PURPOSE: Peritumoral brain edema (PTBE) is a serious causative factor that contributes the morbidity or mortality of brain tumors. The development of PTBE is influenced by many factors, including such tight junction proteins as occludin. We evaluated the PTBE volume and survival time with respect to the occludin expression in various pathological types of brain tumors. MATERIALS AND METHODS: Fresh-frozen specimens from sixty patients who had brain tumors were obtained during surgery and the tumors were confirmed pathologically. The occludin expression was investigated by Western blot analysis. The PTBE volume was measured by using preoperative magnetic resonance (MR) imaging, and the survival time in each patient was estimated retrospectively. RESULTS: Occludin was detected in 41 (68.3%) of the cases with brain tumors and it was not expressed in the other 19 (31.7%) cases. Although the lowest expression was revealed in high-grade gliomas, its expression was variable according to the pathology of the brain tumors (p>0.05). The difference of PTBE volume between occludin-positive and negative brain tumors was statistically significant (2072.46+/-328.73 mm3 vs. 7452.42+/-1504.19 mm3, respectively, p=0.002). The mean survival time was longer in the occludin-positive tumor group than in the occludin-negative group (38.63+/-1.57 months vs. 26.16+/-3.83 months, respectively; p=0.016). CONCLUSIONS: This study suggests that the occludin expression is highly correlated to the development of PTBE in brain tumors and it might be a prognostic indicator for patient survival.
Blotting, Western ; Brain Edema ; Brain Neoplasms* ; Brain* ; Edema* ; Glioma ; Humans ; Mortality ; Occludin* ; Pathology ; Retrospective Studies ; Survival Rate ; Tight Junction Proteins

Severe ischemic stroke carries a high rate of disability and death. The severity of stroke is often assessed by the degree of neurological deficits or the extent of brain infarct, defined as severe stroke and large infarction, respectively. Critically severe stroke is a life-threatening condition that requires neurocritical care or neurosurgical intervention, which includes stroke with malignant brain edema, a leading cause of death during the acute phase, and stroke with severe complications of other vital systems. Early prediction of high-risk patients with critically severe stroke would inform early prevention and treatment to interrupt the malignant course to fatal status. Selected patients with severe stroke could benefit from intravenous thrombolysis and endovascular treatment in improving functional outcome. There is insufficient evidence to inform dual antiplatelet therapy and the timing of anticoagulation initiation after severe stroke. Decompressive hemicraniectomy (DHC) <48 h improves survival in patients aged <60 years with large hemispheric infarction. Studies are ongoing to provide evidence to inform more precise prediction of malignant brain edema, optimal indications for acute reperfusion therapies and neurosurgery, and the individualized management of complications and secondary prevention. We present an evidence-based review for severe ischemic stroke, with the aims of proposing operational definitions, emphasizing the importance of early prediction and prevention of the evolution to critically severe status, summarizing specialized treatment for severe stroke, and proposing directions for future research.
Humans ; Ischemic Stroke/pathology* ; Brain Edema/surgery* ; Stroke/prevention & control* ; Brain/pathology* ; Brain Infarction/pathology* ; Treatment Outcome

So a considerable amount of work on the cerebral edema has been done by numerous investigator hat it is difficult to summarize the research works of cerebral edema on this paper. Cerebral edema is a well-recognized clinical entity. It was also quite obvious around many cerebral tumors and injured brains of the post-mortem materials. Further, in 1937, Stewart-Wallace considered that the fluid increase of the cerebral edema was in the intercellular or interstitial space. This was accepted by histologic using the light microscope and biochemists for the next two decades. Since 1957 electron microscope has been used to study, the concept of cerebral edema has been changes. So the author selected and introduced the following experimental studies and their occlusions from number of different clinical and experimental research works of cerebral edema that have been carried out since 1957. 1) Cold induced cerebral edema. 2) Experimental cerebral swelling produced by supratentorial extradural compression (implanted balloons). 3) Triethyltin-induced cerebral edema. 4) Cerebral edema due to implantation of foreign substances. 5) Cerebral edema associated with experimental intracerebal tumors. 6) Experimental ischemic brain swelling and experimental intracranial hypertension due toe vascular blockade. 7) Ouabeininduced cerebral edema. 8) Serotonin-induced cerebral edema. 9) Cerebral edema due to radiofrequency lesion. 10) The effect of laser irradiation. By these experimental cerebral edema numerous conclusions were reported, but the important results were as follows: 1) In the cortex there is enlargement of astrocytes. 2) Axonal and myeline changes occur. 3) Ultrastuructural studies indicate that edema was entirely intracellular. 4) Basically cerebral edema is an extracellular phenomenon of the white matter accompanied by marked swelling of the astrocytes. 5) An increase in water and sodium and decrease in potassium content of white matter, resulting in a sharp rise of Na: K ratio is evident. 6) Radioactive amino acid incorporation into protein of edematous brain is increased. 7) The depressed respiratory control, depressed P:O radio and accelerated state 4 respiration are present. Moreover, it has become apparent that these are some disadvantages in the experimentally induced cerebral edema. It may not involve the entire brain uniformly: different agents produce different types of edema; patterns are subject to variations of animal species and cerebral topography; the extent of damage is not controllable and reproducible; consistency of damage is uncertain no all experimental edema are artificial and not completely analogous to those occurring in human pathology. Nonetheless, cold induced edema and extradural compression method can be considered as a prototype of traumatic brain swelling. And the experimental intracerebral tumors can be exact counterparts in human pathology also. The laser irradiation and radio frequency lesion can produce standardized lesion and edema, further they will be appreciable to study the efficacy of various agents in reducing intracranial damage and edema.
Animals ; Astrocytes ; Axons ; Brain ; Brain Edema* ; Edema ; Humans ; Intracranial Hypertension ; Myelin Sheath ; Pathology ; Potassium ; Research Personnel ; Respiration ; Sodium ; Toes ; Water

OBJECTIVETo investigate the influence of therapeutic bloodletting at Jing-well points and hypothermia on acute cerebral edema after traumatic brain injury (TBI) in rats.

METHODSSeventy-five SD rats were randomly divided into sham-operation group (Sham), TBI group (TBI), bloodletting group (BL), mild-induced hypothermia group (MIH), and bloodletting plus MIH group (BL + MIH) (n = 15). The model of TBI was established by electric controlled cortical impactor (eCCI). The rats of BL group were bloodletting at Jing-well points immediately after injury, twice daily. While the MIH group was settled on a hypothermia blanket promptly after TBI for 6 hours, so that the temperature dropped to 32 degrees. Each of measurement was performed after 48 hours. Magnetic resonance imaging (MRI) was used to evaluate the dynamic impairment of cerebral edema after TBI (n = 3). In addition, mNSS score, measurements of wet and dry brain weight, and Evans Blue assay were performed to investigate the neurologic deficit, cerebral water content (n = 8), and blood-brain barrier permeability (BBB), (n = 4), respectively.

RESULTSMRI analysis showed that the cerebral edema, hematoma and midline shifting of rats in TBI group was more serious than other treatment group. Meanwhile compared with TBI group, the mNSS scores of every treatment group were meaningfully lower (all P < 0.05). Furthermore, treatment with BL+ MIH group was superior to the separated BL and MIH group (all P < 0.01). In addition, brain water content of each intervention group reduced to varying degrees (all P < 0.05), especially that of MIH group and BL + MIH group (P <0.01). BBB permeability of each treatment group was also significantly improved (all P < 0.01), and the improvement in MIH group and BL + MIH group was much better than the BL alone group (P < 0.05, P < 0.01).

CONCLUSIONOur major finding is that bloodletting at Jing-well points and MIH can reduce cerebral edema and BBB dysfunction and exert neuroprotective effects after TBI. The results suggest that the combination of BL and MIH is more effective than other treatment being used alone.

Animals ; Blood-Brain Barrier ; Bloodletting ; Brain ; pathology ; Brain Edema ; prevention & control ; Brain Injuries ; therapy ; Hypothermia, Induced ; Rats ; Rats, Sprague-Dawley

The authors analyzed the clinical and pathological characteristics of 66 meningioma patients, operated and pathologically confirmed at the Department of Neurosurgery > Pathology, Yeungnam University Hospital from 1984 to 1992. The results are as follows: 1) Meningioma was the most common in the 6th decase(39.4%) and the overall ratio of male to female was 1:2.5. 2) The most common pathologic types were meningothelial type(30.3%) and transitional type(30.3%). 3) The predilection sites were convexity, parasagittal and falx in order of frequency. 4) The most common clinical features were IICP signs(57.6%). 5) The marginal contour of the tumor on brain CT wre more irregular, mushrooming and fringing pattern in the case of angioblastic and atypical type. The brain edema was more severe in the case of these types. However, these findings had no correlation with prognosis. 6) Thre were 9 atypical cases(13.6%). 7) The total removal was done in 53 cases(80.3%) and the postoperative mortality rate was 7.5%. 8) The recurrence rate was 9.0% and the mean duration of recurrence was 36.5 months. The recurrence depended on grade of the surgical removal rather than the pathological type.
Agaricales ; Brain ; Brain Edema ; Female ; Humans ; Male ; Meningioma* ; Mortality ; Neurosurgery ; Pathology ; Prognosis ; Recurrence

OBJECTIVETo establish a new macrophotographic measurement of brain surface area to evaluate brain edema after focal cerebral ischemia in mice.

METHODSPermanent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in mice. The brains were removed 10,30 min,1,3,6,12 and 24 h after MCAO, and photographed in dorsal and lateral views by a digital camera. Then, 6 coronal slices of 1 mm thick were cut and photographed. Finally, the water content of brain tissue was measured by heating at 110 degrees C for 24 h. The left and right hemisphere areas of the brains and the brain slices were analyzed and calculated by MedBrain 2 imaging analyzer to evaluate brain edema.

RESULTThe macrophotographic measurement showed that the ischemic hemisphere areas significantly increased from 1 h after focal cerebral ischmia, which was similar to the measurement of water content. This measurement for brain edema correlated well with those of water content and brain slice volume.

CONCLUSIONThe macrophotographic measurement is an objective and quantitative method for evaluating brain edema after focal cerebral ischemia.

Animals ; Brain Edema ; diagnosis ; pathology ; Brain Ischemia ; complications ; psychology ; Female ; Mice ; Mice, Inbred ICR ; Photography

It is the intent of this study to estimate the progression or regression of edema at the bedside continuously. Based on the theoretic model, the Adaptive Genetic Algorithm (AGA) has been applied in the calculation of conductivity reconstruction. Dynamic crossover and mutation operators which are based on Haiming Distance are brought forward in this paper to maintain generation's diversity. Then, both AGA and Standard GA (SGA) have been applied in the conductivity reconstruction of edema in human brain. It is shown that AGA not only has attained a higher degree of efficiency but also has enhanced the capability to converge to the best answer.
Algorithms ; Brain Injuries ; complications ; pathology ; Computer Simulation ; Edema ; pathology ; Electric Impedance ; Humans ; Models, Biological

OBJECTIVETo assess the morphologic changes in traumatic cerebral infarction and to discuss its mechanism.

METHODSSpecimens from seventeen cases of cerebral infarction were selected from 81 patients with severe brain injury, and subject to routine gross and histological examinations.

RESULTS(1) The cerebral infarction in all cases was hemorrhagic in nature with a wedged or irregular shape upon gross inspection. The lesions were found in occipital gyrus (8 cases), occipital lobes (3 cases), basal nuclei (3 cases), cingulate gyrus (2 cases), and lateral occipitotemporal gyrus (1 case). Histologically, the lesions were located at the junction between the cortex and medulla, showing congestion, edema, hemorrhage, necrotic nerve tissue and blood vessels. In severe cases, the lesion extended into the entire cortex and subarachnoid spaces. (2) Swelling of the brain and cerebral hernia were found in all cases, 8 of which demonstrated that the posterior cerebral artery was compressed and stenotic within the space between the crus cerebri and uncus.

CONCLUSIONBrain tissue necrosis in traumatic cerebral infarction is the result of brain swelling and cerebral hernia formation, following congestion, bleeding and ischemia due to vasculature compression.

Adolescent ; Adult ; Brain ; pathology ; Brain Edema ; complications ; Cerebral Infarction ; etiology ; pathology ; Craniocerebral Trauma ; complications ; Encephalocele ; complications ; Female ; Humans ; Male

BACKGROUNDThe dialysis disequilibrium syndrome is characterized by neurologic deterioration and cerebral edema which occurs after hemodialysis. The purpose of this study was to investigate the pathogenesis of acute cerebral and pulmonary edema induced by hemodialysis.

METHODSWe evaluated the effects of hemodialysis on the biochemical and hemodynamic parameters of the plasma and cerebrospinal fluid, including the intracranial pressure, dry/wet ratio, and pulmonary edema index, and we also examined the pathological changes of the brain and lung tissue in dogs suffering from uremia.

RESULTSSeventy-two hours after bilateral ureteral ligation, 10 uremic dogs were hemodialyzed for 2 hours, yielding a 73.6% and 60.1% decrease in the plasma urea and creatinine, respectively, a decrease in the plasma osmolality from (359 +/- 18) mOsm/kg H(2)O to (304 +/- 6) mOsm/kg H(2)O (P < 0.01), a decrease in the dry/wet ratio of the lung and brain tissue, and an increase in the hemodynamic parameters (right atrial pressure, right ventricular pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and central venous pressure), intracranial pressure, total pulmonary resistance index, and pulmonary edema index. Moreover, the pathological examination revealed lung and brain edema in the dialyzed dogs. This group was compared to 3 control groups: 6 uremic dogs which were sham dialyzed without dialysate so that no fall in the plasma urea occurred, and 12 uremic and 12 nonuremic animals that were not dialyzed. However, the parameters mentioned above were not significantly changed among these 3 control groups.

CONCLUSIONSThe acute brain and lung edema in our model appeared to be primarily due to a large osmotic gradient between the plasma and the brain and lung. This is the "urea reverse effect" which promoted the osmotically-induced lung and brain swelling.

Acute Disease ; Animals ; Brain ; pathology ; Brain Edema ; etiology ; Dogs ; Intracranial Pressure ; Lung ; pathology ; Pulmonary Edema ; etiology ; Radiography, Thoracic ; Renal Dialysis ; adverse effects ; Urea ; metabolism

OBJECTIVETo study the clinicopathologic features of fatal enterovirus 71 (EV71) infection.

METHODSAutopsy was performed in 5 neonates died of EV71 infection. Tissue samples from major organs were collected, formalin-fixed and examined under light microscopy. Immunohistochemical study was carried out in selected examples.

RESULTSFour of the 5 cases showed predominant changes in central nervous system, with encephalitis and encephalomyelitis identified mainly in brainstem and upper cervical spinal cord. Histologic findings included neuronal degeneration and necrosis, neuronophagia, perivascular cuffing and diffuse or nodular hyperplasia of macrophages/microglia. Cerebral edema, brain herniation and aseptic meningitis were also noted. The lungs showed mainly pulmonary congestion, neurogenic pulmonary edema and focal hemorrhage. There were minimal changes in the intestinal epithelium. The intestinal lymphoid tissue however was hyperplastic and associated with apoptosis of follicular center cells. The remaining case had cerebral edema and mild meningitis. The lung alveolar septa were thickened with lymphocytic infiltrates. Some alveolar cells were hyperplastic and associated with diffuse hyaline membrane formation. No specific abnormalities were identified in gastrointestinal tract. In all the 5 cases studied, there was enlargement of lung hilar and mesenteric lymph nodes, coupled with apoptosis of follicular center cells. In general, no significant pathologic changes were demonstrated in heart, liver and kidneys.

CONCLUSIONSIn fatal EV71 infection, the major pathologic changes lie in the central nervous system. The pulmonary lesions are mainly secondary in nature. The usual cause of death is cerebral edema complicated by brain herniation and pulmonary edema. It is also noteworthy that some cases show only lung damages, without classic neurologic changes.

Autopsy ; Brain Edema ; etiology ; pathology ; Brain Stem ; pathology ; Child, Preschool ; Encephalitis, Viral ; etiology ; pathology ; Encephalomyelitis ; etiology ; pathology ; Enterovirus A, Human ; isolation & purification ; Enterovirus Infections ; complications ; pathology ; virology ; Female ; Humans ; Infant ; Male ; Pulmonary Edema ; etiology ; pathology ; Spinal Cord ; pathology