Do women fare worse: a metaanalysis of gender differences in traumatic brain injury outcome

2000 ◽  
Vol 93 (4) ◽  
pp. 539-545 ◽  
Author(s):  
Elana Farace ◽  
Wayne M. Alves
Keyword(s):  
Gender Differences ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Case Fatality ◽  
Average Effect ◽  
Opposite Pattern ◽  
Quantitative Review ◽  
Men And Women ◽  
Content Type ◽  
Fine Print

Object. The purpose of this metaanalysis was to investigate possible gender differences in traumatic brain injury (TBI) sequelae. The case fatality rates in patients after TBI have previously been shown to be significantly higher in women as compared with men.Methods. A quantitative review of published studies of TBI outcome revealed eight studies (20 outcome variables) of TBI, in which outcome was reported separately for men and women.Conclusions. Outcome was worse in women than in men for 85% of the measured variables, with an average effect size of −0.15. Although clinical opinion is often that women tend to experience better outcomes than men after TBI, the opposite pattern was suggested in the results of this metaanalysis. However, this conclusion is limited by the fact that, in only a small percentage of the total published reports on TBI outcome, was outcome described separately for each sex. A careful, prospective study of sex differences in TBI outcome is clearly needed.

scholarly journals Do women fare worse? A metaanalysis of gender differences in outcome after traumatic brain injury

2000 ◽  
Vol 8 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Elana Farace ◽  
Wayne M. Alves
Keyword(s):  
Gender Differences ◽  
Traumatic Brain Injury ◽  
Sex Differences ◽  
Brain Injury ◽  
Prospective Study ◽  
Case Fatality ◽  
Average Effect ◽  
Opposite Pattern ◽  
Quantitative Review ◽  
Men And Women

The purpose of this metaanalysis was to investigate possible gender differences in TBI sequelae. The case fatality rates in patients after TBI have previously been shown to be significantly higher in women as compared with men. A quantitative review of published studies of TBI outcome revealed eight studies (20 outcome variables) of TBI in which outcome was reported separately for men and women. Outcome was worse in women than in men for 85% of the measured variables, with an average effect size of −0.15. Although clinical opinion is often that women tend to experience better outcomes than do men after TBI, the opposite pattern was suggested in the results of this metaanalysis. However, this conclusion is limited by the fact that in only a small percentage of the total published reports on TBI outcome was outcome described separately for each sex. A careful, prospective study of sex differences in TBI outcome is clearly needed.

Flushing in relation to a possible rise in intracranial pressure: documentation of an unusual clinical sign

2000 ◽  
Vol 92 (6) ◽  
pp. 1040-1044 ◽  
Author(s):  
Gregory W. Hornig
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intraventricular Hemorrhage ◽  
Pneumococcal Meningitis ◽  
Clinical Importance ◽  
Neurological Deterioration ◽  
Content Type ◽  
Transient Nature ◽  
Fine Print

✓ This report documents clinical features in five children who developed transient reddening of the skin (epidermal flushing) in association with acute elevations in intracranial pressure (ICP). Four boys and one girl (ages 9–15 years) deteriorated acutely secondary to intracranial hypertension ranging from 30 to 80 mm Hg in the four documented cases. Two patients suffered from ventriculoperitoneal shunt malfunctions, one had diffuse cerebral edema secondary to traumatic brain injury, one was found to have pneumococcal meningitis and hydrocephalus, and one suffered an intraventricular hemorrhage and hydrocephalus intraoperatively. All patients were noted to have developed epidermal flushing involving either the upper chest, face, or arms during their period of neurological deterioration. The response was transient, typically lasting 5 to 15 minutes, and dissipated quickly. The flushing reaction is postulated to be a centrally mediated response to sudden elevations in ICP. Several potential mechanisms are discussed. Flushing has clinical importance because it may indicate significant elevations in ICP when it is associated with neurological deterioration. Because of its transient nature, the importance of epidermal flushing is often unrecognized; its presence confirms the need for urgent treatment.

Intracranial bone marrow transplantation after traumatic brain injury improving functional outcome in adult rats

2001 ◽  
Vol 94 (4) ◽  
pp. 589-595 ◽  
Author(s):  
Asim Mahmood ◽  
Dunyue Lu ◽  
Yi Li ◽  
Jae Li Chen ◽  
Michael Chopp
Keyword(s):  
Traumatic Brain Injury ◽  
Bone Marrow ◽  
Brain Injury ◽  
Motor Function ◽  
Glial Fibrillary Acid Protein ◽  
Protein Markers ◽  
Adult Rats ◽  
Content Type ◽  
The Impact ◽  
Fine Print

Object. The authors tested the hypothesis that intracranial bone marrow (BM) transplantation after traumatic brain injury (TBI) in rats provides therapeutic benefit. Methods. Sixty-six adult Wistar rats, weighing 275 to 350 g each, were used for the experiment. Bone marrow prelabeled with bromodeoxyuridine (BrdU) was harvested from tibias and femurs of healthy adult rats. Other animals were subjected to controlled cortical impact, and BM was injected adjacent to the contusion 24 hours after the impact. The animals were killed at 4, 7, 14, or 28 days after transplantation. Motor function was evaluated both before and after the injury by using the rotarod test. After the animals had been killed, brain sections were examined using hemotoxylin and eosin and immunohistochemical staining methods. Histological examination revealed that, after transplantation, BM cells survived, proliferated, and migrated toward the injury site. Some of the BrdU-labeled BM cells were reactive, with astrocytic (glial fibrillary acid protein) and neuronal (NeuN and microtubule-associated protein) markers. Transplanted BM expressed proteins phenotypical of intrinsic brain cells, that is, neurons and astrocytes. A statistically significant improvement in motor function in rats that underwent BM transplantation, compared with control rats, was detected at 14 and 28 days posttransplantation. Conclusions. On the basis of their findings, the authors assert that BM transplantation improves neurological outcome and that BM cells survive and express nerve cell proteins after TBI.

Cerebral tissue PO2 and SjvO2 changes during moderate hyperventilation in patients with severe traumatic brain injury

2002 ◽  
Vol 96 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Roberto Imberti ◽  
Guido Bellinzona ◽  
Martin Langer
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Cerebral Perfusion ◽  
Content Type ◽  
Secondary Damage ◽  
Tissue Po2 ◽  
Two Parameters ◽  
Fine Print

Object. The aim of this study was to investigate the effects of moderate hyperventilation on intracranial pressure (ICP), jugular venous oxygen saturation ([SjvO2], an index of global cerebral perfusion), and brain tissue PO2 (an index of local cerebral perfusion). Methods. Ninety-four tests consisting of 20-minute periods of moderate hyperventilation (27–32 mm Hg) were performed on different days in 36 patients with severe traumatic brain injury (Glasgow Coma Scale score ≤ 8). Moderate hyperventilation resulted in a significant reduction in average ICP, but in seven tests performed in five patients it was ineffective. The response of SjvO2 and brain tissue PO2 to CO2 changes was widely variable and unpredictable. After 20 minutes of moderate hyperventilation in most tests (79.8%), both SjvO2 and brain tissue PO2 values remained above the lower limits of normality (50% and 10 mm Hg, respectively). In contrast, in 15 tests performed in six patients (16.6% of the studied population) brain tissue PO2 decreased below 10 mm Hg although the corresponding SjvO2 values were greater than 50%. The reduction of brain tissue PO2 below 10 mm Hg was favored by the low prehyperventilation values (10 tests), higher CO2 reactivity, and, possibly, by lower prehyperventilation values of cerebral perfusion pressure. In five of those 15 tests, the prehyperventilation values of SjvO2 were greater than 70%, a condition of relative hyperemia. The SjvO2 decreased below 50% in four tests; the corresponding brain tissue PO2 values were less than 10 mm Hg in three of those tests, whereas in the fourth, the jugular venous O2 desaturation was not detected by brain tissue PO2. The analysis of the simultaneous relative changes (prehyperventilation — posthyperventilation) of SjvO2 and brain tissue PO2 showed that in most tests (75.5%) there was a reduction of both SjvO2 and brain tissue PO2. In two tests moderate hyperventilation resulted in an increase of both SjvO2 and brain tissue PO2. In the remaining 17 tests a redistribution of the cerebral blood flow was observed, leading to changes in SjvO2 and brain tissue PO2 in opposite directions. Conclusions. Hyperventilation, even if moderate, can frequently result in harmful local reductions of cerebral perfusion that cannot be detected by assessing SjvO2. Therefore, hyperventilation should be used with caution and should not be considered safe. This study confirms that SjvO2 and brain tissue PO2 are two parameters that provide complementary information on brain oxygenation that is useful to reduce the risk of secondary damage. Changes in SjvO2 and brain tissue PO2 in opposite directions indicate that data obtained from brain tissue PO2 monitoring cannot be extrapolated to evaluate the global cerebral perfusion.

Early and persistent impaired percent alpha variability on continuous electroencephalography monitoring as predictive of poor outcome after traumatic brain injury

2002 ◽  
Vol 97 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Paul M. Vespa ◽  
W. John Boscardin ◽  
David A. Hovda ◽  
David L. McArthur ◽  
Marc R. Nuwer ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Eeg Monitoring ◽  
Content Type ◽  
Poor Outcome ◽  
Continuous Electroencephalography ◽  
Continuous Eeg ◽  
Continuous Eeg Monitoring ◽  
Severe Tbi ◽  
Fine Print

Object. Early prediction of outcomes in patients after they suffer traumatic brain injury (TBI) is often nonspecific and based on initial imaging and clinical findings alone, without direct physiological testing. Improved outcome prediction is desirable for ethical, social, and financial reasons. The goal of this study was to determine the usefulness of continuous electroencephalography (EEG) monitoring in determining prognosis early after TBI, while the patient is in the intensive care unit. Methods. The authors hypothesized that the reduced percentage of alpha variability (PAV) in continuous EEG tracings indicates a poor prognosis. Prospective continuous EEG monitoring was performed in 89 consecutive patients with moderate to severe TBI (Glasgow Coma Scale [GCS] Scores 3–12) from 0 to 10 days after injury. The PAV was calculated daily, and the time course and trends of the PAV were analyzed in comparison with the patient's Glasgow Outcome Scale (GOS) score at the time of discharge. In patients with GCS scores of 8 or lower, a PAV value of 0.1 or lower is highly predictive of a poor outcome or death (positive predictive value 86%). The determinant PAV value was obtained by Day 3 after injury. Persistent PAV values of 0.1 or lower over several days or worsening of the PAV to a value of 0.1 or lower indicated a high likelihood of poor outcome (GOS Scores 1 and 2). In comparison with the combination of traditional initial clinical indicators of outcome (GCS score, pupillary response to light, patient age, results of computerized tomography scanning, and early hypotension or hypoxemia), the early PAV value during the initial 3 days after injury independently improved prognostic ability (p < 0.01). Conclusions. Continuous EEG monitoring performed with particular attention paid to the PAV is a sensitive and specific method of prognosis that can indicate outcomes in patients with moderate to severe TBI within 3 days postinjury.

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

2005 ◽  
Vol 103 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Tobias Clausen ◽  
Oscar Luis Alves ◽  
Michael Reinert ◽  
Egon Doppenberg ◽  
Alois Zauner ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Time Course ◽  
Glycerol Concentration ◽  
Significant Information ◽  
Content Type ◽  
Significant Difference ◽  
Fine Print

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 µmol/L on Day 1 to 9 ± 3 µmol/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.

scholarly journals Increased incidence and impact of nonconvulsive and convulsive seizures after traumatic brain injury as detected by continuous electroencephalographic monitoring

1999 ◽  
Vol 91 (5) ◽  
pp. 750-760 ◽  
Author(s):  
Paul M. Vespa ◽  
Marc R. Nuwer ◽  
Valeriy Nenov ◽  
Elisabeth Ronne-Engstrom ◽  
David A. Hovda ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Status Epilepticus ◽  
Brain Injury ◽  
Scale Score ◽  
Eeg Monitoring ◽  
Content Type ◽  
Continuous Eeg ◽  
Nonconvulsive Seizures ◽  
Continuous Eeg Monitoring ◽  
Fine Print

Object. The early pathophysiological features of traumatic brain injury observed in the intensive care unit (ICU) have been described in terms of altered cerebral blood flow, altered brain metabolism, and neurochemical excitotoxicity. Seizures occur in animal models of brain injury and in human brain injury. Previous studies of posttraumatic seizures in humans have been based principally on clinical observations without a systematic approach to electroencephalographic (EEG) recording of seizures. The purpose of this study was to determine prospectively the incidence of convulsive and nonconvulsive seizures by using continuous EEG monitoring in patients in the ICU during the initial 14 days postinjury.Methods. Ninety-four patients with moderate-to-severe brain injuries underwent continuous EEG monitoring beginning at admission to the ICU (mean delay 9.6 ± 5.4 hours) and extending up to 14 days postinjury. Convulsive and nonconvulsive seizures occurred in 21 (22%) of the 94 patients, with six of them displaying status epilepticus. In more than half of the patients (52%) the seizures were nonconvulsive and were diagnosed on the basis of EEG studies alone. All six patients with status epilepticus died, compared with a mortality rate of 24% (18 of 73) in the nonseizure group (p < 0.001). The patients with status epilepticus had a shorter mean length of stay (9.14 ± 5.9 days compared with 14 ± 9 days [t-test, p < 0.03]). Seizures occurred despite initiation of prophylactic phenytoin on admission to the emergency room, with maintenance at mean levels of 16.6 ± 2.8 mg/dl. No differences in key prognostic factors (such as the Glasgow Coma Scale score, early hypoxemia, early hypotension, or 1-month Glasgow Outcome Scale score) were found between the patients with seizures and those without.Conclusions. Seizures occur in more than one in five patients during the 1st week after moderate-to-severe brain injury and may play a role in the pathobiological conditions associated with brain injury.

Loss of forebrain cholinergic neurons following fluid-percussion injury: implications for cognitive impairment in closed head injury

1995 ◽  
Vol 83 (3) ◽  
pp. 496-502 ◽  
Author(s):  
Richard H. Schmidt ◽  
M. Sean Grady
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Neuron Loss ◽  
Content Type ◽  
Fluid Percussion ◽  
Concussive Injury ◽  
Fine Print

✓ Disturbances in memory, concentration, and problem solving are common after even mild to moderate traumatic brain injury. Because these functions are mediated in part by forebrain cholinergic and catecholaminergic innervation, in this study the authors sought to determine if experimental concussive injury produces detectable morphological damage to these systems. Fluid-percussion head injury, sufficient to cause a 13- to 14-minute loss of righting reflex, was produced in rats that had been anesthetized with halothane. Injury was delivered either at midline or 2 mm off midline and compared with appropriate sham-injured controls. After 11 to 15 days, the rat brains were stained in serial sections for choline acetyltransferase, tyrosine hydroxylase, dopamine β-hydroxylase, acetylcholinesterase, and nicotinamide adenine dinucleotide phosphate diaphorase. Cell counts were determined for the entire population of ventrobasal forebrain cholinergic cells. Midline injury produced a bilateral loss of cholinergic neurons averaging 36% in area Ch1 (medial septal nucleus), 45% in Ch2 (nucleus of the diagonal band of Broca), and 41% in Ch4 (nucleus basalis of Meynart), (p ≤ 0.05). Lateralized injury resulted in cholinergic neuron loss of similar magnitude ipsilaterally (p ≤ 0.05), but a smaller contralateral loss of between 11% and 28%. No loss of neurons was detected in the pontomesencephalic cholinergic groups Ch5 and Ch6. There was no visible effect of head injury on forebrain dopamine or noradrenergic innervation. A significant and apparently selective loss of ventrobasal forebrain cholinergic neurons following brief concussive injury in rats is demonstrated in this study. This type of injury is known to produce significant disturbance in cognitive tasks linked to neocortical and hippocampal cholinergic function. It remains to be determined how this neuron loss occurs, whether it can be prevented with neuroprotective agents, how it affects innervation in target tissues, and whether it occurs in human victims of traumatic brain injury.

Patient age and outcome following severe traumatic brain injury: an analysis of 5600 patients

2003 ◽  
Vol 99 (4) ◽  
pp. 666-673 ◽  
Author(s):  
Chantal W. P. M. Hukkelhoven ◽  
Ewout W. Steyerberg ◽  
Anneke J. J. Rampen ◽  
Elana Farace ◽  
J. Dik F. Habbema ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Individual Patient Data ◽  
Patient Data ◽  
Unfavorable Outcome ◽  
Quadratic Term ◽  
Content Type ◽  
Adult Age ◽  
Discrete Manner ◽  
Fine Print

Object. Increasing age is associated with poorer outcome in patients with closed traumatic brain injury (TBI). It is uncertain whether critical age thresholds exist, however, and the strength of the association has yet to be investigated across large series. The authors studied the shape and strength of the relationship between age and outcome, that is, the 6-month mortality rate and unfavorable outcome based on the Glasgow Outcome Scale. Methods. The shape of the association was examined in four prospective series with individual patient data (2664 cases). All patients had a closed TBI and were of adult age (96% < 65 years of age). The strength of the association was investigated in a metaanalysis of the aforementioned individual patient data (2664 cases) and aggregate data (2948 cases) from TBI studies published between 1980 and 2001 (total 5612 cases). Analyses were performed with univariable and multivariable logistic regression. Proportions of mortality and unfavorable outcome increased with age: 21 and 39%, respectively, for patients younger than 35 years and 52 and 74%, respectively, for patients older than 55 years. The association between age and both mortality and unfavorable outcome was continuous and could be adequately described by a linear term and expressed even better statistically by a linear and a quadratic term. The use of age thresholds (best fitting threshold 39 years) in the analysis resulted in a considerable loss of information. The strength of the association, expressed as an odds ratio per 10 years of age, was 1.47 (95% confidence interval [CI] 1.34–1.63) for death and 1.49 (95% CI 1.43–1.56) for unfavorable outcome in univariable analyses, and 1.39 (95% CI 1.3–1.5) and 1.46 (95% CI 1.36–1.56), respectively, in multivariable analyses. Thus, the odds for a poor outcome increased by 40 to 50% per 10 years of age. Conclusions. An older age is continuously associated with a worsening outcome after TBI; hence, it is disadvantageous to define the effect of age on outcome in a discrete manner when we aim to estimate prognosis or adjust for confounding variables.

The effect of brain temperature on hemoglobin extravasation after traumatic brain injury

2002 ◽  
Vol 97 (4) ◽  
pp. 945-953 ◽  
Author(s):  
Kosaku Kinoshita ◽  
Katina Chatzipanteli ◽  
Ofelia F. Alonso ◽  
Mackenzie Howard ◽  
W. Dalton Dietrich
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Injury Severity ◽  
Brain Temperature ◽  
Experimental Studies ◽  
Hemoglobin Concentration ◽  
Contralateral Hemisphere ◽  
Ipsilateral Hemisphere ◽  
Content Type ◽  
Fine Print

Object. Although the benefits of posttraumatic hypothermia have been reported in experimental studies, the potential for therapeutic hypothermia to increase intracerebral hemorrhage remains a clinical concern. The purpose of this study was to quantify the amount of extravasated hemoglobin after traumatic brain injury (TBI) and to assess the changes in intracerebral hemoglobin concentrations under posttraumatic hypothermic and hyperthermic conditions. Methods. Intubated and anesthetized rats were subjected to fluid-percussion injury (FPI). In the first experiment, rats were divided into moderate (1.8–2.2 atm) and severe (2.4–2.7 atm) TBI groups. In the second experiment, the effects of 3 hours of posttraumatic hypothermia (33 or 30°C), hyperthermia (39°C), or normothermia (37°C) on hemoglobin levels following moderate trauma were assessed. The rats were perfused with saline at 24 hours postinjury, and then the traumatized and contralateral hemispheres, including the cerebellum, were dissected from whole brain. The hemoglobin level in each brain was quantified using a spectrophotometric hemoglobin assay. The results of these assays indicate that moderate and severe FPI induce increased levels of hemoglobin in the ipsilateral hemisphere (p < 0.0001). After severe TBI, the hemoglobin concentration was also significantly increased in the contralateral hemisphere (p < 0.05) and cerebellum (p < 0.005). Posttraumatic hypothermia (30°C) attenuated hemoglobin levels (p < 0.005) in the ipsilateral hemisphere, whereas hyperthermia had a marked adverse effect on the hemoglobin concentration in the contralateral hemisphere (p < 0.05) and cerebellum (p < 0.005). Conclusions. Injury severity is an important determinant of the degree of hemoglobin extravasation after TBI. Posttraumatic hypothermia reduced hemoglobin extravasation, whereas hyperthermia increased hemoglobin levels compared with normothermia. These findings are consistent with previous data reporting that posttraumatic temperature manipulations alter the cerebrovascular and inflammatory consequences of TBI.

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