PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Traumatic Brain Injuries”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed1990

Multiple personality disorder: diagnosis after a traumatic brain injury.

A patient is described with memory deficits after a traumatic brain injury; she was eventually diagnosed as having multiple personality disorder. A delay in diagnosis of multiple personality occurred because her cognitive deficits were thought to be secondary to the traumatic brain injury. Neuropsychologic tests were not helpful in establishing the diagnosis. Her EEG was negative, and she had no clinical evidence of complex partial seizures, which have been described in association with this disorder. Only after a process of careful history taking and the establishment of a therapeutic alliance with the patient was the diagnosis established. This case highlights the necessity to consider a "differential diagnosis for amnesia" in all patients with traumatic brain injury. In some patients, both organic and psychogenic causes are discovered.

Adult↗
PubMed1998

Aging effect on psychosocial outcome in traumatic brain injury.

OBJECTIVE: To examine the effects of age on outcome in persons with traumatic brain injury. DESIGN: Longitudinal cohort design. SETTING: Level I trauma center. PATIENTS: A total of 411 hospitalized subjects with mild to severe traumatic brain injury prospectively studied to 1 year; their age range was 18 to 89 years. MAIN OUTCOME MEASURES: Glasgow Outcome Scale, living situation, and employment. RESULTS: Increasing age is associated with increasing levels of psychosocial limitations, especially in persons 60 years of age and older. Part of the reason is the greater severity of injury sustained by older persons as reflected in longer coma (despite equivalent initial coma depth) and greater numbers of complications and surgeries for subdural hematomas. However, the consequences of traumatic brain injuries appear to worsen with increasing age at each level of brain injury severity examined, including the milder injuries. CONCLUSIONS: Older adults clearly show less complete recovery 1 year after brain injury than younger adults, either because they have reduced reserves with which to tolerate brain injury or because their physiologic status creates a more destructive injury. Glasgow Coma Scale alone may underestimate the severity of brain injury in the aged as well as its associated consequences. Caution is advised in generalizing findings based principally on younger individuals to older adults with traumatic brain injuries.

Activities of Daily Living↗
PubMed2004

Neuron-specific-enolase is increased in plasma after hemorrhagic shock and after bilateral femur fracture without traumatic brain injury in the rat.

Neuron-specific enolase (NSE) is an acknowledged marker of traumatic brain injury. Several markers originally considered reliable in the setting of traumatic brain injury have been challenged after having been studied more extensively. The aim of our experimental study was to determine whether NSE is a reliable marker of traumatic brain injury early after trauma. Hemorrhagic shock was achieved by bleeding anesthetized rats to a mean arterial pressure (MAP) of 30-35 mmHg through a femoral catheter until incipient decompensation. MAP was maintained at 30-35 mmHg until 40% of shed blood had been administered as Ringer's solution and was then increased and maintained at 40-45 mmHg for 40 min by further administration of Ringer's solution, mimicking the phase of inadequate preclinical resuscitation. Blood samples were drawn at the end of the 40-min period of inadequate resuscitation. Femur fracture was achieved in anesthetized rats by bilateral application of forceps. Blood samples were drawn 30 and 60 min after fracture. Hemorrhagic shock caused NSE increase versus laboratory controls at the end of inadequate resuscitation (P < 0.01). Bilateral femur fracture caused NSE increase versus laboratory controls 30 min after fracture, which was significant 60 min after fracture (P < 0.01). During femur fracture, MAP remained at a level that is not associated with shock in rats. Our findings show for the first time that NSE increases after hemorrhagic shock as well as after femur fracture without hemorrhagic shock in rats. From a clinical point of view, these findings indicate that NSE cannot be considered a reliable marker of traumatic brain injury early after trauma in cases associated with hemorrhagic shock and/or femur fracture.

Animals↗
PubMed2001

The impact on outcomes in a community hospital setting of using the AANS traumatic brain injury guidelines. Americans Associations for Neurologic Surgeons.

BACKGROUND: Traumatic brain injury poses a serious public health challenge. Treatment paradigms have dramatically shifted with the introduction of the American Association of Neurologic Surgeons (AANS) Guidelines for the Management of Severe Head Injury. Implementation of the AANS guidelines positively affects patient outcomes and can be successfully introduced in a community hospital setting. METHODS: Data were collected both retrospectively and prospectively from the records of all trauma patients between 1994 and 1999. A cohort of 93 patients was selected. Thirty-seven patients were treated before the implementation of the AANS guidelines, and these were statistically compared with 56 patients treated after the implementation of the guidelines. RESULTS: Implementation of the recommendations in the AANS guidelines in a standardized protocol resulted in a 9.13 times higher odds ratio of a good outcome relative to the odds of a poor outcome or death compared with a group managed before the practice change. A Glasgow Coma Scale (GCS) admission score > 8 was associated with a 6.58 times higher odds ratio of a good outcome compared with a GCS admission score < or = 8. Odds ratio of a good outcome decreased by a factor of 0.92 for each year increase in age of patients starting at age 9. A dedicated neurotrauma team and comprehensive treatment algorithms are critical elements to this success. Hospital charges increased by more than $97,000 per patient, but are justifiable in the face of significantly improved outcomes. CONCLUSION: Implementation of a traumatic brain injury protocol in a community hospital setting is practical and efficacious. Appropriate invasive monitoring of systemic and cerebral parameters guides care decisions. The protocol results in an increase in resource usage, but it also results in statistically improved outcomes justifying the increase in expenditures.

Adolescent↗
PubMed2004

Effect of granulocyte colony-stimulating factor on functional and histopathologic outcome after traumatic brain injury in mice.

OBJECTIVE: Granulocyte colony-stimulating factor has been used to reduce the risk of sepsis in patients with traumatic brain injury. However, granulocyte colony-stimulating factor exerts potent pro- and anti-inflammatory effects that could influence secondary injury, and outcome, after traumatic brain injury. Our objective was to determine the effect of granulocyte colony-stimulating factor on histopathologic, motor, and cognitive outcome after experimental traumatic brain injury in mice. DESIGN: Experimental study. SETTING: Research laboratory at the Massachusetts General Hospital, Boston, MA. SUBJECTS: Forty-eight adult male C57Bl/6 mice. INTERVENTIONS: Mice (8 wks of age, n = 16/group) were administered granulocyte colony-stimulating factor or saline subcutaneously twice per day for 7 days after controlled cortical impact or sham injury (n = 16). Absolute neutrophil counts, motor function, Morris water maze performance, and lesion volume were determined after controlled cortical impact or sham injury. MEASUREMENTS AND MAIN RESULTS: At the time of controlled cortical impact, body weight, brain and body temperature, and systemic absolute neutrophil counts did not differ between groups. Compared with control, systemic absolute neutrophil count was increased more than ten-fold in granulocyte colony-stimulating factor-treated mice on posttrauma days 2 and 7 (p < .05, repeated-measures analysis of variance) but did not differ between groups by day 14. There were no differences between groups in tests of motor function or histopathologic outcome. However, compared with control, mice given granulocyte colony-stimulating factor had improved Morris water maze performance after controlled cortical impact (p < .05, repeated-measures analysis of variance) but not sham injury. CONCLUSIONS: The data suggest a small beneficial effect of granulocyte colony-stimulating factor on functional outcome after traumatic brain injury in adult mice but do not show differences in histopathology or motor outcome between treated and control groups.

Analysis of Variance↗
PubMed2001

Effects of the nitrone radical scavengers PBN and S-PBN on in vivo trapping of reactive oxygen species after traumatic brain injury in rats.

In previous studies, the authors showed that the nitrone radical scavenger alpha-phenyl-N- tert -butyl nitrone (PBN) and its sulfo-derivative, 2-sulfo-phenyl-N- tert -butyl nitrone (S-PBN), attenuated cognitive disturbance and reduced tissue damage after traumatic brain injury (TBI) in rats. In the current study, the production of reactive oxygen species (ROS) after TBI was monitored with microdialysis and the 4-hydroxybenzoic acid (4-HBA) trapping method. A single dose of PBN (30 mg/kg) or an equimolar dose of S-PBN (47 mg/kg) was administered intravenously 30 minutes before a controlled cortical contusion injury in rats. Plasma and brain tissue drug concentrations were analyzed at the end of the microdialysis experiment (3 hours after injury) and, in a separate experiment with S-PBN, at 30 and 60 minutes after injury. Traumatic brain injury caused a significant increase in ROS formation that lasted for 60 minutes after the injury as evidenced by increased 3,4-dihydroxybenzoic acid (3,4-DHBA) concentrations in the dialysate. PBN and S-PBN equally and significantly attenuated the posttraumatic increase in 3,4-DHBA formation. High PBN concentrations were found bilaterally in brain tissue up to 3 hours after injury. In contrast, S-PBN was rapidly cleared from the circulation and was not detectable in brain at 30 minutes after injury or at any later time point. The results suggest that scavenging of ROS after TBI may contribute to the neuroprotective properties observed with nitrone spin-trapping agents. S-PBN, which remained undetectable even in traumatized brain tissue, reduced ROS production to the same extent as PBN that readily crossed the blood-brain barrier. This finding supports an important role for ROS production at the blood-endothelial interface in TBI.

Animals↗
PubMed2007

Criterion validity of the California Verbal Learning Test-Second Edition (CVLT-II) after traumatic brain injury.

The California Verbal Learning Test-Second Edition (CVLT-II) was performed by 200 participants, divided into moderate-severe traumatic brain injury (n=43), mild traumatic brain injury (n=57) and demographically matched control (n=100) groups. Participants with complicating premorbid histories or who scored below 15/16 on the CVLT-II forced choice recognition trial were excluded. There were statistically significant (p<.0001) effects of group status on the CVLT-II total recall discriminability and recognition discriminability indices. Logistic regression revealed that, in the classification of control versus moderate-severe traumatic brain injury, CVLT-II variables were accurate 66-71% overall, but false positive rates ranged from 49 to 54%. In conclusion, average scores on the CVLT-II differ meaningfully between patients with various degrees of severity of traumatic brain injury and controls, but this test should not be used in isolation to determine the presence or absence of acquired memory impairment.

Adolescent↗
PubMed1999

Traumatic brain injury and time to onset of Alzheimer's disease: a population-based study.

Controversy continues as to whether traumatic brain injury is a risk factor for Alzheimer's disease. The authors examined a related hypothesis that among persons with traumatic brain injury who develop Alzheimer's disease, time to onset of the disease is reduced. They used data on all documented episodes of traumatic brain injury that occurred from 1935 to 1984 among Olmsted County, Minnesota, residents. Community-based medical records were used to follow traumatic brain injury cases who were aged 40 years or older at last contact prior to June 1, 1988, for Alzheimer's disease until last contact, death, or June 1, 1988. The test of the hypothesis was restricted to those cases who developed Alzheimer's disease. The expected time to onset of Alzheimer's disease was derived from a life table constructed by using age-of-onset distributions within sex groups for a previously identified cohort of Rochester, Minnesota, Alzheimer's disease incidence cases without a history of head trauma. The authors found that of the 1,283 traumatic brain injury cases followed, 31 developed Alzheimer's disease, a number similar to that expected (standardized incidence ratio = 1.2, 95% confidence interval 0.8-1.7). However, the observed time from traumatic brain injury to Alzheimer's disease was less than the expected time to onset of Alzheimer's disease (median = 10 vs. 18 years, p = 0.015). The results suggest that traumatic brain injury reduces the time to onset of Alzheimer's disease among persons at risk of developing the disease.

Adult↗
PubMed2001

Medical treatment and neuroprotection in traumatic brain injury.

The goal of this article is to give an overview about the established current treatment concepts of traumatic brain injury, as well as an outlook on possible future developments in pharmacological neuroprotection. Modern medical treatment modalities of traumatic brain injury (TBI), including the preclinical management of severely head-injured patients, are reviewed. Since an increased intracranial pressure represents the most common complication of severe traumatic brain injury, frequently associated with the development of secondary brain damage, special emphasis was given to an updated treatment algorithm for this important condition. New insight into the pathophysiology of severe traumatic brain injury, especially the realization that brain damage develops sequentially, initiated several new treatment approaches aiming at the interruption of pathophysiological mechanisms leading to secondary brain injury. A high number of pharmacological substances have been tested for their ability to ameliorate secondary damage after TBI, or are currently under clinical trial. Although no drug has achieved this goal so far, the most promising of these therapeutical approaches, glutamate receptor antagonists, calcium channel antagonists, free radical scavengers, and cyclosporin A will be discussed in this review. Although a "magical bullet" for the treatment of traumatic brain injury has not been developed yet, several of the currently investigated neuroprotective strategies seem to be encouraging. A promising future approach might be to evaluate treatment strategies that combine several pharmacological agents, and possibly other treatment modalities, such as mild hypothermia, "tailored" according to the special pathology of patient subgroups, or even to every single patient in order to achieve an improvement in outcome after TBI.

Brain Injuries↗
PubMed2004

Cerebral microdialysis of patients with severe traumatic brain injury exhibits highly individualistic patterns as visualized by cluster analysis with self-organizing maps.

OBJECTIVE: To analyze patterns of cerebral microdialysis in patients with traumatic brain injury and, with a neural network methodology, investigate pattern relationships to intracranial pressure and cerebral perfusion pressure. DESIGN: Retrospective. SETTING: University hospital, adult neurosurgical intensive care unit. PATIENTS: Twenty-six patients with severe traumatic brain injury. All consecutive traumatic brain injured patients (Glasgow Coma Scale < or =8) with microdialysis monitoring, analyzing glutamate, lactate, pyruvate, and glucose in both penumbral and nonpenumbral tissue. INTERVENTIONS: None; patients received the unit's standard neurointensive care procedure. MEASUREMENTS AND MAIN RESULTS: We used 2084 hrs of complete microdialysis data sets (eight markers) to train Kohonen self-organizing maps. The self-organizing map algorithm is a data-clustering method that reduces high-dimensional information to a two-dimensional representation on a grid (map), retaining local relationships in the data. Maps were colored (overlaid) for intracranial pressure, cerebral perfusion pressure, and outcome, to explore relationships with underlying microdialysis patterns. The maps exhibited a striking clustering of patients, with unique microdialysis patterns that were recognizable throughout the analysis period. This also held true for most microdialysis patterns characteristic of ischemia. These patients with ischemic patterns can have good outcomes, suggesting a disparity between microdialysis values and severity of traumatic brain injury. CONCLUSION: Using an artificial neural network-like clustering technique, Kohonen self-organizing maps, we have shown that cerebral microdialysis, in traumatic brain injury, exhibits strikingly individualistic patterns that are identifiable throughout the analysis period. Because patients form their own clusters, microdialysis patterns, during periods of increased intracranial pressure or decreased cerebral perfusion pressure, will be found within these clusters. Consequently, no common pattern of microdialysis can be seen among patients within the range of our data. We suggest that these individualistic patterns reflect not only metabolic states of traumatic brain injury but also local gradients seen with small volume sampling. Future investigation should focus on relating these patterns, and movement within and from clusters, to metabolic states of the complex pathophysiology of traumatic brain injury.

Adolescent↗
PubMed2001

Increased adenosine in cerebrospinal fluid after severe traumatic brain injury in infants and children: association with severity of injury and excitotoxicity.

OBJECTIVES: To measure adenosine concentration in the cerebrospinal fluid of infants and children after severe traumatic brain injury and to evaluate the contribution of patient age, Glasgow Coma Scale score, mechanism of injury, Glasgow Outcome Score, and time after injury to cerebrospinal fluid adenosine concentrations. To evaluate the relationship between cerebrospinal fluid adenosine and glutamate concentrations in this population. DESIGN: Prospective survey. SETTING: Pediatric intensive care unit in a university-based children's hospital. PATIENTS: Twenty-seven critically ill infants and children who had severe traumatic brain injury (Glasgow Coma Scale < 8), who required placement of an intraventricular catheter and drainage of cerebrospinal fluid as part of their neurointensive care. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients ranged in age from 2 months to 14 yrs. Cerebrospinal fluid samples (n = 304) were collected from 27 patients during the first 7 days after traumatic brain injury. Control cerebrospinal fluid samples were obtained from lumbar puncture on 21 infants and children without traumatic brain injury or meningitis. Adenosine concentration was measured by using high-pressure liquid chromatography. Adenosine concentration was increased markedly in cerebrospinal fluid of children after traumatic brain injury vs. controls (p < .001). The increase in cerebrospinal fluid adenosine was independently associated with Glasgow Coma Scale < or = 4 vs. > 4 and time after injury (both p < .005). Cerebrospinal fluid adenosine concentration was not independently associated with either age (< or = 4 vs. > 4 yrs), mechanism of injury (abuse vs. other), or Glasgow Outcome Score (good/moderately disabled vs. severely disabled, vegetative, or dead). Of the 27 patients studied, 18 had cerebrospinal fluid glutamate concentration previously quantified by high-pressure liquid chromatography. There was a strong association between increases in cerebrospinal fluid adenosine and glutamate concentrations (p < .005) after injury. CONCLUSIONS: Cerebrospinal fluid adenosine concentration is increased in a time- and severity-dependent manner in infants and children after severe head injury. The association between cerebrospinal fluid adenosine and glutamate concentrations may reflect an endogenous attempt at neuroprotection against excitotoxicity after severe traumatic brain injury.

Adenosine↗
PubMed2005

Experimental models of traumatic brain injury: do we really need to build a better mousetrap?

Approximately 4000 human beings experience a traumatic brain injury each day in the United States ranging in severity from mild to fatal. Improvements in initial management, surgical treatment, and neurointensive care have resulted in a better prognosis for traumatic brain injury patients but, to date, there is no available pharmaceutical treatment with proven efficacy, and prevention is the major protective strategy. Many patients are left with disabling changes in cognition, motor function, and personality. Over the past two decades, a number of experimental laboratories have attempted to develop novel and innovative ways to replicate, in animal models, the different aspects of this heterogenous clinical paradigm to better understand and treat patients after traumatic brain injury. Although several clinically-relevant but different experimental models have been developed to reproduce specific characteristics of human traumatic brain injury, its heterogeneity does not allow one single model to reproduce the entire spectrum of events that may occur. The use of these models has resulted in an increased understanding of the pathophysiology of traumatic brain injury, including changes in molecular and cellular pathways and neurobehavioral outcomes. This review provides an up-to-date and critical analysis of the existing models of traumatic brain injury with a view toward guiding and improving future research endeavors.

Animals↗
PubMed1996

Antidepressant pharmacotherapy and the treatment of depression in patients with severe traumatic brain injury: a controlled, prospective study.

BACKGROUND: Untreated or poorly treated depression in patients who suffer from traumatic brain injury can result in greater functional disability and prolonged or ineffective hospital and rehabilitation stays. Literature available on the pharmacologic treatment of depression after traumatic brain injury is scarce. This study investigated in a controlled and prospective manner the use of desipramine, a tricyclic antidepressant, in a series of patients with severe traumatic brain injury. METHOD: Ten patients with severe traumatic brain injury and long-standing depression, as diagnosed by DSM-III-R criteria, were admitted to the study because of the intention to be treated with antidepressants. They were randomly assigned to blindly start on either desipramine treatment (N = 6) or placebo lead-in (N = 4). Patients starting with desipramine stayed on that drug; patients starting with placebo lead-in were blindly crossed over to desipramine after 1 month if there was no significant improvement demonstrated by DSM-III-R criteria. All rating clinicians, physicians, and patients were blind to actual treatment and any ratings data. DSM-III-R evaluations were done monthly. An affect/mood scale was done every 2 weeks. RESULTS: Of all patients evaluable using the DSM-III-R, 6 (86%) of 7 demonstrated resolution of depression and depressed mood during desipramine treatment. (Three received desipramine throughout the study; 3 others started taking placebo and crossed over to desipramine,) One patient refused evaluation on DSM-III-R throughout; 2 patients, both on desipramine, dropped out because of adverse effects (seizure, mania). In addition, there was statistically significant (p = .001) improvement over time and different rates of improvement over time in the treated and untreated groups for the affect/mood scale data. CONCLUSION: Results from this small study, utilizing a blinded, placebo lead-in design appear to (1) demonstrate the clinically significant effectiveness of desipramine in treating long-standing depression in a series of patients with severe traumatic brain injury, as rated with DSM-III-R criteria; (2) show statistically significant improvement on the affect/mood scale data, favoring the treated versus untreated (placebo lead-in) group.

Accidents, Traffic↗
PubMed1996

Cisapride as a treatment for gastroparesis in traumatic brain injury.

Gastroparesis is a well-documented finding among patients with severe traumatic brain injuries. The treatment of choice has been metoclopramide, but it is less than ideal given its central dopaminergic blocking activity. Cisapride is a newer prokinetic agent without side effects on the central nervous system and might be a superior treatment. The case of a healthy 22-year-old man who suffered a severe traumatic brain injury and multiple trauma in a motor vehicle accident is reported. The patient required gastrostomy tube placement but developed recurrent aspiration pneumonia once feedings were initiated. Despite receiving metoclopramide, barium studies revealed gastroparesis, a significant decrease in gastric peristalsis, and reflux. A jejunostomy tube was placed to prevent further aspiration. The administration of cisapride was begun, and 2 days later the patient was changed back to G-tube feedings with no evidence of residual aspirates. Repeat barium study showed definite improvement in peristalsis. This case demonstrates the potential usefulness of cisapride in patients with traumatic brain injury. Although further research is necessary, efficacy without central dopamine blockage may make cisapride the treatment of choice for gastroparesis and reflux in traumatic brain injury.

Adult↗
PubMed2001

Long-term life quality and family needs after traumatic brain injury.

OBJECTIVES: This investigation assessed the life quality and long-term family needs of caregivers of persons with brain injury. DESIGN: Respondents completed the Virginia Traumatic Brain Injury Family Needs Assessment Survey. SETTING: Community-based sample. PARTICIPANTS: Respondents included 57 caregivers of persons with traumatic brain injury who were at least 4 years after injury and who resided in Virginia. Respondents ranged in age from 19 to 82 years and were primarily women and Caucasian. OUTCOME MEASURES: The Family Needs Questionnaire (FNQ) and quality of life questions. RESULTS: Results indicate diminished life quality after injury. With regard to family needs, Health Information (51.43%) and Involvement with Care (47.93%) needs were most often rated as met. Instrumental Support (31.52%) and Professional Support (28.38%) needs were most often rated as not met. CONCLUSIONS: Family needs and support systems for those needs change over time. This investigation provides evidence that unmet family needs extend well beyond the acute setting and that caregiver life quality diminishes over time. The importance of appreciating long-term family needs and other life quality issues should not be underestimated.

Adult↗
PubMedDate not supplied

Prediction of outcome at discharge from acute care following traumatic brain injury.

OBJECTIVE: To compute outcome probabilities for persons with traumatic brain injury at discharge from acute care. PARTICIPANTS: Three hundred thirty-nine patients with traumatic brain injury (239 mild, 48 moderate, 52 severe). SETTING: Level I trauma center. MAIN MEASURES: Predictor variables considered were age, education, Glasgow Coma Scale score, duration of posttraumatic amnesia, cerebral imaging results, and need for neurosurgical intervention. Outcome measures were Extended Glasgow Outcome Scale and discharge destination. RESULTS: Logistic regressions showed that a shorter posttraumatic amnesia decreased the probability of moderate to severe disability. Moreover, discharge home was less probable for patients with positive cerebral imaging. CONCLUSION: This model can help predict rehabilitation needs upon discharge from an acute care hospital.

Adult↗
PubMed2000

Impaired autoregulation of cerebral blood flow in an experimental model of traumatic brain injury.

In order to study the pathophysiology and the intracranial hemodynamics of traumatic brain injury, we have developed a modified closed-head injury model of impact-acceleration that expresses several features of severe head injury in humans, including acute and long-lasting intracranial hypertension, diffuse axonal injury, neuronal necrosis, bleeding, and edema. In view of the clinical relevance of impaired autoregulation of cerebral blood flow after traumatic brain injury, and aiming at further characterization of the model, we investigated the autoregulation efficiency 24 h after experimental closed-head injury. Cortical blood flow was continuously monitored with a laser-Doppler flowmeter, and the mean arterial blood pressure was progressively decreased by controlled hemorrhage. Relative laser-Doppler flow was plotted against the corresponding mean arterial blood pressure, and a two-line segmented model was applied to determine the break point and slopes of the autoregulation curves. The slope of the curve at the right hand of the break point was significantly increased in the closed head injury group (0.751 +/- 0.966%/mm Hg versus -0.104 +/- 0.425%/mm Hg,p = 0.028). The break point tended towards higher values in the closed head injury group (62.2 +/- 20.8 mm Hg versus 46.9 +/- 12.7 mm Hg; mean +/- SD, p = 0.198). It is concluded that cerebral autoregulation in this modified closed head injury model is impaired 24 h after traumatic brain injury. This finding, in addition to other characteristic features of severe head injury established earlier in this model, significantly contributes to its clinical relevance.

Animals↗