Therapeutic effect of mild hypothermia on severe traumatic head injury

ldhypothermia (33 35℃ )isbeneficialforbrainprotectionandthusreducesthemortalityofthepatientswithseveretraumaticbraininjury (TBI) ,whichhasbeen provedbyclinicalandexperimentalevidences .1,2 However ,hypothermialeadstosuchcomplicationsasseveresecondaryinfectionsandshockduringrewarming .1InordertofurtherevaluatetheeffectofhypothermiaonsevereTBI ,wetreatedsuch patientswithmildhypothermiaandnormothermia ,respectively ,ananalyzedtheirclinicaleffectsprospectively .METHODSClinicaldataBetween 199…     

S-100 beta reflects the extent of injury and outcome, whereas neuronal specific enolase is a better indicator of neuroinflammation in patients with severe traumatic brain injury

It has been hypothesized that immunoactivation may contribute to brain damage and affect outcome after traumatic brain injury (TBI). In order to determine the role of inflammation after TBI, we studied the interrelationship of the immune mediators sICAM-1 and IL-6 with the levels of S-100beta and neuronal specific enolase (NSE), both recognized markers of brain damage. In addition, the extent and type of cerebral injury and the neurological outcome were related to these measured markers of injury. An evident elevation of S-100beta (range of means: 2.7-81.4 ng/mL) and NSE (range of means: 2.0-81.3 ng/mL) was observed in CSF of all 13 patients during the first 3 posttraumatic days and decreased over 2 weeks. In parallel, the production of sICAM-1 (range of means: 0.7-11.9 ng/mL) and IL-6 (range of means: 0.1-8.2 ng/mL) was also markedly enhanced in CSF. The CSF means of S-100beta and NSE per patient correlated with IL-6 (r = 0.60, p < 0.05; and r = 0.64, p < 0.05, respectively), whereas the corresponding means in serum showed a significant correlation only between NSE and IL-6 (r = 0.56, p < 0.05). Maximal CSF values of NSE and sICAM-1 correlated with each other (r = 0.57, p < 0.05). The contusion sizes assessed on the CT scans correlated with the means of S-100beta (r = 0.63, p < 0.05) and NSE (r = 0.71, p < 0.05) in CSF and with the mean of S-100beta in serum, although not statistically significant (r = 0.52, p = 0.06), but not with serum NSE. Interestingly, linear regression analysis demonstrated that means of S-100beta in CSF (r = 0.78, p = 0.002) and serum (r = 0.82, p < 0.001) correlated with the GOS. These results indicate that the elevation of these parameters in CSF depends on the extent of injury and that S-100beta may be a predictor of outcome after TBI, whereas NSE reflects better the inflammatory response.     

Neurocognitive outcome and serum biomarkers in inflicted versus non-inflicted traumatic brain injury in young children

Traumatic brain injury (TBI) in infants and toddlers is frequently explained by child abuse. This study compared 6-month outcome in children with inflicted TBI (iTBI) or non-inflicted TBI (nTBI) who were injured before 3 years of age, and assessed the relationship between outcome and serum concentrations of neuron-specific enolase (NSE), S100B, and myelin-basic protein (MBP). Children with iTBI (n = 15) or nTBI (n = 15) of varying severity were assessed 6 months after injury using the Glasgow Outcome Scale (GOS), Vinel and Adaptive Behavior Scale (VABS), and an intelligence quotient (IQ) measure. Serum concentrations of NSE, S100B, and MBP were measured soon after injury and every 12 h, for up to 5 days. Groups were matched by ethnicity, gender, socioeconomic status, and injury severity. Student's t-tests, analysis of covariance, or nonparametric tests assessed between-group differences for GOS, IQ, and biomarkers; correlation coefficients assessed relationships between outcome and biochemical markers. Functional and cognitive tests showed significant between-group differences (p < or = 0.05); the iTBI group performed more poorly (GOS, 2.00 +/- 1.00 vs.1.23 +/- 0.60; VABS, 95.92 +/- 14.05 vs. 115.80 +/- 20.02; IQ, 69.00 +/- 20.85 vs. 97.33 +/- 23.66). Significant between-group differences (iTBI vs. nTBI) were found for time to peak NSE (66.48 +/- 53.56 vs.8.11 +/- 11.58), S100B (43.30 +/- 51.41 vs. 8.21 +/- 8.29), and MBP (77.66 +/- 56.77 vs. 21.63 +/- 28.39). Time to peak concentrations were significantly correlated with outcome measures. Children with iTBI are at risk for poorer outcome. Acute measurement of NSE, S100B, and MBP serum concentrations may provide a quantitative predictor of outcome after TBI in young children. Outcome may be due to the mechanism of iTBI, cumulative effects of unreported TBI, and/or other unidentified risk factors.     

F2-isoprostane and neuron-specific enolase in cerebrospinal fluid after severe traumatic brain injury in infants and children

It has been hypothesized that oxidative stress plays an important role in mediating secondary damage after traumatic brain injury (TBI). To study the relationship between lipid peroxidation, clinical variables, and neuronal damage in pediatric TBI, we measured levels of F2-isoprostane, a marker of lipid peroxidation, and neuron-specific enolase (NSE), a marker of neuronal damage, in serial cerebrospinal fluid (CSF) samples from 23 infants and children with severe TBI (Glasgow Coma Scale score <8). These were compared to CSF samples from 10 uninjured pediatric controls. On d1 after injury, F2-isoprostane was increased 6-fold vs. control (36.59+/-8.96 pg/ml vs. 5.64+/-8.08 pg/ml, p=0.0035) and NSE was increased 10-fold (100.62+/-17.34 ng/ml vs. 8.63+/-2.76 ng/ml, p=0.0002). Multivariate analysis of F2-isoprostane levels and selected clinical variables showed a trend toward an inverse association with time after injury (p=0.0708). Multivariate analysis of NSE levels and selected variables showed a positive association between d1 NSE and F2-isoprostane (p=0.0426). CSF F2-isoprostane increases early after TBI in infants and children and is correlated with NSE, supporting a role for oxidative stress in the evolution of secondary damage early after severe TBI in infants and children.     

Cerebrospinal fluid apolipoprotein E concentration decreases after traumatic brain injury

The APOE epsilon4 allele has been associated with unfavorable outcome after several types of acute brain injury, yet the biological mechanisms underlying this observation are poorly understood. Postmortem and experimental brain injury studies suggest the presence of increased amounts of apolipoprotein E (apoE) within the neuropil after acute brain injury. We assayed the concentration of apolipoprotein E in the cerebrospinal fluid (CSF) of non-injured controls and patients with traumatic brain injury (TBI) to determine whether differences exist, and if these differences correlate with injury severity and clinical outcome. CSF apoE and S100B, a marker of injury severity, were measured by enzyme linked immunosorbant assay. CSF was sampled from 27 traumatic brain injury patients (mean age 32, median 25, range 16-65 years) within 3 days of injury, and 28 controls (mean age 40, median 37, range 19-73 years). The TBI patients all had a Glasgow Coma Score (GCS) of less than eight (i.e., severe head injury). Clinical outcome was determined using the Glasgow Outcome Score (GOS). The average concentration of apoE in the CSF of controls was 12.4 mg/L (95% CI: 10.5-14.3 mg/L) and in TBI patients was 3.7 mg/L (95% CI: 2.1-4.1 mg/L; Mann-Whitney: p < 0.0001). In contrast, the concentration of S100B in the CSF of TBI patients was significantly higher than that of controls (Mann-Whitney: p < 0.0001). We speculate that apoE is retained within the parenchyma of the central nervous system in response to injury where in view of previous data, it may have a protective role.     

Computed tomography-estimated specific gravity of noncontused brain areas as a marker of severity in human traumatic brain injury

In this study, we assessed the relationship between brain estimated specific gravity (eSG) and clinical symptoms, therapeutic intensity level, and outcome in human traumatic brain injury (TBI). Brain weight, volume, and eSG of the noncontused hemispheric areas were measured from computed tomography (CT) DICOM images on the initial (5 +/- 6 h) CT of 120 patients with severe TBI. Control values were obtained from 40 healthy patients. The eSG of the noncontused hemispheric areas was significantly higher in TBI patients than in controls. eSG was higher in patients having a Marshall CT classification of 3 or 4 or a low initial Glasgow coma score. Two groups were defined according to the eSG of the noncontused hemispheric areas: less than (n = 83, 69%) or more than (n = 37, 31%) the threshold of normality (defined as 1.96 sd above normal = 1.0355 g/mL). The occurrence of mydriasis, use of osmotherapy at the scene of the accident, and therapeutic intensity level were higher in the increased eSG group. The outcome at intensive care unit discharge was worse in patients with an increased eSG although the difference was no longer significant at 1 yr. eSG determination by CT analysis might be relevant in the early management of TBI.     

Coagulation abnormalities associated with severe isolated traumatic brain injury: cerebral arterio-venous differences in coagulation and inflammatory markers

Although coagulopathy is known to be the major contributor to a poor outcome of traumatic brain injury (TBI), the mechanisms that trigger coagulation abnormalities have not been studied in detail. We undertook a prospective observational study at a neurosurgical ICU (NICU) in a university hospital. We examined 11 patients with severe isolated TBI, at admittance to the hospital and during the next 3 days. We collected cerebrovenous blood samples from a jugular bulb catheter, arterial blood, and cerebrospinal fluid (CSF) samples. We measured concentrations of thrombin-antithrombin complex (TAT), fibrin D-dimer (DD), prothrombin fragment 1 + 2 (F1 + 2), interleukin-6 (IL-6), and complement complex (C5b-9). All patients had some degree of consumption coagulopathy at the study start and a tendency to thrombocytopenia during the next few days. Levels of DD (3.6 +/- 2.7 mg/L), TAT (86 +/- 72 microg/L) and F1 + 2 (5.9 +/- 6.8 nmol/L) were significantly increased shortly after the trauma compared to reference values, with considerable transcranial gradients for TAT (49 microg/L) and F1 + 2 (3.2 nmol/L). Compared to controls, IL-6 levels were increased more than a hundredfold in both blood (283 +/- 192 ng/L) and CSF (424 +/- 355 ng/L) samples, with a transcranial gradient at the study start (107 ng/L). C5b-9 levels were moderately increased in blood samples, 270 +/- 114 microg/L, versus controls, 184 +/- 39 (p < 0.05). We conclude that activation of the coagulation system takes place during the passage of blood through the damaged brain, and is already evident hours after the trauma. IL-6 and activation of the complement system (C5b-9) co-vary with hemostatic parameters in TBI patients.     

The effect of apolipoprotein E genotype on neuron specific enolase and S-100beta levels after cardiac surgery

We tested the hypothesis that two biochemical markers of brain injury would be increased after cardiac surgery in patients with the apolipoprotein (Apo) epsilon4 allele. Arterial blood samples were drawn before and 8 and 24 h after induction of anesthesia and later assayed for neuron specific enolase (NSE), S-100beta, and apoE genotype. There was a highly significant temporal effect with increases in NSE (2.2 +/- 1.6 ng/L to 11.8 +/- 8.9 ng/L; P < 0.0001) (mean +/- sd) and S-100beta (0.15 +/- 0.1 microg/L to 0.45 +/- 0.42 microg/L, P < 0.0001). At 8 and 24 h after induction of anesthesia S-100beta (0.28 +/- 0.18 microg/L versus 0.91 +/- 0.54 microg/L; P =0.004) and NSE (8.6 +/- 5.6 ng/L versus 19.0 +/- 19.7 ng/L; P = 0.02) levels, respectively, were higher in patients with the Apoepsilon4 allele. Patients with the Apoepsilon4 allele may be more susceptible to perioperative neural insults.     

Predicting late outcome for patients with traumatic brain injury referred to a rehabilitation programme: a study of 508 Finnish patients 5 years or more after injury

Variables were studied which predict at the acute stage the functional and occupational long term outcome for patients with traumatic brain injury (TBI). Glasgow Coma Scale (GCS) score on hospital admission, length of coma (LOC) and duration of post traumatic amnesia (PTA) were studied in a group of 508 TBI rehabilitation patients, age 0·8-71, mean age 19, followed up between five and over 20 years, mean of 12 years. Information from hospital charts and all data available before and after the injury were gathered and reviewed. The study was carried out among a consecutive sample of Finnish patients with TBI referred to a rehabilitation programme at the out patient neurological clinic of Kauniala Hospital, which specializes in brain injuries in Finland. The patients came from various hospital districts in the country for an evaluation of their educational and vocational problems. Main outcome measures were functional outcome, as measured by the Glasgow Outcome Scale GOS at the end of follow up, and post injury occupational outcome. The patients reemployment on the open job marklet, subsidized employment or inability to work was noted. The GCS score on hospital admission correlated clearly with the functional outcome of the patients at the end of follow up. Length of coma and duration of post traumatic amnesia correlated specifically with the patient s work history after the brain injury and with functional outcome measured by the GOS. Outcomes varied among age groups and seemed to be affected by age at injury. Accordingly, the extent of recovery and quality of life for rehabilitation patients with TBI can be estimated early on by prognostic factors reflecting injury severity in the acute phase. The results suggest that the GCS score, LOC and duration of PTA all have a strong predictive value in assessing functional or occupational outcome for TBI patients.     

Post-operative expansion of hemorrhagic contusions after unilateral decompressive hemicraniectomy in severe traumatic brain injury

Decompressive hemicraniectomy is commonly performed in patients with traumatic brain injury (TBI) with diffuse brain swelling or refractory raised intracranial pressure. Expansion of hemorrhagic contusions in TBI patients is common, but its frequency following decompressive hemicraniectomy has not been well established. The aim of this retrospective study was to determine the rate of hemorrhagic contusion expansion following unilateral hemicraniectomy in severe TBI, to identify factors associated with contusion expansion, and to examine whether contusion expansion is associated with worsened clinical outcomes. Computed tomography (CT) scans of 40 consecutive patients with non-penetrating TBI who underwent decompressive hemicraniectomy were analyzed. Hemorrhagic contusion volumes were measured on initial, last pre-operative, and first post-operative CT scans. Mortality and 6-month Glasgow Outcome Scale (GOS) score were recorded. Hemorrhagic contusions of any size were present on the initial head CT scan in 48% of patients, but hemorrhagic contusions with a total volume of >5 cc were present in only 10%. New or expanded hemorrhagic contusions of >or=5 cc were observed after hemicraniectomy in 58% of patients. The mean volume of increased hemorrhage among these patients was 37.1+/-36.3 cc. The Rotterdam CT score on the initial head CT was strongly associated with the occurrence and the total volume of expanded hemorrhagic contusions following decompressive hemicraniectomy. Expanded hemorrhagic contusion volume greater than 20 cc after hemicraniectomy was strongly associated with mortality and poor 6-month GOS even after controlling for age and initial Glasgow Coma Scale (GCS) score. Expansion of hemorrhagic contusions is common after decompressive hemicraniectomy following severe TBI. The volume of hemorrhagic contusion expansion following hemicraniectomy is strongly associated with mortality and poor outcome. Severity of initial CT findings may predict the risk of contusion expansion following hemicraniectomy, thereby identifying a subgroup of patients who might benefit from therapies aimed at augmenting the coagulation system.     

Diffusion-weighted imaging improves outcome prediction in pediatric traumatic brain injury

Diffusion-weighted imaging (DWI) and consequent apparent diffusion coefficient (ADC) maps have been used for lesion detection and as a predictor of outcome in adults with traumatic brain injury (TBI), but few studies have been reported in children. We evaluated the role of DWI and ADC for outcome prediction after pediatric TBI (n=37 TBI; n=10 controls). Fifteen regions of interest (ROIs) were manually drawn on ADC maps that were grouped for analysis into peripheral gray matter, peripheral white matter, deep gray and white matter, and posterior fossa. All ROIs excluded areas that appeared abnormal on T2-weighted images (T2WI). Acute injury severity was measured using the Glasgow Coma Scale (GCS) score, and 6-12-month outcomes were assessed using the Pediatric Cerebral Performance Category Scale (PCPCS) score. Patients were categorized into five groups: (1) controls; (2) all TBI patients; (3) mild/moderate TBI with good outcomes; (4) severe TBI with good outcomes; and (5) severe TBI with poor outcomes. ADC values in the peripheral white matter were significantly reduced in children with severe TBI with poor outcomes (72.8+/-14.4x10(-3) mm2/sec) compared to those with severe TBI and good outcomes (82.5+/-3.8x10(-3) mm2/sec; p<0.05). We also found that the average total brain ADC value alone had the greatest ability to predict outcome and could correctly predict outcome in 84% of cases. Assessment of DWI and ADC values in pediatric TBI is useful in evaluating injury, particularly in brain regions that appear normal on conventional imaging. Early identification of children at high risk for poor outcome may assist in aggressive clinical management of pediatric TBI patients.     

Playing soccer increases serum concentrations of the biochemical markers of brain damage S-100B and neuron-specific enolase in elite players: a pilot study

PRIMARY OBJECTIVE: To analyse serum concentrations of two biochemical markers of brain tissue damage, S-100B and NSE (neurone-specific enolase), in male soccer players in connection to the game. METHODS: Blood samples were taken in players before and after a competitive game and the numbers of headers and of trauma events during soccer play were assessed. RESULTS: Both S-100B and NSE were significantly raised in serum samples obtained after the game in comparison with the pre-game values (S-100B: 0.118 +/- 0.040 microg L(-1) vs 0.066 +/- 0.025 microg L(-1), p < 0.001; NSE: 10.29 +/- 2.16 microg L(-1) vs 8.57 +/- 2.31 microg L(-1), p < 0.001). Only changes in S-100B concentrations (post-game minus pre-game values) were statistically significantly correlated to the number of headers (r = 0.428, p = 0.02) and to the number of other trauma events (r = 0.453, p = 0.02). CONCLUSION: Playing competitive elite soccer was found to cause increase in serum concentrations of S-100B and NSE. Increases in S-100B were significantly correlated to the number of headers, and heading may accordingly have contributed to these increases.     

Diffusion-weighted magnetic resonance imaging improves outcome prediction in adult traumatic brain injury

In patients with traumatic brain injury (TBI), diffuse axonal injury (DAI) accounts for a significant amount of parenchymal injury. Diffusion weighted magnetic resonance imaging (DWI) is known to be sensitive for detecting visible DAI lesions. We focused on detection of non-visible, quantifiable diffusion changes in specific normal-appearing brain regions, using apparent diffusion coefficient (ADC) maps. Thirty-seven adults with TBI were compared to 35 age-matched control patients. DWI was performed and ADC maps were generated. Thirty-one regions of interest (ROI) were manually drawn on ADC maps and ADC values extracted. Brain ROIs were categorized into five zones: peripheral gray matter, peripheral white matter, deep gray matter, deep white matter, and posterior fossa. ADC results were compared with the severity of injury based on the admission Glasgow Coma Scale (GCS 3-8; severe; GSC 9-15 mild/moderate) and with long-term outcome (6-12 months after injury) using the Glasgow Outcome Scale (GOS 1-3, unfavorable; GOS: 4-5, favorable) score. Mean ADC values in all five brain zones were significantly different between TBI subjects and controls (p相似文献   

Effect of AVP on brain edema following traumatic brain injury

Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤8) and moderate traumatic brain injury group ( MTBI, GCS >8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group) and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan. Results: plasma AVP levels (ng/L) were (mean±SD): control, 3. 06±1. 49; MTBI, 38. 12±7. 25; and STBI, 66. 61±17. 10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0. 01). And the AVP level was correlated with the severity (STBI r =0.919, P < 0.01; MTBI r = 0.724, P < 0.01) and the duration of brain edema (STBI r = 0. 790, P < 0. 01; MTBI r = 0. 712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.     

Effect of mild hypothermia on brain dialysate lactate after fluid percussion brain injury in rodents

OBJECTIVE: To investigate the effects of mild hypothermia on brain microdialysate lactate after fluid percussion traumatic brain injury (TBI) in rats. METHODS: Brain dialysate lactate before and after fluid percussion brain injury (2.1 +/- 0.2 atm) was measured in rats with preinjury mild hypothermia (32 degrees C), postinjury mild hypothermia (32 degrees C), injury normothermia (37 degrees C), and the sham control group. Mild hypothermia (32 degrees C) was induced by partial immersion in a water bath (0 degrees C) under general anesthesia and maintained for 2 hours. RESULTS: In the normothermia TBI group, brain extracellular fluid lactate increased from 0.311 +/- 0.03 to 1.275 +/- 0.08 mmol/L within 30 minutes after TBI (P < 0.01) and remained at a high level (0.546 +/- 0.05 mmol/L) (P < 0.01) at 2 hours after injury. In the postinjury mild hypothermic group, brain extracellular fluid lactate increased from 0.303 +/- 0.03 to 0.875 +/- 0.05 mmol/L at 15 minutes after TBI (P < 0.01) and then gradually decreased to 0.316 +/- 0.04 mmol/L at 2 hours after TBI (P > 0.05). In the preinjury mild hypothermic group, brain extracellular fluid lactate remained at normal levels after injury (P > 0.05). CONCLUSION: The cerebral extracellular fluid lactate level increases significantly after fluid percussion brain injury. Preinjury mild hypothermia completely inhibits the cerebral lactate accumulation, and early postinjury mild hypothermia significantly blunts the increase of cerebral lactate level after fluid percussion injury.     

Proton MR spectroscopy detected glutamate/glutamine is increased in children with traumatic brain injury

Adults with traumatic brain injury (TBI) have been shown by invasive methods to have increased levels of the excitatory neurotransmitter glutamate. It is unclear whether glutamate release contributes to primary or secondary injury and whether its protracted elevation is predictive of a poor outcome. Preliminary studies at our institution in adults found that early increases in magnetic resonance spectroscopy (MRS)-detected glutamate/glutamine (Glx) were associated with poor outcomes. We therefore studied 38 children (mean age, 11 years; range, 1.6-17 years) who had TBI with quantitative short-echo time (STEAM, TE = 20 msec) proton MRS, a mean of 7 +/- 4 (range, 1-17) days after injury in order to determine if their occipital or parietal Glx levels correlated with the severity of injury or outcome. Occipital Glx was significantly increased in children with TBI compared to controls (13.5 +/- 2.4 vs. 10.7 +/- 1.8; p = 0.002), but there was no difference between children with good compared to poor outcomes as determined by the Pediatric Cerebral Performance Category Scale score at 6-12 months after injury. We also did not find a correlation between the amount of Glx and the initial Glasgow Coma Scale score, duration of coma, nor with changes in spectral metabolites, including N-acetyl aspartate, choline, and myoinositol. In part, this may have occurred because, in this study, most patients with poor outcomes were studied later than patients with good outcomes, potentially beyond the time frame for peak elevation of Glx after injury. Additional early and late studies of patients with varying degrees of injury are required to assess the importance to the pathophysiology of TBI of this excitatory neurotransmitter.     

Temporal profile of release of neurobiochemical markers of brain damage after traumatic brain injury is associated with intracranial pathology as demonstrated in cranial computerized tomography

This study aimed at the investigation of release patterns of neuron specific enolase (NSE) and protein S-100B after traumatic brain injury (TBI) and their association with intracranial pathologic changes as demonstrated in computerized tomography (CT). We analyzed NSE and S-100B concentrations in serial venous blood samples taken one to three days after TBI in 66 patients by the use of immunoluminometric assays. These markers are considered to be specific neurobiochemical indicators of damage to glial (S-100B) or neuronal (NSE) brain tissue. Standardized neurological examination and plani- and volumetric evaluation of computerized tomography scans were performed in all patients. Patients with medium severe to severe TBI [Glasgow Coma Scale (GCS) score at the site of accident < or =12] exhibited significantly higher NSE and S-100B concentrations and a significantly longer release compared to patients with minor head injury (GCS: 13-15). Both, patients with and without visible intracerebral pathology in CT scans exhibited elevated concentrations of NSE and S-100B after TBI and a significant decrease in the follow-up blood samples. Release patterns of S-100B and NSE differed in patients with primary cortical contusions, diffuse axonal injury (DAI), and signs of cerebral edema (ICP) without focal mass lesions. All serum concentrations of NSE and S-100B were significantly correlated with the volume of contusions. The data of the present study indicate that the early release patterns of NSE and S-100 may mirror different pathophysiological consequences of traumatic brain injury.     

Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries

OBJECT: The edema associated with brain swelling after traumatic brain injury (TBI) has been thought to be vasogenic in origin, but the results of previous laboratory studies by the authors have shown that a cellular form of edema is mainly responsible for brain swelling after TBI. In this study the authors used magnetic resonance (MR) imaging techniques to identify the type of edema that occurs in patients with TBI. METHODS: Diffusion-weighted MR imaging was used to evaluate the apparent diffusion coefficient (ADC) in 44 patients with TBI (Glasgow Coma Scale Score < 8) and in eight healthy volunteers. Higher ADC values have been associated with vasogenic edema, and lower ADC values with a predominantly cellular form of edema. Regional measurements of ADC in patients with focal and diffuse injury were computed. The water content of brain tissue was also assessed in absolute terms by using MR imaging to measure the percentage of water per gram of tissue. Cerebral blood flow (CBF) was measured using stable Xe-computerized tomography (CT) studies to rule out ischemia as a cause of cellular edema. The mean ADC value in the healthy volunteers was 0.82 +/- 0.05 x 10(-3) mm2/second. The ADC values in the patients with diffuse brain injury without swelling were close to the mean for the healthy volunteers. In contrast, the patients with brain swelling had increased brain water content and low ADC values (mean 0.74 +/- 0.05 x 10(-3) mm2/second). The ADC values correlated with CT classifications. In all patients with low ADC values, the CBF values were outside the range for ischemia. CONCLUSIONS: The brain swelling observed in patients with TBI appears to be predominantly cellular, as signaled by low ADC values in brain tissue with high levels of water content.     

Association between elevated brain tissue glycerol levels and poor outcome following severe traumatic brain injury

OBJECT: Glycerol is considered to be a marker of cell membrane degradation and thus cellular lysis. Recently, it has become feasible to measure via microdialysis cerebral extracellular fluid (ECF) glycerol concentrations at the patient's bedside. Therefore the aim of this study was to investigate the ECF concentration and time course of glycerol after severe traumatic brain injury (TBI) and its relationship to patient outcome and other monitoring parameters. METHODS: As soon as possible after injury for up to 4 days, 76 severely head-injured patients were monitored using a microdialysis probe (cerebral glycerol) and a Neurotrend sensor (brain tissue PO2) in uninjured brain tissue confirmed by computerized tomography scanning. The mean brain tissue glycerol concentration in all monitored patients decreased significantly from 206 +/- 31 micromol/L on Day 1 to 9 +/- 3 micromol/L on Day 4 after injury (p < 0.0001). Note, however, that there was no significant difference in the time course between patients with a favorable outcome (Glasgow Outcome Scale [GOS] Scores 4 and 5) and those with an unfavorable outcome (GOS Scores 1-3). Significantly increased glycerol concentrations were observed when brain tissue PO2 was less than 10 mm Hg or when cerebral perfusion pressure was less than 70 mm Hg. CONCLUSIONS: Based on results in the present study one can infer that microdialysate glycerol is a marker of severe tissue damage, as seen immediately after brain injury or during profound tissue hypoxia. Given that brain tissue glycerol levels do not yet add new clinically significant information, however, routine monitoring of this parameter following traumatic brain injury needs further validation.     

Serum S-100B protein and neuron-specific enolase after traumatic brain injury

OBJECTIVE: The aim of this study was to investigate S-100B protein and NSE as a serum marker of brain cell damage after traumatic brain injury. MATERIAL AND METHODS: Forty-one patients with traumatic brain injury were included in this prospective study. Venous blood samples for S-100B protein and NSE were taken after admission and on the next day. Serum levels of S-100 protein and NSE were compared with Glasgow Coma Scale score, computed tomographic findings and outcome after 3 months. RESULTS: Serum S-100B protein and NSE were significantly correlated with Glasgow Coma Scale score and outcome after 3 months. The significant correlation was found between the initial S-100B and NSE (P < 0.001). In patients without parenchymal injuries on computed tomographic scan such as epidural hematoma and concussion, the elevation of S-100B protein and NSE was observed. The initial values of S-100B and NSE in acute subdural hematomas with unfavorable outcome were significantly higher than in those with favorable outcome. Secondary increase of serum markers was associated with the presence of secondary insult such as hypoxia or hypotension, and was found to have an unfavorable outcome. CONCLUSIONS: Serum concentration and kinetics of S-100B protein and NSE provide the clinical assessment of the primary brain damage and have a predictive value for outcome after traumatic brain injury.