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Results for “Traumatic Brain Injuries”

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PubMed2004

Mild traumatic brain injuries presenting to Swedish hospitals in 1987-2000.

OBJECTIVE: To evaluate the incidence and causes of mild traumatic brain injury in Sweden. DESIGN: Retrospective, population-based incidence cohort study. SUBJECTS: All persons presenting to hospitals in Sweden between 1987 and 2000 with a discharge diagnosis of ICD-9 code 850 and ICD-10 code S0.60. METHODS: Data source was the Hospital Discharge Register at the National Board of Health and Welfare (Sweden). Incidence rates are stratified by age, gender, mechanism of injury and length of hospital stay. RESULTS: Men had a mean of 209 mild traumatic brain injuries per 100,000 inhabitants and women averaged 148 per 100,000. Men had more mild traumatic brain injury than women at all ages. There were 2 incidence peaks, in the age strata 16-20 years and those over 65 years. Falls were the most common cause of mild traumatic brain injury overall and occurred commonly under the age of 10 years and over the age of 65 years. Motor vehicle and bicycle injuries were the second and third most common causes of mild traumatic brain injury, and had their peak incidence in those aged 16-35 years. CONCLUSION: Preventative strategies for mild traumatic brain injury should be age and gender specific.

Adolescent↗

PubMed2001

Association of HIF-1alpha expression and cell apoptosis after traumatic brain injury in the rat.

OBJECTIVE: To explore the expression of hypoxia inducible factor-1alpha (HIF-1alpha) and the correlation between HIF-1alpha and apoptosis after traumatic brain injury. METHODS: Using experimental traumatic brain injury in the rats, the expression of HIF-1alpha was studied by immunohistochemistry in cerebral tissue, apoptotic cell death was evaluated with TUNEL (transferase-mediated X-dUTP nick end labeling), and double-labeled immunohistochemistry and TUNEL methods were used to investigate the relationship between HIF-1alpha and apoptosis. RESULTS: There was remarkable difference in the expression of H IF-1alpha between the experimental groups and the control groups (P<0.01), in the experimental groups, the expression of HIF-1alpha at 48 hours was highest; the evidence of apoptotic cell death after experimental traumatic brain injury was found by TUNEL; the apoptotic percentage increased or decreased according to the changes of the positive expression of HIF-1alpha (r=0.99). CONCLUSIONS: The results suggest that secondary brain ischemia plays a crucial role in apoptotic cell death after traumatic brain injury; HIF-1alpha can prompt apoptotic cell death after experimental traumatic brain injury.

Animals↗

PubMed2026

Effectiveness of hyperbaric oxygen in traumatic brain injury patients: A systematic review and meta-analysis.

BACKGROUND: Traumatic brain injury (TBI) is the most common neurological disorder and a leading cause of global mortality and disability. Although growing evidence suggests potential benefits of Hyperbaric Oxygen Therapy (HBOT) for TBI, its efficacy remains controversial. METHODS: We systematically searched PubMed, Embase, Cochrane Library, and Web of Science from inception to March 2026. Randomized controlled trials (RCTs) evaluating HBOT versus any comparator including sham, standard care and no treatment in adults with TBI were included. Two independent reviewers screened records, extracted data, and assessed risk of bias using the Cochrane Risk of Bias tool. Heterogeneity was assessed using the I² statistic. Effect sizes were pooled using random/fixed-effects models per heterogeneity results. RESULTS: 8 studies involving 570 participants were included. HBOT significantly improved computerized cognitive performance (SMD = 0.23, 95% CI: 0.07-0.40, p = 0.004, I² = 0%), executive function and processing speed (SMD = -0.59, 95% CI: -0.93 to -0.26, p = 0.0005, I² = 30%), memory function (SMD = 0.33, 95% CI: 0.03-0.63, p = 0.03, I² = 0%), and sleep quality (MD = 1.98, 95% CI: 0.07-3.88, p = 0.04, I² = 65%). No significant benefits were observed for Glasgow Outcome Scale (RR = 1.57, 95% CI: 0.55-4.44, I² = 87%), PTSD symptoms (MD = -3.05, 95% CI: -7.05-0.95, I² = 67%), neurobehavioral symptoms (MD = -9.06, 95% CI: -32.13-14.00, I² = 97%), and emotional distress (SMD = 0.25, 95% CI: -0.32-0.81, I² = 85%). Most adverse events were mild and transient. CONCLUSION: HBOT demonstrates domain‑specific benefits for cognitive function and sleep quality in TBI patients, predominantly those with mild TBI. However, evidence for PTSD, neurobehavioral symptoms, and emotional distress remains uncertain. Furthermore, the applicability of current evidence to moderate-to-severe TBI populations is restricted.

Humans↗

PubMed2003

Traumatic brain injury.

PURPOSE OF REVIEW: Management of the patient with traumatic brain injury is a rapidly advancing field, characterized in recent years by an improved understanding of intracranial pathophysiology and ways in which outcomes can be improved. Many traditional therapies, such as fluid restriction and hyperventilation, have been called into question and are no longer recommended. Other proposed therapies, such as deliberate hypothermia, remain controversial. This detailed review of the recent literature helps the reader come to an understanding of current scientific and evidence-based practices in this area, with emphasis on those therapies most likely to be of use to the practicing intensivist. RECENT FINDINGS: High-quality care of the traumatic brain injury patient demands the integrated activities of a number of different medical and nursing specialties. The best outcomes today are achieved by those systems that are able to focus as a team on the collective goal of minimizing secondary brain injury, and the respiratory therapist adjusting the patient's mechanical ventilation may be just as important to this effort as the attending neurosurgeon. Although the search for new diagnostic, prognostic, and therapeutic modalities continues (many of the more promising of which are reviewed in this article), it is clear that there exists no "silver bullet" therapy that will help all patients. Instead, it is the systematic integration and application of many small advances that will ultimately lead to better outcomes. SUMMARY: Some issues in traumatic brain injury have now been resolved, and specific recommendations can be made. Fluid therapy directed toward a euvolemic state is now universally recommended, for example, as is the role of intracranial pressure monitoring. Other areas, such as the use of hypertonic saline, remain controversial. In both cases the authors have made an effort to cite the most recent literature, so that readers can draw their own conclusions from the original source material.

Brain Injuries↗

PubMed2003

Mood disorders following traumatic brain injury.

Mood disorders are a frequent complication of traumatic brain injury that exerts a deleterious effect on the recovery process and psychosocial outcome of brain injured patients. Prior psychiatric history and impaired social support have been consistently reported as risk factors for developing mood disorders after traumatic brain injury (TBI). In addition, biological factors such as the involvement of the prefrontal cortex and probably other limbic and paralimbic structures may play a significant role in the complex pathophysiology of these disorders. Preliminary studies have suggested that selective serotonin reuptake inhibitors such as sertraline, mood stabilizers such as sodium valproate, as well as stimulants and ECT may be useful in treating these disorders. Mood disorders occurring after TBI are clearly an area of neuropsychiatry in which further research in etiology as well as treatment is needed.

Adult↗

PubMed1992

Limitations of the Glasgow Coma Scale in predicting outcome in children with traumatic brain injury.

OBJECTIVE: To study the hypothesis that, in the absence of an ischemic-hypoxic state, children with severe traumatic brain injury and with unfavorable Glasgow Coma Scale scores may have good recovery. DESIGN: Retrospective, observational, cross-sectional study with factorial design. SETTING: Inpatient population in a university hospital. PATIENTS: Seventy-nine children with traumatic brain injury admitted to the intensive care unit. INTERVENTIONS: All patients received close monitoring and strict control of intracranial pressure (less than 20 mm Hg) and cerebral perfusion pressure (greater than 60 mm Hg). MEASUREMENTS AND RESULTS: Admission Glasgow Coma Scale score, survival, need for cardiopulmonary resuscitation, presence of shock, peak intracranial pressure, duration of coma, Glasgow Outcome Scale score, and the results of neuropsychologic tests were analyzed. Of 79 children, 70 (89%) survived. Although the mortality rate was higher among patients with Glasgow Coma Scale scores of 3 to 5, 14 (64%) of 22 of these children survived. Nonsurvivors had a significantly higher incidence of shock and need for cardiopulmonary resuscitation. Except for two patients who had prolonged hypoxemia, all children, including those with Glasgow Coma Scale scores of 3 to 5, had a satisfactory outcome (Glasgow Outcome Scale scores of 4 or 5). Neuropsychologic outcome was not significantly different in the survivors with Glasgow Coma Scale scores of 3 to 5 and those with Glasgow Coma Scale scores of 6 or more. CONCLUSIONS: A low Glasgow Coma Scale score does not always accurately predict the outcome of severe traumatic brain injury; in the absence of hypoxic-ischemic injury, children with traumatic brain injury and Glasgow Coma Scale scores of 3 to 5 can recover independent function.

Adolescent↗

PubMed1998

Medroxyprogesterone in the treatment of aggressive hypersexual behavior in traumatic brain injury.

Sexual function is among the many areas affected by traumatic brain injury. The most common change is decreased sexual performance and satisfaction, for the brain injured person and the sexual partner. Hypersexuality, especially inappropriate sexual comments and gestures, is also a common result of traumatic brain injury. A case of hypersexuality in a severely disabled brain injured man is presented. He was successfully treated with medroxyprogesterone acetate after failure of multiple other treatment strategies. The literature is reviewed. An evaluation and treatment strategy for sexual dysfunction post traumatic brain injury is presented.

Accidents, Traffic↗

PubMed2006

How great is willingness to pay for recovery from sequelae after severe traumatic brain injury in Japan?

OBJECTIVE: To evaluate the burden on families with a family member suffering traumatic brain injury sequelae in Japan. DESIGN: Cross-sectional study. METHODS: Family members' burden from the sequelae of traumatic brain injury was estimated by use of willingness-to-pay models and the contingent valuation method. A national survey among 1707 members of the Japan Traumatic Brain Injury Association was conducted by postal questionnaire with open-ended questions. A total of 509 (29.8%) of the family members responded (405 men and 104 women). Mean age of patients with traumatic brain injury was 33.4 (SD 14.3) years and of responding family members 53.3 (SD 14.5) years. RESULTS: Willingness-to-pay for the family member's recovery from sequelae of traumatic brain injury (8,694,502 Japanese yen; 79,134 US dollars/year) was similar to that reported for a family member's survival from incurable terminal disease (8,342,953 Japanese yen; 75,934 US dollars/year). CONCLUSION: The data indicate that family members perceive the burden of a family member with traumatic brain injury sequelae as similar to what would have been caused by an incurable terminal disease.

Adult↗

PubMed2026

Seawater immersion reshapes the temporal dynamics of traumatic brain injury and reveals mitochondrial oxidative stress as a modifiable therapeutic target.

Traumatic brain injury (TBI) evolves through time-dependent secondary injury, but whether seawater (SW) immersion merely amplifies pathology or reshapes the temporal trajectory of post-traumatic biology remains unclear. Here, we applied time-resolved proteomics to mouse brains after controlled cortical impact (CCI) with or without artificial SW immersion at 1, 3, 7, and 28 days post-injury. Trajectory-based proteomic analysis revealed that SW immersion altered the direction, magnitude, timing, persistence, and recovery of protein responses, rather than simply intensifying TBI-induced changes. This remodeled trajectory exhibited phase-specific patterns, including SW-dominant, synergistically enhanced, and attenuated responses, highlighting mitochondrial oxidative stress, inflammatory activation, complement/coagulation disturbance, and impaired structural repair. Phenotypic validation confirmed phase-specific deficits, including acute inflammatory-redox injury, impaired neuronal survival, chronic axon-myelin disruption, and incomplete behavioral recovery. SS-31 partially mitigated selected inflammatory, redox, neuronal, and white matter abnormalities, supporting mitochondrial oxidative stress as a modifiable node rather than the sole driver of trajectory remodeling. These findings identify seawater immersion as a temporal modifier of secondary injury and emphasize that environmental trauma may require trajectory-informed, phase-specific therapeutic interventions.

Animals↗

PubMed2006

One-year follow-up of patients with mild traumatic brain injury: occurrence of post-traumatic stress-related symptoms at follow-up and serum levels of cortisol, S-100B and neuron-specific enolase in acute phase.

OBJECTIVE: To investigate serum levels of cortisol (a biochemical marker of stress), S-100B and neuron-specific enolase (two biochemical markers of brain tissue injury), in acute phase in mild traumatic brain injury patients and the occurrence of post-traumatic stress-related symptoms 1 year after the trauma. METHODS: Blood samples were taken in patients (n = 88) on admission and approximately 7 hours later for analysis. Occurrence of post-traumatic stress-related symptoms was assessed for 69 patients using items from the Impact of Event Scale questionnaire (IES) at follow-up at 15 +/- 4 months after the injury. RESULTS: Serum levels of cortisol were more increased in the first sample (cortisol/1, 628.9 +/- 308.9 nmol L-1) than in the second blood sample (cortisol/2, 398.2 +/- 219.4 nmol L-1). The difference between these samples was statistically significant (p < 0.001). Altogether 12 patients (17%) showed post-traumatic stress related symptoms at the time of the follow-up. Stepwise forward logistic regression analysis of symptoms and serum concentrations of markers revealed that only S-100B in the second sample was statistically significantly (p < 0.05) associated to symptoms (three symptoms of the avoidance sub-set of IES). CONCLUSION: A major increase in serum concentrations of cortisol indicates that high stress levels were reached by the patients, in particular shortly ( approximately 3 hours) after the trauma. The association between the occurrence of post-traumatic stress related symptoms and serum levels of S-100B (generally considered as a biochemical marker of brain injury) seem to reflect the complexity of interactions between brain tissue injury and the ensemble of stress reactions.

Acute Disease↗

PubMed2001

[Traumatic brain injury--the National Trauma Registry].

BACKGROUND: Traumatic Brain Injury (TBI) has been established as a category in reporting systems. Uniform data systems case definition has been suggested for hospital discharge data surveillance systems cases based on ICD-9-CM diagnostic codes. These include fractures and specific mention of intracranial injuries such as contusion, laceration, hemorrhage, and concussion. Inspection of data from the Israel National Trauma Registry suggested that two diagnostic groups of very different severity and outcome were being unjustifiably combined. AIM: To evaluate the validity of categorizing TBI into two discrete groups, using the presence of specific mention of intracranial injury and/or loss of consciousness for more than one hour as the definition of definite TBI. Possible TBI includes skull fractures with no mention of intracranial injury and/or concussion with no loss of consciousness. METHODS: The study population includes all traumatic injuries admitted to hospital, dying in the ER or transferred to other hospitals and recorded in the 1998 Trauma Registry in all 6 level I trauma centers in Israel and two level II centers. RESULTS: The significant difference in severity between groups supports the validity of sub-dividing the TBI classification into definite and possible subcategories. As a result, we obtain two different severity groups without measuring specific severity scores which are limited in the reporting system. CONCLUSION: The groups were significantly different in severity, hospital resource use, immediate outcome, demographic and injury circumstances.

Accidental Falls↗

PubMed2001

Longitudinal outcome of verbal discourse in children with traumatic brain injury: three-year follow-up.

PURPOSE: This study compared changes in discourse ability between two groups of children age 5 to 10 years after brain injury: those with severe traumatic brain injury (TBI) and those with mild/moderate injury over 3-year follow-up testing. MATERIALS AND METHODS: Forty-three children with TBI were recruited from a larger research project examining cognitive and linguistic recovery after injury. Twenty-two of these patients had severe injuries and 21 sustained mild/moderate injuries. All children were presented an ordered sequence of pictures and asked to verbally produce a story/narrative discourse. Each child was then asked to produce a lesson relating to the story. RESULTS: The severe group performed significantly worse than the mild/moderate group when performance across all four discourse domains was considered. Both groups improved across time on selected discourse measures. Qualitative analysis suggested that the severe group showed differential rates of improvement across the individual discourse variables over the 3-year interval. CONCLUSIONS: Severe TBI can have a pernicious effect on discourse abilities in children years after injury compared with children with mild/moderate injuries. The major caveat is that the discourse measures must be sufficiently challenging when used to assess older children and children with milder forms of TBI.

Analysis of Variance↗

PubMed2006

Considering the use of induced hypothermia in a pediatric patient with traumatic brain injury: a critical appraisal of two meta-analyses.

OBJECTIVE: To review whether induced hypothermia after traumatic brain injury affects morbidity and mortality based on the results of two meta-analyses. DESIGN: Critical appraisals of McIntyre et al: Prolonged therapeutic hypothermia after traumatic brain injury in adults: A systematic review. JAMA 2003; 289:2992-2999, and Henderson et al: Hypothermia in the management of traumatic brain injury: A systematic review and meta-analysis. Intensive Care Med 2003; 29:1637-1644. FINDINGS: Both meta-analyses included trials of adult patients with severe traumatic brain injury randomized to induced hypothermia or normothermia and evaluated risk of death and poor neurologic outcomes. McIntyre et al. found the overall relative risk of mortality with induced hypothermia to be 0.81 (95% confidence interval 0.69-0.96). By designing a priori analyses, these authors also found that the relative risk of death was reduced in patients cooled for >48 hrs, and the risk of poor neurologic outcome was reduced with all durations of cooling, cooling to 32-33 degrees C, and rewarming in <24 hrs. In contrast, Henderson et al. found that induced hypothermia did not change the odds of death after traumatic brain injury (odds ratio 0.81; 95% confidence interval 0.59-1.13) and that normothermic controls had an odds ratio of 0.42 (95% confidence interval 0.25-0.70) for developing intercurrent pneumonia. Both analyses found trials to be heterogeneous with respect to neurologic outcome. CONCLUSIONS: The discrepancies in the results of these contemporaneous meta-analyses may stem, in part, from differences in their trial selection strategies as well as from sources of trial heterogeneity. Nevertheless, McIntyre et al. uncovered the equivalent of a dose-dependent reduction in the risk of death with induced hypothermia, supporting further study of this neuroprotective strategy. Although these meta-analyses included trials containing adult patients, a phase II trial of induced hypothermia in pediatric traumatic brain injury has established its feasibility and safety in infants and children. As in adult patients, induced hypothermia for traumatic brain injury in children can be considered an optional therapy for refractory intracranial hypertension but should not be regarded as standard of care.

Comment↗

PubMedDate not supplied

The clinical significance of major depression following mild traumatic brain injury.

OBJECTIVE: The authors assessed the association of major depression with behavioral outcome following mild traumatic brain injury. METHOD: Consecutive patients with mild traumatic brain injury (N=170) were assessed for major depression. Those with major depression were compared with those without on self-report measures of psychosocial dysfunction, psychological distress, and postconcussive symptoms in addition to examiner-rated neurobehavioral disturbance. RESULTS: Major depression was seen in 15.3% (N=26) of the subjects after traumatic brain injury, and these individuals showed subjective and objective evidence of poorer outcome. CONCLUSIONS: Major depression is associated with poor outcome across multiple domains. This study highlights the need for the early diagnosis and prompt treatment of major depression following mild traumatic brain injury.

Adolescent↗

PubMed2006

Critical score of Glasgow Coma Scale for pediatric traumatic brain injury.

The aim of this study is to determine the predictive critical value of the Glasgow Coma Scale for use as a determinant of outcome for children with traumatic brain injuries. A total of 309 children, aged 2-10 years, were enrolled in this study. Each subject underwent the following assessments: Glasgow Coma Scale; clinical data; brain computed tomography; and Glasgow Outcome Scale assessments. The receiver operating characteristic curve indicated that a critical point of the Glasgow Coma Scale set at 5 was most strongly correlated with outcome of pediatric traumatic brain injury. Subarachnoid hemorrhage with brain swelling and edema, subdural, intracerebral hemorrhage, and basal ganglion lesions were associated with severe injury and poor outcome (P < 0.05). However, cortical lesions did not affect injury severity and outcome. In injuries associated with traumatic brain injuries, only chest trauma had a tendency to be associated with poor outcome (P < 0.05). Of the factors analyzed, the score of the Glasgow Coma Scale was the most effective predictor for outcome in pediatric traumatic brain injury. Furthermore, the predictive critical score of the Glasgow Coma Scale should be set at 5 for pediatric traumatic brain injury. The computed tomographic findings also were important in determining injury severity and predicting outcome.

Accidents, Traffic↗

PubMed2006

Soluble amyloid precursor protein alpha reduces neuronal injury and improves functional outcome following diffuse traumatic brain injury in rats.

Amyloid precursor protein (APP) has previously been shown to increase following traumatic brain injury (TBI). Whereas a number of investigators assume that increased APP may lead to the production of neurotoxic Abeta and be deleterious to outcome, the soluble alpha form of APP (sAPPalpha) is a product of the non-amyloidogenic cleavage of amyloid precursor protein that has previously been shown in vitro to have many neuroprotective and neurotrophic functions. However, no study to date has addressed whether sAPPalpha may be neuroprotective in vivo. The present study examined the effects of in vivo, posttraumatic sAPPalpha administration on functional motor outcome, cellular apoptosis, and axonal injury following severe impact-acceleration TBI in rats. Intracerebroventricular administration of sAPPalpha at 30 min posttrauma significantly improved motor outcome compared to vehicle-treated controls as assessed using the rotarod task. Immunohistochemical analysis using antibodies directed toward caspase-3 showed that posttraumatic treatment with sAPPalpha significantly reduced the number of apoptotic neuronal perikarya within the hippocampal CA3 region and within the cortex 3 days after injury compared to vehicle-treated animals. Similarly, sAPPalpha-treated animals demonstrated a reduction in axonal injury within the corpus callosum at all time points, with the reduction being significant at both 3 and 7 days postinjury. Our results demonstrate that in vivo administration of sAPPalpha improves functional outcome and reduces neuronal cell loss and axonal injury following severe diffuse TBI in rats. Promotion of APP processing toward sAPPalpha may thus be a novel therapeutic strategy in the treatment of TBI.

Amyloid beta-Protein Precursor↗

PubMed2006

Efficacy and safety of dexanabinol in severe traumatic brain injury: results of a phase III randomised, placebo-controlled, clinical trial.

BACKGROUND: Traumatic brain injury is a major cause of death and disability. We sought to assess the safety and efficacy of dexanabinol, a synthetic cannabinoid analogue devoid of psychotropic activity, in severe traumatic brain injury. METHODS: 861 patients with severe traumatic brain injury admitted to 86 specialist centres from 15 countries were included in a multi-centre, placebo-controlled, phase III trial. Patients were randomised to receive a single intravenous 150 mg dose of dexanabinol or placebo within 6 h of injury. The primary outcome was the extended Glasgow outcome scale assessed at 6 months, with the point of dichotomisation into unfavourable versus favourable outcome differentiated by baseline prognostic risk. Prespecified subgroup analyses were defined by injury severity, recruitment rate, and time to dosing. Secondary analysis included control of intracranial pressure and quality of life. Analysis were prespecified in the protocol and the statistical analysis plan. This study is registered with ClinicalTrials.gov, number NCT00129857. FINDINGS: 846 patients were included in the efficacy analysis. The extended Glasgow outcome scale at 6 months did not differ between groups; 215 (50%) patients in the dexanabinol group and 214 (51%) patients in the placebo group had an unfavourable outcome (odds ratio for a favourable response 1.04; 95% CI 0.79-1.36). Improvements in the control of intracranial pressure or quality of life were not recorded and subgroup analysis showed no indication of differential treatment effects. Dexanabinol was not associated with hepatic, renal, or cardiac toxic effects. INTERPRETATION: Dexanabinol is safe, but is not efficacious in the treatment of traumatic brain injury.

Adolescent↗

PubMed2001

The hypothalamo-pituitary-adrenal axis response to experimental traumatic brain injury.

Alterations in the hypothalamo-pituitary-adrenal (HPA) axis following traumatic brain injury have not been documented in detail. We used fluid percussion injury (FPI) to evaluate the early changes in components of the HPA axis following experimental traumatic brain injury. Wistar rats were sacrificed at 2 or 4 h following sham or FPI surgery. In situ hybridization histochemistry was used to determine the expression of mRNAs of corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP) in the hypothalamus and pro-opiomelanocortin (POMC) in the pituitary. A group of animals undergoing no surgery were used as control. Repeated blood sampling from an indwelling catheter demonstrated that plasma corticosterone (CORT) levels peaked 30 min following surgery in sham and FPI animals but there was no significant difference in CORT concentration between these groups at any time. Pituitary POMC expression was increased following sham and FPI surgery (compared with control non-operated animals) but with no significant difference between the two groups undergoing surgery. Hypothalamic CRH mRNA expression was significantly higher in animals undergoing FPI compared with sham surgery. Hypothalamic AVP mRNA expression was not significantly increased when compared with control nonoperated animals. These data indicate that the anaesthesia and/or surgery associated with FPI or sham surgery induces a generalised activation of the HPA axis. The selective increase in CRH mRNA in animals undergoing FPI may be due to specific effects of traumatic brain injury rather than a general stress response and may suggest an additional neurotransmitter role for CRH following head injury. The absence of an AVP response suggests that the effects of FPI may be mediated through the CRH-alone-containing subpopulation of neurons.

Animals↗