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Results for “Brain Edema”

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PubMed1994

Formation and resolution of brain edema associated with brain tumors. A comprehensive theoretical model and clinical analysis.

The purpose of this study is to quantify the relative contribution of the mechanisms in the absorption of edema fluid. The convection/diffusion and the comprehensive bulk flow model were applied for the finite element analysis of peritumoral brain edema. For clinical analysis, 90 meningiomas studied by MRI were selected. Serial CT scan and MRI were performed at 0, 2, 4, 6 hours after injection of Iopamidol or Gadpenteic acid respectively. Then the tracer distributions in the edematous brain was analyzed. The tracer movement in the brain is well represented by the convection/diffusion equation. The absence of the preferential fluid flow directing toward the ventricle indicates that a limited role of CSF sink action into the ventricle. From capillary surface area (240 cm2/g brain), capillary hydraulic conductivity (1.8 x 10(-8) ml/cmH2O/cm2/min) and the simulated average tissue pressure of 9.8 mmHg, maximum absorption rate into capillaries was estimated to be 0.003 ml/h/cm3 brain tissue. Considering the limited role of edema fluid clearance into the ventricle, the results indicate a possible role of subarachnoid CSF space for the clearance of edema fluid. The clearance of edema fluid into subarachnoid CSF space should be studied quantitatively. Finally, unification of the convection/diffusion and the comprehensive bulk flow model will provide a more quantitative analysis of edema formation and resolution by using MRI and tracer studies.

Blood-Brain Barrier↗

PubMed1975

Steroid treatment of brain edema.

Experimental brain edema due to extradural compression was studied in rats, and the beneficial effect of a steroid, betamethasone, on this was tested. Immediately following extradural compression, betamethasone therapy was begun by intraperitoneal injection. Three groups of animals received eight divided doses of betamethasone over 48 hours: total doses were 64 mg, 6.4 mg, and 0.64 mg/kg, respectively. Two other groups received doses at zero and 24 hours only, with total doses of 64 mg and 6.4 mg/kg. Water and sodium content of the brain were reduced depending upon dosage. Administration every 6 hours was superior to every 24 hours. Potassium content was not consistently altered. After injection of radioactive steroid, a significant increase in uptake of the drug was observed in the edematous brain.

Animals↗

PubMed1986

Significance of proton relaxation time measurement in brain edema, cerebral infarction and brain tumors.

We examined the proton relaxation times in vitro in various neurological diseases using experimental and clinical materials, and consequently obtained significant results for making a fundamental analysis of magnetic resonance imaging (MRI) as followings. 1) In the brain edema and cerebral infarction, T1 prolonged and T2 separated into two components, one fast and one slow. Prolongation of T1 referred to the volume of increased water in tissue. The slow component of T2 reflects both the volume and the content of increased edema fluid in tissue. 2) In the edematous brain tissue with the damaged Blood-Brain-Barrier (BBB), the slow component of T2 became shorter after the injection of Mn-EDTA. Paramagnetic ion could be used as an indicator to demonstrate the destruction of BBB in the brain. 3) After the i.v. injection of glycerol, the slow component of T2 became shorter in the edematous brain with the concomitant decrease of water content. The effects of therapeutic drug could be evaluated by the measurement of proton relaxation times. 4) Almost all tumor tissue showed a longer T1 and T2 values than the normal rat brain, and many of them showed two components in T2. It was difficult to determine the histology of tumor tissue by the relaxation time alone because of an overlap of T1 and T2 values occurred among various types of brain tumors. 5) In vivo T1 values of various brain tumor were calculated from the data of MRIs by zero-crossing method, and they were compared with the in vitro T1 values which were measured immediately after the surgical operation. Though the absolute value did not coincide with each other due to differences in magnetic field strength, the tendency of the changes was the same among all kinds of tumors. It is concluded that the fundamental analysis of proton relaxation times is essentially important not only for the study of pathophysiology in many diseases but also for the interpretation of clinical MRI.

Animals↗

PubMed1995

The effect of hypertonic fluid resuscitation on brain edema in rabbits subjected to brain injury and hemorrhagic shock.

Small-volume resuscitation with 7.2% NaCl/10% dextran 60 (HHS) restores cardiovascular stability faster than all other therapeutic modalities currently known. This study was undertaken to elucidate the effects of HHS on the brain, specifically on the formation of posttraumatic brain edema. HHS was administered to anesthetized albino rabbits with or without a focal cryogenic brain lesion and hemorrhagic shock. Specific gravity of small tissue samples was determined 4 h after injury and values were topographically assembled to form a color-coded map of both hemispheres, allowing for a high resolution mapping of brain edema. Cerebral blood flow on the side of the lesion, as assessed by the H2 clearance method, increased transiently after injury but remained unchanged from baseline during shock and after infusion of HHS, indicating intact cerebrovascular autoregulation. The cryogenic lesion without subsequent HHS infusion resulted in significant brain edema formation in grey and white matter of the exposed hemisphere. In injured animals, resuscitation with HHS led to a global reduction of brain water content in both hemispheres. We conclude that small-volume resuscitation with HHS does not worsen posttraumatic brain edema. To the contrary, our results show that it decreases cerebral water content even in regions close to the injury. This makes it worthwhile to investigate the benefits of HHS for the treatment of intracranial hypertension.

Animals↗

PubMed1991

[Serum hyposomolarity, brain edema and the bulbar brain syndrome as complications in the course of severe cranio-cerebral injuries in children].

It is reported on a severe craniocerebral trauma in a child with a rarely occurring spontaneously induced serum hypoosmolality which led to brain edema combined with intracranial increase of pressure and bulbar brain syndrome. By means of bedside brain ventricle catheterization for liquor drainage following drill-hole trepanation, the complication could be controlled. Later the recovery was completed under supervision of the outpatient department. Pathophysiological metabolic peculiarities, especially osmolality, are discussed. The necessity of special and repeated controls of the metabolic characteristics osmolality, sodium and potassium in serum and urine as well as the water and sodium balance within 24 hours is emphasized.

Brain Edema↗

PubMed1979

Tissue albumin and water content in the early stages of vasogenic brain edema formation.

Brain edema (BE) research lacks quantitative regional methods. We modified the method of Pappius and McCann (1969), who used radioactive iodinated I125 serum albumin (RISA) as a label for vasogenic BE fluid. To correct for intravascular plasma volume we used Cr51 labelled red blood cells and calculated equivalent extravascular plasma volume (EVPV). The modified RISA method was compared with a standard method for measuring increased tissue water, i.e. the change in wet:dry weights. Anesthetized rabbits were subjected to unilateral cortical freeze injury and sacrificed three hours later. The lesion corresponding to the area of blood brain barrier (BBB) breakdown was delineated by Evan's blue staining. That area and the two adjacent poles were sectioned. The contralateral hemisphere was used as the control. Good agreement was found between the two methods. By the modified RISA method, 4.08% of the wet weight of the injured hemisphere was EVPV while the decrease in dry weight corresponded to 5.56% edema. In the freeze lesion, however, where BBB breakdown occurred extravascular (EV) protein exceeded EV water, while adjacent to the lesion in the area with intact BBB, EV water exceeded EV protein. This suggests that the diffusion rate for water through brain tissue exceeds that of albumin in the early stages of vasogenic BE formation. We conclude that the modified RISA method is a satisfactory measure of regional vasogenic BE in acute animal experiments.

Animals↗

PubMed1989

Oxygen free radicals in the genesis of traumatic and peritumoral brain edema.

This study evaluates the effect of superoxide dismutase, a scavenger of oxygen free radicals, on peritumoral and cold injury edema. Vasogenic brain edema was produced in 39 cats by a standardized cortical freezing lesion. Peritumoral edema was produced by the transplantation of VX2 carcinoma cells into the brain of New Zealand White rabbits. Detection of superoxide radicals was studied by topical application of nitroblue tetrazolium to the cortical injury and by incubation of the VX2 carcinoma cells. The animals were treated with free superoxide dismutase (SOD) and polyethylene glycol superoxide dismutase (PEG-SOD). The following groups were studied: 1) control, 2) untreated tumor group, 3) tumor group treated with PEG-SOD, 4) a group treated with PEG-SOD before injury, and 5) a group treated with free SOD after injury. Brain edema was evaluated by measurement of specific gravity and planimetry study of the spread of Evans blue dye. Preliminary data indicate that superoxide radicals are present in the brain after cold injury and in the cytoplasm and nucleus of VX2 carcinoma cells. Free SOD and PEG-SOD had no beneficial effect upon the vasogenic brain edema produced in either model. It is concluded that intracellular uptake of SOD may be one of the factors necessary for an effect upon either form of edema.

Animals↗

PubMed2004

Hyperammonemia, brain edema and blood-brain barrier alterations in prehepatic portal hypertensive rats and paracetamol intoxication.

AIM: To study the blood-brain barrier integrity, brain edema, animal behavior and ammonia plasma levels in prehepatic portal hypertensive rats with and without acute liver intoxication. METHODS: Adults male Wistar rats were divided into four groups. Group I: sham operation; II: Prehepatic portal hypertension, produced by partial portal vein ligation; III: Acetaminophen intoxication and IV: Prehepatic portal hypertension plus acetaminophen. Acetaminophen was administered to produce acute hepatic injury. Portal pressure, liver serum enzymes and ammonia plasma levels were determined. Brain cortex water content was registered and trypan blue was utilized to study blood brain barrier integrity. Reflexes and behavioral tests were recorded. RESULTS: Portal hypertension was significantly elevated in groups II and IV. Liver enzymes and ammonia plasma levels were increased in groups II, III and IV. Prehepatic portal hypertension (group II), acetaminophen intoxication (group III) and both (group IV) had changes in the blood brain-barrier integrity (trypan blue) and hyperammonemia. Cortical edema was present in rats with acute hepatic injury in groups III and IV. Behavioral test (rota rod) was altered in group IV. CONCLUSION: These results suggest the possibility of another pathway for cortical edema production because blood brain barrier was altered (vasogenic) and hyperammonemia was registered (cytotoxic). Group IV, with behavioral altered test, can be considered as a model for study at an early stage of portal-systemic encephalopathy.

Acetaminophen↗

PubMed1990

Brain edema following an experimental missile wound to the brain.

Brain edema occurs after brain injury and may be life threatening. The occurrence and type of brain edema, its magnitude, and time course have never been ascertained following a missile wound to the brain. We therefore measured the development of brain edema in a series of cats in which a right cerebral hemisphere wound was made with a 2.0 mm, 31.7 mg steel sphere with a velocity of 240-300 m/s (0.9-1.4 J). The entire brain was surveyed for postwounding brain edema by determining the wet weight minus dry weight. Brain edema was seen to develop only in the white matter about the missile wound track in the injured cerebral hemisphere. There, brain water rose from 66 to 73%; white matter sodium also increased significantly from approximately 150 mEq/kg dry weight to 254 mEq/kg dry weight. Potassium levels remained essentially unchanged. This vasogenic edema was relatively mild, peaked at 24-48 h after wounding, and resolved spontaneously within a week without specific treatment. We infer that brain edema following an uncomplicated cerebral missile wound in the human brain is also mild, self-limited, and may resolve spontaneously without special treatment.

Animals↗

PubMed1979

The effect of intracerebral ouabain administration on the composition of edema fluid isolated from cats with cold-induced brain edema.

Brain edema fluid was collected from cats with a freezing lesion in the left parietal cortex by the insertion into the brain of needles containing nylon wicks and connected to polyethylene tubes. The edema fluid samples which accumulated in the polyethylene tubes were regularly analyzed for Na+ and K+ content, colloid osmotic pressure, lactate dehydrogenase and creatine phosphokinase activity, and 99mTc-albumin radioactivity; the albumin tracer being introduced intravenously at the time of cold-injury. One series of cats received an intracerebral injection of ouabain solution, the control series an intracerebral injection of saline, at 100 min after the cold-injury. The ouabain injection was followed by an increase of K+ content, LDH and CPK activities but a decrease of Na+ concentration in the edema fluid, attributable to a concentration of solutes in the edema fluid as presumably water and Na+ were shifted into the cells and hence the extracellular space was reduced.

Animals↗

PubMed1989

Influence of thermal stress and various agents on the brain edema formation in rats following a cryogenic brain lesion.

The influence of cold stress, heat stress, or various agents on the development of brain edema were assessed in rats following a cryogenic brain lesion. Brain edema was induced by local cold injury to the cortex. Cerebral edema was assessed 0.5, 3.0 or 24 h after a cryogenic brain lesion by measuring the water content of two hemispheres. Pretreatment of animals with sodium pentobarbital (15 or 30 mg/kg, i.p.) or lidocaine (15 mg/kg, i.p.) did not influence the development of brain edema. In addition, pretreatment with an external heat stress (heat exposure of 32 degrees C for 6 h) exaggerated significantly the development of brain edema in the rat following a cryogenic brain lesion. On the other hand, pretreatment of animals with either external cold stress (cold exposure of 8 degrees C for 6 h), glycerol (10% 10 ml, i.p.), mannitol (15% 10 ml, i.p.), gamma-hydroxybutyric acid (300 mg/kg, i.p.), metiamide (5 mg/kg, i.p.), dexamethasone (4 mg/kg, i.p.), aminophylline (100 mg/kg, i.p.), or ketamine (30 mg/kg, i.p.) inhibited significantly the brain edema formation.

Animals↗

PubMed2006

Photodynamic therapy increases brain edema and intracranial pressure in a rabbit brain tumor model.

The objective of this study was to evaluate the effect of a single photodynamic therapy (PDT) on brain edema and intracranial pressure (ICP) in a rabbit model of brain tumor. A total of 57 adult New Zealand rabbits were assigned to 3 groups: the PDT group, the tumor group, and the tumor plus PDT group. Rabbits in the PDT group (n = 9) received PDT but no tumor implantation; rabbits in the tumor group (n = 18) received VX2 carcinoma implantation but no PDT; rabbits in the tumor plus PDT group (n = 30) received tumor implantation with subsequent PDT 16 days later. Brain edema and ICP levels were then evaluated. We found that ICP in the PDT group was 7.43 +/- 0.50 mmHg. After tumor implantation, ICP increased rapidly (18.43 +/- 1.10 mmHg, 21 days later). PDT alone did not increase ICP, but compared with that in the tumor group, ICP increased significantly in the tumor plus PDT group (9.55 +/- 1.32 vs. 13.31 +/- 1.13 mmHg, p < 0.01) 24 hours after treatment. Brain water content in the tumor group increased rapidly after tumor implantation. PDT again increased perineoplastic brain edema 24 hours after treatment (81.09 +/- 0.97% vs. 78.32 +/- 0.49%, p < 0.01). It should be noted that PDT alone did not induce brain edema. In conclusion, PDT causes transient brain edema and increases ICP in a rabbit brain tumor model.

Animals↗

PubMed1993

Contributions of ions and albumin to the formation and resolution of ischemic brain edema.

Changes in brain water, sodium, potassium, and albumin contents and blood-brain barrier (BBB) permeability were determined at various times between 1 hour and 6 weeks following occlusion of the middle cerebral artery (MCA) in rats. In the center of the infarct, brain edema increased to a maximum level by 12 hours, remained elevated for 7 days, and then returned to normal. The change in water content was accompanied by a parallel increase in sodium and decrease in potassium contents; however, the increase in sodium always exceeded the decrease in potassium, resulting in a net gain in brain cations during edema formation which returned to normal with edema resolution. The BBB permeability to 3H-alpha-aminoisobutyric acid was increased by 24 hours after MCA occlusion and returned to normal by 1 week after the edema had resolved. The time course for changes in brain albumin content was different than that for brain edema formation. Large increases in brain albumin content were not apparent until 6 hours after the onset of ischemia, rose to a peak at 3 days after occlusion of the MCA, and returned to normal several weeks after the edema had resolved. Albumin appeared to spread from the central infarct zone to surrounding, less ischemic areas. The relative contributions of the osmotic force produced by the increase in brain cations and the oncotic force produced by the increase in brain albumin to the observed change in water content were calculated. At all time points, the increase in brain cations accounted for nearly all of the observed brain edema, while the increase in albumin played essentially no role in edema development.

Albumins↗

PubMed1994

Experimental intracerebral hemorrhage: relationship between brain edema, blood flow, and blood-brain barrier permeability in rats.

There have been few investigations of brain edema formation after intracerebral hemorrhage (ICH), despite the fact that mass effect and edema are important clinical complications. The present study was designed to investigate the time course for the formation and resolution of brain edema and to determine how changes in cerebral blood flow (CBF) and blood-brain barrier (BBB) permeability are temporally related to edema formation following ICH. Anesthetized adult rats received a sterile injection of 100 microliters of autologous blood into the caudate nucleus. Water and ion contents were measured immediately, at 4 and 12 hours, and daily to Day 7 (10 time points, six rats at each time) after experimental ICH. The water content of the ipsilateral basal ganglia increased progressively (p < 0.002) over the first 24 hours, then remained constant until after Day 5, when the edema began to resolve. Edema was most severe in the tissue immediately surrounding the hemorrhage; however, it was also present in the ipsilateral cortex, the contralateral cortex, and the basal ganglia. Measurements of local CBF (using [14C]-iodoantipyrine) and BBB permeability (using [3H]-alpha-aminoisobutyric acid) were obtained in separate groups of six to eight rats at various time intervals between 1 and 48 hours after ICH. Cerebral blood flow was reduced to 50% of control at 1 hour, returned to control values by 4 hours, but then decreased to less than 50% of control between 24 and 48 hours after ICH. The BBB permeability increased significantly prior to the occurrence of significant edema in the tissue surrounding the clot. However, BBB permeability in the more distant structures remained normal despite the development of edema. These results demonstrate a time course for the formation and resolution of brain edema following ICH similar to that observed during focal ischemia. Brain edema forms in the immediate vicinity of the clot as a result of both BBB disruption and the local generation of osmotically active substances and then spreads to adjacent structures. While local ischemia, due to the mass effect of the hemorrhage, may play a role in producing cytotoxic and vasogenic edema, the release of toxic substances from the clot should also be considered. Since edema is nearly maximal by 24 hours after ICH, therapy directed at reducing edema formation must be instituted within the 1st day.

Aminoisobutyric Acids↗

PubMed1984

Radiation induced brain edema in primates, studied with sequential brain cat scanning and histopathology. Protective effect of sodium meclofenamate. A preliminary report.

Four Cynomologous monkeys (Mecaca fascicularis) received 2000 Rad whole brain irradiation. One remained untreated and exhibited loss of hair, facial edema, brain edema and hydrocephalus. There was loss of alertness and motor activity. One was scheduled to be treated with phenobarbital, but died in 24 hours after irradiation. One animal received 2 mg/kg dexamethasone I.M. daily. It died two weeks after irradiation apparently due to treatment related infection. One animal received 20 mg/kg sodium meclofenamate (Meclomen) orally daily. This animal showed no brain edema and only minimal hydrocephalus, delayed and incomplete hair loss and no facial edema. Further studies of this treatment appear to be justified.

Animals↗

PubMed1969

[Biochemical study of brain edema. 1. Changes in tissue electrolytes and proteins in several types of experimentally induced brain edema].

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Animals↗

PubMed1994

Brain edema resolution by CSF pathways and brain vasculature in cats.

Brain edema is a major contributor to the brain swelling process and raised intracranial pressure, yet the specific pathways involved in clearance of brain edema (fluid and proteins) and their relative contribution to the resolution process remain unknown. The objective of this study was to document the temporal course of edema resolution from brain to cerebrospinal fluid (CSF) and by the brain vasculature. Radioiodinated (125I) cat serum albumin (RICSA) was infused continuously into the white matter of anesthetized adult cats for 8 h, and ventriculocisternal perfusion was used to monitor the RICSA activity in CSF at 15-min intervals and to compare with the blood taken at 15-min intervals. The RICSA that cleared from the brain in 8 h measured 29.8% of the amount infused. Of the amount of RICSA leaving the brain, we found that the CSF compartment accounted for 87.14% of the cleared RICSA volume, while only 10.96% of RICSA was found in the blood during the 8-h experiment. The amount of RICSA remaining in the brain when the animal was killed equaled 71.2 +/- 15.9% (mean +/- SD) of the RICSA infused. We conclude that vascular clearance during the acute stage of resolution is minimal and that clearance of RICSA occurs predominantly via the CSF pathways.

Animals↗

PubMed1989

Brain edema: a classification based on blood-brain barrier integrity.

Brain edema is a frequent complication of a variety of brain injuries and disorders. Two primary types of brain edema can be distinguished depending upon the integrity of the blood-brain barrier. With intact-barrier edema, the permeability of the blood-brain barrier is normal and brain edema results from a disturbance in ionic homeostasis. This type of edema is typically associated with swelling of the brain cells and a contraction of the extracellular space. In open-barrier edema, the permeability of the blood-brain barrier is increased and brain edema results from the oncotic forces generated by an influx of serum proteins into brain. In this case, the edema fluid accumulates primarily in the extracellular space. To a greater or lesser extent, both types of edema occur simultaneously in the majority of clinical conditions; however, one form usually predominates and demands the attention of both the scientist and clinician. Furthermore, classification of brain edema based upon blood-brain barrier integrity is useful to focus research on common mechanisms for brain edema formation and to direct therapy. This review considers intact-barrier and open-barrier edema with regard to their (a) histological features, (b) biophysical forces, (c) possible biochemical mediators, (d) mechanisms of resolution, and (e) implications for therapy.

Blood-Brain Barrier↗