A Fatal Case of Valproic Acid-Induced Cerebral Edema
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Valproic Acid
Cerebral edema
Brain Edema
Objective: Prediction of delayed brain edema after spontaneous intracerebral hemorrhage by magnetic resonance spectroscopy combined with diffusion weighted imaging, and to explore the causes and treatment of delayed brain edema after intracerebral hemorrhage. Methods: The patients with spontaneous cerebral hemorrhage diagnosed by CT from January 2015 to June 2018 in our hospital were analyzed. Magnetic resonance spectroscopy and diffusion weighted imaging examinations were performed on the third day after hemorrhage. It was diagnosed as delayed brain edema that the edema range enlarged more than 1 cm in CT scan on the 14th day Compare with the 7th Day. The patients were divided into the delayed brain edema group and the control group(n=27 for each). The NAA/Cr value and rADC value of the edema area in the two groups were analyzed by T test. Results: The NAA/Cr value (1.67±0.38) in the edema area of patients with delayed brain edema was significantly decreased Compare with the control group(1.92±0.42), and the rADC value (2.59±0.42) reduced significantly Compare with the control group (2.93±0.51), the differences were statistically significant (P<0.05). Conclusion: MRS and DWI were susceptive in showing delayed brain edema lesions at hyper-early phase. Combination of MRS and DWI can provide a basis for clinical individual treatment programs selection and prognostic evaluation.目的： 通过磁共振波谱成像联合弥散加权成像技术预测自发性脑出血后迟发性脑水肿的发生，并探讨该病的发生原因及防治措施。 方法： 对湖州市第一人民医院2015年1月至2018年6月收治的头颅CT提示为自发性脑出血的患者进行分析。入院后第3天常规行MRS及DWI检查，动态CT证实14 d内脑内血肿周围水肿较7 d水肿周边直径增大1 cm以上诊断为迟发性脑水肿，设为观察组（27例），未并发迟发性脑水肿的脑出血患者设为对照组（27例），对两组患者水肿区域NAA/Cr值以及rADC值进行统计分析。 结果： 自发性脑出血迟发性水肿患者水肿区域NAA/Cr值（1.67±0.38）较对照组NAA/Cr值（1.92±0.42）明显降低，rADC值（2.59±0.42）较对照组rADC值（2.93±0.51）明显降低，差异均有统计学意义（均P<0.05）。 结论： 通过MRS的脑水肿区域NAA/Cr比值以及DWI检查的rADC值的统计差异变化，可以指导预判自发性脑出血后迟发性脑水肿的发生，更具客观性及科学性。.
Brain Edema
Cerebral edema
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Objective To study the effect of dynamic expression at different time points of metallo proteinase-9 on brain edema after cerebral hemorrhage. Methods Serum levels of MMP-9 in 90 patients with brain hemorrhage and 80 normal patients were detected by radioimmunoassay on 24 h、72 h、7 d and 14 d.The relationship between levels of MMP-9 and brain edema after cerebral hemorrhage.Results Brain edema went up to the peak at 72 h and slowly decline after it. At 24 h, the serum level of MMP-9 were significantly higher, and reached the peak at 72 h according to the peak of cerebral edema, and then decreased significantly after 7 d. Cerebral hemorrhage group compared with the control group were significantly higher(P＜0.01). The level of MMP-9 close to normal levels on 14 d. MMP-9 was positive correlated with edema volume and edema ratioat 24 h and 72 h (P=0.01).Conclusions Serum MMP-9 dynamic changes over time after cerebral hemorrhage. The level of MMP-9 was correlated with the brain edema volume and had more stronger correlation with relative size of brain edema. MMP-9 was correlated with inflammation after cerebral hemorrhage.
Key words:
Cerebral hemorrhage; Brain edema; Matrix metallo proteinases-9
Brain Edema
Cerebral edema
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Cerebral edema contributes significantly to the morbidity and mortality associated with many common neurologic conditions. Clinically, a diagnostic tool that can be used to monitor cerebral edema in real-time and differentiate between different types of cerebral edema is urgently needed. Because there are differences in electrical impedance between normal cortical tissue and cerebral edema tissue, electrical impedance tomography (EIT) can potentially be used to detect cerebral edema. Accurate recording of the electrical impedance properties of cerebral edema tissue at different time points is important when detecting cerebral edema with EIT. In this study, a rat cerebral edema model was established; then, following the onset of ischemic brain injury, variation in the electrical impedance of cerebral edema was measured at different time points within a 24-hour period and the corresponding morphologic variation was analyzed. After the first six hours, following the onset of ischemic brain injury, the resistivity of brain tissue increased (p < 0.05); during this period, brain cell volume increased (p < 0.05) and the intercellular space decreased (p < 0.05) (behaving like cytotoxic cerebral edema). From 6 to 24 hours, the resistivity of brain tissue decreased; during this time, brain cell volume unchanged (p > 0.05) while intercellular space increased (p < 0.05) (behaving like vasogenic cerebral edema). These findings support the notion that EIT can be used to monitor the development of cerebral edema in real-time and differentiate between different types of brain edema.
Cerebral edema
Brain tissue
Brain Edema
Electrical Impedance Tomography
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Cerebral edema is a frequent and challenging problem in the clinical setting and is a major cause of morbidity and mortality in patients with acute brain injury. It is simply defined as an increase in brain water content (normal brain water content is approximately 80%) and is invariably a consequence of a primary brain insult. Etiologies of these neurologic injuries that cause cerebral edema are diverse and commonly include:
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Cerebral edema
Etiology
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Brain Edema
Brain swelling
Cerebral edema
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Although meningiomas are known to cause varying degrees of cerebral edema, the relative importance of their location, size, histological subtype, and other histological features in the production of cerebral edema has not been studied adequately. Therefore, we undertook a retrospective analysis of 43 meningiomas excised between 1975 and 1980. The results indicate that histological subtype has no relationship to the production of cerebral edema, with one exception. Meningiomas containing partly or completely a hemangiopericytic component were the only histological subtype associated consistently with cerebral edema. The location of a meningioma per se may not determine the production of cerebral edema. A relationship between size, aggressive histological features, vascular proliferative changes, and the production of cerebral edema was seen. The need for and the nature of further studies required to explain the cerebral edema that may be associated with small meningiomas are discussed.
Cerebral edema
Brain Edema
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Although meningiomas are known to cause varying degrees of cerebral edema, the relative importance of their location, size, histological subtype, and other histological features in the production of cerebral edema has not been studied adequately. Therefore, we undertook a retrospective analysis of 43 meningiomas excised between 1975 and 1980. The results indicate that histological subtype has no relationship to the production of cerebral edema, with one exception. Meningiomas containing partly or completely a hemangiopericytic component were the only histological subtype associated consistently with cerebral edema. The location of a meningioma per se may not determine the production of cerebral edema. A relationship between size, aggressive histological features, vascular proliferative changes, and the production of cerebral edema was seen. The need for and the nature of further studies required to explain the cerebral edema that may be associated with small meningiomas are discussed. (Neurosurgery 8:428-433, 1981)
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Objective To explore the evolving and vanishing time of brain edema after contusion and laceration in order to provide the guidance for clinically treating the brain edema. Methods The brain edma were judged according to a CT scan at least every 3 days in 174 patients with cerebral contusion and laceration. The change in the brain edema with the lapse of time were re-corded and analyzed. Results The brain edema in all the patients reached to the peak in 3 days after trauma, but the time of the brain edema peak was different among the patients. The peak of the brain edema lasted 3～5 days in 7 patients, 6～8 days in 34, 9～11 days in 112 and more than 12 days in 21. The time of the brain edema peak were significantly associated with the severity of trauma and brain edema. Conclusion The time of the brain edema peak revealed by the present study were longer than that we knew before in most of the patients with cerebral contusion and laceration; therefore the dehydrating agents should be longer administered and carefully selected according to their condition in the patients with cerebral injury, especially in one with severe brain contusion and laceration.
Brain Contusion
Brain Edema
Cerebral contusion
Cerebral edema
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Brain Edema
Etiology
Brain tumor
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Secondary cerebral edema is no less significant than direct injury of the brain parenchyma as a factor to markedly aggravate the prognosis of cerebrovascular disturbance. Accordingly, theorapeutic measures for cerebral edema are very important.For the purpose of studying the anti-cerebral edema effect of dexamethasone, we had cerebral hemorrhage induced experimentally in rabbit and studied the occurrence of cerebral edema, effect of dexamethasone administration on it and the method of administration. Experimental animals used were 197 male rabbits weighing 2.4-2.6 kg about 12 weeks after birth.Experimental lesion of cerebral hemorrhage was prepared by the cold injury method according to Klatzo's method.In order to examine the course of cerebral edema in the acute phase of cerebral hemorrhage, the animals were decapitated on a time-course basis after cold injury ; the brain was taken out and divided into the injured part and intact part ; the brain was dried with a vacuum freezedrier ; the brain weight before and after drying was measured with a chemical balance and the water content of the brain was calculated.The RISA transfer rate was also measured on a tune course basis so as to find the conditions of the blood-brain barrier of the impaired brain which plays an important role in the occurrence of cerebral edema.After cold injury, dexamethasone in doses of 0.4 mg/kg/day and 2 mg/kgiday was administered for three days ; the water content of the brain and RISA transfer rate were measured, and a comparative study was made of the administration group and the non-administration group. The period of administration was set at 1 day, 2 days, 3 days, 4 days and 7 days. On these five groups of administration, measurement was made of the water content of the brain one day after and three days after the final day of administration, results of which are as follows.1) Experimentally, the cerebral edema observable in the acute phase of cerebral hemorrhage began to appear six hours after the onset of the disease and reached a peak 12 to 48 hours after.2) A large-dose administration of dexamethasone had an inhibitory effect on cerebral edema incidental to cerebral hemorrhage. Administration for three to four days was free of rebound phenomenon and appeared to be appropriate as the period of administration.
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