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PubMed2005

Simultaneous glutamate and GABA(A) receptor agonist administration increases calbindin levels and prevents hippocampal damage induced by either agent alone in a model of perinatal brain injury.

Perinatal brain injury is associated with the release of amino acids, principally glutamate and GABA, resulting in massive increases in intracellular calcium and eventual cell death. We have previously demonstrated that independent administration of kainic acid (KA), an AMPA/kainate receptor agonist, or muscimol, a GABA(A) receptor agonist, to newborn rats results in hippocampal damage [Hilton, G.D., Ndubuizu, A., and McCarthy, M.M., 2004. Neuroprotective effects of estradiol in newborn female rat hippocampus. Dev. Brain Res. 150, 191-198; Hilton, G. D., Nunez, J.L. and McCarthy, M.M., 2003. Sex differences in response to kainic acid and estradiol in the hippocampus of newborn rats. Neuroscience. 116, 383-391; Nunez, J.L. and McCarthy, M.M., 2003. Estradiol exacerbates hippocampal damage in a model of preterm infant brain injury. Endocrinology. 144, 2350-2359; Nunez, J.L., Alt, J.J. and McCarthy, M.M., 2003. A new model for prenatal brain damage. I. GABA(A) receptor activation induces cell death in developing rat hippocampus. Exp. Neurol. 181, 258-269]. We now report that KA or muscimol alone administered to immature hippocampal neurons in culture induces significant cell death as evidenced by TUNEL assay. Surprisingly, simultaneous administration of equimolar quantities of these two agonists blocks the effect of either one alone. Moreover, treatment of newborn pups results in less damage compared to either muscimol or KA alone. We further observed that immunoreactivity for the calcium-binding protein, calbindin D(28K), is increased in the brains of pups simultaneously administered KA and muscimol as compared to either alone.

Animals↗

PubMed1998

The role of the primary care physician in maximizing cognitive and behavioral recovery from moderate to severe pediatric traumatic brain injury.

Traumatic brain injury (TBI) is a major cause of death and the most common cause of acquired disability in children. Moderate to severe TBI typically results in cognitive deficits, and behavioral and psychosocial adjustment problems, sometimes compromising long term development. Although variable, considerable recovery can occur, especially over the first one to two years post-injury. Appropriate educational and psychological intervention is critical to positive outcome. The primary care physician (PCP) has a major role in monitoring progress and intervention, and therefore in maximizing outcome. The short term neurocognitive and neurobehavioral sequelae and recovery pattern for traumatic brain injury, and the role of the primary care physician in maximizing recovery based on risk factors are described. Some intervention resources are included.

Achievement↗

PubMed2005

Characterization of a new rat model of penetrating ballistic brain injury.

Penetrating brain injury (PBI) is a leading cause of mortality and morbidity in modern warfare and accounts for a significant number of traumatic brain injuries worldwide. Here we characterize the pathophysiology of a new rat model of PBI that simulates the large temporary cavity caused by energy dissipation from a penetrating bullet round. Male Sprague-Dawley rats (250-300 g) were subjected to a simulated ballistic wound to the right frontal hemisphere implemented by an inflatable penetrating probe. Three levels of injury severity were compared to control animals. Neurological and physiological outcome was assessed over a 3-day recovery period and brain tissue collected at 72 h for histopathological evaluation. Brain-injured regions included the ipsilateral frontal cortex and striatum with volumetric increases in intracranial hemorrhage (5-18 mm3) and lesion size (9-86 mm3) related to severity. Similarly, hemispheric swelling increased (3-14%) following PBI, associated with a significant rise in intracranial pressure. Astrogliosis was present in regions adjacent to the core-injury along with microglial and leukocyte infiltration. Injury remote to the lesion was observed in the cerebral peduncle that may have accounted, in part, for observed neurological deficits. Neurological and balance beam testing revealed sensorimotor deficits that persisted through 72 h. Severe electroencephalographic disturbances included the occurrence of cortical spreading depression, slow-waves, and brain seizure activity. In conclusion, this rat PBI model replicates diverse, salient features of clinical PBI pathology, generates reproducible and quantifiable measures of outcome, and is scalable by injury severity, rendering it an attractive vehicle for experimental brain trauma research.

Animals↗

PubMed1998

Does traumatic subarachnoid hemorrhage caused by diffuse brain injury cause delayed ischemic brain damage? Comparison with subarachnoid hemorrhage caused by ruptured intracranial aneurysms.

OBJECTIVE: To examine whether traumatic subarachnoid hemorrhage (TSAH) caused by severe diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome, as does aneurysmal subarachnoid hemorrhage (ASAH). METHODS: We examined 99 patients with diffuse brain injury with TSAH and 114 patients with ASAH. Computed tomographic (CT) findings, cerebral blood flow, and neurological outcomes were assessed during the acute and subacute phases and were compared between the two groups. RESULTS: The distribution of subarachnoid hemorrhage on the CT scans differed between the two groups. Unlike ASAH, TSAH was not limited to cisterns surrounding the circle of Willis but extended to supratentorial regions and interhemispheric fissures. Computed tomography-detected subarachnoid hemorrhage disappeared very early with TSAH and gradually with ASAH. In the ASAH group, mean cerebral blood flow decreased to 75% of normal during the acute phase and decreased a further 10% during the subacute phase. In the TSAH group, mean cerebral blood flow decreased to 85% of normal during the acute phase and increased slightly during the subacute phase. Neurological deterioration and in-hospital death peaked on Day 0 in association with TSAH and showed twin peaks in association with ASAH. The incidence of low-density areas on the CT scans was significantly higher with ASAH than with TSAH. All low-density areas on the CT scans of patients with ASAH corresponded to vascular territories, but low-density areas on the CT scans of patients with TSAH were rarely associated with vascular territories and contained deep-seated or gliding contusion types. CONCLUSION: The findings suggest that the incidence of vasospasm is low in association with TSAH and that the cause is different compared with ASAH. There is no evidence that the presence of TSAH in cases of diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome.

Acute Disease↗

PubMed2005

[Evidence-based intensive care treatment of intracranial hypertension after traumatic brain injury].

Traumatic brain injury (TBI) occurs frequently and is associated with a poor prognosis. Severe TBI results in substantial disability or death in more than 40% of cases. The major aim of treatment of these patients is to minimize secondary brain injury and in this respect, the prevention of intracranial hypertension plays a key role. In addition to surgical approaches, various conservative treatment options exist, such as the use of osmodiuretics, barbiturates, or corticosteroids, hyperventilation as well as induced therapeutic hypothermia. This review analyzes these treatment options and the therapeutic goals of lowering intracranial pressure (ICP) in patients after TBI using evidence-based criteria, and provides recommendations for clinical practice.

Adrenal Cortex Hormones↗

PubMed2003

Violent traumatic brain injury: occurrence, patient characteristics, and risk factors from the Traumatic Brain Injury Model Systems project.

OBJECTIVES: To examine the occurrence of and characteristics associated with violent traumatic brain injury (TBI) in the Traumatic Brain Injury Model Systems (TBIMS) project for 4 of the 5 original Model Systems centers and to determine the patient characteristics of this group, as well as the risk factors for sustaining such an injury. DESIGN: Prospective evaluation of individuals with violent TBI over a 10-year period. SETTING: Four TBIMS centers. PARTICIPANTS: A total of 1,229 individuals who received acute hospitalization and inpatient rehabilitation care for TBI. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE: The occurrence of a violent TBI. RESULTS: Twenty-six percent of the participants in the TBIMS project sustained a violent TBI. This type of injury was more common in African-American men who were single and slightly older than the average TBI patient, were unemployed before injury, and had had a previous TBI. A higher injury rate was noted in the earlier part of the evaluation period. Those who sustained a violent TBI had higher levels of caregiver burden and disability, as well as decreased productivity and community reintegration at rehabilitation discharge and at 1 and 2 years postinjury. CONCLUSIONS: The occurrence of violent TBI in the TBIMS project is consistent with national trends of decreasing incidence of violent injuries in the 1990s. These results present a profile of those who have been injured through violence. The relative risks for sustaining such an injury appear to be well defined when considering demographic and temporal factors.

Adult↗

PubMed2004

Alzheimer's pathology in human temporal cortex surgically excised after severe brain injury.

Traumatic brain injury (TBI) is a risk factor for the development of Alzheimer's disease (AD). This immunohistochemical study determined the extent of AD-related changes in temporal cortex resected from individuals treated surgically for severe TBI. Antisera generated against Abeta species (total Abeta, Abeta(1-42), and Abeta(1-40)), the C-terminal of the Abeta precursor protein (APP), apolipoprotein E (apoE), and markers of neuron structure and degeneration (tau, ubiquitin, alpha-, beta-, and gamma-synuclein) were used to examine the extent of Abeta plaque deposition and neurodegenerative changes in 18 TBI subjects (ages 18-64 years). Diffuse cortical Abeta deposits were observed in one third of subjects (aged 35-62 years) as early as 2 h after injury, with only one (35-year old) individual exhibiting "mature", dense-cored plaques. Plaque-like deposits, neurons, glia, and axonal changes were also immunostained with APP and apoE antibodies. In plaque-positive cases, the only statistically significant change in cellular immunostaining was increased neuronal APP (P = 0.013). There was no significant correlation between the distribution of Abeta plaques and markers of neuronal degeneration. Diffuse tau immunostaining was localized to neuronal cell soma, axons or glial cells in a larger subset of individuals. Tau-positive, neurofibrillary tangle (NFT)-like changes were detected in only two subjects, both of more advanced age and who were without Abeta deposits. Other neurodegenerative changes, evidenced by ubiquitin- and synuclein-immunoreactive neurons, were abundant in the majority of cases. Our results demonstrate a differential distribution and course of intra- and extra-cellular AD-like changes during the acute phase following severe TBI in humans. Abeta plaques and early evidence of neuronal degenerative changes can develop rapidly after TBI, while fully developed NFTs most likely result from more chronic disease- or injury-related processes. These observations lend further support to the hypothesis that head trauma significantly increases the risk of developing pathological and clinical symptoms of AD, and provide insight into the molecular mechanisms that initiate these pathological cascades very early during severe brain injury.

Adolescent↗

PubMed2005

Neuroprotective anti-apoptosis effect of estrogens in traumatic brain injury.

Traumatic brain injury (TBI) is a leading cause of death and functional disability in western countries, affecting mostly young patients. Despite intense and sustained efforts deployed for the development of new therapeutic strategies, no clinical benefit has been shown by any of the investigated compounds. Increasing attention has been drawn during the past two decades to the neuroprotective effects of estrogens, although most of the available data relate to ischemic brain injury. The purpose of the present study was to investigate the potential neuroprotective value of estrogens in TBI as a therapeutic modality. For this purpose, a contusion was created in the parietal cortex by dynamic cortical deformation in two groups of 10 Sprague-Dawley male rats. Following the injury, treated animals received conjugated estrogens for 3 days, using a subcutaneously implanted osmotic pump. Animals were then sacrificed, and TUNEL, anti-active Caspase 3, bcl-2, and bax labeling were performed in paraffin-embedded brain sections, allowing for comparative and quantitative analysis. In estrogen-treated animals, there was a marked and significant reduction of apoptosis in comparison with non-treated animals. The reduction in TUNEL and active Caspase 3 staining was similar and close to 50%. Optical analysis of histological slides prepared by bcl-2 labeling showed a significant increase in bcl-2 expression in estrogen-treated animals compared to non-treated animals. On the contrary, bax expression was not influenced by hormonal treatment, and no difference could be noticed between the two groups. These results support the potential therapeutic value of estrogens in TBI and further clarify their mode of action.

Animals↗

PubMed2003

BAY 38-7271: a novel highly selective and highly potent cannabinoid receptor agonist for the treatment of traumatic brain injury.

Traumatic brain injury (TBI) is the most common cause of mortality and morbidity in adults under 40 years of age in industrialized countries. Worldwide the incidence is increasing, about 9.5 million people are hospitalized per year due to TBI, and the death rate is estimated to be more than one million people per year. Recently BAY 38-7271 has been characterized as a structurally novel, selective and highly potent cannabinoid CB1/CB2 receptor agonist in vitro and in vivo with pronounced neuroprotective efficacy in a rat traumatic brain injury model, showing a therapeutic window of at least 5 h. Furthermore, neuroprotective efficacy was also found in models of transient and permanent occlusion of the middle cerebral artery and brain edema models as well. In this article we review the in vitro and in vivo pharmacology of BAY 38-7271, the results from acute and subacute toxicity studies, pharmacokinetics and drug metabolism in animals and healthy male volunteers. In phase I studies BAY 38-7271 was safe and well tolerated when administered by i.v. infusion for either 1 or 24 h. As the doses of BAY 38-7271 in animals needed for maximal neuroprotective efficacy were significantly lower than those inducing typical cannabinoid-like side effects, it is to be expected that the compound will offer a novel therapeutic approach with a favorable therapeutic window for the treatment of TBI or cerebral ischemia.

Animals↗

PubMed2003

Psychotic disorder and traumatic brain injury.

Traumatic brain injury (TBI) can result in serious and disabling neuropsychiatric disorders, such as cognitive deficits and personality change, as well as severe and chronic psychosis. This review focuses on the relationship between TBI and schizophrenia-like psychosis (SLP) including its epidemiology, diagnostic criteria, clinical presentation, psychopathology, risk factors, and pathophysiology. The relationships between post-traumatic epilepsy and SLP, and brain trauma and schizophrenia, are also discussed. The risk of SLP does increase after TBI. The clinical presentation has considerable overlap with primary schizophrenic disorder, with a prominence of persecutory and other delusions and auditory hallucinations, as well as a lack of negative symptoms. The onset is often gradual, with a subacute or chronic course. More severe and diffuse brain injury, especially of the temporal and frontal lobes, is the most prominent risk factor. Genetic load may also play a role, but presence of epilepsy could be a protective factor. Further large and systematic longitudinal studies are needed.

Brain Injuries↗

PubMed1981

Creatine kinase isoenzymes in acute brain injury.

Brain-type creatine kinase (CK) isoenzyme (CK-BB) was detected in the serum in 13 out of 26 patients with acute brain injury (50%). The peak of CK-BB activity ranged from 5 to 188 U/liter, constituting, on average, 10.5% of the total CK activity. The highest activities were seen in patients with gunshot wounds. High CK-BB activity was associated with poor prognosis, but minimal CK-BB elevations did not have prognostic significance. Heart-type creatine kinase isoenzyme (CK-MB) was detected in the serum in 17 out of 26 patients (65%). The peak activity ranged from 5 to 115 U/liter, constituting, on average, 6.6% of total CK activity. Electrocardiogram taken from 20 patients revealed transient T-wave inversions in the precordial leads in four patients; three of them also showed serum CK-MB activity. Subendocardial hemorrhage was detected at autopsy in three of the five CK-MB-positive patients, but in none of the four CK-MB-negative cases. Present findings suggest that acute brain injury may be secondarily cause myocardial damage.

Adolescent↗

PubMed2005

Anterior pituitary hormone abnormalities following traumatic brain injury.

Traumatic brain injury (TBI) leads to approximately 100 hospitalizations per 100,000/year. Whereas diabetes insipidus is a well-known complication of TBI, anterior hypopituitarism as a consequence of TBI has been regarded as rare. More recent studies, however, suggest a prevalence of at least 30% of anterior pituitary dysfunction after TBI. Clinical signs of anterior hypopituitarism are often subtle and may be masked by sequalae of TBI. Therefore, post-traumatic anterior pituitary dysfunction may remain undiagnosed and, possibly, aggravate symptoms of brain injury. Moreover it may, if undiagnosed, lead to potentially fatal endocrine crises. This review updates clinical researchers, physicians, and other healthcare providers on the relationship between TBI and subsequent anterior pituitary insufficiency.

Brain Injuries↗

PubMed2005

The effect of the selective NMDA receptor antagonist traxoprodil in the treatment of traumatic brain injury.

Traumatic brain injury (TBI) remains a major public health problem, and there is a great medical need for a pharmacological treatment that could improve long-term outcome. The excitatory neurotransmitter, glutamate, has been implicated in processes leading to neurodegeneration. Traxoprodil (CP-101,606) is a novel and potent glutamate receptor antagonist that is highly selective for the NR2B subunit of the NMDA receptor; it has been shown to be neuroprotective in animal models of brain injury and ischemia. A randomized, double-blind, placebo-controlled study was therefore conducted to assess the efficacy and safety of a 72-h infusion of traxoprodil compared to placebo in subjects with computed tomography scan evidence of severe TBI (GCS 4-8). A total of 404 males and non-pregnant females, aged 16-70, were treated within 8 h of injury. At baseline, subjects were stratified by motor score severity. The results showed that a greater proportion of the traxoprodil-treated subjects had a favorable outcome on the dichotomized Glasgow Outcome Scale (dGOS) at 6 months (delta 5.5%, OR 1.3, p = 0.21, 95% CI:[0.85, 2.06]) and at last visit (delta 7.5%, OR 1.47, p = 0.07, 95% CI:[0.97, 2.25]). The mortality rate with traxoprodil treatment was 7% less than with placebo treatment (OR 1.45, p = 0.08, 95% CI:[0.96, 2.18]). Differences between treatment groups were more pronounced in the severest subset (delta 11.8% for the dGOS at last visit and delta 16.6% for mortality). Traxoprodil was well tolerated. Although these results are intriguing, no definitive claim of efficacy can be made for traxoprodil for the treatment of severe TBI.

Adolescent↗

PubMed2005

Cerebral acid-base homeostasis after severe traumatic brain injury.

OBJECT: Brain tissue acidosis is known to mediate neuronal death. Therefore the authors measured the main parameters of cerebral acid-base homeostasis, as well as their interrelations, shortly after severe traumatic brain injury (TBI) in humans. METHODS: Brain tissue pH, PCO2, PO2, and/or lactate were measured in 151 patients with severe head injuries, by using a Neurotrend sensor and/or a microdialysis probe. Monitoring was started as soon as possible after the injury and continued for up to 4 days. During the 1st day following the trauma, the brain tissue pH was significantly lower, compared with later time points, in patients who died or remained in a persistent vegetative state. Six hours after the injury, brain tissue PCO2 was significantly higher in patients with a poor outcome compared with patients with a good outcome. Furthermore, significant elevations in cerebral concentrations of lactate were found during the 1st day after the injury, compared with later time points. These increases in lactate were typically more pronounced in patients with a poor outcome. Similar biochemical changes were observed during later hypoxic events. CONCLUSIONS: Severe human TBI profoundly disturbs cerebral acid-base homeostasis. The observed pH changes persist for the first 24 hours after the trauma. Brain tissue acidosis is associated with increased tissue PCO2 and lactate concentration; these pathobiochemical changes are more severe in patients who remain in a persistent vegetative state or die. Furthermore, increased brain tissue PCO2 (> 60 mm Hg) appears to be a useful clinical indicator of critical cerebral ischemia, especially when accompanied by increased lactate concentrations.

Acid-Base Equilibrium↗

PubMed1994

Early changes of blood-brain barrier and superoxide scavenging activity in rat cryogenic brain injury.

Cryogenic brain injury results in blood-brain barrier (BBB) disruption which may be mediated in part by oxygen free radicals. In this study, sequential changes of BBB and endogenous superoxide scavenging activity were investigated in brains subjected to cryogenic injury. 92 male Wistar rats were sacrificed at 15, 30 minutes, 1, 2, 3, 4, 6, 24 and 48 hours after the lesion. The extent of BBB disruption was determined by quantitative assessment of Evans blue (EB) uptake based on extraction from tissue using dimethylformamide. Determination of endogenous superoxide scavenging activity in the injured brain was performed by electron spin resonance spectrometry using a spin trapping agent. Superoxide scavenging activity was significantly decreased within one hour after the injury relative to normal rat brain (p < 0.05, student's t test) persisting for at least 6 hours. The EB content in the lesioned hemisphere was significantly increased within one hour after the injury relative to the normal rat brain (p < 0.01) and continued to increase for 24 hours. In conclusion, early changes of BBB and endogenous superoxide scavenging activity in rat cryogenic injured brain indicate that BBB may be an early target for oxygen free radicals in cryogenic brain injury.

Animals↗

PubMedDate not supplied

Endothelial cell activation following moderate traumatic brain injury.

Traumatic brain injury (TBI) initiates a cascade of acute and chronic injury responses which include disturbances in the cerebrovasculature that may result in the activation of the microvascular endothelial development of a dysfunction endothelium. The present study examines endothelial cell (EC) activation in a percussion model of moderate TBI. The criteria for endothelial activation used in these studies was surface expression of a number of markers collectively termed endothelial activation antigens. Temporal induction of the major histocompatibility (MHC) class II molecules, E-selectin (CD62E), vascular cell adhesion molecule (VACM-1) (CD106) as well as altered expression of constitutively expressed intercellular adhesion molecule-1 (ICAM-1) (CD54), the glucose transporter protein (glut-1), the transferrin receptor (tfR) (CD71), and MHC class I molecules was examined at various times following impact. Induction of E-selectin and increased expression of ICAM-1 was seen by 2 h post-impact (PI) and was sustained through 24 h PI. Decreased expression of immunologically reactive glut-1 and tfR was observed by 2-4 h PI and remained low up to 24 h PI. No induction of VCAM-1, MHC class II molecules or altered constitutive expression or MHC class I molecules was seen. Changes in EC activation were observed predominantly at the site of impact and were diminished temporarily. These results indicate that mild concussive injury to the brain results in activation of the endothelium.

ATP-Binding Cassette Transporters↗

PubMed2002

Early IL-6 plasma concentrations correlate with severity of brain injury and pneumonia in brain-injured patients.

BACKGROUND: Brain injury as well as early inflammatory and endocrine responses were found to be indicators for infectious complications in patients with multiple injuries. In this context, brain-derived inflammatory response as well as centrally triggered neuroendocrine activation and systemic immunodepression seem to be of major importance. Therefore, we hypothesize that a circulating index of inflammatory or endocrine function measured soon after brain injury (in patients with admission Glasgow Coma Scale [GCS] score of 4-7) would discriminate severe from moderate injury as indexed by GCS status on postinjury day 7. METHODS: In a retrospective study, 25 patients with either acute traumatic brain injury or cerebral hemorrhage and an initial GCS score of 4 to 7 were examined. Blood samples were obtained at different time points, and different immune variables and neuroendocrine hormones were determined. According to the GCS score on day 7, patients were divided into two groups (GCS score > or = 8, moderate brain injury; and GCS score < 8, severe brain injury or patients who died within the first week) for comparison of variables. Concluding from the results of this retrospective analysis, in a prospective study patients (n = 26) were divided into two groups according to their interleukin (IL)-6 plasma concentrations on day 1 (IL-6 > or = 100 pg/mL and IL 6 < 100 pg/mL). After 7 days, the GCS score, the infection rate, and the mortality were compared between these two groups. RESULTS: In the retrospective study, we could show that severe brain injury (as assessed by GCS score and mortality on day 7) was associated with high plasma levels of pro- and anti-inflammatory cytokines, acute phase proteins, and neuroendocrine hormones within 2 to 6 hours after the acute event. Among the investigated variables, elevated IL-6 plasma concentrations were stable up to 1 day after the acute event with a high predictive value with regard to the short-term prognosis and incidence of infectious complications within the first week. Because of this stability during the first 24 hours, we selected IL-6 for further studies. In the prospective study with a calculated cut-off IL-6 plasma concentration of 100 pg/mL on day 1, the predictive value of this parameter regarding the severity of the brain injury was fully confirmed (positive predictive value, 0.94; this value represents the observed pretest probability of 0.62). All patients who died (n = 5) or developed infectious complications within the first week (n = 8) showed plasma IL-6 levels > or = 100 pg/mL on day 1. CONCLUSION: The IL-6 plasma level 1 day after the acute event with a cut-off of 100 pg/mL (Immulite) seems to be a predictor for short-term prognosis and infectious complications in brain-injured patients.

Adult↗

PubMed2005

Immune pre-activation exacerbates hemorrhagic brain injury in immature mouse brain.

Premature infants with placental infection and adult stroke patients with fever have worse outcomes following intracerebral hemorrhage (ICH). We hypothesized that immune pre-activation would aggravate brain injury in mouse brain following ICH. The immune system of 2-day, 10-day and 7-week young adult CD1 mice was stimulated by intraperitoneal injection of concanavalin A (ConA), lipopolysaccharide (LPS) or polyinosinic-polycytidilic acid (PolyI:C) 12 h prior to intracerebral injection of blood. Two days later, brain damage and inflammation were worse in 2-day mice that had received LPS. The other agents had less consistent effects in 2-day mice. Brain damage in young adults was aggravated less after immune stimulation. These data suggest that immune pre-activation modifies hemorrhagic brain injury in immature mouse brain.

Aging↗