of direct thrombin inhibition in the acute phase after hemorrhage on the long-term histological and functional deficits and (2) the early inhibition of PAR1 activation by thrombin with the selective antagonist SCH79797 on lesion volume at 14 days after ASDH. The effects of thrombin on the lesion size were investigated in two separate experiments via (1) direct thrombin inhibition in the subdural infused blood (Argatroban 600 µg) as well as by (2) intraventricular injection of the PAR-1 antagonist SCH79797 (1 µg or 5 µg). Lesion volume and behavior deficits using a neurological deficit score and a motor function test (beam balance test) were analyzed as outcome parameters at 14 days after injury. RESULTS: 59 Male Sprague-Dawley rats received a subdural infusion of 300 µl autologous blood or sham operation. Lesion volume at 14 days after ASDH tended to be smaller in the Argatroban-treated group when compared to the vehicle group (8.1 ± 1.1 vs. 10.1 ± 2.3 mm2, n.s.). Motor deficits in the beam balance test were not significantly less severe in the Argatroban-treated group. Animals treated with SCH79797 also showed a trend towards dose-dependent decreased lesion volume in comparison to the vehicle-treated group (1 µg: 4.3 ± 0.7 mm3; 5 µg: 3.8 ± 1.1 mm3; vehicle: 6.5 ± 2.0 mm3, n.s). CONCLUSIONS: Thrombin inhibition in the subdural blood and local cerebral blockade of PAR-1 cause a tendency towards reduced lesion volume or functional recovery. All results show a trend in favor of the acute treatment on the outcome parameters. Our results suggests that thrombin could be an important blood-derived factor during acute subdural hemorrhage that translates its deleterious effects in concert with other blood-induced factors.

Aggressive medical management of acute traumatic subdural hematomas before emergency craniotomy in patients presenting with bilateral unreactive pupils. A cohort study.

BACKGROUND: The outcome of patients with severe traumatic brain injury (TBI) and acute traumatic subdural hematoma (aSDH) admitted to the emergency room with bilaterally dilated, unreactive pupils (bilateral mydriasis) is notoriously poor. METHODS: Of 2074 TBI patients consecutively admitted to our facility between 1997 and 2012, 115 had a first CT scan with aSDH, unreactive bilateral mydriasis, and a Glasgow Coma Score of 3 or 4. Sixty-two patients were unoperated and died within hours or a few days. The remaining 53 patients (2.5% of the 2074 consecutive patients) were scheduled for emergent evacuation of the aSDH. We compared three different dosages of mannitol to landmark different comprehensive levels of treatment: (1) a "basic" level of treatment characterized by a single conventional dose (18 to 36 g), (2) "reinforced" treatment landmarked by a single high dose (54 to 72 g), and (3) "aggressive" treatment landmarked by a single high dose (90 to 106 g). Doses above 36 g were administered intravenously over a period of 5 min. RESULTS: Of the 53 selected patients, 7 were aggressively managed (13.2%) and 24 (45.3%) received reinforced treatment. Rates of hyperventilation and barbiturate bolus administration were appropriately associated with increasing doses of mannitol. After adjustment for age, aggressive management was significantly associated with a lower risk of death and persistent vegetative state [adjusted OR 0.016 (95% 0.001-0.405)]. Patients surviving after aggressive management suffered more severe disability at 1 year. CONCLUSION: The study shows an association between reduced mortality and persistent vegetative state, albeit at the cost of increased long-term severe disability in survivors, and aggressive medical preoperative management of mydriatic patients with aSDH following TBI.

Symptomatic Acute-on-Chronic Subdural Hematoma: A Clinicopathological Study.

The pathophysiology of acute-on-chronic subdural hematoma (ACSDH) is complex and incompletely understood. Evidence to date indicates that the overall process is initiated by rotational force with movement of the brain inside the skull, which exerts tensile strain and rupture of bridging veins, leading in turn to acute hemorrhage in the subdural potential space. This is followed by the proliferation of mesenchymal elements with angiogenesis and inflammation, which in turn becomes a substrate for repeated hemorrhage and expansion of the lesion. Given the prevalence of traumatic subdural processes in the forensic setting and the importance of proper assessment of timing, etiology, risk factors, and clinicopathological correlation, we studied 47 patients presenting to the University of Maryland Shock Trauma Center, all of whom underwent craniotomy with resection of the outer membrane due to symptomatic ACSDH. The surgically resected tissue was examined for histopathologic features in all cases. Our findings highlight that ACSDH is a condition precipitated by trauma that affects middle-aged and older adults, is relatively indolent, is unilateral or asymmetric, and has a low in-hospital mortality rate. Pathological analysis demonstrates a substantial outer membrane in all cases with varying degrees of inflammation and organization that cannot be precisely dated as a function of clinical presentation. The extrapolation of adult ACSDH to mixed acute and chronic subdural hemorrhage in the pediatric setting is problematic due to substantial differences in clinical presentation, severity of underlying brain injury, gross and microscopic findings, and outcome.

A case of acute subdural hematoma due to ruptured aneurysm detected by postmortem angiography.

Acute subdural hematoma (ASDH) is mostly caused by head trauma, but intrinsic causes also exist such as aneurysm rupture. We describe here a case involving a man in his 70s who was found lying on the bedroom floor by his family. CT performed at the hospital showed ASDH and a forensic autopsy was requested. Postmortem cerebral angiography showed dilatation of the bifurcation of the middle cerebral artery, which coincided with the dilated part of the Sylvian fissure. Extravasation of contrast medium into the subdural hematoma from this site was suggestive of a ruptured aneurysm. Autopsy revealed a fleshy hematoma (total weight 110 g) in the right subdural space and findings of brain herniation. As indicated on angiography, a ruptured saccular aneurysm was confirmed at the bifurcation of the middle cerebral artery. Obvious injuries to the head or face could not be detected on either external or internal examination, and intrinsic ASDH due to a ruptured middle cerebral artery aneurysm was determined as the cause of death. One of the key points of forensic diagnosis is the strict differentiation between intrinsic and extrinsic onset for conditions leading to death. Although most subdural hematomas (SDH) are caused by extrinsic factors, forensic pathologists should consider the possibility of intrinsic SDH. In addition, postmortem angiography can be useful for identifying vascular lesions in such cases.

[A Case of Ruptured Internal Carotid-Posterior Communicating Artery Aneurysm Associated with Acute Subdural Hematoma, Extending from the Interhemispheric Space to the Posterior Fossa].

A 69-year-old woman was admitted to our hospital because of a sudden severe headache without a history of head trauma. CT and MRI revealed an acute subdural hematoma (ASDH) extending from the right interhemispheric space to the posterior fossa bilaterally, with a small amount of subarachnoid hemorrhage that was predominantly localized to the left side of the basal cistern. CT angiogram demonstrated a long protruding ruptured aneurysm at the junction of the right internal carotid and posterior communicating arteries (IC/PC AN) with a posteroinferior projection, associated with a small bleb located near the tentorial edge close to the ipsilateral posterior clinoid process, for which she received clipping surgery. Though rare, IC/PC AN could cause pure or nearly pure ASDH in the above-mentioned distribution. Therefore, in patients with such ASDH, especially without a history of head injury or precise information regarding the situation at the time of onset, urgent imaging evaluation and early intervention are essential to prevent devastating re-rupture events.

Nail injury to the brain obfuscated by a fall from height - homicide or suicide? a case report.

Penetrating head injuries caused by unconventional objects such as a nail generate speculation and doubt regarding the manner of infliction. We report a case of a 24-year-old woman alleged to have committed suicide by a fall from height. Autopsy revealed an unprecedented penetrating intracranial injury caused by a nail over the right temporal region, confounding the manner of death. The underlying intersecting pattern of fractures determined the chronological sequence of events. In this paper, we discuss the manner, incidence and pathology of nail injuries to the brain.

Optical clearing of the dura mater using glycerol: a reversible process to aid the post-mortem investigation of infant head injury.

PURPOSE: In cases of suspected abusive head trauma, a thorough and systematic study of the cranium and its contents is essential, preferably using the best available methods for observing the brain and its coverings. Building upon recent developments in skull bone removal techniques in infant autopsies, we have assessed the use of two optical clearing agents (OCAs), glycerol and mannitol, on pediatric dura mater in an attempt to increase the transparency of this tissue and thereby enhance the post-mortem assessment of infant head injuries, particularly subdural hematomas. METHODS: Extracorporeal testing revealed glycerol to be the more effective OCA. Therefore, in situ investigations were commenced using glycerol during 33 pediatric post-mortem examinations. RESULTS: An increase in the transparency of the dura was observed in 32 of the 33 cases, within 1 min of application of the OCA. In a 2 year old with cerebral palsy, only partial optical clearance of the dura was seen, most likely due to a significantly atrophic brain, prominent gelatinous leptomeninges, and abnormally thickened dura. This technique allowed for detection of minimal amounts of subdural bleeding over the convexities, before dissection of the dura, avoiding post-mortem blood spillage from artifactually disrupted bridging veins. Optical clearing of the dura aided in the evaluation of patterns of subdural hemorrhage in three cases of non-accidental head injury, three cases of peri-natal head injury and one case of overlaying, apparently resulting in minor crush injury to the head. CONCLUSIONS: We have demonstrated that glycerol is an effective and easy-to-use OCA to effect the readily reversible optical clearing of human infant calvarial dura at autopsy.

Is acute subdural hematoma reduced during the agonal stage and postmortem?

The issue of proper use of postmortem computed tomography (PMCT) in forensic fields is currently being actively discussed. The PMCT image has specific findings that differ from the antemortem image, and it is essential to understand and interpret postmortem changes in order to utilize PMCT properly. In this article, we present two cases of acute subdural hematoma (ASDH) in which images were obtained both ante- and postmortem. These images showed marked reduction of hematoma and diminishing midline shift between the agonal and postmortem periods, without evacuation of the hematoma. Attention should be paid to this phenomenon because key findings in determining cause of death could disappear if investigating the cause of death takes too long in cases that prove to be ASDH. In other words, this phenomenon potentially becomes a risk for misdiagnosis when we decide the cause of death without knowing the details of the circumstances of death.

Cerebral tissue pulmonary embolism after severe head trauma in an infant.

Cerebral tissue pulmonary embolism (CTPE) is a very rare complication of severe head trauma. Nearly 20 cases of CTPE have been reported in neonates after birth trauma and even fewer cases in children and adults. We report a 4-month-old infant boy who sustained severe head trauma when he was accidentally dropped by his stepfather. Autopsy revealed multiple skull fractures, dural venous sinus laceration, subdural and subarachnoid hemorrhages, and brain maceration and extrusion. Microscopically, there was widespread embolism of brain tissue in medium- to small-sized pulmonary arteries.

Spontaneous cortical spreading depression and intracranial pressure following acute subdural hematoma in a rat.

Acute subdural hemorrhage (ASDH) is a frequent and devastating consequence of traumatic brain injury. Tissue damage develops rapidly and makes treatment even more difficult. Management of increased intracranial pressure (ICP) due to extravasated blood volume and brain swelling is often insufficient to control all adverse effects of ASDH. In addition to sheer volume, spontaneously triggered cortical spreading depression (CSD) that leads to cell death following ischemia or trauma may contribute to injury development after ASDH. Therefore, we explored the occurrence of CSD by tissue impedance (IMP) measurement in a rat model subjected to ASDH. IMP and intraventricular and mean arterial pressure were monitored before (baseline), during (blood infusion), and after ASDH for 3 h.Tissue impedance increased by around 203% of baseline during subdural infusion of 300 µl of autologous, venous blood and dropped back to baseline within 22 min. Fifty-six minutes after the start of ASDH a cluster of four short-lasting (3-3.5 min; 140-160% of baseline) IMP increases started that reflected spontaneous CSDs. This pattern presumes that CSD occurs early after ASDH and therefore may contribute to the rapid lesion development in this disease.

Analysis of pituitary lesions in fatal closed head injury.

We analyzed forensic autopsy findings of 66 consecutive patients with fatal closed head injury who survived up to 48 days after trauma to ascertain the causal factors and the time course of development of posttraumatic pituitary lesions. Pituitary lesions were identified in 27 patients. In patients with pituitary lesions, posterior lobe hemorrhage was observed in 21 patients, followed by anterior lobe hemorrhage in 10 patients and anterior lobe infarct in 7 patients. Comparisons between patients with and without pituitary lesions showed that falls and subdural hematoma were significantly frequent in patients with pituitary lesions. Immunohistochemistry of neurophysin showed increased immunoreactivity in the hypothalamus of patients with pituitary lesions and brain edema, providing morphologic evidence of pituitary dysfunction. Hemorrhage in the anterior or posterior lobe was identifiable in patients with short survival periods, whereas infarct in the anterior lobe appeared in patients surviving at least 14 hours. These data further our understanding of the mechanisms of pituitary dysfunctions and help in the estimation of the survival period after head trauma.

Cerebral venous sinus thrombosis in an adult patient presenting as headache and acute subdural hematoma.

We report a 55-year-old man with cerebral venous sinus thrombosis presenting as acute subdural hematoma. He was treated with an intravenous infusion of heparin sodium and the occluded superior sagittal sinus was recanalized. According to our literature review, acute subdural hematoma caused by cerebral venous sinus thrombosis is relatively rare, and only a single case has reported thus far. We speculate that dehydration was the reason for cerebral venous sinus thrombosis in the present case, and the sudden rise in intracranial pressure in addition to hemodynamic stress caused by cerebral venous sinus thrombosis resulted in the collapse of a bridging vein and caused an acute subdural hematoma.

Effects of a small acute subdural hematoma following traumatic brain injury on neuromonitoring, brain swelling and histology in pigs.

An acute subdural hematoma (ASDH) induces pathomechanisms which worsen outcome after traumatic brain injury, even after a small hemorrhage. Synergistic effects of a small ASDH on brain damage are poorly understood, and were studied here using neuromonitoring for 10 h in an injury model of controlled cortical impact (CCI) and ASDH. Pigs (n = 32) were assigned to 4 groups: sham, CCI (2.5 m/s), ASDH (2 ml) and CCI + ASDH. Intracranial pressure was significantly increased above sham levels by all injuries with no difference between groups. CCI and ASDH reduced ptiO(2) by a maximum of 36 ± 9 and 26 ± 11%, respectively. The combination caused a 31 ± 11% drop. ASDH alone and in combination with CCI caused a significant elevation in extracellular glutamate, which remained increased longer for CCI + ASDH. The same two groups had significantly higher peak lactate levels compared to sham. Somatosensory evoked potential (SSEP) amplitude was persistently reduced by combined injury. These effects translated into significantly elevated brain water content and histological damage in all injury groups. Thus, combined injury had stronger effects on glutamate and SSEP when compared to CCI and ASDH, but no clear-cut synergistic effects of 2 ml ASDH on trauma were observed. We speculate that this was partially due to the CCI injury severity.

[The possibility and mechanism of spontaneous redistribution of acute intracranial subdural hematomas].

The author has undertaken the systematic search for the description of isolated and serial cases of spontaneous redistribution of acute intracranial subdural hematomas with their mandatory computed and magneto-resonance neurovisualization. Based on the results of the search and metaanalysis of statistical data, it is concluded that acute intracranial subdural are likely to undergo any possible dislocation over the surface of the large hemispheres of the brain as well as downward transtentorial and spinal migration. The non-linear regression analysis allowed to determine the spinal migration rate of acute intracranial subdural hematomas. At the same time, the analysis gave no evidence of the possibility of the upward transtentorial redistribution of acute intracranial subdural hematomas across the falx of the cerebrum. It is concluded that the results of the present study can be used for the porpose of practical forensic medical expertise and the identification of the sources of spontaneous redistribution of acute intracranial subdural hematomas.

Acute subdural hematoma from ruptured cerebral aneurysm.

PURPOSE: The combination of ruptured aneurysms with acute subdural hematomas (aSDHs) is a rare presentation. Patients with aSDH associated with aneurysmal bleeding represent a subgroup within the spectrum of aneurysmatic hemorrhage. We summarize the clinical characteristics, diagnostic evaluation, and management of a series of cases presenting with aSDH associated with aneurysmal subarachnoid hemorrhage (SAH). METHODS: Medical records and surgical reports of 743 consecutive patients admitted to our institution with SAH from January 1995 to December 2007 were screened to detect cases of associated aSDH. Admission evaluations included the Glasgow Coma Scale (GCS) and the subarachnoid grade of the World Federation of Neurosurgical Societies (WFNS). Radiological assessment included computer tomography (CT) scan, CT angiography (CTA), and digital subtraction angiography (DSA). The presence and volume of SAH, intracerebral hemorrhage (ICH), and aSDH were documented. Outcome was measured in terms of Glasgow Outcome Scale (GOS) and modified Rankin Scale (mRS) at 4-8 months. RESULTS: A total of seven cases (0.9%) presenting with aSDH (mean width: 11.2 mm +/- 4.8 mm, range: 5-20 mm) attributable to SAH were documented. Three of these patients were admitted with a suspicion of trauma. Five patients presented with WFNS grade 5, one patient with WFNS grade 3, and one patient with WFNS grade 1. All patients underwent evacuation of the aSDH. In four patients, surgical obliteration of the aneurysm was achieved in the same procedure. Two patients underwent delayed occlusion of the aneurysm: one by coiling and one by clipping. Three of the seven patients recovered completely from their neurological deficits (GOS 5, mRS 0-1), three recovered with mild disability (GOS 4, mRS 2-3), and one died within 8 h after the decompressive procedure. CONCLUSIONS: The incidence of aSDH associated with SAH is low. Most of the patients with aSDH due to a ruptured aneurysm present in exceptionally poor neurological condition. Nevertheless, rapid surgical treatment of the hematoma and aneurysm obliteration can lead to a favorable outcome. Routine CTA should be performed in all patients presenting with an aSDH associated with SAH and no clear history of trauma.

Collagen fibre orientation in human bridging veins.

Bridging veins (BVs) drain the blood from the cerebral cortex into dural sinuses. BVs have one end attached to the brain and the other to the superior sagittal sinus (SSS), which is attached to the skull. Relative movement between these two structures can cause BV to rupture producing acute subdural haematoma, a head injury with a mortality rate between 30 and 90%. A clear understanding of the BVs microstructure is required to increase the biofidelity of BV models when simulating head impacts. Twelve fresh BV samples draining in the superior sagittal sinus (SSS) from a single human cadaver were cut open along their length and placed on an inverted multiphoton microscope. To ensure that the BVs were aligned with the axial direction an in-house built, uniaxial tension set-up was used. Two scans were performed per sample. Before the first scan, a minor displacement was applied to align the tissue; then, a second scan was taken applying 50% strain. Each BV was scanned for a length of 5 mm starting from the drainage site into the SSS. Imaging was performed on a Zeiss LSM780 microscope with an 25[Formula: see text] water immersion objective (NA 0.8), coupled to a tunable MaiTai DS (Spectraphysics) pulsed laser with the wavelength set at 850 nm. Second harmonic and fluorescence signals were captured in forward and backward direction on binary GaAsP (BiG) detectors and stored as four colour Z-stacks. Prior to the calculation of the local orientations, acquired Z-stacks were denoised and enhanced to highlight fibrillar structures from the background. Then, for each Z-plane of the stack, the ImageJ plugin OrientationJ was used to extract the local 2D orientations of the fibres based on structure tensors. Two kinds of collagen architectures were seen. The most common (8[Formula: see text]12 samples) was single layered and had a uniform distribution of collagen. The less common (4[Formula: see text]12 samples) had 2 layers and 7 to 34 times thicker collagen bundles on the outer layer. Fibre angle analysis showed that collagen was oriented mainly along the axial direction of the vessel. The von Mises fittings showed that in order to describe the fibre distribution 3 components were needed with mean angles [Formula: see text] at [Formula: see text] 0.35, 0.21, [Formula: see text] 0.02 rad or [Formula: see text] 20.2[Formula: see text], 12.1[Formula: see text], [Formula: see text] 1.2[Formula: see text] relative to the vessel's axial direction which was also the horizontal scan direction.