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PubMed2002

Cytochrome c release and caspase activation after traumatic brain injury.

Experimental traumatic brain injury (TBI) results in a rapid and significant necrosis of cortical tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the primary damage resulting in significant neurological dysfunction. The identification of cell death pathways that mediate this secondary traumatic injury have not been elucidated, however recent studies have implicated a role for apoptosis in the neuropathology of traumatic brain injury. The present study utilized a controlled cortical impact model of brain injury to assess the involvement of apoptotic pathways: release of cytochrome c from mitochondria and the activation of caspase-1- and caspase-3-like proteases in the injured cortex at 6, 12 and 24 h post-injury. Collectively, these results demonstrate cytochrome c release from mitochondria and its redistribution into the cytosol occurs in a time-dependent manner following TBI. The release of cytochrome c is accompanied by a time-dependent increase in caspase-3-like protease activity with no apparent increase in caspase-1-like activity. However, pretreatment with a general caspase inhibitor had no significant effect on the amount of cortical damage observed at 7 days post-injury. Our data suggest that several pro-apoptotic events occur following TBI, however the translocation of cytochrome c itself and/or other events upstream of caspase activation/inhibition may be sufficient to induce neuronal cell death.

Analysis of Variance↗

PubMed1999

Neuroprotective effect of hypothermia on neuronal injury in diffuse traumatic brain injury coupled with hypoxia and hypotension.

It is well established in mechanical head trauma that posttraumatic secondary insults, such as hypoxia and hypotension exacerbate neuronal injury and lead to worse outcome. In this study, the neuroprotective effect of hypothermia on the reduction of supraventricular subcortical neuronal damage was evaluated using an impact-acceleration model of diffuse traumatic brain injury coupled with both moderate and severe periods of hypoxia and hypotension. A total of 135 adult male Sprague-Dawley rats (340-375 g) were divided into three experimental studies: (I) physiological evaluation (n = 36); (II) quantitative analysis of the effect of trauma coupled with moderate and severe hypotension on neuronal damage assessed at 4 (n = 39) and 24 h (n = 24); and (III) the neuroprotective effect of hypothermia following moderate secondary insult (n = 36). Induction of hypothermia occurred at 15 min postinjury, to a level of 30 degrees C for 60 min. At the designated time points (4 and 24 h), the animals were sacrificed via standard transcardial perfusion techniques for histological processing. Quantitative assessment of neuronal damage using routine H&E staining at 4 hours showed neuronal damage which correlated with the severity of secondary insult. Animals exposed to trauma alone had a mean number of damaged neurons of 7.61 +/- 3.08/high powered field (hpf) compared with a mean of 1.21 +/- 0.30/hpf in the sham operated group (p = 0.015). Animals exposed to trauma with 10 min of hypoxia and hypotension (THH-10) showed a statistically significant number of damaged neurons compared to the sham-operated animals (7.50 +/- 2.15 damaged neurons/hpf, p = 0.013), whereas, neuronal damage in animals undergoing trauma with a 30-min secondary insult of hypoxia and hypotension (THH-30) was markedly increased (100 +/- 30.20/hpf, p = 0.002). Statistical analysis showed no significant difference in neuronal damage in animals subjected to secondary insult alone. At 24 h, the evolution of neuronal damage in the trauma alone group (5.08 +/- 1.63/hpf) was relatively static; however, there was a remarkable increase in the neuronal damage of the THH-10 group (29.88 50 +/- 8.20/hpf). However, hypothermia provided nearly complete protection against secondary insults, and neuronal damage was equal to that of the trauma alone group (p = 0.42). The results of this study confirm that hypothermia provides remarkable protection against the adverse effects of neuronal damage exacerbated by secondary injury. This study also presents a new model of secondary insult, which can be used experimentally to further define the mechanism of increased vulnerability of the injured brain.

Animals↗

PubMed2003

Respiratory care in spinal cord injury with associated traumatic brain injury: bridging the gap in critical care nursing interventions.

Spinal cord injury (SCI) is a devastating and challenging condition. The events that lead to SCI, such as road traffic accidents, falls, sports and violence [Top. Spinal Cord Inj. Rehabil. 5 (1999) 83], are also the common aetiologies of traumatic brain injury (TBI). It's not surprising then, that 20-50% of those with cervical SCI have TBI [J. Trauma 46 (1999) 450]. The literature pertaining to the management of either injury in isolation is vast, but lacking where the two conditions are experienced together and require distinct adaptations to interventions. Consequently, a gap in the literature exists. This paper focuses on those patients with SCI of the cervical spine with associated head injury, and pay particular attention to respiratory difficulties, and presents interventions required to minimise and treat the effects of such pulmonary compromise.

Brain Injuries↗

PubMed2000

The role of tumor necrosis factor-alpha in diffuse axonal injury following fluid-percussive brain injury in rats.

The immunolocalization of tumor necrosis factor-alpha (TNF alpha) after diffuse axonal injury (DAI) is demonstrated using a midline fluid percussion rat model (moderate brain injury of 1000 mm Hg was generated) and the effects of TNF alpha on the axolemmal permeability using horseradish peroxidase as a tracer. In addition, the accumulation of beta-amyloid precursor protein (beta-APP) was investigated, which has recently been shown to be a reliable marker for the diagnosis of DAI in cases with fatal head injury. TNF alpha levels in brain tissues from the impact site and the cortex including the corpus callosum, gradually increased during the first 1 h, rose to a maximal elevation at 3 h, gradually decreased at 6 h and decreased further at 24 h. Horseradish peroxidase (HRP) tracer experiments revealed that primary axonal damage appeared as early as 15 min after impact but rapidly recovered and that 1 h after impact, secondary axonal damage occurred in the corpus callosum and the brain stem. By immunoelectron microscopy it was seen that beta-APP accumulated in the axon from 1 h after impact demonstrating that there was functional axonal damage. TNF alpha reactions were detected in the lysosomes of microglia 30 min after impact and 1 h after impact these reactions were mainly detected in the glial cells (such as microglia, astrocytes and oligodendrocytes) in the corpus callosum and the brain stem. It is generally accepted that TNF alpha directly induces primary demyelination and oligodendrocyte apoptosis. Therefore, TNF alpha conveyed from the microglial cells is one cofactor contributing to the formation of the delayed axonal damage observed at these sites. The present study suggests that TNF alpha conveyed from the glial cells may contribute to the pathogenic mechanism of DAI formation following fluid percussive brain injury.

Amyloid beta-Protein Precursor↗

PubMed1994

Phenobarbital modifies seizure-related brain injury in the developing brain.

To investigate the potential role of drug therapy in preventing or exacerbating seizure-related brain injury in the prepubescent brain, we administered kainic acid to rats at postnatal day 35. Therapy with daily phenobarbital was started directly before or 1 day after kainic acid was administered, and was continued through postnatal day 153. Rats receiving phenobarbital had therapeutic concentrations during most of the 24-hour dosing period, but also experienced supratherapeutic peak concentrations. The animals were subsequently tested using the water maze (a measure of visuospatial memory), open field (a measure of activity level), and handling tests (a measure of emotionality). The frequency of spontaneous recurrent seizures was monitored during and after phenobarbital therapy. Kainic acid resulted in status epilepticus on postnatal day 35 in all the rats that received it but those receiving phenobarbital first manifested a shorter and less severe status epilepticus as compared to the rats given kainic acid alone. Rats starting phenobarbital immediately before kainic acid was administered did not differ from control rats on behavioral testing and had no subsequent spontaneous recurrent seizures and no histological lesions. Rats receiving kainic acid alone performed significantly poorer than did control rats in the water maze, were more aggressive, had histological lesions, and manifested spontaneous recurrent seizures. As compared to the group treated only with kainic acid, rats receiving kainic acid followed by phenobarbital at postnatal days 36 to 153 manifested similar aggressiveness and histological lesions, similar frequency of spontaneous recurrent seizures after phenobarbital taper, and even greater disturbances in memory, learning, and activity level.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed2003

The role of thrombin and thrombin receptors in ischemic, hemorrhagic and traumatic brain injury: deleterious or protective?

In the last two decades it has become apparent that thrombin has many extravascular effects that are mediated by a family of protease-activated receptors (PARs). PAR-1, -3 and -4 are activated via cleavage by thrombin. The importance of extravascular thrombin in modulating ischemic, hemorrhagic and traumatic injury in brain has recently become clear. Thus, in vitro, thrombin at low concentration protects neurons and astrocytes from cell death caused by a number of different insults. In vivo, pretreating the brain with a low dose of thrombin (thrombin preconditioning), attenuates the brain injury induced by a large dose of thrombin, an intracerebral hemorrhage or by focal cerebral ischemia. Thrombin may also be an important mediator of ischemic preconditioning. In contrast, high doses of thrombin kill neurons and astrocytes in vitro and cause disruption of the blood-brain barrier, brain edema and seizures in vivo. This review examines the role of thrombin in brain injury and the molecular mechanisms and signaling cascades involved.

Animals↗

PubMed2004

Multimodality monitoring in severe traumatic brain injury: the role of brain tissue oxygenation monitoring.

Traumatic brain injury (TBI) is a major cause of morbidity and mortality with widespread social, personal, and financial implications for those who survive. TBI is caused by four main events: motor vehicle accidents, sporting injuries, falls, and assaults. Similarly to international statistics, annual incidence reports for TBI in Australia are between 100 and 288 per 100,000. Regardless of the cause of TBI, molecular and cellular derangements occur that can lead to neuronal cell death. Axonal transport disruption, ionic disruption, reduced energy formation, glutamate excitotoxicity, and free radical formation all contribute to the complex pathophysiological process of TBI-related neuronal death. Targeted pharmacological therapy has not proved beneficial in improving patient outcome, and monitoring and maintenance of various physiological parameters is the mainstay of current therapy. Parameters monitored include arterial blood pressure, blood gases, intracranial pressure, cerebral perfusion pressure, cerebral blood flow, and direct brain tissue oxygen measurement (ptiO2). Currently, indirect brain oximetry is used for cerebral oxygenation determination, which provides some information regarding global oxygenation levels. A newly developed oximetry technique, has shown promising results for the early detection of cerebral ischemia. ptiO2 monitoring provides a safe, easy, and sensitive method of regional brain oximetry, providing a greater understanding of neurophysiological derangements and the potential for correcting abnormal oxygenation earlier, thus improving patient outcome. This article reviews the current status of bedside monitoring for patients with TBI and considers whether ptiO2 has a role in the modern intensive care setting.

Brain↗

PubMed2006

The use of controlled mild hypothermia and immune system status in patients with severe brain injury.

INTRODUCTION: Severe brain injuries pose one of the most important problems on our health care because of their high morbidity and mortality. MATERIAL AND METHODS: A group of 89 patients after severe brain injury (Glasgow Coma Scale< or =8) was included into our research of detecting the changes of immune system parameters and their relation to the application of mild hypothermia during the early period after the insult. RESULTS: In both of the groups CD3+ and CD4+ lymphocytic levels decreased significantly after the insult and gradually got to normal (p<0.01). The NK cells levels have changed in correlation with the course of infection. Immunoglobulin (IgA, IgG) levels were normal or slightly increased. IgM levels changes had a close relation to the occurrence of inflammatory complications, especially that of pneumonia (p<0.01). The most surprising moment in our research was the level of IgE antibodies. They had been high and got even higher. They achieved the values typical for atopic reactions or parasitic diseases. 77.52 % of the patients with decreased parameters of immune system developed extra cranial complications. Immune system disorders appeared more frequently in the patients with lower Glasgow Coma Scale after admission (p<0.01). The application of mild hypothermia caused an unimportant increase in extra cranial complications (p>0.05) having no relation to immunity disorders. CONCLUSION: Intensive treatment of intracranial hypertension fundamentally affects results of our treatment (Glasgow Outcome Score). The application of controlled mild hypothermia doesn't escalate the occurrence of extra cranial inflammatory complications after severe brain injury (Tab. 2, Fig. 11, Ref. 15).

Adult↗

PubMed1998

Effects of olfactory stimulation on the vigilance performance of individuals with brain injury.

Observers with brain injury and control participants performed a vigilance task during which they received periodic whiffs of unscented air or air scented with peppermint. Under both fragrance conditions, controls reduced the frequency of commissive errors (false alarms) over the course of the vigil, an adaptive strategy given the low probability of signals employed (0.04). The false alarm rate of observers with brain injury increased precipitously toward the end of the vigil in the unscented air condition. However, exposure to the scent of peppermint rendered the false alarm scores of observers with brain injury similar to that of controls, a result which is consistent with evidence that olfactory stimulation activates brain areas vital for planning and judgment.

Adolescent↗

PubMedDate not supplied

Peripheral nerve injuries in children with traumatic brain injury.

The relationship between traumatic brain injuries and associated peripheral nerve injuries has not been previously studied in children in the rehabilitation setting. One hundred and fifty-seven consecutive admissions of brain-injured children were included in this prospective study to determine the frequency and pattern of recovery of peripheral nerve injuries in such patients. Twelve patients met the clinical diagnostic criteria for peripheral nerve injury. Electrodiagnostic studies confirmed the clinical diagnosis in 11 (7%) patients. Grading of spontaneous activity and electrodiagnostic study of the contralateral limb were used to differentiate electromyographic abnormalities due to upper motor neuron lesion and nerve injury. Electrodiagnostic study was useful to confirm clinical diagnosis and predict prognosis of nerve injuries. Two patients developed preventable pressure neuropathy. Eight patients showed moderate or full recovery in 9-10 months post-injury. All children with severe brain injuries should be evaluated for concomitant peripheral nerve injuries.

Adolescent↗

PubMed1998

Relationship of neuron specific enolase and protein S-100 concentrations in systemic and jugular venous serum to injury severity and outcome after traumatic brain injury.

Neuron specific enolase (NSE) and protein S-100 have previously been described as markers of brain injury. We aimed to discover whether concentrations of either were raised in arterial and jugular venous serum after traumatic brain injury, and whether serum profiles were related to injury severity and neurological outcome. We recruited 22 patients with a traumatic brain injury who were admitted to the intensive care unit. Paired arterial and jugular venous blood samples were taken on admission, and at 24, 48 and 96 hrs after injury. Samples were analysed for NSE and S-100 by RIA. Concentrations of both NSE and S-100 were increased above controls--mean NSE concentration was highest on admission, whilst mean S-100 peaked at 24 hours after injury. There was a small, but significant difference between jugular venous and arterial concentrations of S-100 (p = 0.022). High NSE and S-100 concentrations were significantly related to poor neurological outcome (p = 0.004 and p < 0.001 respectively). Both serum NSE and S-100 may be of some value in helping to predict outcome after a traumatic brain injury.

Adolescent↗

PubMed1992

[Transorbital penetrating brain injury].

Transorbital penetrating brain injury is rare during this time of peace. In our paper, we reported seven cases of these injuries and discussed the mechanism and treatment of intracranial complications. Transorbital penetrating brain injuries were caused by thin, long and relative hard objects such as chop-stick (case 3), pencil (case 6), bamboo stick (case 1, 2, 7) and a piece of metal (case 4, 5). CT scan, MRI and angiography demonstrated a large variety of intracranial complications. For instance, intracerebral hematoma, cerebral contusion, intraventricular hemorrhage, pneumocephalus, brain stem injury and carotid cavernous sinus fistula. We had no case of infectious complications such as meningitis and brain abscess. If the direction of the injuring object runs parallel to the orbital roof, it penetrates the cranial cavity commonly via the superior orbital fissure or the optic canal, which routes provide direct access without bone fracture. This direction will cause critical intracranial complications such as CCF or brain stem injury. If the injuring object runs upward and across the orbital roof which has thin bone and therefore offers little resistance, the frontal lobe will be easily damaged, and it will cause intracerebral hematoma. But the prognosis for this type of injury is not so poor because we can easily remove the hematoma and the foreign body. With our treatment policy of "pull and see", all our cases but one recovered well. The one exception was a case in which a large intracerebral hematoma was over-looked in an ophthalmological clinic. This patient died. Nowadays, CT scan and MRI give clear information about the anatomical location of injuring objects and intracranial complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2005

The membrane-associated progesterone-binding protein 25-Dx is expressed in brain regions involved in water homeostasis and is up-regulated after traumatic brain injury.

After traumatic brain injury, progesterone has important neuroprotective effects in the nervous system. There is better functional outcome and less oedema formation in pseudopregnant rat females (high levels of endogenous progesterone) than in males. In addition to intracellular progesterone receptors, membrane binding sites of the hormone such as 25-Dx may also be involved in neuroprotection. In the present study we investigated the distribution of the membrane-associated progesterone-binding protein 25-Dx in rat brain. Immunohistochemical analysis showed that 25-Dx is particularly abundant in the hypothalamic area, circumventricular organs, and ependymal cells of the lateral walls of the third and lateral ventricles. A strong signal was also detected in the meninges. Double immunofluorescence immunolabelling and confocal microscopy showed that 25-Dx is co-expressed with vasopressin in neurones of the paraventricular, supraoptic and retrochiasmatic nuclei. Levels of 25-Dx expression were higher in pseudopregnant females than in males. After traumatic brain injury, 25-Dx expression was up-regulated in neurones and induced in astrocytes, which play an important role in regulating water and ion homeostasis. The expression of 25-Dx in structures involved in CSF production (choroid plexus) and in osmoregulation (circumventricular organs, hypothalamus and meninges), and its up-regulation after brain damage, point to a novel and potentially important role of this progesterone-binding protein in the maintenance of water homeostasis after traumatic brain injury.

Animals↗

PubMed1999

Effects of dopaminergic combination therapy for frontal lobe dysfunction in traumatic brain injury rehabilitation.

Traumatic brain injury poses significant and diverse challenges to rehabilitation efforts. Neurobehavioural deficits represent a particularly difficult barrier to rehabilitative progress and societal reintegration. Early studies have identified dopaminergic drugs such as amantadine, bromocriptine and sinemet as potentially assistive in countering these deficits. To date, side effect profiles have been relatively benign, noted most frequently in small-scale case trials. The case of a 40-year-old patient with bilateral frontal traumatic brain injuries, and previous arteriovenous malformation (AVM) bleed with significant ataxia, dysarthria and neurobehavioural deficits is presented. This long range study demonstrates, through multiple varied dosing schedules, a trade off between the benefits and side effects of dopaminergic therapy, with implications for a larger brain injury population.

Accidental Falls↗

PubMed2006

[Diffuse axonal injury in traumatic brain injury].

BACKGROUND: Head trauma of varying severity may induce diffuse axonal injury. More attention is now given to this important type of injury, as examinations of head-injured patients with MRI have given us more knowledge. MATERIAL AND METHODS: We present a review of diffuse axonal injury with the main focus on clinical presentation and radiology, based on a Pubmed search and own experience. RESULTS AND INTERPRETATION: Axons seldom rupture at the moment of injury. It is more common that it takes hours or a few days until the axons are detached. Areas most commonly affected are white matter in the hemispheres, corpus callosum and the brain stem. Half of the patients with severe head injury have diffuse axonal injury, but this type of injury also occurs in patients with moderate and mild head injury. The clinical presentation and prognosis will therefore vary. Diffuse axonal injury can present with typical signs revealed by CT, but the CT scan may also be normal, especially when there is no bleeding. New MRI techniques are more sensitive and show that diffuse axonal injury occurs more often than previously assumed. MRI is therefore necessary to give the patients correct diagnoses and adequate rehabilitation and follow-up.

Brain Injuries↗

PubMed2005

NOC/oFQ activates ERK and JNK but not p38 MAPK to impair prostaglandin cerebrovasodilation after brain injury.

Fluid percussion brain injury (FPI) elevates the CSF concentration of the opioid nociceptin/orphanin FQ (NOC/oFQ), which contributes to impairment of pial artery dilation to the prostaglandins (PG) PGE2 and PGI2. This study investigated the role of the ERK, p38, and JNK isoforms of mitogen-activated protein kinase (MAPK) in impaired PG cerebrovasodilation after FPI, and the relationship of brain injury induced release of NOC/oFQ to MAPK in such vascular impairment in newborn pigs equipped with a closed cranial window. FPI blunted PGE2 pial artery dilation, but U 0126 and SP 600125 (10(-6) M) (ERK and JNK MAPK inhibitors, respectively) partially prevented such impairment (7 +/- 1, 12 +/- 1, and 17 +/- 1 vs. 2 +/- 1, 3 +/- 1, and 5 +/- 1 vs. 4 +/- 1, 7 +/- 1, and 12 +/- 1% for 1, 10, and 100 ng/ml PGE2 in control, FPI, and FPI + U 0126 pretreated animals, respectively). In contrast, administration of SB 203580 (10(-5) M) (p38 MAPK inhibitor) did not prevent FPI impairment of PGE2 dilation. Co-administration of NOC/oFQ at the dose of 10(-10) M, the cerebrospinal fluid concentration observed after FPI, with PGE2 under non-brain injury conditions blunted PG dilation, but U 0126 or SP 600125 partially prevented such impairment (7 +/- 1, 11 +/- 1, and 16 +/- 2 vs. 0 +/- 1, 1 +/- 1, and 2 +/- 1, vs. 5 +/- 1, 9 +/- 1, and 13 +/- 2 for responses to PGE2 in control, NOC/oFQ, and NOC/oFQ + U 0126 treated animals, respectively). Administration of SB 203580 did not prevent impairment of PG pial artery dilation by NOC/oFQ. These data show that activation of ERK and JNK but not p38 MAPK contributes to impairment of PG cerebrovasodilation after FPI. These data suggest that NOC/oFQ induced ERK and JNK but not p38 MAPK activation contributes to impaired cerebrovasodilation to PG after FPI.

Animals↗

PubMed2003

Inhibiting caspase-8 after injury reduces hypoxic-ischemic brain injury in the newborn rat.

A broad spectrum caspase inhibitor reduces brain injury. Will a caspase-8 inhibitor provide protection? Seven-day-old rat pups had the right carotid artery ligated, then were subjected to 2.5 h of 8% oxygen. Caspase-8 activity in the right cortex was measured enzymatically. Caspase-8 activity was increased at 12 and 24 h after injury and IETD-CHO, (Ac-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Pro-Ile-Glu-Thr-Asp-CHO, CHO is aldehyde) a cell permeable caspase-8 inhibitor, given by i.c.v. injection after the hypoxic period eliminated this increase with significant effect at 15 and 50 microg/pup (1.7 micromol/kg). Thirty pups were randomly assigned to receive 50 microg/pup of IETD-CHO or vehicle i.c.v. immediately after the hypoxic period. The loss of brain weight in the right hemisphere 22 days after injury was 29+/-5% in the vehicle-treated animals and 12+/-5% in the IETD-CHO-treated animals (P<0.05). Inhibiting caspase-8 activity after hypoxic-ischemic brain injury reduces brain injury.

Animals↗

PubMed2004

Subcortical white matter metabolic changes remote from focal hemorrhagic lesions suggest diffuse injury after human traumatic brain injury.

OBJECTIVE: We used positron emission tomographic studies to prospectively examine the relationship between glucose and oxidative metabolism in the subcortical white matter (WM) acutely after traumatic brain injury (TBI). The objective was to determine the nature, extent, and degree of metabolic abnormalities in subcortical brain regions remote from hemorrhagic lesions. METHODS: Sixteen normal volunteers and 10 TBI patients (Glasgow Coma Scale score, 4-10; age, 17-64 yr; 6 with focal and 4 with diffuse injury) were studied. Each subject underwent dynamic positron emission tomographic studies using [(15)O]CO, (15)O(2), [(15)O]H(2)O, and fluorodeoxyglucose plus a magnetic resonance imaging scan acutely after TBI. Parametric images of the metabolic rate of oxygen and metabolic rate of glucose were generated, and a molar oxygen-to-glucose utilization ratio was calculated. Data from gray matter and WM remote from hemorrhagic lesions, plus whole brain, were analyzed. RESULTS: There was a significant reduction in the subcortical WM oxygen-to-glucose utilization ratio after TBI compared with normal values (3.99 +/- 0.77 versus 5.37 +/- 1.00; P < 0.01), whereas the mean cortical gray matter and whole-brain values remained unchanged. WM metabolic changes, which were diffuse throughout the hemispheres, were characterized by a reduction in the metabolic rate of oxygen without a concomitant drop in the metabolic rate of glucose. CONCLUSION: The extent and degree of subcortical WM metabolic abnormalities after moderate and severe TBI suggest that diffuse WM injury is a general phenomenon after such injuries. This pervasive finding may indicate that the concept of focal traumatic injury, although valid from a computed tomographic imaging standpoint, may be misleading when considering metabolic derangements associated with TBI.

Adolescent↗