The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform
Yoichi Katayama - One of the best experts on this subject based on the ideXlab platform.
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Tissue hyperosmolality and brain edema in Cerebral Contusion.
Neurosurgical focus, 2007Co-Authors: Tatsuro Kawamata, Tatsuro Mori, Shoshi Sato, Yoichi KatayamaAbstract:Severe Cerebral Contusion is often associated with nonhemorrhagic mass effect that progresses rapidly within 12 to 48 hours posttrauma. The mechanisms underlying such a rapid progression of mass effect cannot be fully explained by classic concepts of vasogenic and cytotoxic brain edema. Data from previous clinical trials, including diffusion-weighted magnetic resonance imaging studies, have indicated that cells in the central (core) area of the Contusion undergo shrinkage, disintegration, and homogenization, whereas cellular swelling is located predominately in the peripheral (rim) area during this period. The authors hypothesized that high osmolality within the contused brain tissue generates an osmotic potential across the central and peripheral areas or causes blood to accumulate a large amount of water. To elucidate the role of tissue osmolality in Contusion edema, they investigated changes in tissue osmolality, specific gravity, and ion concentration in contused brain in both experimental and clinical settings. Their results demonstrated that Cerebral Contusion induced a rapid increase in tissue osmolality from a baseline level of 311.4 +/- 11.3 to 402.8 +/- 15.1 mOsm at 12 hours posttrauma (p < 0.0001). Specific gravity in tissue significantly decreased from 1.0425 +/- 0.0026 to 1.0308 +/- 0.0028 (p < 0.01), reflecting water accumulation in contused tissue. The total ionic concentration [Na+] + [K+] + [Cl-] did not change significantly at any time point. Inorganic ions do not primarily contribute to this elevation in osmolality, suggesting that the increase in colloid osmotic pressure through the metabolic production of osmoles or the release of idiogenic osmoles can be a main cause of Contusion edema.
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Cerebral Contusion: a role model for lesion progression.
Progress in brain research, 2007Co-Authors: Tatsuro Kawamata, Yoichi KatayamaAbstract:The early massive edema caused by severe Cerebral Contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 h post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In this chapter, we review the results of our clinical studies regarding the pathophysiology of Contusion edema and evaluate the effects of surgical treatment, i.e. Contusion necrotomy, by analyzing the data from the Japan Neurotrauma Data Bank.
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Surgical management of early massive edema caused by Cerebral Contusion in head trauma patients.
Acta neurochirurgica. Supplement, 2006Co-Authors: Tatsuro Kawamata, Yoichi KatayamaAbstract:Early massive edema caused by severe Cerebral Contusion results in elevation of intracranial pressure (ICP) and clinical deterioration within 24–72 hours post-trauma. Previous studies indicate that cells in the central area of the Contusion undergo shrinkage, disintegration, and homogenization, whereas cellular swelling is predominant in the peripheral area, suggesting that early massive edema is attributable to high osmolality within necrotic brain tissue and may generate an osmotic potential across central and peripheral areas.
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Edema fluid accumulation within necrotic brain tissue as a cause of the mass effect of Cerebral Contusion in head trauma patients.
Acta neurochirurgica. Supplement, 2003Co-Authors: Yoichi Katayama, Tatsuro KawamataAbstract:The early massive edema caused by severe Cerebral Contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24–72 hours post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In order to elucidate the mechanisms underlying the early massive edema, we have carried out a series of detailed clinical studies. Diffusion magnetic resonance (MR) imaging and apparent diffusion co-efficient (ADC) mapping suggest that cells in the central area of Contusion undergo shrinkage, disintegration and homogenization, whereas cellular swelling is predominant in the peripheral area during the period of 24–72 hours post-trauma. The ADC values in the central and peripheral areas are maximally dissociated during this period. A large amount of edema fluid accumulates within the necrotic brain tissue of the central area beginning at approximately 24 hours post-trauma. We have found that fluid-blood interface formation within the central area does not represent an uncommon finding in various neuroimaging examinations of Cerebral Contusions, indicating layering of red blood cells within the necrotic brain tissue accumulating voluminous edema fluid. Intravenous slow infusion of gadolinium-DTPA and delayed MR imaging revealed that the central area of Contusion can be enhanced at 24–48 hours posttrauma, implying that water supply from the blood vessels is not completely interrupted. Necrotic brain tissue sampled from the central area of Contusion during surgery demonstrates a very high osmolality. It appears that the capacitance for edema fluid accumulation increases in the central area, whereas cellular swelling in the peripheral area elevates the resistance for edema fluid propagation. Combination of these circumstances may facilitate edema fluid accumulation in the central area. We also suggest that the dissociation of ADC values and high osmolality within the necrotic brain tissue may generate an osmotic potential across the central and peripheral areas and contribute to the early massive edema caused by Cerebral Contusion.
Abel Pohao Huang - One of the best experts on this subject based on the ideXlab platform.
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Cavitation-induced traumatic Cerebral Contusion and intraCerebral hemorrhage in the rat brain by using an off-the-shelf clinical shockwave device
Scientific reports, 2019Co-Authors: Abel Pohao Huang, Dar-ming Lai, Yi-hua Hsu, Yi Kung, Chiang Lan, Chia-shan Yeh, Hsin-han Tsai, Chih-feng Lin, Wen-shiang ChenAbstract:Traumatic Cerebral Contusion and intraCerebral hemorrhages (ICH) commonly result from traumatic brain injury and are associated with high morbidity and mortality rates. Current animal models require craniotomy and provide less control over injury severity. This study proposes a highly reproducible and controllable traumatic Contusion and ICH model using non-invasive extracorporeal shockwaves (ESWs). Rat heads were exposed to ESWs generated by an off-the-shelf clinical device plus intravenous injection of microbubbles to enhance the cavitation effect for non-invasive induction of injury. Results indicate that injury severity can be effectively adjusted by using different ESW parameters. Moreover, the location or depth of injury can be purposefully determined by changing the focus of the concave ESW probe. Traumatic Contusion and ICH were confirmed by H&E staining. Interestingly, the numbers of TUNEL-positive cells (apoptotic cell death) peaked one day after ESW exposure, while Iba1-positive cells (reactive microglia) and GFAP-positive cells (astrogliosis) respectively peaked seven and fourteen days after exposure. Cytokine assay showed significantly increased expressions of IL-1β, IL-6, and TNF-α. The extent of brain edema was characterized with magnetic resonance imaging. Conclusively, the proposed non-invasive and highly reproducible preclinical model effectively simulates the mechanism of closed head injury and provides focused traumatic Contusion and ICH.
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early parenchymal contrast extravasation predicts subsequent hemorrhage progression clinical deterioration and need for surgery in patients with traumatic Cerebral Contusion
Journal of Trauma-injury Infection and Critical Care, 2011Co-Authors: Abel Pohao Huang, Chungwei Lee, Hong Jen Hsieh, Chicheng Yang, Yi Hsin Tsai, Fonyih Tsuang, Luting Kuo, Yuan Shen Chen, Sheng Jean Huang, Honman LiuAbstract:Background:This study aimed to identify early radiologic signs that are predictive of hemorrhage progression and clinical deterioration in patients with traumatic Cerebral Contusion. We hypothesized that contrast extravasation (CE) and blood-brain barrier disruption might be associated with hemorrha
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Early parenchymal contrast extravasation predicts subsequent hemorrhage progression, clinical deterioration, and need for surgery in patients with traumatic Cerebral Contusion.
The Journal of trauma, 2011Co-Authors: Abel Pohao Huang, Chungwei Lee, Hong Jen Hsieh, Chicheng Yang, Yi Hsin Tsai, Fonyih Tsuang, Luting Kuo, Yuan Shen Chen, Sheng Jean HuangAbstract:This study aimed to identify early radiologic signs that are predictive of hemorrhage progression and clinical deterioration in patients with traumatic Cerebral Contusion. We hypothesized that contrast extravasation (CE) and blood-brain barrier disruption might be associated with hemorrhage progression, brain edema, and clinical deterioration in these patients. Twenty-two patients with traumatic Cerebral Contusion (diagnosed on initial noncontrast head computed tomography [CT]) who initially did not require surgical intervention were enrolled in this study. Contrast-enhanced and perfusion CT scans were performed within 6 hours of injury, and follow-up noncontrast CT scans were performed at 24 hours and 72 hours. In each noncontrast CT scan, the volumes of the Contusion hemorrhage and edema were calculated using computerized planimetric techniques. The initial Glasgow Coma Scale, hemorrhage progression, clinical deterioration, and the need for subsequent surgery were recorded. The early radiologic findings were compared with these parameters and functional outcome at 6 months to identify predictive radiologic signs. CE was present in 9 of 22 patients (41%) and was highly associated with hemorrhage progression (p < 0.05), clinical deterioration (p < 0.01), and need for subsequent surgery (p < 0.01). In addition, patients with CE had a greater volume of edema at 24 hours (p < 0.01) and 72 hours (p < 0.01) than those who did not have CE. However, CE was not found to be associated with poor outcome. Early parenchymal CE is associated with hemorrhage progression, Cerebral edema, clinical deterioration, and need for subsequent surgery. These patients should be monitored closely, and early surgery may be needed if deterioration occurs. Further elucidation of the pathophysiology is needed to formulate effective treatment for these high-risk patients.
Tatsuro Kawamata - One of the best experts on this subject based on the ideXlab platform.
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Tissue hyperosmolality and brain edema in Cerebral Contusion.
Neurosurgical focus, 2007Co-Authors: Tatsuro Kawamata, Tatsuro Mori, Shoshi Sato, Yoichi KatayamaAbstract:Severe Cerebral Contusion is often associated with nonhemorrhagic mass effect that progresses rapidly within 12 to 48 hours posttrauma. The mechanisms underlying such a rapid progression of mass effect cannot be fully explained by classic concepts of vasogenic and cytotoxic brain edema. Data from previous clinical trials, including diffusion-weighted magnetic resonance imaging studies, have indicated that cells in the central (core) area of the Contusion undergo shrinkage, disintegration, and homogenization, whereas cellular swelling is located predominately in the peripheral (rim) area during this period. The authors hypothesized that high osmolality within the contused brain tissue generates an osmotic potential across the central and peripheral areas or causes blood to accumulate a large amount of water. To elucidate the role of tissue osmolality in Contusion edema, they investigated changes in tissue osmolality, specific gravity, and ion concentration in contused brain in both experimental and clinical settings. Their results demonstrated that Cerebral Contusion induced a rapid increase in tissue osmolality from a baseline level of 311.4 +/- 11.3 to 402.8 +/- 15.1 mOsm at 12 hours posttrauma (p < 0.0001). Specific gravity in tissue significantly decreased from 1.0425 +/- 0.0026 to 1.0308 +/- 0.0028 (p < 0.01), reflecting water accumulation in contused tissue. The total ionic concentration [Na+] + [K+] + [Cl-] did not change significantly at any time point. Inorganic ions do not primarily contribute to this elevation in osmolality, suggesting that the increase in colloid osmotic pressure through the metabolic production of osmoles or the release of idiogenic osmoles can be a main cause of Contusion edema.
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Cerebral Contusion: a role model for lesion progression.
Progress in brain research, 2007Co-Authors: Tatsuro Kawamata, Yoichi KatayamaAbstract:The early massive edema caused by severe Cerebral Contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 h post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In this chapter, we review the results of our clinical studies regarding the pathophysiology of Contusion edema and evaluate the effects of surgical treatment, i.e. Contusion necrotomy, by analyzing the data from the Japan Neurotrauma Data Bank.
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Surgical management of early massive edema caused by Cerebral Contusion in head trauma patients.
Acta neurochirurgica. Supplement, 2006Co-Authors: Tatsuro Kawamata, Yoichi KatayamaAbstract:Early massive edema caused by severe Cerebral Contusion results in elevation of intracranial pressure (ICP) and clinical deterioration within 24–72 hours post-trauma. Previous studies indicate that cells in the central area of the Contusion undergo shrinkage, disintegration, and homogenization, whereas cellular swelling is predominant in the peripheral area, suggesting that early massive edema is attributable to high osmolality within necrotic brain tissue and may generate an osmotic potential across central and peripheral areas.
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Ultra-early study of edema formation in Cerebral Contusion using diffusion MRI and ADC mapping.
Acta neurochirurgica. Supplement, 2003Co-Authors: Takeshi Maeda, Y. Katayama, Tatsuro Kawamata, S. Koyama, J. SasakiAbstract:Objective Our previous studies have reported that heterogeneous mechanisms exist in early edema formation in Cerebral Contusion, and cytotoxic edema plays an important role within 48 hours posttrauma. It is remains unclear, when edema begins to develop following injury. In order to determine the time course of edema development, diffusion imaging and ADC (apparent diffusion coefficient) mapping was performed in 10 patients within 24 hours posttrauma with Cerebral Contusion.
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Edema fluid accumulation within necrotic brain tissue as a cause of the mass effect of Cerebral Contusion in head trauma patients.
Acta neurochirurgica. Supplement, 2003Co-Authors: Yoichi Katayama, Tatsuro KawamataAbstract:The early massive edema caused by severe Cerebral Contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24–72 hours post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In order to elucidate the mechanisms underlying the early massive edema, we have carried out a series of detailed clinical studies. Diffusion magnetic resonance (MR) imaging and apparent diffusion co-efficient (ADC) mapping suggest that cells in the central area of Contusion undergo shrinkage, disintegration and homogenization, whereas cellular swelling is predominant in the peripheral area during the period of 24–72 hours post-trauma. The ADC values in the central and peripheral areas are maximally dissociated during this period. A large amount of edema fluid accumulates within the necrotic brain tissue of the central area beginning at approximately 24 hours post-trauma. We have found that fluid-blood interface formation within the central area does not represent an uncommon finding in various neuroimaging examinations of Cerebral Contusions, indicating layering of red blood cells within the necrotic brain tissue accumulating voluminous edema fluid. Intravenous slow infusion of gadolinium-DTPA and delayed MR imaging revealed that the central area of Contusion can be enhanced at 24–48 hours posttrauma, implying that water supply from the blood vessels is not completely interrupted. Necrotic brain tissue sampled from the central area of Contusion during surgery demonstrates a very high osmolality. It appears that the capacitance for edema fluid accumulation increases in the central area, whereas cellular swelling in the peripheral area elevates the resistance for edema fluid propagation. Combination of these circumstances may facilitate edema fluid accumulation in the central area. We also suggest that the dissociation of ADC values and high osmolality within the necrotic brain tissue may generate an osmotic potential across the central and peripheral areas and contribute to the early massive edema caused by Cerebral Contusion.
S. Scott Lollis - One of the best experts on this subject based on the ideXlab platform.
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Outpatient follow-up of nonoperative Cerebral Contusion and traumatic subarachnoid hemorrhage: does repeat head CT alter clinical decision-making?
Journal of neurosurgery, 2014Co-Authors: Sebastian Rubino, Rifat A Zaman, Caleb R Sturge, Jessica G Fried, Atman Desai, Nathan E. Simmons, S. Scott LollisAbstract:Object Many neurosurgeons obtain repeat head CT at the first clinic follow-up visit for nonoperative Cerebral Contusion and traumatic subarachnoid hemorrhage (tSAH). The authors undertook a single-center, retrospective study to determine whether outpatient CT altered clinical decision-making. Methods The authors evaluated 173 consecutive adult patients admitted to their institution from April 2006 to August 2012 with an admission diagnosis of Cerebral Contusion or tSAH and at least 1 clinic follow-up visit with CT. Patients with epidural, subdural, aneurysmal subarachnoid, or intraventricular hemorrhage, and those who underwent craniotomy, were excluded. Patient charts were reviewed for new CT findings, new patient symptoms, and changes in treatment plan. Patients were stratified by neurological symptoms into 3 groups: 1) asymptomatic; 2) mild, nonspecific symptoms; and 3) significant symptoms. Mild, nonspecific symptoms included minor headaches, vertigo, fatigue, and mild difficulties with concentration,...
Lin Mengqiang - One of the best experts on this subject based on the ideXlab platform.
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perioperative application of large dose of mannitol and methylprednisolone for severe Cerebral Contusion and laceration combined with brain hernia patients
Chinese Journal of General Practice, 2013Co-Authors: Lin MengqiangAbstract:Objective To explore the therapeutic efficacy of perioperative large dose of mannitol and methylprednisolone on the control of intracranial pressure in severe Cerebral Contusion and laceration combined with brain hernia patients undergoing a large decompressive craniotomy(large bone flaps).Methods Thirty five patients with severe Cerebral Contusion and laceration combined brain hernia early received 20% mannitol 250-375 ml fast IV drip,followed by normal saline 100 ml + methylprednisolone 500 mg IV drip immediately,again 20% mannitol 250 ml fast IV drip(observation group).The first two application of mannitol was finished in 2 to 3 hours.The second IV drip of mannitol was perioperative used half an hour before the dural incision.Another 35 cases receiving 20% mannitol 250 ml fast IV drip were selected as control(control gorup).The therapeutic efficacy was compared between the two groups.Results In the observation group,the intracranial pressure was out of control only in 1 old patient due to malignant brain swelling,other cases got a well perioperative control in the intracranial pressure and prepared a good condition for the surgery.The routine perioperative fluid supplementation was performed to maintain effective circulation.The monitoring for kidney function did not find an acute renal failure case.The effect in the observation group was obviously superior to the control group,and the difference was significant.(P 0.01).Conclusion The perioperative large dose of mannitol and methylprednisolone for severe Cerebral Contusion and laceration merger brain hernia patients can effectively control the cranial pressure,create the timing of surgery,and avoid the occurrence of acute renal failure.