[Pathophysiology of intracranial injuries]. / Pathophysiologie intrakranieller Verletzungen.

Traumatic brain injury (TBI) constitutes a heterogeneous condition that affects the most complex organ of the human body. It is commonly classified by its location as focal injury (e.g. epidural hematoma) and diffuse injury (e.g. diffuse axonal shearing injury) as well as by primary and secondary tissue injury. Accordingly, direct mechanical force causes the primary insult. The tissue damage occurring afterwards is subsumed under the term secondary brain damage. Some of these processes are overlapping and include in the early phase local cerebral ischemia resulting in excitotoxicity, which together with the triggered neuroinflammatory cascade causes the formation of cerebral edema and ultimately increased intracranial pressure once the intracranial compliance is exhausted. In survivors the long-term sequelae of the late stage include seizures caused by synaptic reorganization (incidence depending on the severity of TBI), persistent neuroinflammation promoting further neurodegeneration and increased risk for Alzheimer's disease probably because of TBI-related protein misfolding (tauopathy). Acute phase biomarkers of TBI should ideally originate from the injured brain. They should help distinguish disease severity and predict morbidity and mortality; however, the most commonly used biomarkers (S-100ß and neurone-specific enolase) show a low specificity. In theory their successors (i. e. GFAP, pNF-H) seem more specific; however, these "new kids on the block" still need to be thoroughly investigated in large scale studies.

Spectrum and potential pathogenesis of reversible posterior leukoencephalopathy syndrome.

BACKGROUND: Controversy still exists over the etiology and pathophysiology of reversible posterior leukoencephalopathy syndrome (RPLS). This large single-center case series aims to describe the clinical and imaging features of RPLS in an attempt to deduce the etiology of the disorder and the mechanisms of brain injury. METHODS: A retrospective chart and imaging review was conducted on 59 cases of RPLS in 55 patients. RESULTS: Five RPLS imaging patterns were observed: posterior predominant (n = 40), anterior predominant (n = 7), diffuse lesion (n = 7), basal ganglia predominant (n = 3), and brainstem/cerebellum predominant patterns (n = 2). RPLS resulted in permanent neurologic deficits in 14 patients and death in 4 patients. Hypertension was seen in 57 (97%) cases, and mean arterial blood pressure exceeded 140 mm Hg in 30 (51%) cases. Follow-up magnetic resonance imaging scans revealed a significant worsening of vasogenic edema in 2 cases, both with persistent hypertension. Magnetic resonance imaging scans revealed areas of ischemia in 14 cases, all within or at areas closely adjacent to vasogenic edema. Diffuse vasculopathy was seen in 8 cases. There was a lack of correlation between the presence of vasculopathy and the degree of vasogenic edema (P = .62), but a correlation was suggested between ischemia and vasculopathy (P = .02). CONCLUSIONS: This study strongly suggests that hypertension-induced vasodilation rather than vasoconstriction-mediated hypoxia is likely the major mechanism responsible for the development of vasogenic edema, and that vasoconstriction may contribute to the development of ischemia in RPLS.

[Effects of alcohol consumption on traumatic brain injury].

It has been well known that alcohol consumption affects traumatic brain injury. The mechanism of detrimental effect of ethanol on traumatic brain injury has not been clarified. This review focused on the relationship among traumatic brain injury, ethanol and aquaporin-4. We have reported that ethanol increased brain edema after brain contusion and decreased survival rates in rats. It was suggested that increasing brain edema by ethanol after brain contusion may be caused by oxidative stress. Brain edema consists of cytotoxic brain edema, vasogenic brain edema, interstitial brain edema and osmotic edema. Ethanol mainly increases cytotoxic brain edema. Both alcohol consumption and brain contusion cause oxidative stress. Antioxidant treatment decreases cytotoxic brain edema. Aquaporin-4, an water channel, was increased by ethanol 24 hr after traumatic brain injury in rat. The aquaporin-4 inhibitor decreased brain edema after brain contusion and increased survival rates under ethanol consumption. Aquaporin-4 may have strict relation between ethanol and brain edema increasing after brain contusion.

Analysis of changes in the volume of edema around brain contusions and the influencing factors: A single-center, retrospective, observational study.

ABSTRACT: Traumatic brain injury (TBI), a common neurosurgical condition, has well-known treatment guidelines. However, the mechanisms underlying the varying severity of brain edema secondary to TBI are largely unknown, leading to controversial treatments.This study seeks to measure edema volumes around brain contusions in different regions, analyze factors related to differences in edema volume and provide a theoretical basis for brain edema treatment.Data from 113 brain contusion patients treated at the Department of Neurosurgery of Fuzhou General Hospital from January 2017 to November 2019 were analyzed retrospectively. Based on computed tomography (CT) data, the patients were divided into the venous group (brain contusion in regions with large cortical veins, n = 47) and the nonvenous group (brain contusions in other regions, n = 66). Here, 3D Slicer software was used to calculate the brain contusion volume on the first CT obtained after injury and the brain contusion volume and its surrounding edema on the 5th day after injury. The brain contusion volume to surrounding edema volume ratio was calculated, and the number of patients who showed brain contusion progression requiring surgery was determined. Hematocrit (Hct), fibrinogen (Fg), and d-dimer levels within 6 hours and on the 5th day after admission were also compared.Patients in the venous group had a significantly increased percentage of area with edema around the brain contusion compared with patients in the nonvenous group (P < .05), and the 2 groups showed no significant difference in the number of patients with brain contusion progression or surgical treatment (P > .05) or Hct, Fg, or d-dimer (D-D) levels. For all patients, Hct, Fg, and D-D levels within 6 hours after admission were significantly different from those on the 5th day (P < .05 for all).Cortical venous obstruction may be the most important factor influencing edema around brain contusions. The Fg level decreased slightly, and the D-D level increased to its peak rapidly after mild-moderate TBI. This change was followed by a gradual increase in the former and a gradual decrease in the latter.

Determinants of brain swelling in pediatric and adult cerebral malaria.

Cerebral malaria (CM) affects children and adults, but brain swelling is more severe in children. To investigate features associated with brain swelling in malaria, we performed blood profiling and brain MRI in a cohort of pediatric and adult patients with CM in Rourkela, India, and compared them with an African pediatric CM cohort in Malawi. We determined that higher plasma Plasmodium falciparum histidine rich protein 2 (PfHRP2) levels and elevated var transcripts that encode for binding to endothelial protein C receptor (EPCR) were linked to CM at both sites. Machine learning models trained on the African pediatric cohort could classify brain swelling in Indian children CM cases but had weaker performance for adult classification, due to overall lower parasite var transcript levels in this age group and more severe thrombocytopenia in Rourkela adults. Subgrouping of patients with CM revealed higher parasite biomass linked to severe thrombocytopenia and higher Group A-EPCR var transcripts in mild thrombocytopenia. Overall, these findings provide evidence that higher parasite biomass and a subset of Group A-EPCR binding variants are common features in children and adult CM cases, despite age differences in brain swelling.

Pathology and new players in the pathogenesis of brain edema.

Brain edema continues to be a major cause of mortality after diverse types of brain pathologies such as major cerebral infarcts, hemorrhages, trauma, infections and tumors. The classification of edema into vasogenic, cytotoxic, hydrocephalic and osmotic has stood the test of time although it is recognized that in most clinical situations there is a combination of different types of edema during the course of the disease. Basic information about the types of edema is provided for better understanding of the expression pattern of some of the newer molecules implicated in the pathogenesis of brain edema. These molecules include the aquaporins, matrix metalloproteinases and growth factors such as vascular endothelial growth factors A and B and the angiopoietins. The potential of these agents in the treatment of edema is discussed. Since many molecules are involved in the pathogenesis of brain edema, effective treatment cannot be achieved by a single agent but will require the administration of a "magic bullet" containing a variety of agents released at different times during the course of edema in order to be successful.

[Conservative treatment of brain edema--which way is leading to Rome?]. / Konservative Therapie bei Hirnödem--welche Wege führen nach Rom?

In patients with brain edema the pathophysiology of the different forms of edema have to be considered to ensure the prompt, sensible and consistent use of the limited treatment modalities available. Brain edema may be classified into cytotoxic and vasogenic edema, these two types often coexist in one patient. Head elevation, hyperventilation, osmotic therapy and reduction of brain metabolism by sedation or hypothermia should be used closely monitoring ICP and blood pressure. In the future considering the autoregulatory capacity of the individual patient will possibly lead to a more effective action of the treatment modalities described. Further research will open new perspectives how aquaporines are involved in the genesis and mobilisation of brain edema.

Predictors of oedema type in reversible posterior leukoencephalopathy syndrome with preeclampsia or eclampsia.

OBJECTIVE: To explore the predictive factors of oedema types in reversible posterior leukoencephalopathy syndrome (RPLS) with preeclampsia (PE) and eclampsia, which is closely related to reversible lesions and clinical recovery. METHOD: We collected data from 44 consecutive patients diagnosed with RPLS in PE or eclampsia between 2013 and 2017. All patients were classified into vasogenic oedema (n = 31) or cytotoxic oedema (n = 13) groups according to magnetic resonance imaging (MRI) results. General information, clinical data, biochemical indicators and imaging features were collected retrospectively to explore the differences between the groups. Furthermore, we analysed potential predictive factors by logistic regression. RESULTS: The occurrence rates of immune disease and stillbirth, hospitalization time and the levels of serum albumin (ALB), lactate dehydrogenase (LDH), aspartate transaminase (AST) and alanine aminotransferase (ALT) were higher, while the values of systolic blood pressure (SBP), mean arterial pressure (MAP) and 24-h urine protein were lower in the cytotoxic oedema patients than those in the vasogenic oedema patients (p < .05). The ALB concentration was closely correlated with vasogenic oedema, while AST and ALT were closely correlated with cytotoxic oedema by logistic regression (p < .05). CONCLUSION: The levels of ALB, AST and ALT are potential predictors for the development of oedema in RPLS. ALB is related to vasogenic oedema by a possible mechanism of decreased colloid osmotic pressure, while AST and ALT are related to cytotoxic oedema by a possible mechanism of endothelial dysfunction.

[Cerebral edema and its treatment]. / Smegenu edema ir jos gydymas.

Cerebral edema is a life-threatening condition that develops as a result of an inflammatory reaction. Most frequently, this is the consequence of cerebral trauma, massive cerebral infarction, hemorrhages, abscess, tumor, allergy, sepsis, hypoxia, and other toxic or metabolic factors. At present, the following types of cerebral edema are differentiated: the vasogenic cerebral edema resulting from an increased permeability of the endothelium of cerebral capillaries to albumin and other plasma proteins; the cytotoxic cerebral edema resulting from the exhaustion of the energy potential of cell membranes without damage to the barrier; the hydrostatic cerebral edema resulting from disturbance of the autoregulation of cerebral blood circulation; the osmotic cerebral edema resulting from dilution of blood; and the interstitial cerebral edema resulting from acute hydrocephaly. Some authors also differentiate ischemic cerebral edema. At present, when various traumas and traumatic cerebral injuries are frequent causes of death in young people, treatment strategy for cerebral edema is of utmost importance. Monitoring of the patient's condition in the intensive care unit is a necessity. It is important to ensure proper positioning of the patient--the head should be tilted at 30 degrees in order to optimize the cerebral perfusion pressure and control of the increase in intracranial pressure. Hyperventilation should be applied. Controlled hypothermia decreases the rate of metabolism in the brain. Slightly positive fluid balance should be maintained using crystalloid or colloid (hypertonic-hyperoncotic) solutions, at the same time maintaining cerebral perfusion pressure exceeding 70 mmHg. The treatment includes administration of antihypertensive medications, nonsteroidal antiinflammatory drugs, and barbiturates. Steroids decrease the permeability of capillaries and the hemato-encephalic barrier, promoting the movement of Na(+)/K(+) ions and water through the main endothelial membrane, and therefore they are used in the treatment of vasogenic cerebral edema as well as edema caused by a cerebral tumor. Glutamate and N-methyl-D-aspartate receptor antagonists improve cerebral microcirculation and metabolism. Trometamol corrects cerebral acidosis. Extended cerebral edema is treated surgically via a bilateral decompressive craniotomy, sometimes including craniotomy of lateral and posterior fossae. The treatment of cerebral edema is complex, and positive results may be expected only if the diagnosis and the provision of assistance are timely.

[Brain edema--historical aspects and contemporary suggestions].

The aim of this article was to show the historical aspects of elaboration of the brain edema study. To draft the main stages of study development from naive medievals suggestions till the creation of modern technologies and the possibility of the brain edema neurovisualization. The possibility to watch and control these processes grants the real perspective to enhance the effectiveness of the brain edema therapy.

Space-Occupying Tumor Bed Cysts as a Complication of Modern Treatment for High-Grade Glioma.

BACKGROUND: The management of high-grade glioma (HGG) has been affected by recent landmark trials and is now more proactive. More aggressive treatment leads to hospitalization due to side effects, however. Space-occupying tumor bed cysts have been described, but not systematically assessed. We sought to analyze this complication in a contemporary HGG cohort. METHODS: We performed a retrospective review of patients with HGG treated between 2007 and 2013, identified patients with space-occupying tumor bed cysts, and reviewed their hospital notes for relevant variables. Statistical analyses were performed, and odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. RESULTS: Tumor bed cysts were found in 12 of 282 patients (4%). The main symptoms were increased intracranial pressure (n = 11), new focal deficits (n = 6), and pseudomeningocele (n = 3), presenting at a median of 19 days since the last resection. Cysts were treated with cystoperitoneal (n = 7) and ventriculoperitoneal (n = 5) shunts, resulting in clinical benefit in 75% of those treated. Intraoperative opening of ventricles is a risk factor, with an OR of 39.339. We propose a classification system comprising 3 cyst types: isolated cyst, cyst with local cerebrospinal fluid (CSF) disturbance, and cyst with global CSF disturbance. CONCLUSIONS: In modern neuro-oncology, the rate of tumor bed cysts complicating HGG management appears stable compared with historical data. Shunt implantation is feasible and effective. We propose a classification system as a common data element for comparison across future studies.

Traumatic brain edema in diffuse and focal injury: cellular or vasogenic?

The objective of this study was to confirm the nature of the edema, cellular or vasogenic, in traumatic brain injury in head-injured patients using magnetic resonance imaging techniques. Diffusion-weighted imaging methods were quantified by calculating the apparent diffusion coefficients (ADC). Brain water and cerebral blood flow (CBF) were also measured using magnetic resonance and stable Xenon CT techniques. After obtaining informed consent, 45 severely injured patients rated 8 or less on Glasgow Coma Scale (32 diffuse injury, 13 focal injury) and 8 normal volunteers were entered into the study. We observed that in regions of edema, the ADC was reduced, signifying a predominantly cellular edema. The ADC values in diffuse injured patients without swelling were close to normal and averaged 0.89 +/- 0.08. This was not surprising, as ICP values for these patients were low. In contrast, in patients with significant brain swelling ADC values were reduced and averaged 0.74 +/- 0.05 (p < 0.0001), consistent with a predominantly cellular edema. We also found that the CBF in these regions was well above ischemic threshold at time of study. Taking these findings in concert, it is concluded that the predominant form of edema responsible for brain swelling and raised ICP is cellular in nature.

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.

MR imaging correlates of survival in patients with high-grade gliomas.

BACKGROUND AND PURPOSE: For patients with malignant gliomas, clinical data-including age, perioperative Karnofsky Performance Status (KPS), and tumor resection-and tumor imaging features-including necrosis and edema-have been found to correlate with survival. The purpose of this study was to assess the validity of these results and determine whether other imaging features are useful in predicting survival. METHODS: We analyzed the relationship between 15 imaging variables obtained from contrast-enhanced MR imaging scans and survival in patients with grade III (n = 43) and grade IV (n = 110) glioblastoma multiforme (GBM) gliomas. Image analysis was performed by 2 neuroradiologists who were blinded to clinical data. The Kaplan-Meier method was used to estimate survival probabilities. Univariable Cox models were used to assess the impact of imaging features on survival. A recursive partitioning analysis also was performed. RESULTS: As expected, age and KPS scores had significant prognostic value for both tumor grades. The extent of resection was not a statistically meaningful predictor of survival. For GBM, univariable analysis revealed the following imaging features to be significant, (hazard ratios in parentheses): noncontrast-enhancing tumor (nCET, 0.55), edema (1.62), satellites (1.74), and multifocality (4.34). For grade III tumors, the Cox hazard ratio for necrosis was 4.43 (P = .014) and correlated with a poor outcome and survival rates comparable to GBM patients. Lack of nCET, multifocality, and satellite lesions also were correlated with shortened survival. CONCLUSION: Of 15 tumor imaging features in GBM patients, only nCET, edema, and multifocality/satellites are statistically significant prognostic indicators. The survival advantage of nCET is a novel finding.

Clinical and radiologic features of cerebral edema in fulminant hepatic failure.

OBJECTIVE: To describe a series of consecutive patients with fulminant hepatic failure (FHF) and to present a new classification system for brain edema, an important cause of mortality in such patients. DESIGN: We reviewed 22 computed tomographic (CT) scans of the brain in 12 patients with FHF and classified the severity of cerebral edema by using predefined criteria. RESULTS: No cerebral edema was detected on CT scans in four patients with stage 1 or 2 hepatic encephalopathy at the time of admission, but it was noted in seven of eight patients with stage 3 or 4 hepatic encephalopathy. The severity of brain edema on CT scans was significantly correlated (P < 0.001) with the stage of hepatic encephalopathy. Three of the four patients who had stage 1 or 2 hepatic encephalopathy at the time of initial assessment ultimately had a good outcome. Of seven patients with stage 3 encephalopathy, two had rapid deterioration to brain death, three died of nonneurologic causes, and two had a good outcome after liver transplantation. One patient with stage 4 hepatic encephalopathy died, and autopsy showed cerebral edema. CONCLUSION: Stage 3 or 4 hepatic encephalopathy is associated with cerebral edema that can be detected on CT scans. The clinical and radiologic signs of cerebral edema in patients who have progression to stage 3 hepatic encephalopathy can be reversed with conventional treatment of increased intracranial pressure. Whether early recognition and treatment of cerebral edema result in increased survival of patients with FHF remains to be determined.

Characterization of multiple sclerosis plaques with T1-weighted MR and quantitative magnetization transfer.

PURPOSE: To investigate the relationship between the appearance of multiple sclerosis lesions identified on unenhanced T1-weighted images and their corresponding magnetization transfer ratios. METHODS: A total of 119 white matter lesions seen on T2-weighted images in 17 patients with multiple sclerosis were evaluated. Axial T1-weighted images were used to classify the lesions as isointense to white matter (10 lesions), hypointense to white matter but hyperintense to gray matter (44 lesions), hypointense to gray matter (59 lesions), and relatively isointense to cerebrospinal fluid (6 lesions). The magnetization transfer ratio of each lesion was calculated, and an average magnetization transfer ratio for each subcategory was determined. RESULTS: The magnetization transfer ratio values became progressively lower with increasing hypointensity of lesions on T1-weighted images. The average magnetization transfer ratio for lesions isointense to white matter, hypointense to white matter but hyperintense to gray matter, hypointense to gray matter, and relatively isointense to cerebrospinal fluid was 34.90 +/- 2.67 mean +/- SD), 30.93 +/- 3.57, 27.27 +/- 3.56, and 23.62 +/- 2.83, respectively. All groups were significantly different from each other. CONCLUSION: Lesions isointense to white matter exhibited higher magnetization transfer ratio values than lesions that were hypointense. These findings are consistent with relative preservation of the myelin structure in the former, perhaps indicating that these lesions are predominantly inflammatory (edematous) in nature. The proportionately lower magnetization transfer ratio values of lesions that appear progressively more hypointense on T1-weighted images may reflect varying degrees of demyelination, with increasing lesion hypointensity corresponding to more breakdown in the macromolecular structure. These results suggest that T1-weighted images may be useful in characterizing the underlying pathologic substrate in multiple sclerosis plaques.

A simple practical classification of cerebral infarcts on CT and its interobserver reliability.

PURPOSE: To test the interobserver reliability of a simple method of classifying cerebral infarcts as seen on CT brain scans, which might allow differentiation of the site and size of the infarct from infarct swelling and hemorrhagic transformation. METHOD: Two experienced neuroradiologists independently reviewed 119 CT brain scans showing recent small to large cortical and subcortical cerebral infarcts and classified each for site and size, amount of swelling, and hemorrhagic transformation blind to clinical information. Six less experienced general radiologists in training classified 33 of the CT scans blind to clinical information. Interobserver agreement was calculated using unweighted kappa statistics. RESULTS: The kappa statistics between the two experienced neuroradiologists were: (a) 0.78 for site and size (95% confidence interval 0.69-0.87); (b) 0.8 for swelling (95% confidence interval, 0.68-0.92); and (c) 0.3 for hemorrhagic transformation (95% confidence interval, 0-0.77); indicating "good," "excellent," and "fair" agreement, respectively. Agreement for the less experienced radiologists was fair to excellent. CONCLUSION: The cerebral infarct morphologic classification is simple, quick, and reliable and therefore practical. It usefully distinguishes between infarcts of similar site and size but with different amounts of swelling and hemorrhagic transformation, thus facilitating study of factors such as the influence of drug treatment on infarct swelling, which might influence clinical outcome. Although developed for CT, it could be used equally for MR imaging and has applications in research and clinical practice.

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

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 (r(s) = 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 x 0.7, which can be used to predict the chance of recurrence based on findings on CT scans (r(s) = 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.

Role of cerebral endothelium in brain oedema.

The view that cerebral endothelial cells represent the cellular basis of the blood-brain barrier has been generally accepted. The regulation of transport processes operating in the cerebral endothelial cells is currently of great interest. Our knowledge of these regulatory mechanisms is briefly reviewed here with special regard to the molecular processes involved in the formation of brain oedema and emphasis on new therapeutic means for its prevention.

Brain edema -- a new classification.

Brain edema is a reaction to any brain injury and can be the first stage in the beginning of intracranial hypertension. This paper puts forth a modern classification of brain edema types, based on a etiopathogenic interpretation. The hydroelectrolitic and/or proteinic buildup can occur within cells and/or in the extracellular space and differentiates three types of brain edema: cellular brain edema; extracellular brain edema and combined brain edema. Cellular brain edema (cytotoxic brain edema) occurs through intracellular hyperosmolarity or extracellular hypotonicity. Extracellular brain edema (interstitial) appears as a result of the buildup of edema fluid in the extracellular space of the brain parenchyma and can be: hydrostatic extracellular brain edema (through ultrafiltration), oncotical extracellular brain edema (vasogen brain edema) and hydrocephalic extracellular brain edema. Combined brain edema includes in variable ratios both types of brain edema, cellular and extracellular; they can be present together from the beginning or can appear successively.