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PubMed2000

Magnetization transfer imaging of traumatic brain injury.

Magnetization transfer imaging (MTI) has been shown to be sensitive for the detection of white matter abnormalities in entities such as multiple sclerosis, progressive multifocal leukoencephalopathy, and wallerian degeneration. Our hypothesis was that MTI would detect traumatic white matter abnormalities (TWMA) and provide information additional to that obtainable with routine spin- and gradient-echo imaging. We hypothesized that the presence of TWMA defined by MTI would correlate with outcome following TBI. Twenty-eight victims of head trauma and 15 normal controls underwent magnetic resonance imaging including MTI. Magnetization transfer ratios (MTR) were calculated for areas of shearing injury and for normal-appearing white matter (NAWM) in locations frequently subject to diffuse axonal injury. Abnormal MTRs were detected in NAWM in eight patients. All eight had persistent neurologic deficits, including cognitive deficits, aphasia, and extremity weakness. Seven of the 28 patients had no abnormal findings on neurologic exam at discharge, transfer, or follow-up. None of these patients had an abnormal MTR in NAWM. In the remaining 13 patients, who had persistent neurologic deficits, no regions of abnormal MTR were detected in NAWM. MTI is a sensitive method for the detection of TWMA. Detection of abnormal MTR in NAWM that is prone to axonal injury may predict a poor patient outcome. The presence of normal MTR in NAWM in these areas does not necessarily confer a good outcome, however.

Adult↗
PubMed1997

CT findings in persistent vegetative state following blunt traumatic brain injury.

The use of linear measurements in the analysis of CT scans of TBI patients was found to contribute to the understanding of brain damage and were correlated with outcome in severe traumatic close brain injured patients. The purpose of the present study was to analyse the data obtained by the linear measurements on CT studies of TBI patients who remained in persistent vegetative state following blunt head trauma. All 27 patients included in the study were reported to be neurologically normal prior to injury. Thirteen patients, 11 remaining in persistent vegetative state (responsive but unaware) and two who died, constituted the worst outcome group. Fourteen patients who regained consciousness, underwent multidisciplinary evaluation when their recovery reached a plateau and were ranked according to severity of residual symptoms and outcome. The degree of correlation with the overall vocational outcome parameter with the various radiological indices was calculated as the Spearman rank correlation coefficient, with correction for tied scores. Fisher's z transformation was used to combine results with those of our previous analysis. Three radiological parameters showed a statistically significant correlation with clinical outcome. These were the right and left septum-caudate distance and the cerebroventricular index 2; these showed Spearman rank coefficients of 0.52, 0.45 and 0.48; with two-tailed p-values under 0.01, 0.02 and 0.01 respectively. The width of the third ventricle suggested correlation with the clinical scoring. The findings of the present study point to the importance of loss of deep gray matter of the caudate nuclei and widening of the adjacent part of the lateral ventricles in catastrophic brain injury. This finding may highlight the role of localized ischemic changes, in addition to diffuse axonal injury. Values of over 8 mm for the width of the third ventricle and over 11 mm for septum caudate distance are suggestive of catastrophic and poor prognosis for recovery.

Activities of Daily Living↗
PubMedDate not supplied

On-the-field management of athletic head injuries.

Head injuries are prevalent in collision sports. Concussions represent the relatively benign end of the spectrum of injuries. Severe closed head injuries include epidural hematomas, acute subdural hematomas, intracerebral hematomas, intraventricular hematomas, subarachnoid hemorrhages, and diffuse axonal injuries. Second impact syndrome represents a severe cerebral autoregulatory dysfunction that can lead to death in an athlete who sustains a second (often minor) closed head trauma while still symptomatic from a previous head injury. Generally, athletes who have suffered a severe closed head injury should not return to play. Exceptions include athletes asymptomatic for 1 year who return to a noncontact sport and those who recover completely from an epidural hematoma without underlying brain injury. Several guidelines for returning athletes to play have been proposed and are commonly used. The team physician has the responsibility of on-the-field evaluation and management of athletes with head injuries, as well as of advising them when it is safe to return to play.

Athletic Injuries↗
PubMedDate not supplied

[Autonomic dysfunction in children with traumatic brain injury].

INTRODUCTION: Autonomic dysfunction syndrome following traumatic brain injury is a situation involving adrenergic hyperactivity produced by the lack of control over the autonomous nervous system at a central level. The difficulties involved in its therapeutic management make it even more important. CASE REPORTS: We report the cases of a boy and a girl aged 6 and 12 years, respectively, who had suffered a severe traumatic brain injury with important brain damage that included diencephalic and mesencephalic compromise and areas of diffuse axonal injury. From the acute phase onwards, they presented episodes of hypertension, tachycardia, excessive sweating and spasticity in the form of attacks that initially led to a differential diagnosis between sepsis, opiate and/or benzodiazepine withdrawal syndrome and epilepsy. The length of time spent in coma was very long and the attacks went on throughout the awakening phase almost until the moment they were discharged from hospital, despite trying different treatments. In our cases, orally administered baclofen and midazolam seemed to be the most effective. CONCLUSIONS: Autonomic dysfunction is difficult to manage. There are no standardised treatments and speculation continues with regard to its true promoter. We might think that the central injury is the cause of the process and that the autonomic dysfunction increases the secondary lesion and contributes to the functional worsening. If we take into account that the survival rate of the children is high despite the severity of the injuries and although the dysautonomia can be self-limiting with time, we believe that its treatment is essential if the ultimate aim is to minimise the sequelae.

Autonomic Nervous System Diseases↗
PubMed1992

[Magnetic resonance imaging in diffuse brain injury].

Forty cases diagnosed as diffuse brain injury (DBI) were studied by magnetic resonance imaging (MRI) performed within 3 days after injury. These cases were divided into two groups, which were the concussion group and diffuse axonal injury (DAI) group established by Gennarelli. There were no findings on computerized tomography (CT) in the concussion group except for two cases which had a brain edema or subarachnoid hemorrhage. But on MRI, high intensity areas on T2 weighted imaging were demonstrated in the cerebral white matter in this group. Many lesions in this group were thought to be edemas of the cerebral white matter, because of the fact that, on serial MRI, they were isointense. In mild types of DAI, the lesions on MRI were located only in the cerebral white matter, whereas, in the severe types of DAI, lesions were located in the basal ganglia, the corpus callosum, the dorsal part of the brain stem as well as in the cerebral white matter. As for CT findings, parenchymal lesions were not visualized especially in mild DAI. Our results suggested that the lesions in cerebral concussion were edemas in cerebral white matter. In mild DAI they were non-hemorrhagic contusion; and in severe DAI they were hemorrhagic contusions in the cerebral white matter, the basal ganglia, the corpus callosum or the dorsal part of the brain stem.

Adolescent↗
PubMed1992

Outcome prediction in early management of severe head injury: an experience in Malaysia.

The outcome of 109 patients with severe head injury was studied in relation to clinical and computed tomographic (CT) criteria on admission, after resuscitation. Age, Glasgow Coma Score (GCS) and state of pupils strongly correlated with outcome. The presence of hypothalamic disturbances, hypoxia and hypotension were associated with an adverse outcome. The CT indicators associated with poor outcome were perimesencephalic cistern (PMC) obliteration, subarachnoid haemorrhage, diffuse axonal injury and acute subdural haematoma. The prognostic value of midline shift and mass effect were influenced by concomitant presence of diffuse brain injury. For the subset of patients aged < 20 years, with GCS 6-8 and patent PMC (n = 21), 71.4% correct predictions were made for a good outcome. For the subset of patients aged > 20 years, with GCS 3-5 and partial or complete obliteration of PMC (n = 28), 89.3% correct predictions were made for a poor outcome.

Adolescent↗
PubMed1990

Acute tissue tear hemorrhages of the brain: computed tomography and clinicopathological correlations.

Tissue tear hemorrhages (TTHs) are often seen on high-resolution computed tomographic scans after closed head injury. Generally, TTHs have been thought to be visible manifestations of more severe forms of diffuse axonal injury and thus portend a poor prognosis. Computed tomographic scans from 600 patients with head injuries were reviewed; 48 (8%) were found to have TTHs. The clinical spectrum of TTHs was characterized. No direct relationship could be established between either the presence or the number of TTHs and the severity and/or outcome from the head injury in this group, except that patients with TTHs in both the brain stem and the corpus callosum uniformly had a poor outcome. Magnetic resonance imaging provided more sensitive information than computed tomography in evaluating TTHs.

Adult↗
PubMed2001

The state of head injury biomechanics: past, present, and future: part 1.

This article is the first of two parts of a comprehensive survey of the biomechanics of head injury since its inception in 1939 in the United States, the separation being made for temporal and spatial reasons. The second portion of this material will be published at a later time in this journal. The discussion will be almost exclusively limited to nonpenetrating events. The topics presented in the following sections include an introduction that discusses the magnitude of the problem, the basic tools of biomechanics, and significant major reference sources covering this subject. This is succeeded by a brief description of the components of the head, classification of head injuries, early experimental investigations and human tolerance considerations, measurement techniques of kinetic parameters, and head motion and head injury investigations prior to 1966. A Head Injury Conference sponsored by the National Institutes of Neurological Diseases and Stroke in 1966 changed the landscape of investigations in this area. While informal collaboration between neurosurgeons and engineers had existed prior to this time, the conference established a permanent mechanism of synergism between these disciplines, produced the first zero-order realistic model of biomechanical head injury investigation, and established a 4-year program of federally funded research into the mechanical properties of the tissues of the cranium. While a recession precluded a continuation of the national sponsorship of such work, this 4-year period of intensive research resulted in a nationwide individual effort to develop further knowledge in this area. The current presentation, then, covers the mechanical and structural properties of solid and fluid tissues of the head, emphasizing progress during the past 3 decades; fetal cranial properties; analytical and numerical head injury models; experimental cranial loads applied to human volunteers and cadaver heads, dynamic loading of surrogate heads; and, finally, head injury mechanisms. The future publication will encompass experimental, analytical, and some numerical and regulatory information and that will be divided into the following sections: 1. head injury experimentation involving translatory and rotational motion: equipment, subjects and mechanical and physiological consequences 2. diffuse axonal injury: production and traumatic effects; mechanical properties at the axonal and neuronal level 3. vehicular crash investigation and simulation: reconstruction methodologies, staging, surrogate validation, and occupant protection, including vehicular design 4. injury thresholds and tolerances, including skull and vessel failure and brain and brainstem damage, including consideration of loading directions 5. criteria for head injury: governmental and industry regulations, including effects of combined motion- and tissue-level loading 6. further discussions of cranial component properties and injury mechanisms 7. sports head injury considerations: boxing, baseball, softball, football, ice hockey, and skiing activities; protective head devices for these activities 8. vehicular protective devices: design, efficacy, standards, and limitations; models for helmets and experimental validation. This presentation is based on my nearly 4 decades of head injury research, continuous collaboration and discussions with prominent members of the neurosurgical and orthopedic community, and an exhaustive, 2-year search of the literature. While every effort has been made to include all relevant information, it is inevitable that some important research has not come to my attention, and I apologize for any such omissions. It is hoped that this survey will serve as a resource for researchers and practitioners in the area of traumatic head injury and provide a roadmap for further investigations that are urgently needed. For example, this could include a determination of the rate of absorption of blood emitted from broken vessels, and, hopefully, some correlation between mechanical failure and physiological dysfunction of the various relevant tissues of the head. Although a good beginning has been initiated, additional information at the neuronal and axonal level concerning the effect of loading on function as well as age-related changes in geometry and tissue properties is also needed.

Biomechanical Phenomena↗
PubMedDate not supplied

Clinicopathologic observations in 100 consecutive patients with fatal head injury admitted to a neurosurgical unit.

A neuropathologic study of 100 patients with fatal head injuries admitted to a neurosurgical unit revealed hypoxic-ischaemic brain damage in 74% and diffuse axonal injury in 42% of patients respectively. Of the seven patients who died as a result of extracerebral injuries, there were four in whom death due to hypovolaemic shock, was considered potentially avoidable. This study indicates that there is scope for improvement in the management of patients with acute head injury, particularly in the prevention of secondary brain damage, and in the need to increase awareness of potentially life threatening extracerebral injuries as a cause of coma.

Adolescent↗
PubMed1991

Focal axonal injury: the early axonal response to stretch.

The development of a model for axonal injury in the optic nerve of the guinea pig has allowed analysis of early morphological changes within damaged axons. We provide evidence that the initial site of damage after stretch is the nodes of Ranvier, some of which develop 'nodal blebs'. The development of nodel blebs is correlated with the loss of subaxolemmal density, disruption of the neurofilament cytoskeleton and aggregation of membranous profiles of smooth endoplasmic reticulum. Nodal blebs are numerous 15 min after injury but less so at later survivals. The glial-axonal junction is intact at early survivals in damaged nodes. Marked accumulation of membranous organelles occurs in the paranodal and internodal regions adjacent to damaged nodes between two and six hours and is correlated with disruption of the myelin sheath. Axotomy and the formation of degeneration bulbs occurs between 24 and 72 h. The area of axonal injury is invaded by phagocytic cells by 72 h and large numbers of myelin figures occur within the neuropil until 14 days. The results are compared with those of other studies of diffuse axonal injury and other neuropathies. The time course of axonal changes is more rapid than during Wallerian degeneration. Our data from longer surviving animals is exactly comparable with published data. We are confident that the principal site of axonal injury is the node of Ranvier. We suggest that damage at the node results in disruption of axonal transport, which in turn leads to a cascade of events, culminating in axotomy between 24 and 72 h after the initial insult.

Animals↗
PubMed2002

Biomechanics and neuropathology of adult and paediatric head injury.

The objective of this study was to understand the biomechanics in age-related primary traumatic brain injuries (TBI) causing initial severity and secondary progressive damage and to develop strategy reducing TBI outcome variability using biomechanical reconstruction to identify types of causal mechanisms prior to clinical trials of neuro-protective treatment. The methods included the explanation of TBI biomechanics and physiopathological mechanisms from dual perspectives of neurosurgery and biomechanical engineering. Scaling of tolerances for skull failure and brain injuries in infants, children and adults are developed. Diagnostic assumptions without biomechanical considerations are critiqued. Methods for retrospective TBI reconstruction for prevention are summarized. Mechanisms of TBI are based on the differences between the mechanical properties of the head and neck related to age. Skull fracture levels correlate with increasing cranial bone thickness and in the development of the cranial sutures in infants and in adults. Head injury tolerance levels at three age categories for cerebral concussion, skull fracture and three grades of diffuse axonal injuries (DAI) are presented. Brain mass correlates inversely for TBI caused by angular head motions and locations of injurious stresses are predictable by centripetal theory. Improved quantitative diagnosis of TBI type and severity levels depend primarily on age and biomechanical mechanisms. Reconstruction of the biomechanics is feasible and enables quantitative stratification of TBI severity. Experimental treatment has succeeded in preventing progressive damage in animal TBI models. In humans this has failed, because the animal model received biomechanically controlled TBI and humans did not. Clinical similarities of human TBI patients do not necessarily predict equivalent biomechanics because such trauma can be produced in various ways. We recommend 'reverse engineering' for in-depth reconstruction of the TBI injury mechanism for qualitative diagnoses and reduction of outcome variability.

Accidental Falls↗
PubMed2000

Reduction of corpus callosum growth after severe traumatic brain injury in children.

OBJECTIVE: To study effects of closed head injury (CHI) severity on development of corpus callosum (CC) in children, using MRI. BACKGROUND: Vulnerability of CC to diffuse axonal injury has been shown in adults and children by neuropathologic and MRI studies. Given continued development of CC through the second decade, serial MRI could characterize effects of CHI on CC growth in children. METHOD: MRI performed at 3 and 36 months after severe (mean age = 10.3 years, n = 25) and mild to moderate (mean age = 9.7 years, n = 28) CHI. Mild to moderate and severe CHI groups did not differ in demographic features. Morphometry of T1-weighted midsagittal CC by two operators with satisfactory interrater reliability yielded uncorrected and corrected CC volume. RESULTS: An interaction of occasion with CHI severity was present as CC area decreased from 3 to 36 months in severely injured children and increased in the mild to moderate CHI group. Uncorrected CC area was correlated with acute CHI severity and functional outcome at 36 months postinjury. CONCLUSIONS: Morphometric measurement of CC area provides a useful index of diffuse injury, which is related to functional outcome of CHI in children.

Brain Injuries↗
PubMed2000

The neuropathology of the vegetative state after an acute brain insult.

The vegetative state is often described clinically as loss of function of the cortex while the function of the brainstem is preserved. In an attempt to define the structural basis of the vegetative state we have undertaken a detailed neuropathological study of the brains of 49 patients who remained vegetative until death, 1 month to 8 years after an acute brain insult. Of these, 35 had sustained a blunt head injury and 14 some type of acute non-traumatic brain damage. In the traumatic cases the commonest structural abnormalities identified were grades 2 and 3 diffuse axonal injury (25 cases, 71%). The thalamus was abnormal in 28 cases (80%), and in 96% of the cases who survived for more than 3 months. Other abnormalities included ischaemic damage in the neocortex (13 cases, 37%) and intracranial haematoma (nine cases, 26%). In the non-traumatic cases there was diffuse ischaemic damage in the neocortex in nine cases (64%) and focal damage in four (29%); the thalamus was abnormal in every case. There were cases in both groups where the cerebral cortex, the cerebellum and the brainstem were of structurally normal appearance. In every case, however, there was profound damage to the subcortical white matter or to the major relay nuclei of the thalamus, or both. These lesions render any structurally intact cortex unable to function because connections between different cortical areas via the thalamic nuclei are no longer functional, and there is also extensive damage to afferent and efferent cerebral connections.

Adolescent↗
PubMed2000

Rehabilitation of a person with severe traumatic brain injury.

A case study report of a long and intensive rehabilitation programme for a young woman after she sustained a severe diffuse axonal injury in a motor vehicle accident is described in detail. The purpose of this paper is to encourage specialist brain injury rehabilitation services to offer extended rehabilitation programmes to patients, even with very severe injuries. Significant functional improvements and enhanced quality of life frequently reward the high cost and hard work involved.

Accidents, Traffic↗
PubMed1998

Neuropathology of the Head Injuries.

Structural abnormalities develop progressively after trauma to the central nervous system suggesting that injury is a process of events rather than a singular event. Thus, numerous types of neuropathologies can occur, depending on the exact nature of the processes of cellular damage that are set into motion after injury. Four general interrelated processes of delayed cellular damage occur in different amounts and in different locations to result in the numerous types of traumatic brain damage. These include direct damage caused by calcium influx into cells, free radical-mediated damage, receptor-mediated damage, and inflammation. By these mechanisms, the general response of the brain to mechanical energy causes damage to vascular or neural components of the brain, and results in principally focal or diffuse brain damage, respectively. These form the phenotypic types of damage to the brain and the resulting clinically associated traumatic syndromes. Focal brain damage consists principally of vascular injury that results in confusions and hemorrhages in various locations. Diffuse brain damage mainly involves scattered damage to axons in the white matter (diffuse axonal injury) or secondary damage attributable to raised intracranial pressure, hypoxia, or ischemia.

Journal Article↗
PubMed1992

Magnetic resonance applications in cerebral injury.

CT and MR imaging are complementary in the evaluation of cerebral head trauma. CT is still more useful for the initial evaluation of the acutely unstable patient who has a head injury. However, many lesions are identified by MR imaging such as cortical contusions, small subdural hematomas, and diffuse axonal injuries that may not be seen on CT examinations. In addition, MR angiography can play an important role in the diagnostic evaluation of the trauma patient. MR angiography can be clinically useful in delineating vascular abnormalities such as arterial occlusions, arteriovenous fistulae, dissecting aneurysms, and venous sinus occlusion. In pediatric trauma, MR imaging appears to be superior to CT in assessing head injuries, particularly those due to child abuse.

Adult↗
PubMed1992

Degenerative changes in traumatic brain injury: post-injury magnetic resonance identified ventricular expansion compared to pre-injury levels.

Magnetic resonance (MR) scans obtained 42 days and 10 months post-injury were compared to scans obtained in similar planes three months prior to injury. In comparison to pre-injury scans, post-injury MR scan analysis demonstrated significant ventricular volume increase which is considered a measure of the degree of diffuse axonal injury. Most important, the trauma induced degenerative effects appeared to be quite complete by 42 days post-injury as there was little further degeneration that occurred between the 6 week and 10 month post-injury scans. This study demonstrates that in humans the majority of gross trauma-induced degenerative changes are complete by 6 weeks post-trauma.

Adult↗