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PubMed2004

Proton MRS in acute traumatic brain injury: role for glutamate/glutamine and choline for outcome prediction.

Proton magnetic resonance spectroscopy (MRS) is being used to evaluate individuals with acute traumatic brain injury and several studies have shown that changes in certain brain metabolites (N-acetylaspartate, choline) are associated with poor neurologic outcomes. The majority of previous MRS studies have been obtained relatively late after injury and none have examined the role of glutamate/ glutamine (Glx). We conducted a prospective MRS study of 42 severely injured adults to measure quantitative metabolite changes early (7 days) after injury in normal appearing brain. We used these findings to predict long-term neurologic outcome and to determine if MRS data alone or in combination with clinical outcome variables provided better prediction of long-term outcomes. We found that glutamate/glutamine (Glx) and choline (Cho) were significantly elevated in occipital gray and parietal white matter early after injury in patients with poor long-term (6-12-month) outcomes. Glx and Cho ratios predicted long-term outcome with 94% accuracy and when combined with the motor Glasgow Coma Scale score provided the highest predictive accuracy (97%). Somatosensory evoked potentials were not as accurate as MRS data in predicting outcome. Elevated Glx and Cho are more sensitive indicators of injury and predictors of poor outcome when spectroscopy is done early after injury. This may be a reflection of early excitotoxic injury (i.e., elevated Glx) and of injury associated with membrane disruption (i.e., increased Cho) secondary to diffuse axonal injury.

Adolescent↗
PubMed1995

Role of apnea in nonaccidental head injury.

We hypothesize that apnea induced by shaking or by shaking combined with impact plays a major role in the pathophysiology of nonaccidental head trauma and accounts for the poor outcome in this subgroup of patients. In a retrospective study of 28 children who suffered significant nonaccidental head injury, 57% had a history of apnea prior to hospitalization, 82% were intubated upon admission, and 71% had early seizures. For further evidence of ischemia and hypoxia, the first recorded blood pressure was < 80 in 50% and the arterial pH < 7.3 in 54%. Seventy-one percent had diffuse brain swelling which is characteristic of cerebral hypoxia and/or ischemia on the first CT scan. None of the children who had clinical evidence of cerebral hypoxia or ischemia had a good outcome. We conclude that trauma-induced apnea causes cerebral hypoxia and/or ischemia which is more fundamental to outcome than the mechanism of injury (shaken vs. shaken with impact), subdural hemorrhage, subarachnoid hemorrhage, diffuse axonal injury, parenchymal shear, or brain contusion.

Apnea↗
PubMed2006

Bench to bedside: evidence for brain injury after concussion--looking beyond the computed tomography scan.

The emergency management of cerebral concussion typically centers on the decision to perform a head computed tomography (CT) scan, which only rarely detects hemorrhagic lesions requiring neurosurgery. The absence of hemorrhage on CT scan often is equated with a lack of brain injury. However, observational studies revealing poor long-term cognitive outcome after concussion suggest that brain injury may be present despite a normal CT scan. To explore this idea further, the authors reviewed the evidence for objective neurologic injury in humans after concussion, with particular emphasis on those with a normal brain CT. This evidence comes from studies involving brain tissue pathology, CT scanning, magnetic resonance image (MRI) scanning, serum biomarkers, formal cognitive and balance tests, functional MRI, positron emission tomography, and single-photon emission computed tomography scanning. Each section is accompanied by technical information to help the reader understand what these tests are, not to endorse their use clinically. The authors discuss the strengths and weaknesses of the evidence in each case. These reports make a compelling case for the existence of concussion as a clinically relevant disease with demonstrable neurologic pathology. Areas for future emergency medicine research are suggested.

Axons↗
PubMed1993

Cranial MR imaging and cerebral 99mTc HM-PAO-SPECT in patients with subacute or chronic severe closed head injury and normal CT examinations.

Eighteen patients in the subacute or chronic state following severe closed head injury with normal cranial CT scans were examined by MR and 99mTc HM-PAO SPECT. Correlations were sought between these 2 imaging modalities and the clinical outcome, as defined by the Glasgow Outcome Scale (GOS) score. Both MR and SPECT revealed cerebral damage in all patients examined but structural and functional alterations did not coincide topographically in 64.9% of lesions. Nevertheless, complementary injury patterns suggesting poor recovery were found; cortical contusions and diffuse axonal injury (MR) in conjunction with cortical and thalamic hypoperfusion (SPECT) were noticed in 8 out of 12 patients with unfavorable outcome (GOS = III and IV). The synthesis of MR and SPECT information clearly enhanced the ability both to accurately assess posttraumatic brain damage and to improve patients' outcome prediction.

Adolescent↗
PubMed2000

Neuroimaging correlates of cognitive and functional outcome after traumatic brain injury.

Magnetic resonance imaging (MRI) may provide an estimate of the severity of diffuse axonal injury by quantitative measurements of atrophy of white matter tracts (such as corpus callosum) and of ventricular enlargement (particularly the third ventricle). However, most MRI studies failed to reveal consistent relationships between the pattern of neuropsychological impairments and the site and extent of focal structural lesions after traumatic brain injury. Functional neuroimaging techniques, such as positron emission tomography or functional MRI, may reveal areas of cerebral dysfunction in regions that look structurally intact on MRI. Studies using these techniques have suggested that the cognitive and behavioural disturbances of traumatic brain injury could be related to a defective activation of a prefrontal-cingulate network.

Animals↗
PubMed1993

Ultrastructural evidence of axonal shearing as a result of lateral acceleration of the head in non-human primates.

The concept of shearing of axons at the time of non-impact injury to the head was first suggested in the middle of this century. However, no experimental model of diffuse axonal injury (DAI) has provided morphological confirmation of this concept. Evidence from experiments on invertebrate axons suggests that membrane resealing after axonal transection occurs between 5 and 30 min after injury. Thus, ultrastructural evidence in support of axonal shearing will probably only be obtained by examination of very short-term survival animal models. We have examined serial thin sections from the corpus callosum of non-human primates exposed to lateral acceleration of the head under conditions which induce DAI. Tearing or shearing of axons was obtained 20 and 35 min after injury, but not at 60 min. Axonal fragmentation occurred more frequently at the node/paranode but also in the internodal regions of axons. Fragmentation occurred most frequently in small axons. Axonal shearing was associated with dissolution of the cytoskeleton and the occurrence of individual, morphologically abnormal membranous organelles. There was no aggregation of membranous organelles at 20 and 35 min but small groups did occur in some axons at 60 minutes. We suggest that two different mechanisms of injury may be occurring in non-impact injury to the head. The first is shearing of axons and sealing of fragmented axonal membranes within 60 min. A second mechanism occurs in other fibres where perturbation of the axon results in axonal swelling and disconnection at a minimum of 2 h after injury.

Acceleration↗
PubMed2000

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

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

Animals↗
PubMed2003

Neurogenic fever after traumatic brain injury: an epidemiological study.

OBJECTIVES: To determine the incidence of neurogenic fever (NF) in a population of patients in the acute phase following severe traumatic brain injury (TBI); to identify factors associated with the development of NF following severe TBI in adults. METHODS: Charts of patients admitted from 1996 to 1999 with severe TBI at a large, urban mid-Atlantic teaching hospital were retrospectively evaluated based on diagnostic criteria for each episode of hyperthermia to determine the diagnosis of NF. Data were collected regarding mechanism and area of injury, severity of injury, and demographic factors to determine potential predictors of NF. RESULTS: Diffuse axonal injury (DAI) (OR 9.06, 95% CI 0.99 to 82.7) and frontal lobe injury of any type (OR 6.68, 95% CI 1.1 to 39.3) are independently predictive of an increased risk of development of NF following severe TBI. The presence of a skull fracture and lower initial Glasgow Coma Score (GCS) were individual predictors of development of NF, but did not contribute to the final model. CONCLUSIONS: These findings examine known and novel risk factors for this phenomenon in comparison to previously published literature on NF. A set of predictor variables was identified to help clinicians target patients at high risk for development of NF following severe TBI. It is hoped that earlier diagnosis and appropriate intervention for fever in the TBI patient will lead to improved outcomes.

Acute-Phase Reaction↗
PubMed2005

Familiarity effect on retrieval: a neuropsychological case study.

NM, who suffered traumatic brain injury (TBI) to the prefrontal cortex (PFC), was compared with a diffuse axonal injury (DAI) patient on tasks of free recall, cued recall and recognition memory. We manipulated the familiarity of items to explore the effects of item strength on retrieval. On free recall, NM performed best during the high-familiarity picture condition. On cued recall, he performed best during the high-familiarity word condition. Although high familiarity improved his accuracy on picture items in free recall, low familiarity improved his recognition of words. The patient with DAI did not show these patterns. The role of the PFC in memory is discussed in terms of plausible recognition processes.

Adult↗
PubMed2000

Optic nerve damage in shaken baby syndrome: detection by beta-amyloid precursor protein immunohistochemistry.

BACKGROUND: Rapid acceleration-deceleration of an infant's head during intentional shaking should in theory exert stretch or shear forces upon the optic nerves sufficient to cause axonal injury. beta-Amyloid precursor protein (beta-APP) immunohistochemistry recently has been shown to be a highly effective method for identifying diffuse axonal injury in the brains of infants with shaken baby syndrome. In this study, we investigated the utility of beta-APP in identifying optic nerve damage in infants who have sustained fatal whiplash shaking. MATERIALS AND METHODS: beta-Amyloid precursor protein immunohistochemistry was performed on formalin-fixed, paraffin-embedded sections of eyes (including optic disc and distal optic nerve) from infants less than 1 year of age with shaken baby syndrome (5 cases), combined shaken baby syndrome/blunt head trauma (3 cases), and "pure" blunt head trauma (1 case). Nontraumatic control cases included infants who died of suffocation (1 case), sudden infant death syndrome (1 case), and positional asphyxia (1 case) and an enucleation from a child with a retinoblastoma (1 case). Matched hematoxylin-eosin-and neurofilament-stained sections were used for comparison. RESULTS: Three of the 5 shaken baby cases and all 3 combined shaken baby/blunt head trauma cases had optic nerve axonal injury identified by the presence of strongly beta-APP-immunoreactive beaded or swollen axonal segments. Axonal injury could not be detected in the corresponding hematoxylin-eosin-or neurofilament-stained sections. Optic nerve axonal injury was not seen in the case involving pure blunt head trauma or in the nontraumatic control cases. CONCLUSIONS: Optic nerve axonal injury is a prominent feature of intentional fatal whiplash head trauma in infants less than 1 year of age. beta-Amyloid protein precursor immunohistochemistry appears to be the most effective method for demonstrating axonal damage in the optic nerve.

Amyloid beta-Protein Precursor↗
PubMedDate not supplied

Update of neuropathology and neurological recovery after traumatic brain injury.

This review focuses on the potential for traumatic brain injury to evoke both focal and diffuse changes within the brain parenchyma, while considering the cellular constituents involved and the subcellular perturbations that contribute to their dysfunction. New insight is provided on the pathobiology of traumatically induced cell body injury and diffuse axonal damage. The consequences of axonal damage in terms of subsequent deafferentation and any potential retrograde cell death and atrophy are addressed. The regional and global metabolic sequelae are also considered. This detailed presentation of the neuropathological consequences of traumatic brain injury is used to set the stage for better appreciating the neurological recovery occurring after traumatic injury. Although the pathological and clinical effects of focal and diffuse damage are usually intermingled, the different clinical manifestations of recovery patterns associated with focal versus diffuse injuries are presented. The recognizable patterns of recovery, involving unconsciousness, posttraumatic confusion/amnesia, and postconfusional restoration, that typically occur across the full spectrum of diffuse injury are described, recognizing that the patient's long-term recovery may involve more idiosyncratic combinations of dysfunction. The review highlights the relationship of focal lesions to localizing syndromes that may be embedded in the evolving natural history of diffuse pathology. It is noted that injuries with primarily focal pathology do not necessarily follow a comparable pattern of recovery with distinct phases. Potential linkages of these recovery patterns to the known neuropathological sequelae of injury and various reparative mechanisms are considered and it is proposed that potential biological markers and newer imaging technologies will better define these linkages.

Brain Injuries↗
PubMed1997

Strong expression of GFAP mRNA in rat hippocampus after a closed-head injury.

We investigated the spatiotemporal GFAP mRNA expression over a period of 11 days following brain injury in rats caused by impact acceleration, which is known to produce diffuse axonal injury (DAI). We observed widespread GFAP mRNA expression throughout the brain, which was more rapid and intense in the hippocampus. This expression was obvious in most animals 2 days after injury and appeared maximal at day 6. Although it decreased by day 11, the level of expression remained high compared with control levels. We noted slight differences in time of onset and the magnitude of the response between hippocampus and white matter structures or cortical areas. The different mechanisms able to trigger this response are discussed in regard to histopathological changes observed in DAI models.

Analysis of Variance↗
PubMed2003

On the Development of the SIMon Finite Element Head Model.

The SIMon (Simulated Injury Monitor) software package is being developed to advance the interpretation of injury mechanisms based on kinematic and kinetic data measured in the advanced anthropomorphic test dummy (AATD) and applying the measured dummy response to the human mathematical models imbedded in SIMon. The human finite element head model (FEHM) within the SIMon environment is presented in this paper. Three-dimensional head kinematic data in the form of either a nine accelerometer array or three linear CG head accelerations combined with three angular velocities serves as an input to the model. Three injury metrics are calculated: Cumulative strain damage measure (CSDM) - a correlate for diffuse axonal injury (DAI); Dilatational damage measure (DDM) - to estimate the potential for contusions; and Relative motion damage measure (RMDM) - a correlate for acute subdural hematoma (ASDH). During the development, the SIMon FEHM was tuned using cadaveric neutral density targets (NDT) data and further validated against the other available cadaveric NDT data and animal brain injury experiments. The hourglass control methods, integration schemes, mesh density, and contact stiffness penalty coefficient were parametrically altered to investigate their effect on the model's response. A set of numerical and physical parameters was established that allowed a satisfactory prediction of the motion of the brain with respect to the skull, when compared with the NDT data, and a proper separation of injury/no injury cases, when compared with the brain injury data. Critical limits for each brain injury metric were also established. Finally, the SIMon FEHM performance was compared against HIC15 through the use of NHTSA frontal and side impact crash test data. It was found that the injury metrics in the current SIMon model predicted injury in all cases where HIC15 was greater than 700 and several cases from the side impact test data where HIC15 was relatively small. Side impact was found to be potentially more injurious to the human brain than frontal impact due to the more severe rotational kinematics.

Journal Article↗
PubMed1997

[Cooperative multicentre study on posttraumatic epilepsy].

A multicentre cooperative prospective study have been conducted to investigate the factors influencing posttraumatic epilepsy (PTE) and to evaluate the prophylactic effect of anticonvulsants. Since April 1994, patients with head injury have been observed following our protocol as follows; anticonvulsants are administered only to the patients with brain parenchymal injury for one month just after head trauma and no anticonvulsants are administered after one month after trauma to any patients except those with posttraumatic epilepsy (PTE). Brain parenchymal injury included traumatic subarachnoid hemorrhage, acute subdural hematoma, contusion, intracerebral hematoma, and diffuse axonal injury. To April 1996, 635 patients with head injury have been registered and analyzed. During the follow-up period, 14 patients (2.2%) developed PTEs, which had only been observed in patients with brain parenchymal injury. Multiple regression analysis revealed that two factors, early epilepsy and brain parenchymal injury, could contribute to the prediction of PTE. The frequency of PTE in this study was compared with that in our previous retrospective study (Nakamura, 1995), in which anticonvulsants were administered to the patients with head injury. There was no significant difference in the percentage of patients having PTE between the group treated without anticonvulsants in this study and the untreated group in previous retrospective study. Anticonvulsants treatment after head injury was not likely to have a prophylactic effect against the development of PTE.

Adolescent↗
PubMed2005

CT for acute stage of closed head injury.

Brain damage after head injury can be classified by its time course. Primary damage that includes acute subdural hematoma (SDH), acute epidural hematoma (EDH), and intraaxial lesions that include contusions, diffuse axonal injury (DAI), and intracranial hemorrhage (ICH), occurs at the moment of impact and is thought to be irreversible. Secondary damage that includes herniations, diffuse cerebral swelling, and secondary infarction and hemorrhage, evolves hours or days after injury as a consequence of systemic or intracranial complications. The duration and severity of secondary damage influence outcome. Head injury management is focused on preventing, detecting, and correcting such secondary damage. CT has been widely used for the neuromonitoring of head trauma. CT is the gold standard for the detection of intracranial abnormalities and is a safe method for survey. While MRI is more sensitive and accurate in diagnosing cerebral pathology, CT is considered the most critical imaging technique for the management of closed head-injured patients in the acute stage. In this article, we review the imaging findings and literature of various lesions of closed head injury in the acute stage.

Acute Disease↗
PubMed2005

New developments in the neuroradiological diagnosis of craniocerebral trauma.

Accurate radiographic diagnosis is a cornerstone of the clinical management and outcome prediction of the head-injured patient. New technological advances, such as multi-detector computed tomography (MDCT) scanning and diffusion-weighted magnetic resonance imaging (MRI) have influenced imaging strategy. In this article we review the impact of these developments on the neuroradiological diagnosis of acute head injury. In the acute phase, multi-detector CT has supplanted plain X-ray films of the skull as the initial imaging study of choice. MRI, including fluid-attenuated inversion recovery, gradient echo T2* and diffusion-weighted sequences, is useful in determining the severity of acute brain tissue injury and may help to predict outcome. The role of MRI in showing diffuse axonal injuries is emphasized. We review the different patterns of primary and secondary extra-axial and intra-axial traumatic brain lesions and integrate new insights. Assessment of intracranial hypertension and cerebral herniation are of major clinical importance in patient management. We discuss the issue of pediatric brain trauma and stress the importance of MRI in non-accidental injury. In summary, new developments in imaging technology have advanced our understanding of the pathophysiology of brain trauma and contribute to improving the survival of patients with craniocerebral injuries.

Brain Injuries↗
PubMed1997

Shaken adult syndrome.

A 30-year-old Palestinian collapsed when under interrogation by the Israeli General Security Service and was declared brain dead 3 days later. Information on the circumstances and interrogation methods was denied on security grounds. Autopsy disclosed extensive anterior chest and shoulder bruising and acute subdural haemorrhage but no other trauma. On this evidence, violent shaking was postulated as the mechanism of injury. Later, this was admitted by Israeli investigators and corroborated by histopathologically proved diffuse axonal injury and retinal haemorrhages. This is the first reported case of fatal shaken adult syndrome.

Adult↗
PubMed1996

The prognostic value of the Glasgow Coma Scale, hypoxia and computerised tomography in outcome prediction of pediatric head injury.

The outcome of 151 children less than 15 years of age and admitted within 24 h of head injury was studied in relation to clinical and computed tomography (CT) scan features. Thirty one (20.5%) had a poor outcome (24 died, 6 were severely disabled at 6 months after injury and 1 was in a persistent vegetative state) while 120 (79.5%) had a good outcome (89 recovered well and 31 were moderately disabled). Factors associated with a poor outcome were Glasgow Coma Scale (GCS) score 24 h following injury, presence of hypoxia on admission and CT scan features of subarachnoid haemorrhage, diffuse axonal injury and brain swelling. GCS scores alone, in the absence of other factors, had limited predictive value. The prognostic value of GCS scores < 8 was enhanced two-to fourfold by the presence of hypoxia. The additional presence of the CT scan features mentioned above markedly increased the probability of a poor outcome to > 0.8, modified only by the presence of GCS scores > 12. Correct predictions were made in 90.1% of patients, indicating that it is possible to estimate the severity of a patient's injury based on a small subset of clinical and radiological criteria that are readily available.

Adolescent↗