Role of hydrodynamic processes in the pathogenesis of peritumoral brain edema in meningiomas

2000 ◽  
Vol 93 (4) ◽  
pp. 594-604 ◽  
Author(s):  
Michael Bitzer ◽  
Thomas Nägele ◽  
Beverly Geist-Barth ◽  
Uwe Klose ◽  
Eckardt Grönewäller ◽  
...  
Keyword(s):  
Contrast Agent ◽  
Brain Edema ◽  
Brain Tissue ◽  
Magnetic Resonance Images ◽  
Content Type ◽  
Extracellular Contrast Agent ◽  
Peritumoral Brain Edema ◽  
Hydrodynamic Processes ◽  
Fine Print

Object. In a prospective study, 28 patients with 32 intracranial meningiomas were examined to determine the role of hydrodynamic interaction between tumor and surrounding brain tissue in the pathogenesis of peritumoral brain edema.Methods. Gadolinium—diethylenetriamine pentaacetic acid (Gd-DPTA), an extracellular contrast agent used for routine clinical imaging, remains strictly extracellular without crossing an intact blood—brain barrier. Therefore, it is well suited for investigations of hydrodynamic extracellular mechanisms in the development of brain edema. Spin-echo T1-weighted magnetic resonance images were acquired before and after intravenous administration of 0.2 mmol/kg Gd-DPTA. Additional T1-weighted imaging was performed 0.6, 3.5, and 6.5 hours later. No significant Gd-DPTA diffused from tumor into peritumoral brain tissue in 12 meningiomas without surrounding brain edema. In contrast, in 17 of 20 meningiomas with surrounding edema, contrast agent in peritumoral brain tissue was detectable after 3.5 hours and 6.5 hours. In three of 20 meningiomas with minimum surrounding edema (< 5 cm3), contrast agent effusion was absent. After 3.5 hours and 6.5 hours strong correlations of edema volume and the maximum distance of contrast spread from the tumor margin into adjacent brain parenchyma (r = 0.84 and r = 0.87, respectively, p < 0.0001) indicated faster effusion in larger areas of edema.Conclusions. The results of this study show that significant contrast agent effusion from the extracellular space of the tumor into the interstitium of the peritumoral brain tissue is only found in meningiomas with surrounding edema. This supports the hypothesis that hydrodynamic processes play an essential role in the pathogenesis of peritumoral brain edema in meningiomas.

Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients

2000 ◽  
Vol 93 (2) ◽  
pp. 183-193 ◽  
Author(s):  
Anthony Marmarou ◽  
Panos P. Fatouros ◽  
Pal Barzó ◽  
Gennarina Portella ◽  
Masaaki Yoshihara ◽  
...  
Keyword(s):  
Brain Edema ◽  
Brain Tissue ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Brain Swelling ◽  
Tissue Water ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The pathogenesis of traumatic brain swelling remains unclear. The generally held view is that brain swelling is caused primarily by vascular engorgement and that edema plays a relatively minor role in the swelling process. The goal of this study was to examine the roles of cerebral blood volume (CBV) and edema in traumatic brain swelling.Methods. Both brain-tissue water and CBV were measured in 76 head-injured patients, and the relative contribution of edema and blood to total brain swelling was determined. Comparable measures of brain-tissue water were obtained in 30 healthy volunteers and CBV in seven volunteers. Brain edema was measured using magnetic resonance imaging, implementing a new technique for accurate measurement of total tissue water. Measurements of CBV in a subgroup of 31 head-injured patients were based on consecutive measures of cerebral blood flow (CBF) obtained using stable xenon and calculation of mean transit time by dynamic computerized tomography scanning after a rapid bolus injection of iodinated contrast material. The mean (± standard deviation) percentage of swelling due to water was 9.37 ± 8.7%, whereas that due to blood was −0.8 ± 1.32%.Conclusions. The results of this study showed that brain edema is the major fluid component contributing to traumatic brain swelling. Moreover, CBV is reduced in proportion to CBF reduction following severe brain injury.

Effect of magnesium given 1 hour after head trauma on brain edema and neurological outcome

1996 ◽  
Vol 85 (1) ◽  
pp. 131-137 ◽  
Author(s):  
Zeev Feldman ◽  
Boris Gurevitch ◽  
Alan A. Artru ◽  
Arieh Oppenheim ◽  
Esther Shohami ◽  
...  
Keyword(s):  
Brain Edema ◽  
Brain Tissue ◽  
Head Trauma ◽  
Neurological Outcome ◽  
Edema Formation ◽  
Content Type ◽  
Standard Curve ◽  
Baseline Values ◽  
Brain Edema Formation ◽  
Fine Print

✓ Excitatory amino acids (EAA), mainly glutamate and aspartate, are released in excessive amounts from terminals of ischemic or traumatically injured neurons. These excessive levels of EAAs initiate a cascade of events believed to lead to secondary delayed damage to the surrounding brain. The N-methyl-d-aspartate receptor antagonists MK-801 and ketamine are reported to suppress excessive EAA release and to attenuate the development of focal brain edema following neuronal injury. Magnesium is also reported to work at the postsynaptic receptor to reduce the neurotoxic effect of glutamate. The present study was undertaken to examine the effect of postinjury treatment with Mg++ on brain edema and neurological outcome after traumatic brain injury. Sixty-nine rats that survived halothane anesthesia and closed head trauma (CHT) were randomly assigned to one of seven experimental groups: sham, CHT, and CHT with administration of Mg++ 1 hour postinjury. At 48 hours, brain tissue Mg++ concentration (calculated from optical density using a standard curve) was significantly increased compared to baseline levels (10.06 ± 2.44 mg/g vs. 6.83 ± 0.81 mg/g, p < 0.01 calculated by one-way analysis of variance). Also at 48 hours postinjury, brain tissue specific gravity in the contused hemisphere of Mg++-treated rats was significantly greater than that in the contused hemisphere of untreated rats, indicating attenuation of brain edema formation by Mg++. The neurological severity score (NSS) of rats treated with Mg++ improved significantly at both 18 and 48 hours, compared to baseline values obtained 1 hour after CHT but prior to administration of Mg++ (11.2 ± 2.5 vs. 15.2 ± 4.1, p = 0.03; and 12.3 ± 6.1 vs. 17.3 ± 3.6, p = 0.004, respectively). In the untreated groups, the NSS at 18 and 48 hours was not significantly different from baseline values (that is, no neurological improvement). The present study indicates that postinjury treatment with Mg++ attenuates brain edema formation and improves neurological outcome after experimental CHT.

Effects of tromethamine and hyperventilation on brain injury in the cat

1991 ◽  
Vol 74 (1) ◽  
pp. 87-96 ◽  
Author(s):  
Kazuo Yoshida ◽  
Anthony Marmarou
Keyword(s):  
Water Content ◽  
Brain Edema ◽  
Brain Tissue ◽  
Mr Spectroscopy ◽  
Content Type ◽  
Fluid Percussion Injury ◽  
Brain Ph ◽  
The Brain ◽  
Brain Lactate ◽  
Fine Print

✓ The metabolic brain acidosis after trauma has been thought to be harmful and to contribute to neurological deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore with magnetic resonance (MR) spectroscopy the metabolic changes in brain that occur with the use of hyperventilation, THAM (tromethamine; tris[hydroxymethyl]aminomethane), and a combination (THAM and hyperventilation) therapy in experimental fluid-percussion injury. Brain lactate, brain pH, inorganic phosphate (Pi), and adenosine triphosphate levels were measured by 1H and 31P MR spectroscopy. Arterial and cerebrovenous lactate and water content in brain tissue was determined in 29 cats using the specific gravimetric technique. Following injury, the phosphocreatine (PCr)/Pi ratio, which is an index of cerebral energy depletion, decreased to 76% in four untreated animals, to 79% in 11 THAM-treated animals, to 68% in seven animals receiving hyperventilation, and to 66% in seven animals with combination THAM and hyperventilation therapy. The PCr/Pi ratio returned to a normal level in 8 hours in animals treated with THAM and THAM in combination with hyperventilation. The brain lactate index increased to 157% in the hyperventilation group after trauma. In cats receiving THAM plus hyperventilation, the brain lactate index was reduced to 142%, while the minimum rise of 126% was associated with treatment of THAM alone. In the THAM-treatment and combination-treatment groups, the water content of the white and gray matter was significantly decreased compared with that in untreated cat brains. Prolonged hyperventilation provided relative ischemia in brain tissue and promoted more production of brain lactate, no recovery of the PCr/Pi ratio, and no decrease in brain edema. On the other hand, administration of THAM decreased production of brain lactate and brain edema and promoted the recovery of cerebral energy dysfunction. It was found that THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and that it also decreases brain edema. The authors conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

1999 ◽  
Vol 91 (3) ◽  
pp. 375-383 ◽  
Author(s):  
Ross E. Mantle ◽  
Boleslaw Lach ◽  
Mauricio R. Delgado ◽  
Salleh Baeesa ◽  
Gerard Bélanger
Keyword(s):  
Brain Edema ◽  
Computerized Tomography ◽  
Statistical Significance ◽  
Ct Scanning ◽  
Complete Resection ◽  
Content Type ◽  
Brain Invasion ◽  
Peritumoral Brain Edema ◽  
The Mean ◽  
Fine Print

Object. The goal of this study was to determine whether the quantity of peritumoral brain edema displayed on computerized tomography (CT) scanning could be correlated with brain invasion and subsequent recurrence of meningiomas.Methods. One hundred thirty-five patients who underwent resection of intracranial meningiomas at the Ottawa Civic Hospital were followed during the period 1980 to 1998. A complete resection was defined as one in which tumor, invaded bone, and involved dura were removed. Tumors were examined microscopically for evidence of brain invasion. The mean follow-up period was 9 ± 4 years (standard deviation [SD]) and the mean time to recurrence was 5 ± 4 years (SD). The authors used a simple grading system based on the average thickness (in centimeters) of edema seen on an axial CT slice showing the most tumor.Edema grade was linearly related to edema volume determined by digitizing the scans (r = 0.96; 29 cases). The chance of brain invasion increased by 20% for each centimeter of edema (rs = 1, p < 0.0001; 124 cases). The presence of brain invasion was predictive of recurrence after complete resection with an accuracy of 83%, a sensitivity of 89%, and a specificity of 82%. The chance of recurrence within 10 years after complete resection was given by the equation: percentage chance of recurrence = (centimeter of edema)3 × 0.7, which can be used to predict the chance of recurrence based on findings on CT scans (rs = 1, p < 0.0001; 86 patients). Statistical significance was confirmed using Kaplan—Meier and univariate and multivariate analyses. Completeness of resection was the most powerful predictor of recurrence (p < 0.00001, r = 0.6), followed by edema grade and brain invasion (both p = 0.02, r = 0.1). Patient age and gender and tumor location, size, and histological subtype were nonsignificant factors.Conclusions. Brain invasion causes peritumoral edema. Invaded brain tissue is also the source of residual cells in cases of tumor recurrence after gross-total resection.

scholarly journals Direct evidence for a key role of protein kinase C in the development of vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (4) ◽  
pp. 635-639 ◽  
Author(s):  
Shigeru Nishizawa ◽  
Nobukazu Nezu ◽  
Kenichi Uemura
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Direct Evidence ◽  
Control Group ◽  
Content Type ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Fine Print

✓ Vascular contraction is induced by the activation of intracellular contractile proteins mediated through signal transduction from the outside to the inside of cells. Protein kinase C plays a crucial role in this signal transduction. It is hypothesized that protein kinase C plays a causative part in the development of vasospasm after subarachnoid hemorrhage (SAH). To verify this directly, the authors measured protein kinase C activity in canine basilar arteries in an SAH model with (γ-32P)adenosine triphosphate and the data were compared to those in a control group. Protein kinase C is translocated to the membrane from the cytosol when it is activated, and the translocation is an index of the activation; thus, protein kinase C activity was measured both in the cytosol and in the membrane fractions. Protein kinase C activity in the membrane in the SAH model was remarkably enhanced compared to that in the control group. The percentage of membrane activity to the total was also significantly greater in the SAH vessels than in the control group, and the percentage of cytosol activity in the SAH group was decreased compared to that in the control arteries. The results indicate that protein kinase C in the vascular smooth muscle was translocated to the membrane from the cytosol and was activated when SAH occurred. It is concluded that this is direct evidence for a key role of protein kinase C in the development of vasospasm.

Long-term hearing preservation after surgery for vestibular schwannoma

2005 ◽  
Vol 102 (1) ◽  
pp. 6-9 ◽  
Author(s):  
Simone A. Betchen ◽  
Jane Walsh ◽  
Kalmon D. Post
Keyword(s):  
Hearing Preservation ◽  
Magnetic Resonance Images ◽  
Class I ◽  
Repeated Testing ◽  
Content Type ◽  
Factors Influencing ◽  
Long Term Preservation ◽  
Fine Print

Object. Vestibular schwannomas (VSs) are now amenable to resection with excellent hearing preservation rates. It remains unclear whether immediately postoperative hearing is a durable result and will not diminish over time. The aim of this study was to determine the rate of long-term preservation of functional hearing following surgery for a VS and to examine factors influencing hearing preservation. Methods. All patients eligible for hearing preservation (Gardner—Robertson Class I or II) who had undergone resection of a VS by a single surgeon were reviewed retrospectively. Follow-up audiograms and magnetic resonance images were obtained. Of 142 patients deemed eligible for hearing preservation surgery, 38 had immediate postoperative hearing confirmed by an audiogram. In these patients with preserved hearing, the audiographic results demonstrated functional hearing in 30 (85.7%) of 35 patients who underwent repeated testing at a mean follow-up time of 7 years. Delayed hearing loss occurred in five (14.3%) of the 35 patients and did not correlate significantly with the size of the tumor. Hearing improved one Gardner—Robertson class postoperatively in three (7.9%) of the 38 patients. Conclusions. Long-term functional hearing was maintained in 85.7% of patients when it was preserved immediately postoperatively and the result was independent of tumor size. The results of this study emphasize that long-term preservation of functional hearing is a realistic goal following VS surgery and should be attempted in all patients in whom preoperative hearing is determined to be Gardner—Robertson Class I or II.

Preliminary results of linear accelerator radiosurgery for acoustic schwannomas

1996 ◽  
Vol 85 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
William M. Mendenhall ◽  
William A. Friedman ◽  
John M. Buatti ◽  
Francis J. Bova
Keyword(s):  
Stereotactic Radiosurgery ◽  
Local Control ◽  
Linear Accelerator ◽  
Local Control Rate ◽  
Magnetic Resonance Images ◽  
High Rate ◽  
Content Type ◽  
Treatment Volume ◽  
Fine Print

✓ In this paper the authors evaluate the results of linear accelerator (LINAC)—based stereotactic radiosurgery for acoustic schwannomas. Fifty-six patients underwent LINAC-based stereotactic radiosurgery for acoustic schwannomas at the University of Florida between July 1988 and November 1994. Each patient was followed for a minimum of 1 year or until death; no patient was lost to follow up. One or more follow-up magnetic resonance images or computerized tomography scans were obtained in 52 of the 56 patients. Doses ranged between 10 and 22.5 Gy with 69.6% of patients receiving 12.5 to 15 Gy. Thirty-eight patients (68%) were treated with one isocenter and the dose was specified to the 80% isodose line in 71% of patients. Fifty-five patients (98%) achieved local control after treatment. The 5-year actuarial local control rate was 95%. At the time of analysis, 48 patients were alive and free of disease, seven had died of intercurrent disease, and one was alive with disease. Complications developed in 13 patients (23%). The likelihood of complications was related to the dose and treatment volume: 10 to 12.5 Gy to all volumes, three (13%) of 23 patients; 15 to 17.5 Gy to 5.5 cm3 or less, two (9%) of 23 patients; 15 to 17.5 Gy to more than 5.5 cm3, five (71%) of seven patients; and 20 to 22.5 Gy to all volumes, three (100%) of three patients. Linear accelerator—based stereotactic radiosurgery results in a high rate of local control at 5 years. The risk of complications is related to the dose and treatment volume.

Incidence of silent hemorrhage and delayed deterioration after stereotactic brain biopsy

1998 ◽  
Vol 89 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Abhaya V. Kulkarni ◽  
Abhijit Guha ◽  
Andres Lozano ◽  
Mark Bernstein
Keyword(s):  
Ct Scan ◽  
Neurological Deficit ◽  
Stereotactic Biopsy ◽  
Brain Biopsy ◽  
Ct Scanning ◽  
Ct Scans ◽  
Stereotactic Brain Biopsy ◽  
Content Type ◽  
Fine Print

Object. Many neurosurgeons routinely obtain computerized tomography (CT) scans to rule out hemorrhage in patients after stereotactic procedures. In the present prospective study, the authors investigated the rate of silent hemorrhage and delayed deterioration after stereotactic biopsy sampling and the role of postbiopsy CT scanning. Methods. A subset of patients (the last 102 of approximately 800 patients) who underwent stereotactic brain biopsies at the Toronto Hospital prospectively underwent routine postoperative CT scanning within hours of the biopsy procedure. Their medical charts and CT scans were then reviewed. A postoperative CT scan was obtained in 102 patients (aged 17–87 years) who underwent stereotactic biopsy between June 1994 and September 1996. Sixty-one patients (59.8%) exhibited hemorrhages, mostly intracerebral (54.9%), on the immediate postoperative scan. Only six of these patients were clinically suspected to have suffered a hemorrhage based on immediate postoperative neurological deficit; in the remaining 55 (53.9%) of 102 patients, the hemorrhage was clinically silent and unsuspected. Among the clinically silent intracerebral hemorrhages, 22 measured less than 5 mm, 20 between 5 and 10 mm, five between 10 and 30 mm, and four between 30 and 40 mm. Of the 55 patients with clinically silent hemorrhages, only three demonstrated a delayed neurological deficit (one case of seizure and two cases of progressive loss of consciousness) and these all occurred within the first 2 postoperative days. Of the neurologically well patients in whom no hemorrhage was demonstrated on initial postoperative CT scan, none experienced delayed deterioration. Conclusions. Clinically silent hemorrhage after stereotactic biopsy is very common. However, the authors did not find that knowledge of its existence ultimately affected individual patient management or outcome. The authors, therefore, suggest that the most important role of postoperative CT scanning is to screen for those neurologically well patients with no hemorrhage. These patients could safely be discharged on the same day they underwent biopsy.

Deflation of metrizamide-filled balloon used to occlude a carotid-cavernous fistula

1983 ◽  
Vol 59 (3) ◽  
pp. 524-528 ◽  
Author(s):  
Thomas J. Leipzig ◽  
Sean F. Mullan
Keyword(s):  
Contrast Agent ◽  
Vascular Wall ◽  
Carotid Cavernous Fistula ◽  
Technical Problems ◽  
Content Type ◽  
Cavernous Fistula ◽  
Short Summary ◽  
Carotid Cavernous Fistulas ◽  
Fine Print

✓ A carotid-cavernous fistula was occluded by a detachable latex balloon. Because of technical problems, the contrast-filled balloon was left in a precarious position in the ostium of the fistula. Premature deflation of the balloon would have resulted in intra-arterial migration of the device. Approximately 1 week is required for the balloon to become secured in place by fibrous attachment to the vascular wall. For success, if the ligature is adequate, a detachable Debrun balloon should remain inflated for this period of time. The deflation process was monitored radiographically in this patient. The balloon remained inflated for at least 2 weeks. A short summary of the experience with deflation of various contrast-containing balloon devices in the treatment of carotid-cavernous fistulas is given. Metrizamide may be the best contrast agent for use in these devices.

Complement activation in the brain after experimental intracerebral hemorrhage

2000 ◽  
Vol 92 (6) ◽  
pp. 1016-1022 ◽  
Author(s):  
Ya Hua ◽  
Guohua Xi ◽  
Richard F. Keep ◽  
Julian T. Hoff
Keyword(s):  
Brain Edema ◽  
Complement Activation ◽  
Autologous Blood ◽  
Complement Cascade ◽  
Edema Formation ◽  
Content Type ◽  
Erythrocyte Lysis ◽  
The Brain ◽  
Brain Edema Formation ◽  
Fine Print

Object. Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related to erythrocyte lysis and hemoglobin release. Erythrocyte lysis may be mediated by the complement cascade, which then triggers parenchymal injury. In this study the authors examine whether the complement cascade is activated after ICH and whether inhibition of complement attenuates brain edema around the hematoma.Methods. This study was divided into three parts. In the first part, 100 µl of autologous blood was infused into the rats' right basal ganglia, and the animals were killed at 24 and 72 hours after intracerebral infusion. Their brains were tested for complement factors C9, C3d, and clusterin (a naturally occurring complement inhibitor) by using immunohistochemical analysis. In the second part of the study, the rats were killed at 24 or 72 hours after injection of 100 µl of blood. The C9 and clusterin proteins were quantitated using Western blot analysis. In the third part, the rats received either 100 µl of blood or 100 µl of blood plus 10 µg of N-acetylheparin (a complement activation inhibitor). Then they were killed 24 or 72 hours later for measurement of brain water and ion contents. It was demonstrated on Western blot analysis that there had been a sixfold increase in C9 around the hematoma 24 hours after the infusion of 100 µl of autologous blood. Marked perihematomal C9 immunoreactivity was detected at 72 hours. Clusterin also increased after ICH and was expressed in neurons 72 hours later. The addition of N-acetylheparin significantly reduced brain edema formation in the ipsilateral basal ganglia at 24 hours (78.5 ± 0.5% compared with 81.6 ± 0.8% in control animals, p < 0.001) and at 72 hours (80.9 ± 2.2% compared with 83.6 ± 0.9% in control animals, p < 0.05) after ICH.Conclusions. It was found that ICH causes complement activation in the brain. Activation of complement and the formation of membrane attack complex contributes to brain edema formation after ICH. Blocking the complement cascade could be an important step in the therapy for ICH.

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