The human head is identified as the body region most frequently involved in life-threatening injuries. Extensive research based on experimental, analytical and numerical methods has sought to quantify the response of the human head to blunt impact in an attempt to explain the likely injury process. Blunt head impact arising from vehicular collisions, sporting injuries, and falls leads to relative motion between the brain and skull and an increase in contact and shear stresses in the meningeal region, thereby leading to traumatic brain injuries. In this paper the properties and material modeling of the subarachnoid space (SAS) as it relates to Traumatic Brain Injuries (TBI) is investigated. This was accomplished using a simplified local model and a validated 3D finite element model. First the material modeling of the trabeculae in the Subarachnoid Space (SAS) was investigated and validated, then the validated material property was used in a 3D head model. In addition, the strain in the brain due to an impact was investigated. From this work it was determined that the material property of the SAS is approximately E = 1150 Pa and that the strain in the brain, and thus the severity of TBI, is proportional to the applied impact velocity and is approximately a quadratic function. This study reveals that the choice of material behavior and properties of the SAS are significant factors in determining the strain in the brain and therefore the understanding of different types of head/brain injuries.
The features of seizure-related brain injuries in rats poisoned i.p. with diisopropylfiuorophosphate were investigated. Pyridostigmine bromide (0.1 mg/kg) and atropine methylnitrate (20 mg/kg), which are centrally inactive, were pretreated i.m. 30 min and 10 min, respectively. before diisopropylfluorophosphate (10 mg /kg, $2LD_50$) poisoning to reduce the mortality and eliminate peripheral signs. Diisopropylfluorophosphate induced severe limbic seizures, and early necrotic and delayed apoptotic brain injuries. The necrotic brain injury, which was closely related to seizure intensity, was exerted as early as 1 hr predominently in hippocampus and piriform cortex. showing spongiform change (malacia) of neurophils in severe cases, in contrast to a typical apoptotic (TUNEL-positive)pattern after 12 hr in thalamus, and a mixed type in amygdala. Nitric oxide content in cerebrospinal fiuid significantly increased after 2 hr, reaching a maximal level at 6 hr. Pretreatment with $_L-N^G$-nitroarginine, an inhibitor of nitric oxide synthase, reduced nitric oxide content and attenuated only apoptotic brain injury in all four brain regions examined without affecting seizure intensity and necrotic injury. Taken together, early necrotic and delayed apoptotic brain injuries induced by diisopropylfiuorophosphate poisoning in rats may be related to seizure intensity and nitric oxide production, respectively.
Purpose: The purpose of the study is to analyze the results of surgical treatment of patients with brain and torso injury for 5 years in a single regional trauma center. Methods: We analyzed multiple trauma patients who underwent brain surgery and torso surgery for chest or abdominal injury simultaneously or sequentially among all 14,175 trauma patients who visited Dankook University Hospital Regional Trauma Center from January 2015 to December 2019. Results: A total of 25 patients underwent brain surgery and chest or abdominal surgery, with an average age of 55.4 years, 17 men and eight women. As a result of surgical treatment, there were 14 patients who underwent the surgery on the same day (resuscitative surgery), of which five patients underwent surgery simultaneously, four patients underwent brain surgery first, and one patient underwent chest surgery first, four patients underwent abdominal surgery first. Among the 25 treated patients, the 10 patients died, which the cause of death was five severe brain injuries and four hemorrhagic shocks. Conclusions: In multiple damaged patients require both torso surgery and head surgery, poor prognosis was associated with low initial Glasgow Coma Scale and high Injury Severity Score. On the other hand, patients had good prognosis when blood pressure was maintained and operation for traumatic brain injury was performed first. At the same time, patients who had operation on head and torso simultaneously had extremely low survival rates. This may be associated with secondary brain injury due to low perfusion pressure or continuous hypotension and the traumatic coagulopathy caused by massive bleeding.
Oleanolic acid (OA), a natural pentacyclic triterpenoid, has been reported to exert protective effects against several neurological diseases through its anti-oxidative and anti-inflammatory activities. The goal of the present study was to evaluate the therapeutic potential of OA against acute and chronic brain injuries after ischemic stroke using a mouse model of transient middle cerebral artery occlusion (tMCAO, MCAO/reperfusion). OA administration immediately after reperfusion significantly attenuated acute brain injuries including brain infarction, functional neurological deficits, and neuronal apoptosis. Moreover, delayed administration of OA (at 3 h after reperfusion) attenuated brain infarction and improved functional neurological deficits during the acute phase. Such neuroprotective effects were associated with attenuation of microglial activation and lipid peroxidation in the injured brain after the tMCAO challenge. OA also attenuated NLRP3 inflammasome activation in activated microglia during the acute phase. In addition, daily administration of OA for 7 days starting from either immediately after reperfusion or 1 day after reperfusion significantly improved functional neurological deficits and attenuated brain tissue loss up to 21 days after the tMCAO challenge; these findings supported therapeutic effects of OA against ischemic stroke-induced chronic brain injury. Together, these findings showed that OA exerted neuroprotective effects against both acute and chronic brain injuries after tMCAO challenge, suggesting that OA is a potential therapeutic agent to treat ischemic stroke.
Kim, Tae-Won;Lee, Jung-Kil;Moon, Kyung-Sub;Joo, Sung-Pil;Kim, Jae-Hyoo;Kim, Soo-Han
Journal of Korean Neurosurgical Society
/
v.41
no.1
/
pp.16-21
/
2007
Objective : Civilian gunshot injuries to the brain are relatively rare and study of these injuries has been neglected in South Korea. We present our experience with penetrating gunshot injuries to the brain and review the outcome of surgical management, as well as other clinical predictors influencing the prognosis. Methods : We present a retrospective analysis of 13 patients with penetrating gunshot injuries to the brain who were treated at our hospital over a period of 22 years. Results : The Glasgow Coma Scale[GCS] score on admission was recorded to be : 3-5 in 1 patient, 6-8 in 3 patients, 9-12 in 2 patients and 13-15 in 7 patients. There were 11 patients who underwent surgical treatment, and the surgical mortality rate was 0%. The admission GCS score was the most valuable prognostic factor. The best results were found to be in patients admitted with an initial GCS higher than 13. There were no favorable outcomes in patients admitted with a GCS of 8 or lower. There was a correlation between the presence of a transventricular or bihemispheric trajectory and poor outcome. The patients admitted with unilobar wounds resulted in better outcome than those with bilobar or multilobar wounds. Retained deep intracranial bone or metal fragments were the most common postoperative complication. However, retained fragments did not increase the risk of infection or seizure. Conclusion : Our results suggest that a less aggressive approach, consisting of minimal local debridement and removal of the bone and metal fragments that are easily accessible, can be successfully used in civilian gunshot wounds to the brain.
Mahn Jeong Ha;Seung Han Yu;Jung Hwan Lee;Hyuk Jin Choi;Byung Chul Kim
Journal of Trauma and Injury
/
v.36
no.1
/
pp.8-14
/
2023
Purpose: The aim of this study was to assess the agreement between intraoperative transcranial sonography (TCS) and postoperative computed tomography (CT) in patients with traumatic brain injuries. Methods: We performed a retrospective cross-sectional study of 35 patients who underwent TCS during surgery, among those who presented to a regional trauma center and underwent decompressive craniectomy between January 1, 2017 and April 30, 2020. Results: The mean difference between TCS and CT in measuring the midline shift was -1.33 mm (95% confidence interval, -2.00 to -0.65; intraclass correlation coefficient [ICC], 0.96; P<0.001). An excellent correlation was found between TCS and CT in assessing contralateral subdural hematomas (ICC, 0.96; P<0.001) and focal hematoma lesions (ICC, 0.99; P<0.001). A very good correlation between TCS and CT was found for measurements of ventricle width (ICC, 0.92; P<0.001). Conclusions: TCS during surgery is considered an effective diagnostic tool for the detection of intraoperative parenchymal changes in patients with traumatic brain injuries.
Objectives: The purpose of this study is to evaluate the effect of Gonjadaesungchimjoongbang on spatial learning abilities and memories in ischemic brain injury. Methods: Rats were separated into three groups; (1) Normal, (2) Saline medication after ischemic brain injuries (control), (3) Gonjadaesungchimjoongbang medication after ischemic brain injuries (experiment). Ischemic brain injuries was induced by MCA occlusion and reperfusion. Morris water maze test was conducted for spatial learning and memory tests. Then, the change of BDNF in the hippocampus($7^{th}$, $14^{th}$ day) was examined by immunohistoche- mistry. Results: In Morris water maze test, spatial learning abilities and memory functioning were considerably increased in the experiment group as oppose to control group on $7^{th}$ and $14^{th}$ day(p<0.01). Moreover, immunohistochemistric response of BDNF in the hippocampus indicated that the more increased immune reaction was found in the experiment group as oppose to the control group on $7^{th}$ and $14^{th}$ day. Conclusions: Gonjadaesungchimjoongbang can improve the learning abilities and memories in ischemic brain injury.
Objective : Intraoperative ventriculostomy is widely adopted to make the slack brain. However, there are few reports about hemorrhagic or parenchymal injuries after ventriculostomy. We tried to analyze and investigate the incidence of these complications in a consecutive series of patients with aneurysmal subarachnoid hemorrhage (SAH). Methods : From September 2006 to June 2007, 43 patients underwent surgical clipping for aneurysmal SAH at our hospital. Among 43 patients, we investigated hemorrhagic or parenchymal injuries after intraoperative ventriculostomy using postoperative computed tomographic scan in 26 patients. After standard pterional craniotomy, ventriculostomy catheter was inserted perpendicular to the cortical surface along the bisectional imaginary line from Paine's point. Results : Hemorrhagic injuries were detected in 12 of 26 patients (46.2%). Mean systolic blood pressure during anesthesia was with in statistically significant parameter related to hemorrhage (p=0.006). On the other hand, parenchymal injuries were detected in 11 of 26 patients (42.3%). Female and the amount of infused mannitol during anesthesia showed statistically significant parameters related to parenchymal injury (p=0.005, 0.04, respectively). However, there were no ventriculostomy-related severe complications. Conclusion : In our series, hemorrhagic or parenchymal injuries after intraoperative ventriculostomy occurred more commonly than previously reported series in aneurysmal SAH patients. Although the clinical outcomes of complications are generally favorable, neurosurgeon must keep in mind the frequent occurrence of brain injury after intraoperative ventriculostomy in the acute stage of aneurysmal SAH.
Jung, Jun-Sub;Kho, A Ra;Lee, Song Hee;Choi, Bo Young;Kang, Shin-Hae;Koh, Jae-Young;Suh, Sang Won;Song, Dong-Keun
The Korean Journal of Physiology and Pharmacology
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v.24
no.2
/
pp.165-171
/
2020
Ischemic and traumatic brain injuries are the major acute central nervous system disorders that need to be adequately diagnosed and treated. To find biomarkers for these acute brain injuries, plasma levels of some specialized pro-resolving mediators (SPMs, i.e., lipoxin A4 [LXA4], resolvin [Rv] E1, RvE2, RvD1 and RvD2), CD59 and interleukin (IL)-6 were measured at 0, 6, 24, 72, and 168 h after global cerebral ischemic (GCI) and traumatic brain injuries (TBI) in rats. Plasma LXA4 levels tended to increase at 24 and 72 h after GCI. Plasma RvE1, RvE2, RvD1, and RvD2 levels showed a biphasic response to GCI; a significant decrease at 6 h with a return to the levels of the sham group at 24 h, and again a decrease at 72 h. Plasma CD59 levels increased at 6 and 24 h post-GCI, and returned to basal levels at 72 h post-GCI. For TBI, plasma LXA4 levels tended to decrease, while RvE1, RvE2, RvD1, and RvD2 showed barely significant changes. Plasma IL-6 levels were significantly increased after GCI and TBI, but with different time courses. These results show that plasma LXA4, RvE1, RvE2, RvD1, RvD2, and CD59 levels display differential responses to GCI and TBI, and need to be evaluated for their usefulness as biomarkers.
The incidence and distribution of necrotic and apoptotic neural cells, and activated astrocytes in the brain of rats intoxicated intra peritoneally with diisopropylfluorophosphate were investigated. Pyridostigmine bromide (0.1 mg/kg) and atropine methylnitrate (20 mg/kg) were pretreated intramuscularly 30 min and 10 min, respectively, prior to diisopropylfluorophosphate (4-10 mg/kg) administration. Diisopropylfluorophosphate induced severe limbic seizures, early necrotic and delayed apoptotic brain injuries, and rapid astrocytic responses. The necrosis, which was closely related to seizure intensity, was observed as early as 1 hr after intoxication predominently in hippocampal pyramidal cells, cerebellar Purkinje cells and neurons in pyriform/entorhinal cortices, showing malacia of neurophils. In contrast, apoptosis started to appear 12 hr after intoxication in neurons in thalamus, amygdala and neocortex, and ephendymal cells surrounding the 4th ventricle. Since marked apoptosis was induced in rats exhibiting relatively-low seizure intensity, the degree of necrosis and apoptosis was shifted to each type of injury according to the seizure intensity. Activated astrocytes, observed within 1 hr along the limbic system, were suggested to affect the neural injury patterns by producing high level of nitric oxide. However, the distribution of activated astrocytes was not in parallel with those of necrotic or apoptotic injuries, implying that the astrocytic responses resulted from seizure activity rather than neural injuries. Furthermore, astrocytes in malacic tissues disappeared during the severe limbic seizures. Therefore, it would be one of the cautionary notes on the expression of glial fibrillary acidic protein in astrocytes as a biochemical marker of brain injuries following acute exposure to organophosphates.
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