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At least 595 records · Page 33Linked to original sources
PubMed2004

Multiphasic helical computed tomography predicts subsequent development of severe brain edema in acute ischemic stroke.

OBJECTIVE: To evaluate the use of multiphasic helical computed tomography (CT) in predicting subsequent development of severe brain edema in patients with acute middle cerebral artery (MCA) stroke. DESIGN: Case-control study. SETTING: Tertiary referral hospital. PATIENTS: We studied 31 patients with acute MCA stroke who had a baseline National Institutes of Health Stroke Scale score of 15 or higher within 6 hours of symptom onset. Sequential 4-phasic enhanced helical CT scans were performed after taking precontrast CT scans. The severity of perfusion deficit was graded as "severe" or "moderate" depending on collateral blood flow. MAIN OUTCOME MEASURES: Patients were classified as having severe brain edema if they showed signs of uncal herniation or deterioration with mass effect leading to hemicraniectomy. RESULTS: Severe brain edema developed in 10 patients (32%). Severe perfusion deficit greater than 50% of the presumed MCA territory on multiphasic helical CT was more often found in patients with severe brain edema than in those without (8 of 10 vs 4 of 21, P =.002). In contrast, parenchymal hypodensity greater than 50% on precontrast CT was observed only in 5 patients with severe brain edema (5 of 10 vs 4 of 21, P =.10). Additional involvement of the anterior or posterior cerebral artery territory was found on multiphasic CT (6 of 10 vs 0 of 21, P <.001) and on precontrast CT (4 of 10 vs 0 of 21, P =.007) only in patients with severe brain edema. CONCLUSION: Multiphasic helical CT is more useful than precontrast CT for predicting subsequent severe brain edema in acute MCA stroke based on the findings of severe perfusion deficit greater than 50% of the MCA territory and additional involvement of the anterior or posterior cerebral artery territory.

Academic Medical Centers↗
PubMed2004

Intravitreal triamcinolone for the management of macular edema due to nonischemic central retinal vein occlusion.

OBJECTIVE: To evaluate the efficacy of intravitreal triamcinolone acetonide in the management of persistent macular edema secondary to nonischemic central retinal vein occlusion (CRVO). METHODS: Twenty consecutive patients were selected with a 3- to 4-month history of nonischemic CRVO and persistent macular edema. These patients received a single intravitreal injection of 4 mg of triamcinolone acetonide (40 mg/mL). The follow-up period ranged from 10 to 12 months. The amount of macular edema was assessed by the amount of retinal thickening on clinical examination using the Goldmann contact lens and by the area and intensity of staining on fluorescein angiography. Treated patients were compared with a retrospectively matched group of patients who were managed with observation only. MAIN OUTCOME MEASURES: Changes in visual acuity and amount of macular edema were assessed in the treated patients and compared with the observation group. RESULTS: The mean baseline visual acuity in the treatment group was 20/132 vs 20/123 for the observation group (P =.57). After 1 week, the treated group had a mean visual acuity of 20/51. At final follow-up, the treated group had a mean visual acuity of 20/37 while the observation group had a mean visual acuity of 20/110 (P =.001). Sixty percent of treated patients had a final visual acuity of 20/40 or better vs only 20% in the observation group (P =.01). Forty percent of the untreated patients had a final visual acuity worse than 20/200 while none of the treated patients did (P<.001). At final follow-up, 75% of treated patients had complete resolution of macular edema on clinical examination vs only 20% of the untreated patients (P<.001). Two of the treated patients had recurrence of macular edema at 6 months, and 3 had elevated intraocular pressure. CONCLUSION: This study shows a treatment benefit from intravitreal triamcinolone in terms of visual acuity and macular edema for nonischemic CRVO.

Aged↗
PubMed1997

Subretinal fibrosis in diabetic macular edema. ETDRS report 23. Early Treatment Diabetic Retinopathy Study Research Group.

OBJECTIVE: To describe the characteristics of and risk factors for subretinal fibrosis (SRF) in patients with diabetic macular edema. PATIENTS AND METHODS: A total of 109 eyes (in 96 persons) with SRF, defined as a mound or sheet of gray to white tissue beneath the retina at or near the center of the macula, were identified during the Early Treatment Diabetic Retinopathy Study, which is a randomized clinical trial of photocoagulation and aspirin treatment in patients with mild to severe nonproliferative or early proliferative diabetic retinopathy. The patients and the ocular characteristics of these 109 eyes, all of which had clinically significant macular edema, were compared with those of 5653 eyes in which clinically significant macular edema, but not SRF, was observed during the trial. RESULTS: In 9 of 109 eyes, the development of SRF may have been directly related to focal photocoagulation. Seventy-four percent of the eyes in which SRF developed had very severe hard exudates in the macula prior to the development of SRF, while this level of hard exudates was seen in only 2.5% of the eyes with clinically significant macular edema in which SRF did not develop (P < .001). Of the 264 eyes with this level of hard exudates at baseline (n = 29) or during follow-up (n = 235), SRF developed in 30.7% of the eyes, while this complication developed in only 0.05% of 5498 eyes with clinically significant macular edema without this level of hard exudates. CONCLUSIONS: Subretinal fibrosis is an infrequent complication of diabetic macular edema. Although it has been reported to be associated with photocoagulation burn intensity, in only 9 of 109 eyes in which SRF developed was it located adjacent to a photocoagulation-related scar (among 4823 eyes that received focal photocoagulation for treatment of macular edema). The strongest risk factor for the development of SRF is very severe hard exudate.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Does labetalol predispose to pulmonary edema in severe pregnancy-induced hypertensive disease?

We investigated whether use of labetalol, a beta adrenoreceptor blocking antihypertensive agent commonly employed as an alternative to hydralazine, is independently associated with pulmonary edema in women with severe preeclampsia. We retrospectively evaluated women with severe preeclampsia who were given labetalol by intravenous bolus for MAP > 120 mm Hg. Outcome variables included: achieving MAP < 120 mm Hg with < 300 mg of labetalol, incidence of adverse effects of the drug, including pulmonary edema, hypotension, and maternal bradycardia. Total intravenous fluid intake exceeding output (+ delta I/O) and presence or absence of preeclamptic liver involvement were noted. Statistical analysis included unpaired t-tests and Fisher's exact test. Fifty-one women were studied, 7 (13.7%) of whom developed pulmonary edema. Demographic and pregnancy characteristics were not different between patients who did or did not develop pulmonary edema. No patient had detectable underlying heart disease. Patients with or without pulmonary edema did not differ as regards entry MAP (130 +/- 14 vs. 129 +/- 18 mm Hg), total dose of labetalol (209 +/- 83 vs. 193 +/- 39 mg/24 hours), incidence of bradycardia or hypotension (0/7 vs. 8/44), or presence of hepatic involvement (1/7 vs. 9/44). However, there was a significant difference in degree of positive fluid balance. Patients developing pulmonary edema had a net gain of 1,466 +/- 429 mL of fluid in the 24 hours in which they received labetalol than those who did not (659 +/- 1152 mL, P = .003). Initial central hemodynamic monitoring data revealed no impairment of cardiac performance (mean cardiac output 7.7 +/- 1.8 L/min, cardiac index 4.0 +/- 0.8 L/min/m2, left ventricular stroke work index 73 +/- 9 g.m.m-2) despite high pulmonary capillary wedge pressures (22 +/- 4 mm Hg). We conclude that the incidence of pulmonary edema in patients with severe preeclampsia who are treated with labetalol appears to be a result of an increase in third space fluid accumulation as a manifestation of the severity of their disease, not a direct effect of the drug on cardiac performance.

Adult↗
PubMed1984

Galactose neuropathy: impact of chronic endoneurial edema on nerve blood flow.

Peripheral neuropathy induced by galactose feeding results in endoneurial edema with increased tissue pressure and ultimate demyelination of nerve fibers. To assess the role of ischemia in the pathogenesis of this neuropathy, nerve blood flow was measured 6 months after the start of galactose ingestion, between the onset of edema and nerve fiber changes. Measurement was carried out by a noninvasive technique involving the use of [14C]iodoantipyrine as a radioactive tracer of tissue perfusion. A significant decline in nerve blood flow was found, which correlated positively with increased nerve water content as quantified by a microgravimetric technique. We sought to establish the pathogenic role of nerve edema in the development of schwannopathy and demyelination by morphological examination. It was found that Schwann cells appeared normal in areas of the peripheral nervous system in which edema does not occur, such as spinal ganglia and roots, whereas in regions in which there was edema, massive glycogen accumulation in Schwann cells and demyelination occurred. These findings suggest that edema, rather than hyperactivity in the sorbitol pathway, is responsible for the pathological changes in galactosemic neuropathy and that ischemia resulting from edema and increased endoneurial fluid pressure is the mechanism responsible for fiber injury.

Animals↗
PubMed1986

Increased leukotriene C4 and vasogenic edema surrounding brain tumors in humans.

Leukotrienes are pharmacologically active compounds that promote vascular permeability. In this study we sought to determine whether tissue leukotriene-like immunoreactivity was increased in intracranial tumors associated with peritumoral edema. In 20 patients undergoing craniotomy tissue specimens were immediately frozen after removal and tissue leukotriene C4 levels were determined by radioimmunoassay. An index of peritumoral edema was estimated from preoperative contrast-enhanced computed tomographic scans. There was a significant correlation between brain edema and tissue leukotriene levels (p less than 0.003). Metastatic tumors (n = 8) had the highest leukotriene C4 level at 13.8 +/- 8.5 pg/mg tissue (mean +/- SE) and the highest index of edema 5.7 +/- 1.8. The mean leukotriene C4 level in the gliomas (n = 5) was 6.2 +/- 2.3 pg/mg tissue and the edema index was 2.1 +/- 0.6. There was no edema and no neoplasm in the temporal lobes removed for seizure (n = 2), and their level of leukotriene C4 was 0.4 +/- 0.1 pg/mg tissue. The formation of leukotriene C4 is stimulated by intracranial tumors. Leukotrienes increase blood-brain barrier permeability and may be important in the formation of vasogenic edema surrounding tumors.

Brain Chemistry↗
PubMed1995

Sacral edema: computed tomographic and anatomical observations.

Sacral edema is a widely recognized clinical sign. Hitherto there has been no method of radiological confirmation, nor has the anatomy of this sign been well described. In a prospective study of 100 patients referred for abdominopelvic computed tomography (CT), 17 showed radiological evidence of sacral edema. It was demonstrated clinically in 12 of these 17 patients, leaving five patients with apparent CT evidence of sacral edema in whom this was not demonstrated clinically. In two patients with clinical evidence of sacral edema, their tissue planes in this region appeared normal on CT. The edema fluid accumulates in an intermediate plane of fibrous tissue within the subcutaneous fatty layer of the trunk. In those 17 patients with CT evidence of edema, the center of the fluid accumulation was situated over the lumbar rather than the sacral spine, suggesting that the term "sacral" edema is something of a misnomer.

Adolescent↗
PubMed1989

Preliminary studies on phospholipase A2-induced mouse paw edema as a model to evaluate antiinflammatory agents.

Phospholipase A2 (PLA2) is a key component of the inflammatory process because of its role in the generation of eicosanoids and platelet-activating factor (PAF). Manipulation of PLA2 activity offers a novel therapeutic approach for the development of antiinflammatory agents; however, there is a need for a suitable in vivo model. Injection of 1 microgram of snake venom PLA2 (A. piscivorus piscivorus, D-49) into the mouse hind footpad produced a significant three- to four-fold rise in paw edema within 10 min, compared to the saline control. Edema formation depended on enzyme concentration and appeared specific for PLA2 since edema was negated by enzyme pretreatment with p-bromophenacyl bromide, a nonspecific PLA2 inhibitor. Moreover, injection of a protein such as bovine serum albumin did not result in significant edema. Coinjection of phenidone (lipoxygenase inhibitor, 50 micrograms), indomethacin (cyclooxygenase inhibitor, 50 micrograms), cyproheptadine (antihistamine/antiserotonin, 50 micrograms), aristolochic acid (putative PLA2 inhibitor, 100 micrograms), or kadsurenone (PAF antagonist, 50 micrograms) with PLA2 (1 microgram/paw) resulted in partial reduction (44.5, 34.2, 54.7, 64, and 50% inhibition, respectively) of edema formation. Oral administration of cyproheptadine (10 mg/kg), indomethacin (10 mg/kg), BW 755c (100 mg/kg), or dexamethasone (1 mg/kg) 1-3 h before challenge also decreased PLA2-induced edema (63.0, 30.1, 47.8, or 62.5% inhibition, respectively). The data suggest that mouse paw edema resulting from PLA2 injection is a multicomponent event, influenced by both autacoids and lipid mediators of inflammation.

Animals↗
PubMed2005

Quantitative apparent diffusion coefficients and T2 relaxation times in characterizing contrast enhancing brain tumors and regions of peritumoral edema.

PURPOSE: To investigate the potential value and relationship of in vivo quantification of apparent diffusion coefficients (ADCs) and T2 relaxation times for characterizing brain tumor cellularity and tumor-related edema. MATERIALS AND METHODS: A total of 26 patients with newly diagnosed gliomas, meningiomas, or metastases underwent diffusion-weighted and six-echo multisection T2-preparation imaging. Regions of interest (ROIs) were drawn on conventional MR images to include tumor (as defined by contrast agent enhancement) and immediate and peripheral edema. Areas of necrosis were excluded. Median values of ADCs and T2 in the ROIs were calculated. RESULTS: ADCs for gliomas were similar to those for meningiomas or metastases in all regions. Tumor T2 values for gliomas (159.5+/-30.6 msec) were significantly higher than those for meningiomas or metastases (125.0+/-31.1 msec; P=0.005). Immediate-edema T2 values for meningiomas or metastases (226.0+/-44.1 msec) were significantly higher than those for gliomas (203.5+/-32.8 msec; P=0.033). Peripheral-edema T2 values for gliomas (219.5+/-41.9 msec) were similar to those for meningiomas or metastases (202.5+/-26.5 msec; P=0.377). Both immediate- and peritumoral-edema ADCs and T2 values were significantly higher than those in tumor for both tumor types. ADCs and T2 values from all regions correlated significantly for gliomas (r=0.95; P<0.0001) and for meningiomas or metastases (r=0.81; P<0.0001). CONCLUSION: The higher immediate-edema T2 values for nonglial tumors than for gliomas suggest tumor-related edema (vasogenic vs. infiltrated) can be further characterized by using T2 values. There were significant correlations between ADC and T2 values.

Adult↗
PubMed2007

In vivo brain edema classification: New insight offered by large b-value diffusion-weighted MR imaging.

PURPOSE: To assess the role of large b-value diffusion weighted imaging (DWI) in the characterization of the physicochemical properties of the water in brain edema under experimental and clinical conditions. MATERIALS AND METHODS: Vasogenic brain edema was induced in mice by means of cold injury. A total of 17 patients with extensive peritumoral brain edema were also investigated. The longitudinal relaxation time (T(1)) and apparent diffusion coefficient (D) were measured in the edematous area both in humans and in mice. D was calculated by using both mono- (D(mono)) and biexponential (D(fast) and D(slow)) approaches in the low and overall range of b-values, respectively. The D values were correlated with the T(1) values. RESULTS: A strong linear correlation was found between T(1) and D(mono) in vasogenic brain edema, both in humans and in mice. After breakdown of D(mono) into fast and slow diffusing components, only D(fast) exhibited a strong correlation with T(1); D(slow) was unchanged in vasogenic brain edema. CONCLUSION: Large b-value DWI can furnish a detailed characterization of vasogenic brain edema, and may provide a quantitative approach for the differentiation of edema types on the basis of the physicochemical properties of the water molecules. Application of the DWI method may permit prediction and follow-up of the effects of antiedematous therapy.

Animals↗
PubMed2001

Correlation between increased airway responsiveness and severity of pulmonary edema.

To determine whether the severity of the pulmonary edema in sheep models of cardiogenic and non-cardiogenic pulmonary edema correlate with concomitant alterations in airway responsiveness using three separate measures of pulmonary edema: post-mortem wet-to-dry lung weight ratio (W/D), chest radiograph (CXR) scores, and small airway wall area. Cardiogenic pulmonary edema was induced by increasing left atrial pressure (increase PLA) and non-cardiogenic pulmonary edema was induced by intravenous administration of Perilla ketone (PK). There was a significant negative correlation between changes in airway responsiveness and changes in CXR grade (r=-0.749, P<0.05), W/D (r=-0.662, P<0.05), airway wall areas (r=0.784, P<0.05) after increases in both PLA and PK. Chest radiograph score, W/D, and airway wall area correlated with each other (CXR score and W/D r=0.657, P<0.05; CXR score and airway wall area r=0.678, P<0.05; airway wall area and W/D r=0.704, P<0.05). We speculate that the increased airway responsiveness observed during pulmonary edema may result from the mechanical effects of edema formation within the airways.

Airway Resistance↗
PubMed2006

The temporal profile of edema formation differs between male and female rats following diffuse traumatic brain injury.

Although female hormones are known to influence edema formation following traumatic brain injury (TBI), no studies have actually compared the temporal profile of edema formation in both male and female rats following diffuse TBI. In this study, male, female, and female ovariectomized rats were injured using the 2 m impact acceleration model of diffuse TBI. The temporal profile of brain water content was assessed over 1 week post-trauma. Male animals demonstrated increased (p < 0.05) edema at 5 hours, 24 hours, 3 days, 4 days, and 5 days after TBI with a peak at 5 hours post-injury. This time point was associated with increased blood-brain barrier (BBB) permeability. In contrast, intact females showed increased levels of edema (p < 0.05) at 5 hours, 24 hours, 3 days, and 4 days post-TBI, with a peak at 24 hours. No BBB opening was present in intact females at 5 hours. Female animals demonstrated more edema than male animals at 24 hours, but less at 5 hours, 3 days, and 5 days. Ovariectomy produced an edema profile that was similar to that observed in males. The temporal profile of edema formation after TBI seems to depend on endogenous hormone levels, a difference which may have an influence on clinical management.

Animals↗
PubMed2006

Increased substance P immunoreactivity and edema formation following reversible ischemic stroke.

Previous results from our laboratory have shown that neurogenic inflammation is associated with edema formation after traumatic brain injury (TBI). This neurogenic inflammation was characterized by increased substance P (SP) immunoreactivity and could be attenuated with administration of SP antagonists with a resultant decrease in edema formation. Few studies have examined whether neurogenic inflammation, as identified by increased SP immunoreactivity, occurs after stroke and its potential role in edema formation. The present study examines SP immunoreactivity and edema formation following stroke. Experimental stroke was induced in halothane anaesthetized male Sprague-Dawley rats using a reversible thread model of middle cerebral artery occlusion. Increased SP immunoreactivity at 24 hours relative to the non-infarcted hemisphere was observed in perivascular, neuronal, and glial tissue, and within the penumbra of the infarcted hemisphere. It was not as apparent in the infarct core. This increased SP immunoreactivity was associated with edema formation. We conclude that neurogenic inflammation, as reflected by increased SP immunoreactivity, occurs following experimental stroke, and that this may be associated with edema formation. As such, inhibition of neurogenic inflammation may represent a novel therapeutic target for the treatment of edema following reversible, ischemic stroke.

Animals↗
PubMed2006

CT prediction of contusion evolution after closed head injury: the role of pericontusional edema.

BACKGROUND: Cerebral contusions have a 51% incidence of evolution in the first hours after injury. Evolution is associated with clinical deterioration and is the reason for ICP monitoring or surgical intervention. We sought to define CT features that predict cerebral contusion evolution. METHODS: Patients treated for cerebral contusion who had 2 CT scans within 24 hours after injury were evaluated (n = 21). CT scans were analyzed for area of contusion, hemorrhagic components, and edema. Increase (%) in contusion size was recorded. Contusion evolution was defined as > 5% size increase. Ratios of hemorrhagic components to surrounding edema were calculated. RESULTS: Ten patients (47.6%) showed contusion evolution and 11 (52.4%) did not. Age, sex ratio, or injury severity between the 2 groups did not differ. Eight of 10 patients with evolving contusions had minimal or no perilesional edema on first CT; only 2 of 11 nonevolution patients had perilesional edema (p < 0.005). Mean ratio of area of surrounding edema to area of hemorrhagic products on first CT was 0.770 in evolution group versus 2.22 in non-evolution group (p = 0.055). CONCLUSIONS: A higher proportion of patients without contusion evolution had perilesional edema present on first CT scan. The absence of pericontusional edema on early CT may be a useful marker to predict contusion evolution.

Adult↗
PubMed2003

Chronological changes of perihematomal edema of human intracerebral hematoma.

Recent investigations have indicated the importance of secondary brain damage in the pathophysiology of intracerebral hemorrhage (ICH), which includes ischemic brain damage and edema formation around a hematoma. The purpose of the current study is to investigate chronological changes of perihematomal edema in patients with human ICH and also the correlation between volume of perihematomal edema and neurological status. Fourteen patients with medium-sized putaminal hemorrhage (29.4 +/- 13.2 ml) without hematoma enlargement were included in this study. To investigate chronological changes of perihematomal edema, we performed CT scans prospectively on the day of hemorrhage and repeated them on days 1, 3, 7, 14, and 28. We evaluated the patients neurologically using the NIH stroke scale on the day a CT scan was performed. The volume of perihematomal edema in human ICH increased rapidly three days after hemorrhage and the score on the NIH stroke scale showed a deterioration. The volume of perihematomal edema then increased slowly until day 14 after hemorrhage, and decreased thereafter. Despite progression of perihematomal edema, the score on the NIH stroke scale improved gradually after day 3.

Aged↗
PubMed2000

LF16-0687 a novel non-peptide bradykinin B2 receptor antagonist reduces vasogenic brain edema from a focal lesion in rats.

Head injury world wide is still the most frequent cause of morbidity and mortality among the population under 45 years. Approximately 50% of patients dying from severe head injury have a therapy refractory intracranial pressure rise (Baethmann 1998). Traumatic brain edema, e.g. resulting from disruption of the blood-brain barrier is viewed as an important factor of the increased intracranial pressure. Bradykinin, an active peptide of the kallikrein-kinin system is considered to enhance brain edema formation which is attributed to its permeabilizing effect on the blood-brain barrier and on dilation of arterial blood vessels in the brain mediated by B2-receptors facilitating extravasation. Currently, LF16-0687, a novel non-peptide bradykinin B2 receptor antagonist was experimentally tested as to its therapeutical potential on vasogenic brain edema from a cortical focal lesion. Following trephination of the skull in anaesthesia, male Sprague-Dawley rats were subjected to a focal cold injury of the left parietal cortex. Animals of two experimental groups were receiving either LF16-0687 as high or low dose, whereas one group of untreated animals with trauma was treated with 0.9% NaCl as continuous infusion beginning 10 min before until 24 h after lesion. 24 h after trauma the brain was removed from the skull, and the cerebral hemispheres were separated in the median plane for gravimetric assessment of hemispheric swelling. No significant reduction of hemispheric brain swelling (+7.4 +/- 2.9%) was found in animals receiving high-dose LF16-0687 as compared to the untreated controls. Brain swelling, however was significantly attenuated by the low-dose treatment, i.e. to +6.4 +/- 1.3%; vs. +9.3 +/- 1.1% found in the controls, (p < 0.05). The current data confirm that blocking of bradykinin B2-receptors by LF16-0687 is significantly attenuating vasogenic brain edema from a focal cold lesion. The therapeutical properties of the antagonist on brain edema formation cannot be attributed to a lowering of the blood pressure. Rather, specific blocking effects of B2-receptors in the brain appear to be involved. In conclusion, the understanding of secondary brain damage including brain edema in head injury has been markedly enhanced by the discovery of pathophysiologically active mediator compounds playing a role in its various manifestations. The current data confirm a pathophysiological function of bradykinin in vasogenic brain edema mediated by activation of B2-receptors. Currently it is studied whether LF16-0687 also reduces brain swelling when given after an insult.

Animals↗
PubMed2000

Time course of trace of diffusion tensor [Trace(D)] and histology in brain edema.

We examined the correlation between changes in the trace of diffusion tensor [Trace(D)], regional water content and tissue ultrastructure relating to cellular (cytotoxic) and vasogenic brain edema. Cellular edema was induced by left middle cerebral artery occlusion in cats (Kuroiwa T et al., 1998). Vasogenic edema was induced in the white matter of cats by a cold lesion (Kuroiwa T et al., 1999). In cellular edema, the water content increase correlated linearly with the Trace(D) decrease in both the gray and white matter. However, both the slopes and intercepts of the correlation lines were significantly different. Hydropic astrocytic swelling was seen in both structures, and in the white matter, oligodendrocytic and myelinated axonal swelling were observed. In vasogenic edema, the increase in Trace(D) showed a significant linear correlation with the increase in tissue water content. Histologically, nerve fibers were dissociated and the extracellular space was markedly enlarged with protein-rich fluid. These result showed that the different slopes and intercepts of the water content--Trace(D) correlation lines for different subtype of brain edema, which reflect different ultrastructural localization of water, should be taken into account when evaluating brain edema using Trace(D) mapping.

Animals↗
PubMed1998

Resolution of experimental vasogenic brain edema at different intracranial pressures.

Resolution of vasogenic brain edema was examined using the infusion edema model in rabbits. Texas Red-albumin (MW 66,000 D) and sodium fluorescein (MW 376 D) dissolved in artificial cerebrospinal fluid (aCSF) were infused into the white matter of the left frontal lobe of the brain. To quantify the edema fluid cleared by the ventricular system, ventriculo-cisternal perfusion was performed with aCSF. A closed cranial window, implanted above the left parietal brain, served for studying resolution of the artificial edema fluid via the subarachnoid space. CSF-samples were collected in 30 minutes-intervals and analysed with a spectrophotometer. Clearance of edema fluid was examined under low (2-5 mm Hg), medium (9-12 mm Hg), or high (14-17 mm Hg) intracranial pressures (ICP). In the low pressure-group, both edema fluid markers were found in the ventriculo-cisternal and subarachnoid perfusate at 60 and 90 min, in the group with moderately increased ICP at 90 and 120 min, respectively. In the high ICP-group both fluorescence dyes appeared not less than 90 min in the ventricular system, while no increase at all could be found in the subarachnoid space. Our results imply that resolution of edema fluid via both the ventricular system and the subarachnoid space depends on the actual ICP level.

Animals↗