[Therapy of space-occupying intracranial processes (brain edema, brain tumor) and low cerebrospinal fluid pressure].
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Adrenal Cortex Hormones↗
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Intraoperative monitoring of brain tissue oxygen and carbon dioxide pressures reveals low oxygenation in peritumoral brain edema.
Brain edema and swelling often complicate surgery for brain tumors. Its pathophysiology is unclear, as is the relationship with brain tissue oxygenation. Our hypothesis was that brain edema around tumor is cytotoxic type caused by impaired local tissue oxygenation due to increased local tissue pressure. Therefore, we monitored brain tissue oxygen pressure (p(ti)O2) and carbon dioxide pressure (p(ti)CO2) in 19 patients undergoing craniotomy for removal of a brain tumor and specifically studied the effect of decompression by dura opening and by tumor removal with respect to the presence of brain swelling. Before craniotomy, multiparameter sensors were inserted into the peritumoral brain tissue guided by MRI-based stereotaxy. In eight patients who had severe brain swelling upon opening of the dura mater, p(ti)O2 immediately rose from 7 +/- 8 mm Hg to 24 +/- 15 mm Hg ( < 0.05), whereas in patients who did not have swelling, p(ti)O2 went from 16 +/- 9 to 18 +/- 10 mm Hg after opening of the dura. The mean p(ti)O2 of all patients at the start of resection of the tumor was 18 +/- 11 mm Hg, and increased to 30 +/- 15 mm Hg after resection was completed ( < 0.05). The effect on p(ti)O2 of raising the FiO2 to 1.0 was limited in this group of patients, as an increase greater than 50% was found in only six of twelve patients. Notably, in six patients, sensor malfunctions or associated hardware problems occurred, prohibiting useful data acquisition. We conclude that brain tissue oxygenation is reduced in the peritumoral area and improves after local tissue pressure relief, especially in patients with brain swelling. Thus, ischemic processes may contribute to brain edema around tumors. Intraoperative p(ti)O2 monitoring may enhance the safety of neuroanesthesia, but the high incidence of failures with this type of sensor remains a matter of concern.
Adult↗
Glutamine, myo-inositol, and organic brain osmolytes after portocaval anastomosis in the rat: implications for ammonia-induced brain edema.
Brain myo-inositol, an organic osmolyte, is decreased in cirrhotic patients with hepatic encephalopathy but appears unchanged in fulminant hepatic failure. An osmoregulatory response to the increase in brain glutamine may explain the decrease in brain myo-inositol; if this is the case, organic osmolytes may account for differences in the development of brain edema seen in acute or chronic liver failure. The response of myo-inositol and nine other organic osmolytes to the increase in brain glutamine at different time intervals after portacaval anastomosis (PCA) in the rat was studied. Organic osmolytes were measured in brain tissue and cerebrospinal fluid. Water in cerebral cortex was measured after ammonia infusion with the gravimetric method. Six weeks after PCA, despite an increase in brain glutamine (PCA, 16.4 +/- 2 mmol.kg wt-1.kg wt-1; sham, 5 +/- 1 mmol.L-1.kg wt-1), the content of total organic osmolytes did not increase (PCA, 44.1 +/- 3; sham, 43 +/- 4) because of a decrease of other osmolytes (myo-inositol, 54%; urea, 39%; taurine, 33%; and glutamate, 8%). Brain myo-inositol was lower at 3 weeks (3.4 +/- 0.5 kg wt-1) than at 1 day after PCA (4.7 +/- 0.5 kg wt-1). An ammonia infusion resulted in brain edema at both time points. In conclusion, the reduction in brain myo-inositol in PCA rats is accompanied by the decrease of other organic osmolytes, supporting the view that changes in myo-inositol reflect an osmoregulatory response. The decrease in brain myo-inositol is more marked as time elapses after PCA. In a model in which short-term and large doses of ammonia were infused, the decrease in brain myo-inositol did not prevent the development of brain swelling. Understanding brain osmoregulatory mechanisms may provide new insights into hepatic encephalopathy and brain edema in fulminant hepatic failure.
Ammonia↗
Blood-to-brain sodium transport in ischemic brain edema.
Brain edema is a frequent complication of cerebral ischemia; however, its mechanism of formation is not well understood. Sodium is known to accumulate in brain during the early stages of partial ischemia. Therefore, the present studies were undertaken to determine the relation among BBB sodium transport, integrity of the BBB, and development of brain edema during the first 24 hr after the onset of cerebral ischemia. Partial cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. After recovery from the anesthetic, animals were scored for the presence of symptoms, and those with scores greater than 10 of 25 (n = 87) were chosen for this study. Measurements of tissue water, sodium, and potassium contents, and brain uptake of 22Na and 3H-mannitol were made in each group at 1.5, 3, 6, 12, and 24 hr after carotid ligation. Accumulation of sodium and water in the ischemic compared with the nonischemic cerebral cortex was progressive. This edema formation was not of the vasogenic type because the permeability of the BBB to mannitol was unchanged. Blood-to-brain sodium transport was reduced by 30% to 40% at all time points in the ischemic cortex. Nevertheless, the remaining sodium transport activity appeared to play a role in the development of brain edema because Na accumulated in the tissue at a rate that was approximately the same as the rate of 22Na uptake from blood.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Physiopathology of brain edema].
Brain edema (BE), defined as an increase in tissue water content leading to an increase in tissue volume, is a common histopathologic response associated with a number of acute and subacute brain lesions. In some cases BE is a result of an unbalance of physical forces, hydrostatic or osmotic gradients driving the water in the tissue (hypertensive encephalopathy, hydrocephaly, plasma hypoosmolarity). In most cases however BE is associated with complex brain tissue alterations. According to Klatzo (1967) two physiopathological types can be described: vasogenic edema follows a breakdown of blood brain barrier to proteins. Edema fluid enlarges the extra-cellular space and spreads within the white matter; cytotoxic edema is an intra-cellular retention of water due to various disorders of ionic balance across the plasmic cell membrane. In both cases the hydrostatic gradient between the vascular lumen and the tissue plays a major role in the amount and spread of the edema fluid. In both cases also, toxic substances produced by tissue destruction act as factors of secondary damage causing more blood brain barrier lesions and/or cellular membrane alterations and eventually enhance edema. In various pathological conditions vasogenic and cytotoxic edema are associated: edema around circumscribed lesions such as hematomas, traumatic contusions, tumors, abscesses is basically a vasogenic edema with a secondary cytotoxic component. Ischemic edema is initially a pure cytotoxic phenomenon with a secondary osmotic edema and lately a vasogenic component. The formation of BE leads to an increase in tissue pressure which may reduce local cerebral blood flow. If blood supply is already impaired this can lead to energy shortage and further tissue destruction. If the bulk of edema is large enough intracranial pressure rises up, brain shifts and herniations may occur. Hypertonic solutions and corticoids are the more widely used drugs against brain edema. Hypertonic solutions remove water from the normal brain and hence may reduce intracranial pressure rather than treat edema. Corticoids, through various discrete mechanisms interfere with some toxic substances, enhance energetic metabolism and allow tissue restitution with a rather limited effect on edema itself.
Brain Edema↗
Evolution of brain abscess in cats formation of capsule and resolution of brain edema.
Brain abscess evolution was studied in an experimental model in the cat correlating the computed tomographic scan appearance with intracranial pressure, brain edema and histopathological findings. Brain inflammation was produced by direct inoculation of Staphylococcus aureus into the white matter. Abscesses developed in all animals. The ring enhancement around the necrotic focus seen at an early stage after contrast-medium injection cannot be equated with capsule formation as long as the abscess diameter increased. Parallel to the acute stage of abscess, the intraventricular pressure increased due to the rising mass effect and the spreading edma. The morphological investigations revealed on the seventh day an extreme enlargement of extracellular spaces with immense amount of edema fluid, rich in protein and fibrin. Some blood vessels in the close vicinity of the abscess showed gaps within the endothelial cell layer. When encapsulation developed, ring enhancement became more homogeneous and decreased in diameter. In spite of encapsulation, a circumscribed disturbance of the blood-brain barrier persisted which was responsible for a belated resolution of edema and a slow decrease of intracranial pressure. Only therapy with dexamethasone could effect a marked change in the course of the disease.
Animals↗
Ischemic brain edema.
Brain edema is a life-threatening complication of cerebral infarction. The molecular cascade initiated by cerebral ischemia includes the loss of membrane ionic pumps and cell swelling. Secondary formation of free radicals and proteases disrupts brain-cell membranes, causing irreversible damage. New diagnostic methods based on magnetic resonance imaging have markedly improved diagnostic accuracy. Cytotoxic and vasogenic edema is maximal by 24 to 72 hours after the ischemic event. Thrombolytics reperfuse tissue and improve outcome; when treatment is delayed, they can increase edema and blood-brain barrier opening. Although osmotherapy reduces brain water, and is used to treat ischemic edema, its efficacy remains to be proven. As the molecular events become clearer, novel treatments that block different stages of the injury cascade will be available for clinical testing.
Animals↗
The management of brain edema in brain tumors.
This review focuses on pathophysiology, clinical signs, and imaging of brain edema associated with intracranial tumors and its treatment. Brain edema in brain tumors is the result of leakage of plasma into the parenchyma through dysfunctional cerebral capillaries. The latter type of edema (ie, vasogenic edema) and the role of other types in brain tumors is discussed. Vascular endothelial growth factor-induced dysfunction of tight junction proteins probably plays an important role in the formation of edema. Corticosteroids are the mainstay of treatment of brain edema. When possible, corticosteroids should be used in a low dose (eg, 4 mg dexamethasone daily) to avoid serious side effects such as myopathy or diabetes. Higher doses of dexamethasone (16 mg/day or more), sometimes together with osmotherapy (mannitol, glycerol) or surgery, may be used in emergency situations. On tapering, one should be aware of the possible development of corticosteroid dependency or withdrawal effects.Novel therapies include vascular endothelial growth factor receptor inhibitors and corticotropin releasing factor, which should undergo further clinical testing before they can be recommended in practice.
Blood-Brain Barrier↗
Aquaporin water channels and brain edema.
Brain edema accounts for much of the morbidity and mortality associated with common neurological conditions such as head trauma, brain tumors, stroke and liver failure. Treatment options are limited to osmotic agents such as mannitol, surgical decompression, and other maneuvers, none of which correct the molecular-level mechanisms responsible for brain swelling. Recent data suggest that aquaporin (AQP) water-transporting proteins may provide a key route for water movement in the brain. AQP1 is expressed in choroid plexus and probably facilitates cerebrospinal fluid secretion. AQP4 is expressed in astrocyte foot processes near capillaries and in ependymal cells lining the ventricles -- key sites for water movement between the cellular, vascular, and ventricular compartments. AQP4 expression is markedly altered in experimental models of brain injury and swelling, and transgenic mice lacking AQP4 are partially protected from brain swelling in response to acute hyponatremia and ischemic stroke. Aquaporins and regulators of brain aquaporin expression are thus potential targets for discovery of compounds for treatment of brain swelling.
Animals↗
Relationship between changes of N-methyl-D-aspartate receptor activity and brain edema after brain injury in rats.
OBJECTIVE: To investigate the relationship between the changes of N-methyl-D aspartate (NMDA) receptor activity and brain edema after injury in rats. METHODS: The brain injury models were made by using a free-falling body. The treatment model was induced by means of injecting AP5 into lateral ventricle before brain injury; water contents in brain cortex were measured with dry-wet method; and NMDA receptor activity was detected with a radio ligand binding assay. RESULTS: The water contents began to increase at 30 minutes and reached the peak at 6 hours after brain injury. The maximal binding (B(max)) of NMDA receptor increased significantly at 15 minutes and reached the peak at 30 minutes, then decreased gradually and had the lowest value 6 hours after brain injury. Followed the treatment with AP5, NMDA receptor activity in the injured brain showed a normal value; and the water contents were lower than that of AP5-free injury group 24 hours after brain injury. CONCLUSIONS: It suggests that excessive activation of NMDA receptor may be one of the most important factors to induce the secondary cerebral impairments, and AP5 may protect the brain from edema after brain injury.
Animals↗
[Effect of glycerol administration on experimental cerebral ischemia--Part 1. Studies on lipid peroxides, prostaglandins, brain edema and brain metabolites].
Using two different models of non ischemic and transient cerebral ischemia in SHR, the effect of hyperosmolar solution with intravenous 10% glycerol on serum lipid peroxides, plasma prostaglandins (TXA2, PGI2), brain water content and brain metabolites were studied. Glycerol did not influence the levels of lipid peroxides, plasma prostaglandins and brain water content in the non ischemic rats. In the transient ischemia group, on the other hand, serum lipid peroxides were significantly reduced in the glycerol administrated group. On the study of plasma prostaglandins, there was no difference of TXA2 levels between two groups, but PGI2 levels were significantly increased in the glycerol administrated group. Brain water content was significantly decreased. And on the study of brain metabolites, ATP concentrations remained higher and lactate concentrations were lower in the glycerol administrated group compared with those in the control group. But there was no difference with pyruvate concentrations between two groups, furthermore L/P ratio improved in the glycerol administrated group. Besides the effect on reduction of brain edema as for hyperosmolar solution, glycerol may indicate improvement of ischemic impediments on brain by the action of antioxidation and reinforcement of PGI2.
Animals↗
[ON THE TREATMENT OF BRAIN EDEMA AND BRAIN SWELLING].
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Brain Edema↗
[Pathophysiology and clinical aspects of brain edema].
Brain oedema is defined as an abnormal accumulation of fluid in the brain tissue accompanied by an increased volume of the brain. It results in the intracranial hypertension directly endangering the patient's life. No causal treatment of the brain oedema is known at present. The brain oedema is not a disease, but it is a symptom of various clinical states. That is why experimental studies of its pathophysiology become the centre of attention. Though the classification of brain oedema according to the pathogenesis is still used (the vasogenic type--resulting from the increased permeability of blood-brain barrier; the cytotoxic type--caused by the cell metabolism impairment), recent papers has shown a definite retraction from such categorisation. It has been shown that neither type of brain oedema comes alone, but both can occur simultaneously during the development of the pathological state of the brain. The most important appears to be the primary insult. It affects the state of blood-brain barrier and brings about the vasogenic extracellular oedema or it can influence the cell metabolism with subsequent cytotoxic, cellular oedema. Categorisation of oedema into extracellular and cellular reflects more precisely the impairment of the homeostasis of the internal environment of the brain. Contemporary view on the classification and pathophysiological mechanisms of the brain oedema is discussed in our review.
Brain Edema↗
Transport of sodium from blood to brain in ischemic brain edema.
Brain water and sodium increase during ischemia, suggesting that the blood-brain barrier permeability to sodium is increased. To test this hypothesis we measured the permeability-surface area products of 22Na and [3H]sucrose in gerbils following 3 hours of unilateral ischemia. In animals with neurologic symptoms, unilateral carotid occlusion reduced the cerebral blood flow in the ipsilateral cerebral hemisphere to 13 +/- 4 ml/100 g/min (n = 6). The water content of the ischemic hemisphere increased from 79.0 +/- 0.6 to 80.8 +/- 0.2% (n = 7, p less than 0.001) and tissue sodium content increased from 231 +/- 17 to 359 +/- 23 mEq/kg (p less than 0.0001). However, there was a 40% reduction in the sodium permeability-surface area product of the ischemic hemisphere compared with the control side (1.65 +/- 0.44 vs 2.79 +/- 0.29 microliter/g/min, n = 6, p less than 0.001). The sucrose permeability-surface area product, a measure of blood-brain barrier integrity, was unchanged. Although ischemia was less severe in the diencephalon, the tissue water and sodium contents increased significantly on the ischemic side. In contrast to the cerebral hemisphere, however, the permeability-surface area products for both sodium and sucrose were unchanged in the ischemic diencephalon. These results suggest that the increase in tissue sodium seen in ischemic edema is not due to enhanced sodium uptake; we speculate that it results, in part, from a reduction in sodium and water clearance from the tissue.
Animals↗
Proceedings of the 12th International Symposium on Brain Edema and Brain Tissue Injury. November 10-13, 2002. Hakone, Japan.
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Animals↗
[Acute brain swelling, brain edema and brain stem function].
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Animals↗
Effect of neutropenia and granulocyte colony stimulating factor-induced neutrophilia on blood-brain barrier permeability and brain edema after traumatic brain injury in rats.
OBJECTIVE: Granulocyte colony stimulating factor (GCSF) has been used to increase systemic absolute neutrophil count (ANC) in patients with severe traumatic brain injury to reduce nosocomial infection risk. However, the effect of increasing systemic ANC on the pathogenesis of experimental traumatic brain injury has not been studied. Thus, we evaluated the effect of systemic ANC on blood-brain barrier (BBB) damage and brain edema after traumatic brain injury in rats. DESIGN: Experimental study. SETTING: Research laboratory at the University of Pittsburgh, PA. SUBJECTS: Forty-three adult male Sprague-Dawley rats. INTERVENTIONS: Protocol I: rats were randomized to receive either vinblastine sulfate to reduce ANC, GCSF to increase ANC, or saline before controlled cortical impact (CCI) of moderate overall severity. Evans blue was used to assess BBB damage at 4-24 hrs after CCI. Protocol II: rats received GCSF or saline before CCI. Brain edema was estimated at 24 hrs using wet - dry) / wet weight method. Protocol III: rats received GCSF or saline before CCI. Brain neutrophil accumulation was estimated at 24 hrs using a myeloperoxidase assay. MEASUREMENTS AND MAIN RESULTS: Physiologic variables were controlled before CCI was maintained at normal in all animals before traumatic brain injury. No rats were anemic, hypoglycemic, or hypotensive before CCI. Protocol I: compared with control, systemic ANC decreased in vinblastine-treated rats and increased in GCSF-treated rats. BBB damage correlated with systemic ANC. Protocol II: mean systemic ANC before traumatic brain injury increased 15-fold in rats given GCSF vs. control; however no difference in brain edema was observed at 24 hrs after injury between groups. Protocol III: median systemic ANC at the time of CCI was increased ten-fold in rats given GCSF vs. control. No difference in brain myeloperoxidase activity 24 hrs after CCI was observed in rats treated with GCSF vs. control. CONCLUSIONS: Systemic ANC influences BBB damage after traumatic brain injury produced by CCI. Because BBB damage and brain edema are discordant, mechanisms other than BBB damage likely predominate in the pathogenesis of brain edema after contusion. The implications of increased BBB permeability with the administration of GCSF in our model remains to be determined. Increasing systemic ANC before CCI with GCSF administration does not increase posttraumatic brain neutrophil accumulation or brain edema after CCI in rats. The finding that neutrophil infiltration is not enhanced by systemic neutrophilia suggests that the ability of GCSF-stimulated neutrophils to migrate into injured tissue may be impaired. Further studies are needed to evaluate the effects of GCSF administration on secondary injury and functional outcome in experimental models of traumatic brain injury.
Animals↗
Ultrasonic diagnosis of subdural hematomas, epidural hematomas, brain edema and brain atrophy.
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Atrophy↗