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The Passage of S100B from Brain to Blood Is Not Specifically Related to the Blood-Brain Barrier Integrity  [PDF]
Andrea Kleindienst,Christian Schmidt,Hans Parsch,Irene Emtmann,Yu Xu,Michael Buchfelder
Cardiovascular Psychiatry and Neurology , 2010, DOI: 10.1155/2010/801295
Abstract: Following brain injury, S100B is released from damaged astrocytes but also yields repair mechanisms. We measured S100B in the cerebrospinal fluid (CSF) and serum (Cobas e411 electrochemiluminescence assay, Roche) longitudinally in a large cohort of patients treated with a ventricular drainage following traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH). Statistical analysis was performed with SPSS software applying the Mann-Whitney rank sum test or chi-test where appropriate. S100B in CSF and serum was significantly increased following TBI ( ) and SAH ( ) for at least one week following injury. High S100B levels in CSF and serum were inconsistent associated with outcome. The passage of S100B from CSF to blood ( ) was significantly decreased although the albumin quotient suggested an “open” blood-CSF barrier. Events possibly interfering with the BBB did not affect the S100B passage ( ). In conclusion, we could not confirm S100B measurements to reliably predict outcome, and a compromised blood-CSF barrier did not affect the passage of S100B from CSF to serum. 1. Introduction There is a desire for a reliable indicator to accurately determine the extent of brain injury and consequent prognosis. The measurement of putative biochemical markers, such as the S100B protein, has been proposed in this role. Furthermore, such a biomarker would aid in identifying events contributing to secondary brain damage and monitoring the success of therapeutic interventions. Over the past decade, numerous studies have reported a positive correlation between S100B levels in blood or cerebrospinal fluid (CSF) and impaired neurological function following traumatic brain injury (TBI) [1], intracerebral hemorrhage [2], stroke [3], perinatal brain damage [4], septic encephalopathy [5], bacterial meningitis [5], or even in major depression [6], and extracranial injuries [7]. Furthermore, S100B levels have been used to monitor therapeutic effects such as the application of hypertonic saline in TBI [8] or of naloxone in epilepsia [9]. However, considerable evidence indicates that S100B is not only a biomarker of brain damage but also represents ongoing neuroregeneration [10]. Moreover, contradictory data interpretation exists with regard to the contribution of an altered blood-brain barrier (BBB) to S100B serum levels [11, 12]. Although in cell cultures the injury-induced S100B release continues to increase up to 48 hours [13, 14], in patients S100B serum levels have been reported to be highest directly after the injury and become normalized within 24 hours in a high
Advanced Neuromonitoring and Imaging in Pediatric Traumatic Brain Injury  [PDF]
Stuart H. Friess,Todd J. Kilbaugh,Jimmy W. Huh
Critical Care Research and Practice , 2012, DOI: 10.1155/2012/361310
Abstract: While the cornerstone of monitoring following severe pediatric traumatic brain injury is serial neurologic examinations, vital signs, and intracranial pressure monitoring, additional techniques may provide useful insight into early detection of evolving brain injury. This paper provides an overview of recent advances in neuromonitoring, neuroimaging, and biomarker analysis of pediatric patients following traumatic brain injury. 1. Introduction Pediatric traumatic brain injury (TBI) remains one of the leading causes of acquired disability and death, with the highest combined rates of TBI-related emergency room visits, hospitalizations, and deaths occurring in the youngest children [1]. Monitoring intracranial pressure (ICP) and cerebral perfusion pressure (CPP), repeat neurological assessments, CT scanning, and vital signs are considered the standard part of care following severe pediatric TBI. However, these assessments may not be sufficient to detect subtle and early secondary insults to the brain, such as ischemia, cerebral cytotoxic or vasogenic edema, and metabolic crisis. With the advent of newer methods of neuromonitoring, neuroimaging, and biomarker development, the concept of advanced neuromonitoring in neurocritical care has evolved in adults following severe TBI and is beginning to be explored in children. In this paper, we will discuss the role of advanced neuromonitoring in children following TBI. 2. Materials and Methods We performed an extensive review of the medical literature regarding advanced neuromonitoring in children following TBI utilizing Pubmed. Search terms included “pediatric,” “child,” “neonate,” “brain,” “traumatic brain injury,” “multimodality,” “monitoring,” “brain oxygen,” “licox,” “jugular venous saturation,” “microdialysis,” “transcranial doppler,” “neuroimaging,” “diffusion weighted imaging,” “susceptibility weighted imaging,” “diffusion tensor imaging,” “ magnetic resonance spectroscopy,” “biospecimen,” “biomarker,” “common data elements,” “S100B,” “neuron specific enolase,” “myelin basic protein,” and “glial fibrillary acidic protein,” and the period of search was from 1987 to 2011. The authors are pediatric neurocritical care specialists and have extensive clinical experience caring for pediatric patients with TBI and research experience in clinical pediatric TBI and experimental animal models of pediatric TBI. 3. Results and Discussion 3.1. Neuromonitoring following Severe TBI in Children 3.1.1. Brain Tissue Oxygen Monitoring One of the primary management goals of the severely head injured child is to minimize
Insulin, intracerebral glucose and bedside biochemical monitoring utilizing microdialysis
Carl-Henrik Nordstr?m
Critical Care , 2008, DOI: 10.1186/cc6826
Abstract: The study published by Schlenk and colleagues in the previous issue of Critical Care was initiated by clinical experience that, after subarachnoid hemorrhage, hyperglycemia is strongly associated with complications and impaired neurological recovery. Utilizing intracerebral microdialysis and bedside biochemical monitoring, Schlenk and colleagues made the unexpected observation that insulin caused a significant decrease in the interstitial cerebral glucose concentration although the blood glucose level remained unaffected [1].The technique of microdialysis was introduced more than 30 years ago for monitoring the animal brain, and has become a standard technique in neuroscience with well over 11,000 publications [2,3]. Microdialysis was introduced as a routine technique within neurointensive care in 1995. The chemical variables generally analyzed and displayed at the bedside are those related to glycolysis (glucose, pyruvate, lactate) as well as those of glycerol and glutamate. A simplified diagram of intermediary metabolism is shown in Figure 1. The figure also shows data for these chemical variables in the normal human brain during wakefulness [4].Since glucose is the main – or sole – substrate for cerebral energy metabolism under normal conditions, the possibility of measuring the glucose interstitial concentration is of obvious clinical interest. The calculated lactate/pyruvate ratio indicates the cytoplasmatic redox state, which reflects tissue oxygenation and the efficacy of oxidative metabolism. The ratio can be expressed in terms of the lactate dehydrogenase equilibrium: [NADH] [H+]/[NAD+] = [lactate]/[pyruvate] × KLDH.As indicated in Figure 1, glycerol is related to intermediary energy metabolism. The glycerol level will accordingly vary with the cerebral metabolic rate [4]. The changes in the glycerol concentration caused by variations in the glycolytic rate are limited, however, and a marked increase in the cerebral glycerol level indicates degradation of t
A Model for Mild Traumatic Brain Injury that Induces Limited Transient Memory Impairment and Increased Levels of Axon Related Serum Biomarkers  [PDF]
Elham Rostami,Johan Davidsson,Kian Chye Ng,Jia Lu,John Walker,Stefan Plantman,Bo-Michael Bellander,Denes V. Agoston,M?rten Risling
Frontiers in Neurology , 2012, DOI: 10.3389/fneur.2012.00115
Abstract: Mild traumatic brain injury (mTBI) is one of the most common neuronal insults and can lead to long-term disabilities. mTBI occurs when the head is exposed to a rapid acceleration-deceleration movement triggering axonal injuries. Our limited understanding of the underlying pathological changes makes it difficult to predict the outcome of mTBI. In this study we used a scalable rat model for rotational acceleration TBI, previously characterized for the threshold of axonal pathology. We have analyzed whether a TBI just above the defined threshold would induce any detectable behavioral changes and/or changes in serum biomarkers. The effect of injury on sensory motor functions, memory and anxiety were assessed by beam walking, radial arms maze and elevated plus maze at 3–7 days following TBI. The only behavioral deficits found were transient impairments in working and reference memory. Blood serum was analyzed at 1, 3, and 14 days after injury for changes in selected protein biomarkers. Serum levels of neurofilament heavy chain and Tau, as well as S100B and myelin basic protein showed significant increases in the injured animals at all time points. No signs of macroscopic injuries such as intracerebral hematomas or contusions were found. Amyloid precursor protein immunostaining indicated axonal injuries at all time points analyzed. In summary, this model mimics some of the key symptoms of mTBI, such as transient memory impairment, which is paralleled by an increase in serum biomarkers. Our findings suggest that serum biomarkers may be used to detect mTBI. The model provides a suitable foundation for further investigation of the underlying pathology of mTBI.
Pharmacokinetics of BPA in Gliomas with Ultrasound Induced Blood-Brain Barrier Disruption as Measured by Microdialysis  [PDF]
Feng-Yi Yang, Yi-Li Lin, Fong-In Chou, Yu-Chuan Lin, Yen-Wan Hsueh Liu, Lun-Wei Chang, Yu-Ling Hsieh
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0100104
Abstract: The blood-brain barrier (BBB) can be transiently disrupted by focused ultrasound (FUS) in the presence of microbubbles for targeted drug delivery. Previous studies have illustrated the pharmacokinetics of drug delivery across the BBB after sonication using indirect visualization techniques. In this study, we investigated the in vivo extracellular kinetics of boronophenylalanine-fructose (BPA-f) in glioma-bearing rats with FUS-induced BBB disruption by microdialysis. After simultaneous intravenous administration of BPA and FUS exposure, the boron concentration in the treated brains was quantified by inductively coupled plasma mass spectroscopy. With FUS, the mean peak concentration of BPA-f in the glioma dialysate was 3.6 times greater than without FUS, and the area under the concentration-time curve was 2.1 times greater. This study demonstrates that intracerebral microdialysis can be used to assess local BBB transport profiles of drugs in a sonicated site. Applying microdialysis to the study of metabolism and pharmacokinetics is useful for obtaining selective information within a specific brain site after FUS-induced BBB disruption.
Technical aspects of an impact acceleration traumatic brain injury rat model with potential suitability for both microdialysis and PtiO2 monitoring  [PDF]
Emilie Carré,Emmanuel Cantais,Olivier Darbin,Jean-Pierre Terrier,Michel Lonjon,Bruno Palmier,Jean-Jacques Risso
Quantitative Biology , 2007, DOI: 10.1016/j.jneumeth.2004.04.037
Abstract: This report describes technical adaptations of a traumatic brain injury (TBI) model-largely inspired by Marmarou-in order to monitor microdialysis data and PtiO2 (brain tissue oxygen) before, during and after injury. We particularly focalize on our model requirements which allows us to re-create some drastic pathological characteristics experienced by severely head-injured patients: impact on a closed skull, no ventilation immediately after impact, presence of diffuse axonal injuries and secondary brain insults from systemic origin...We notably give priority to minimize anaesthesia duration in order to tend to banish any neuroprotection. Our new model will henceforth allow a better understanding of neurochemical and biochemical alterations resulting from traumatic brain injury, using microdialysis and PtiO2 techniques already monitored in our Intensive Care Unit. Studies on efficiency and therapeutic window of neuroprotective pharmacological molecules are now conceivable to ameliorate severe head-injury treatment.
Intracerebral haemorrhage pathophysiology: time is brain  [cached]
Anna Poggesi,Domenico Inzitari
Reviews in Health Care , 2011, DOI: 10.7175/rhc.v2i1s.46
Abstract: Intracerebral haemorrhage is associated with high mortality and morbidity. Cerebral small vessel disease, either due to hypertensive small vessel disease or to amyloid angiopathy, is the common substrate for primary spontaneous intracerebral haemorrhage. The current understanding of brain injury induced by intracerebral haemorrhage is based on both clinical and experimental studies. The initial injury immediately after its onset is from the direct mechanical force of the expanding hematoma, resulting in cytotoxic edema and cellular necrosis. After this, the degrading hematoma releases its breakdown products, which lead to the activation of oxygen free radicals, matrix metalloproteinases, complement proteins and inflammatory markers, thus determining an increase of the BBB permeability, the recruitment of inflammatory cells, apoptosis, and ultimately the exacerbation of cerebral edema and neuronal death. Evidence suggests that early and aggressive medical management and specialist care can improve the overall outcome in patients with intracerebral haemorrhage. The growing insight into the molecular pathophysiological mechanisms may contribute to the development of neuroprotective strategies.
Analyses of cerebral microdialysis in patients with traumatic brain injury: relations to intracranial pressure, cerebral perfusion pressure and catheter placement
David W Nelson, Bj?rn Thornquist, Robert M MacCallum, Harriet Nystr?m, Anders Holst, Anders Rudehill, Michael Wanecek, Bo-Michael Bellander, Eddie Weitzberg
BMC Medicine , 2011, DOI: 10.1186/1741-7015-9-21
Abstract: Cerebral MD, ICP and CPP were monitored in 90 patients with TBI. Data were extensively analyzed, using over 7,350 samples of complete (hourly) MD data sets (glucose, lactate, pyruvate and glycerol) to seek representations of ICP, CPP and MD that were best correlated. MD catheter positions were located on computed tomography scans as pericontusional or nonpericontusional. MD markers were analyzed for correlations to ICP and CPP using time series regression analysis, mixed effects models and nonlinear (artificial neural networks) computer-based pattern recognition methods.Despite much data indicating highly perturbed metabolism, MD shows weak correlations to ICP and CPP. In contrast, the autocorrelation of MD is high for all markers, even at up to 30 future hours. Consequently, subject identity alone explains 52% to 75% of MD marker variance. This indicates that the dominant metabolic processes monitored with MD are long-term, spanning days or longer. In comparison, short-term (differenced or Δ) changes of MD vs. CPP are significantly correlated in pericontusional locations, but with less than 1% explained variance. Moreover, CPP and ICP were significantly related to outcome based on Glasgow Outcome Scale scores, while no significant relations were found between outcome and MD.The multitude of highly perturbed local chemistry seen with MD in patients with TBI predominately represents long-term metabolic patterns and is weakly correlated to ICP and CPP. This suggests that disturbances other than pressure and/or flow have a dominant influence on MD levels in patients with TBI.Cerebral microdialysis (MD) has been used to monitor patients with traumatic brain injury (TBI) for over a decade, but the methodology has not yet found a clear place in the neurointensive care unit (NICU) arsenal of multimodal monitoring [1,2]. The commonly monitored parameters that are advocated to follow dynamic metabolic changes in viable but vulnerable tissue (and their current predominant int
Preclinical care of children with traumatic brain injury (TBI)
Sefrin, Peter,Brandt, Michael,Kredel, Markus
GMS German Medical Science , 2004,
Abstract: The fact that injuries caused by accidents are the most common cause of death in children and adolescents in Germany gave rise to the study, which mainly deals with traffic accidents in this group. 200,221 records of emergency-service physicians in Bavaria which cover the period 1995-1999 were analysed with respect to the importance of traumatic brain injury (TBI) in children and adolescents (n = 721 - representing 45.8% of traffic injuries in this age group). The highest incidence of TBI was in summer (34.3%) and in the evening between 16.00 and 18.00 (23.7%). The time taken between accident and arrival of the emergency services was 8.8 ± 3.1 minutes. The preclinical phase lasted 19.3 ± 5.8 minutes. The probability of having an accident with TBI increases with age, the maximum being in the age-range 7 - 14 years (61.6%). Boys (63.2%) were almost twice as susceptible to injury as girls. 36.8% of all cases had no noticeable neurological disorder, 71.1% resulted in a Glasgow Coma Scale (GCS) score of 15. Only 6.3% had most severe neurological disorders, resulting in a GCS score of 3 - 5. Circulation parameters in the form of adapted hypotension were abnormal in only 3.4%, 21.9% of the children had a bradycardia and in 12.3% the blood oxygen saturation fell below 94%. The most frequent intervention was the laying of an i.v. line for infusions. 8.6% of the patients were intubated to allow for ventilation with oxygen. Analgesics were given in 16.7% of the cases. In 84.7% of all cases, the condition was stable and in only 3.3% was a severe deterioration to be observed. The assessments were made using both the National Advisory Committee for Aeronautics (NACA) and Glasgow Coma Scales (GCS). Discrepancies occurred, as a NACA scale of I - III and a GCS score of < 9 was reported in 4.9% of cases. In contrast a NACA scale of IV - VI was reported with a GCS score of 15 in 30% of all cases. TBI symptoms in children are less obvious than in adults, which leads to an age-dependent restriction in implementing therapeutic measures. If these restrictions are a result of misinterpretation of the situation or due to a lack of practice in the preclinical phase, then further training and education of the physicians involved in emergency service work are necessary.
Cerebral perfusion pressure, microdialysis biochemistry and clinical outcome in patients with traumatic brain injury
Theoniki Paraforou, Konstantinos Paterakis, Konstantinos Fountas, George Paraforos, Achilleas Chovas, Anastasia Tasiou, Maria Mpakopoulou, Dimitrios Papadopoulos, Antonios Karavellis, Apostolos Komnos
BMC Research Notes , 2011, DOI: 10.1186/1756-0500-4-540
Abstract: Thirty four individuals with severe brain injury hospitalized in an intensive care unit participated in this study. Microdialysis data were collected, along with ICP and CPP values. Glasgow Outcome Scale (GOS) was used to evaluate patient outcome at 6 months after injury. Fifteen patients with a CPP greater than 75 mmHg, L/P ratio lower than 37 and Glycerol concentration lower than 72 mmol/l had an excellent outcome (GOS 4 or 5), as opposed to the remaining 19 patients. No patient with a favorable outcome had a CPP lower than 75 mmHg or Glycerol concentration and L/P ratio greater than 72 mmol/l and 37 respectively. Data regarding L/P ratio and Glycerol concentration were statistically significant at p = 0.05 when patients with favorable and unfavorable outcome were compared. In a logistic regression model adjusted for age, sex and Glasgow Coma Scale on admission, a CPP greater than 75 mmHg was marginally statistically significantly related to outcome at 6 months after injury.Patients with favorable outcome had certain common features in terms of microdialysis parameters and CPP values. An individualized approach regarding CPP levels and cut -off points for Glycerol concentration and L/P ratio are proposed.Traumatic Brain Injury (TBI) is a major cause of death and disability [1]. Beyond the primary injury, the secondary insults account for an unfavorable outcome [2]. It is now feasible to monitor and record physiological variables with computerized multimodality monitoring systems in the neurointensive care unit patients. Monitoring assists the physician to implement the appropriate therapy and gives information about the expected outcome [3,4]. It has been shown that poor outcome is related to high Intracranial Pressure (ICP), and low Cerebral Perfusion Pressure (CPP) [5-7]. Besides that, brain metabolic status, as it is expressed via glucose, glycerol and lactate-pyruvate (L/P) ratio has also been correlated to clinical outcome in various studies. High values of L
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