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.

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.

[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.

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.

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.

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.

Differentiation between classic and atypical meningiomas with use of diffusion tensor imaging.

BACKGROUND AND PURPOSE: The differentiation between classic and atypical meningiomas may have implications in preoperative planning but may not be possible on the basis of conventional MR imaging. Our hypothesis was that classic and atypical meningiomas have different patterns of intratumoral water diffusion that will allow for differentiation between them. MATERIALS AND METHODS: Preoperative diffusion tensor imaging (DTI) was performed in 12 classic and 12 atypical meningiomas. Signal intensity of solid-enhancing tumor regions on diffusion-weighted trace images and apparent diffusion coefficient (ADC) and fractional anisotropy (FA) maps was assessed. Regions of interest (ROIs) were placed in solid-enhancing regions, peritumoral edema, and contralateral normal-appearing white matter (NAWM) to measure tensor metrics including major (lambda(1)), intermediate (lambda(2)) and minor eigenvalues (lambda(3)) and FA and ADC values. Distribution of tensor shapes within enhancing tumors was calculated for all tumors. Differences between classic and atypical meningiomas in tumor signal intensity, intratumoral and peritumoral tensor metrics, as well as tensor shapes distribution were statistically analyzed. RESULTS: A significantly greater proportion of atypical meningiomas were isointense and hypointense on ADC maps (P = .007). Classic meningiomas had significantly lower FA (P = .012), higher ADC (P = .011), greater lambda(2) (P = .020) and lambda(3) (P = .003). There was significantly more spherical diffusion in classic than in atypical meningiomas (P = .020). All diffusion tensor metrics for peritumoral edema of the 2 tumor groups did not differ. CONCLUSION: DTI showed that intratumoral microscopic water motion is less organized in classic than in atypical meningiomas. This feature may allow for noninvasive differentiation between classic and atypical meningiomas.

[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.

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.

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.

[Identification of high-risk patients after minor craniocerebral trauma. Measurement of nerve tissue protein S 100]. / Identifikation von Hochrisikopatienten nach leichtem Schädel-Hirn-Trauma. Messung des neuroglialen Proteins S100.

The indication for an initial cranial computed tomography (CCT) in minor head trauma (MHT) patients remains the subject of discussion. The aim of this study was to investigate whether a newly developed, rapid test system (ELECSYS S100, Roche Diagnostics) might allow a diagnostically valid, reproducible measurement of S 100 in MHT patients. Blood samples were drawn from 75 MHT patients, a CCT scan was performed, and those with a post-traumatic intracranial lesion counted as CCT+. Results were compared to a healthy control group (n=17). Of the 75 patients included in the study, 14 were stratified as CCT+. The systemic concentration of S 100 in these CCT+ patients was significantly increased (0.31 microg/l) compared to the healthy control group (0.04 microg/l) as well as to the CCT-negative patients (0.08 microg/l). The ELECSYS S100 system allows a rapid, valid, and reproducible assessment of S 100B in patient serum and this concentration is significantly elevated in patients suffering from intracranial lesions as shown by initial CCT scan. Hence, this study is the basis for a multicenter trial currently underway to confirm the results of our pilot study.