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PubMed1996

Cobalt-55 positron emission tomography in traumatic brain injury: a pilot study.

Traumatic brain injury is usually assessed with the Glasgow coma scale (GCS), CT, or MRI. After such injury, the injured brain tissue is characterised by calcium mediated neuronal damage and inflammation. Positron emission tomography with the isotope cobalt-55 (Co-PET) as a calcium tracer enables imaging of affected tissue in traumatic brain injury. The aim was to determine whether additional information can be gained by Co-PET in the diagnosis of moderate traumatic brain injury and to assess any prognostic value of Co-PET. Five patients with recent moderately severe traumatic brain injury were studied. CT was performed on the day of admission, EEG within one week, and MRI and Co-PET within four weeks of injury. Clinical assessment included neurological examination, GCS, neuropsychological testing, and Glasgow outcome scale (GOS) after one year. Co-PET showed focal uptake that extended beyond the morphological abnormalities shown by MRI and CT, in brain regions that were actually diagnosed with EEG. Thus Co-PET is potentially useful for diagnostic localisation of both structural and functional abnormalities in moderate traumatic brain injury.

Brain Injuries↗

PubMedDate not supplied

Diffuse axonal injury associated with chronic traumatic brain injury: evidence from T2*-weighted gradient-echo imaging at 3 T.

BACKGROUND AND PURPOSE: Diffuse axonal injury is frequently accompanied by tissue tear hemorrhages. We examined whether high field strength T2*-weighted gradient-echo imaging performed during the chronic stage of traumatic brain injury may have advantages in the evaluation of diffuse axonal injury as compared with T1- and T2-weighted MR imaging. METHODS: Prospective MR imaging of 66 patients (age range, 17-57 years) was performed using a 3-T system 3 to 292 months (median, 23.5 months) after traumatic brain injury. T1-, T2-, T2*-hypointense and T2-hyperintense foci of 1- to 15-mm diameter were registered in 10 brain regions by two readers separately. Foci that appeared hypointense both on the T1- and T2- and/or on the T2*-weighted images were defined as traumatic microbleeds. RESULTS: For 46 (69.7%) of the patients, T2*-weighted gradient-echo imaging revealed traumatic microbleeds. Hyperintense foci were observed on the T2-weighted images of only 15 (22.7%) patients. T2*-weighted imaging showed significantly more traumatic microbleeds (P =.000) than did T1- and T2-weighted imaging. Interobserver agreement was strong (kappa = 0.79, tau = 0.749, P =.000). For 14 (21.2%) of the patients, T2*-weighted gradient-echo imaging revealed traumatic microbleeds in the corpus callosum, whereas for only two (3%), hyperintense callosal lesions were seen on the T2-weighted images. Although a significant correlation existed between the total amount and callosal appearance of traumatic microbleeds and Glasgow Coma Scale scores (P =.000), no correlation existed with extended Glasgow Outcome Scale scores. CONCLUSION: T2*-weighted gradient-echo imaging at high field strength is a useful tool for the evaluation of diffuse axonal injury during the chronic stage of traumatic brain injury. Diffuse axonal injury-related brain lesions are mainly hemorrhagic. The relevance of diffuse axonal injury for long-term clinical outcome is uncertain.

Adolescent↗

PubMed2005

Traumatic brain injury and hypopituitarism.

Results of recent and ongoing studies have made it clear that brain injuries like traumatic brain injury (TBI) pose substantial risk to pituitary function, perhaps even greater risk than previously believed. Patients with TBI should be screened both prospectively and retrospectively for isolated, multiple and even total pituitary deficits. It is well known that, patients with "classical" hypopituitarism (due to primary hypothalamic-pituitary pathologies) do benefit from hormonal replacement therapy. It has been suggested that patients with TBI-induced hypopituitarism may benefit with appropriate hormonal replacement receiving replacement therapy such as anti-diuretic hormone (ADH), glucocorticoid and thyroid hormones when needed. Gonadal and recombinant human growth hormone (rhGH) replacement therapy should also be introduced if there are deficiencies demonstrated and even reconfirmed in a second step. The signs and symptoms of post-TBI hypopituitarism may be masked by what has been assumed to be merely the post-traumatic syndrome. By increasing awareness among physicians of the risks of brain injuries-induced endocrinopathies and the need for appropriate endocrinological testing, it may be possible to improve the quality of life and enhance the rehabilitation prospects for these patients. In most instances, these patients are first seen and treated by trauma surgeons and neurosurgeons, and subsequently by rehabilitation physicians; they must be knowledgeable about the risks of hypopituitarism so that they can determine which patients are candidates for screening for hypopituitarism. In addition, endocrinologists and internists must be educated about TBI-induced hypopituitarism and encouraged to actively share their expertise with other physicians.

Brain Injuries↗

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↗

PubMed2006

Impaired fibrinolysis and traumatic brain injury in mice.

Traumatic brain injury (TBI) has been associated with intravascular coagulation, which may be a result of thromboplastin released following brain injury. Clots thus formed are lysed by plasmin, which is activated by tissue-type and urokinase-type plasminogen activators (uPA). To evaluate the association between traumatic intravascular coagulation and post-traumatic outcome, uPA knockout (uPA-/-) transgenic mice (n=12) or wild-type littermates (WT; n=12) were anesthetized and subjected to controlled cortical impact (CCI) brain injury. A second group of uPA-/- (n=12) and WT mice (n=12) were subjected to sham injury. Motor function was assessed over 2 weeks using the composite neuroscore test and cognition (learning) was assessed with the Morris Water Maze (MWM) at 2 weeks post-injury, whereupon the animals were sacrificed for cortical lesion volume analysis. Motor function was significantly worse in the brain-injured uPA-/- mice when compared to brain-injured WT mice at 48 h (p<0.05) and one week post-injury (p<0.05). These differences resolved by 2 weeks post-injury. There was no significant difference in post-injury cognitive function between uPA-/- mice and WT mice. However, at 2 weeks post-injury, the brain-injured uPA-/- had a significantly larger volume of cortical tissue loss than their WT counterparts (p<0.05). These results demonstrate that the absence of uPA in mice aggravates acute motor deficit and exacerbates cortical tissue loss following CCI brain injury, and suggests a neuroprotective role of the fibrinolytic process following TBI.

Animals↗

PubMed2006

A clinical report of adverse health effects due to bed sharing in two children with spinal cord injury and traumatic brain injury.

This paper explores the possibility that bed sharing may carry particular risks for children with special healthcare needs (CSHCN). Two cases of CSHCN who may have sustained adverse health effects from bed sharing are described. These two case reports indicate that CSHCN may be particularly susceptible to risks associated with bed sharing. Healthcare providers for CSHCN may need to inquire about patients' sleeping arrangements and, when bed sharing is acknowledged, provide counseling regarding the potential risks and benefits. They may need to monitor more closely for adverse events when bed sharing is a factor and should consider reporting health problems that may have occurred in concurrence with bed sharing.

Beds↗

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↗

PubMed1999

Relations between traumatic brain injury and the environment: feedback reduces maladaptive behaviour exhibited by three persons with traumatic brain injury.

Feedback is a commonly used technique in neurorehabilitation. It functions to strengthen or weaken select relations between individuals' behaviour and their environment. The study of behaviour-environment relations is a focus of operant psychology, commonly referred to as behaviour analysis. Central to behaviour analysis is the analysis of interrelations among stimuli, behaviour, and consequences. The focus on behaviour-environment relations may have considerable benefits for designing clinical treatments and accounting for successful and unsuccessful treatments, especially psychological interventions for maladaptive behaviour. In the present investigation, three persons with traumatic brain injuries, diagnosed with depression and presenting mild cognitive impairments, received feedback about their maladaptive behaviour. Weekly feedback resulted in general reductions in the variability and frequency of maladaptive behaviour. The results support the utility of giving equal consideration to relations between persons with traumatic brain injury and their environment, despite existing psychological or cognitive impairments. Future research on variables that influence the development and maintenance of behaviour-environment relations, and more generally operant behaviour, may provide a unique perspective on the effects of traumatic brain injury.

Adaptation, Psychological↗

PubMed1992

The treatment of agitation during initial hospitalization after traumatic brain injury.

Agitation after traumatic brain injury is disruptive for patient care, distressing, and difficult to treat. The use of propranolol has been advocated to control agitation after brain injury. It reportedly lacks some of the deleterious cognitive and emotional effects of other medications and physical restraints. This study was designed to test if propranolol is effective in reducing agitated behavior. Subjects had traumatic closed-head injury treated at a combined Level I Trauma Center and Rehabilitation Center. Twenty-one subjects met the criteria of agitation and were treated with propranolol or placebo in a double-blind fashion. The intensity of agitation was significantly lower in the treatment group although the number of episodes were similar. The use of restraints was also significantly lower in the treatment group. The results support the effectiveness of propranolol in reducing the intensity of agitation during the initial hospitalization after closed-head injury.

Aggression↗

PubMed2002

Expression profiling following traumatic brain injury: a review.

Traumatic brain injury (TBI) elicits a complex sequence of putative autodestructive and neuroprotective cellular cascades. It is hypothesized that the genomic responses of cells in the injured brain serve as the basis for these cascades. Traditional methods for analyzing differential gene expression following brain trauma demonstrate that immediate early genes, cytokines, transcription factors, and neurotrophic factors can all participate in the brain's active and directed response to injury, and may do so concurrently. It is this complexity and multiplicity of interrelated molecular mechanisms that has demanded new methods for comprehensive and parallel evaluation of putative as well as novel gene targets. Recent advances in DNA microarray technology have enabled the simultaneous evaluation of thousands of genes and the subsequent generation of massive amounts of biological data relevant to CNS injury. This emerging technology can serve to further current knowledge regarding recognized molecular cascades as well as to identify novel molecular mechanisms that occur throughout the post-traumatic period. The elucidation of the complex alterations in gene expression underlying the pathological sequelae following TBI is of central importance in the design of future therapeutic agents.

Animals↗

PubMed2004

Relationship between flow-metabolism uncoupling and evolving axonal injury after experimental traumatic brain injury.

Blood flow-metabolism uncoupling is a well-documented phenomenon after traumatic brain injury, but little is known about the direct consequences for white matter. The aim of this study was to quantitatively assess the topographic interrelationship between local cerebral blood flow (LCBF) and glucose metabolism (LCMRglc) after controlled cortical impact injury and to determine the degree of correspondence with the evolving axonal injury. LCMRglc and LCBF measurements were obtained at 3 hours in the same rat from 18F-fluorodeoxyglucose and 14C-iodoantipyrine coregistered autoradiographic images, and compared to the density of damaged axonal profiles in adjacent sections and in an additional group at 24 hours using beta-amyloid precursor protein (beta-APP) immunohistochemistry. LCBF was significantly reduced over the ipsilateral hemisphere by 48 +/- 15% compared with sham-controls, whereas LCMRglc was unaffected, apart from foci of elevated LCMRglc in the contusion margin. Flow-metabolism was uncoupled, indicated by a significant 2-fold elevation in the LCMRglc/LCBF ratio within most ipsilateral structures. There was a significant increase in beta-APP-stained axons from 3 to 24 hours, which was negatively correlated with LCBF and positively correlated with the LCMRglc/LCBF ratio at 3 hours in the cingulum and corpus callosum. Our study indicates a possible dependence of axonal outcome on flow-metabolism in the acute injury stage.

Amyloid beta-Protein Precursor↗

PubMed1998

Pharmacotherapy for traumatic brain injury: a review.

Traumatic brain injury in the United States is a serious health problem: it is a significant factor in approximately half of all trauma-related deaths, and, leads to persistent, long-term neurologic dysfunction in survivors. Physiological changes that accompany brain trauma such as cardiovascular alterations, hypercapnia, hypoxiaischemia, metabolic dysfunction, and alterations in the endogenous neurochemical systems are associated with poor clinical outcome. Using a variety of animal models, experimental studies have begun to elucidate these neurochemical disturbances that underlie the behavioral deficits and the pathologic outcome. Modification of the post-traumatic neurochemical milieu can promote functional recovery. While a number of currently available pharmaceutical compounds have been reported to be effective in various animal models of TBI, their utility in the clinical setting has been disappointing [119]. New hope has arisen for the treatment of TBI, based upon new research findings regarding the development of novel pharmacological therapies for brain trauma. Reduction of brain temperature can maintain relative tissue homeostasis by lowering metabolic activity. Hypothermia has been attempted in patients over the past 50 years and recent experimental evidence suggests that posttraumatic hypothermia can attenuate EAA release and free-radical production [120]. In animal models, hypothermic treatment has attenuated post-traumatic neurologic motor dysfunction [121,122], improved histopathologic damage [123,124], and reduced the extent of cytoskeletal damage [120]. In addition, the armamentarium of potentially neuroprotective compounds, which has increased rapidly in the recent years, provides promising pharmacological therapies for the treatment of TBI.

Animals↗

PubMed1997

Expression of endothelial adhesion molecules and recruitment of neutrophils after traumatic brain injury in rats.

Traumatic brain injury (TBI) is often accompanied by an acute inflammatory reaction mediated initially by neutrophils. Adhesion molecules expressed on vascular endothelium are requisite elements during recruitment of leukocytes at sites of inflammation. In a rat model of TBI the induction and persistent expression of E-selectin (CD62E) on cerebrovascular endothelium ipsilateral, but not contralateral, to the site of contusion was demonstrated (P < 0.05 at 4 and 48 h posttrauma). In addition, these studies confirmed up-regulation and prolonged expression of ICAM-1 (CD54) on endothelium in the traumatized hemisphere (P < 0.05 at 4, 24, 48, and 72 h posttrauma). It is of interest that increased expression of CD54 was noted on blood vessels in the contralateral, non-traumatized hemisphere 48 h posttrauma. Expression of a third endothelial adhesion molecule, PECAM-1 (CD31), was unchanged following trauma. Administration of a murine monoclonal antibody (TM-8) that inhibits the adhesive function of CD54 blocked a significant portion (37.9%) of neutrophil recruitment 24 h posttrauma (P = 0.04). Employing immunocytochemistry and a monoclonal antibody specific for rat neutrophils (RP-3), peak infiltration of neutrophils was shown to occur 48 h after trauma. In contrast to emigration of neutrophils from blood vessels within the contusion, however, entry of neutrophils occurred from the surrounding leptomeninges and choroidal vessels. These studies demonstrate the relevance of CD54 (ICAM-1) in recruitment of neutrophils following TBI. However, the majority of neutrophil influx relies on endothelial adhesion molecules other than CD54. Because emigration of neutrophils was shown to occur predominantly from vessels within the leptomeninges and choroid plexus, intrathecal delivery of agents that inhibit the adhesive interactions between neutrophils, endothelial CD54, and other endothelial adhesion molecules to be defined may offer a novel form of therapy to prevent the acute inflammatory response that follows TBI.

Animals↗

PubMed1997

Nerve growth factor attenuates cholinergic deficits following traumatic brain injury in rats.

Traumatic brain injury (TBI) results in chronic derangements in central cholinergic neurotransmission that may contribute to posttraumatic memory deficits. Intraventricular cannula (IVC) nerve growth factor (NGF) infusion can reduce axotomy-induced spatial memory deficits and morphologic changes observed in medial septal cholinergic neurons immunostained for choline acetyltransferase (ChAT). We examined the efficacy of NGF to (1) ameliorate reduced posttraumatic spatial memory performance, (2) release of hippocampal acetylcholine (ACh), and (3) ChAT immunoreactivity in the rat medial septum. Rats (n = 36) were trained prior to TBI on the functional tasks and retested on Days 1-5 (motor) and on Day 7 (memory retention). Immediately following injury, an IVC and osmotic pump were implanted, and NGF or vehicle was infused for 7 days. While there were no differences in motor performance, the NGF-treated group had significantly better spatial memory retention (P < 0.05) than the vehicle-treated group. The IVC cannula was then removed on Day 7, and a microdialysis probe was placed into the dorsal hippocampus. After a 22-h equilibration period, samples were collected prior to and after administration of scopolamine (1 mg/kg), which evoked ACh release by blocking autoreceptors. The posttraumatic reduction in scopolamine-evoked ACh release was completely reversed with NGF. Injury produced a bilateral reduction in the number and cross-sectional area of ChAT immunopositive medial septal neurons that was reversed by NGF treatment. These data suggest that cognitive but not motor deficits following TBI are, in part, mediated by chronic deficits in cholinergic systems that can be modulated by neurotrophic factors such as NGF.

Acetylcholine↗

PubMed2007

Medical-legal issues of mild traumatic brain injury.

Numerous concussions/mild traumatic brain injuries occur each year during athletic participation by a variety of athletes not only in the United States but around the globe. A variety of standards-type statements have been developed by various athletic and sports medicine groups that can be used to improve and standardize the diagnosis and treatment of these injuries. These standards can also be used to assist practitioners in sports medicine clearance for participation and return-to-play decisions. In a medical-legal arena these statements can be used to support the care that is provided to athletes and thus serve as a "shield" to medical-legal claims and suits. However, these standards can also be used to attack the service that is provided and then be used as a "sword." Legal issues surrounding standards statements regarding these injuries and the diagnosis and management of them should be recognized and appreciated by sports medicine providers and used to balance the applicable medical and legal risks associated with their practices.

Athletic Injuries↗

PubMed2004

Progesterone and allopregnanolone reduce inflammatory cytokines after traumatic brain injury.

Following a traumatic brain injury (TBI), the excessive release of interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) is a major cause of cerebral edema, which, in turn, can cause permanent neuronal loss and cognitive deficits in laboratory rats. This study examined the changes in expression of the proinflammatory cytokines IL-1beta and TNF-alpha after progesterone (8 mg/kg) or allopregnanolone (4 mg/kg) treatment in brain-injured rats at 3, 8, and 12 h and 6 days post-injury. Adult male rats received either bilateral prefrontal cortical contusion or sham surgery. The hormones were given intraperitoneally at 1 and 6 h, and continued once per day for up to 5 days. The gene expression of IL-1beta and TNF-alpha was measured by mRNA using real-time quantitative reverse transcripted polymerase chain reaction (RT-PCR). The protein concentrations of IL-1beta and TNF-alpha were measured using enzyme-linked immunosorbent assay (ELISA) to confirm the translation from mRNA to protein. The results indicated that progesterone and allopregnanolone reduce both IL-1beta and TNF-alpha at 3 h post-injury, when the expression of these cytokines peaks. At 8 and 12 h post-injury, IL-1beta and TNF-alpha gene expression in injured rats was still elevated compared to shams. By the sixth day post-injury, cytokine expression was back to the level of intact rats. We conclude that progesterone and allopregnanolone may attenuate the production of proinflammatory cytokines early after TBI, and this may be one mechanism by which progesterone and allopregnanolone reduce cerebral edema and promote functional recovery from TBI.

Animals↗

PubMed2006

Chronic ibuprofen administration worsens cognitive outcome following traumatic brain injury in rats.

Traumatic brain injury (TBI) can induce progressive neurodegeneration in association with chronic inflammation. Since chronic treatment with the non-steroidal anti-inflammatory drug (NSAID), ibuprofen, improves functional and histopathologic outcome in a mouse model of Alzheimer's disease (AD), we investigated whether it would also improve long-term outcome following TBI. Anesthetized adult rats were subjected to fluid percussion brain injury. Over the following 4 months the injured animals received ibuprofen per os (formulated in feed) at the approximate doses of 20 mg/kg body wt/day (n=13), 40 mg/kg body wt/day (n=13), or control (feed only, n=12). Sham animals underwent surgery without injury or ibuprofen treatment (n=9). At 4 months post-injury, a Morris water maze task revealed a profound learning dysfunction in all three injured groups compared to the sham group. Surprisingly, the learning ability of injured animals treated with either chronic ibuprofen regimen was significantly worsened compared to non-treated injured animals. However, there was no difference in the extent of progressive atrophy of the cortex or hippocampus between treated and non-treated injured animals. These data may have important implications for TBI patients who are often prescribed NSAIDs for chronic pain.

Analysis of Variance↗

PubMed2004

Increased expression and processing of caspase-12 after traumatic brain injury in rats.

Traumatic brain injury (TBI) disrupts tissue homeostasis resulting in pathological apoptotic activation. Recently, caspase-12 was reported to be induced and activated by the unfolded protein response following excess endoplasmic reticulum (ER) stress. This study examined rat caspase-12 expression using the controlled cortical impact TBI model. Immunoblots of fractionalized cell lysates found elevated caspase-12 proform (approximately 60 kDa) and processed form (approximately 12 kDa), with peak induction observed within 24 h post-injury in the cortex (418% and 503%, respectively). Hippocampus caspase-12 proform induction peaked at 24 h post-injury (641%), while processed form induction peaked at 6 h (620%). Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis confirmed elevated caspase-12 mRNA levels after TBI. Injury severity (1.0, 1.2 or 1.6 mm compression) was associated with increased caspase-12 mRNA expression, peaking at 5 days in the cortex (657%, 651% and 1259%, respectively) and 6 h in the hippocampus (435%, 451% and 460%, respectively). Immunohistochemical analysis revealed caspase-12 induction in neurons in both the cortex and hippocampus as well as in astrocytes at the contusion site. This is the first report of increased expression of caspase-12 following TBI. Our results suggest that the caspase-12-mediated ER apoptotic pathway may play a role in rat TBI pathology independent of the receptor- or mitochondria-mediated apoptotic pathways.

Animals↗