Fatal head injury in children.

A comprehensive neuropathological study was undertaken on 87 children aged between 2 and 15 years with fatal head injuries to identify those features which occurred at the time of head injury (fractured skull, contusions, intracranial haematoma and diffuse axonal injury) and those which were subsequently produced by complicating processes (hypoxic brain damage, raised intracranial pressure, infection and brain swelling). The types of brain brain damage identified were remarkably similar to those seen in adults. The only difference was the prevalence of diffuse brain swelling in children.     

Evaluation of Three Animal Models for Concussion and Serious Brain Injury

Three animal models were evaluated in this study involving head impacts of the rat, including the Marmarou drop-weight and two momentum-exchange techniques. In series 1, 36 Wistar rats were hit on the side of the free-moving head using Marmarou’s 450 g impact mass at 4.4, 5.4, and 6.3 m/s. Head acceleration was measured and injuries were observed. The 6.3-m/s side impact resulted in no deaths, no skull fractures, infrequent contusions, and some injuries consistent with diffuse axonal injury. In series 2, 57 Marmarou drop-weight tests were conducted to study head biomechanical responses. Marmarou’s technique involves a head impact followed by prolonged loading into a foam pad under the animal. Based on the literature, the 2 m (6.3 m/s) Marmarou drop causes death, skull fracture, brain and spinal cord contusions, and diffuse axonal injury. These injuries are more severe than that occurring with impact of similar mass and velocity to the free-moving head. Impacts to the free-moving head provide more realistic animal models to study concussion and severe brain injury.     

Intracranial diffuse axonal injury at autopsy

An illustrative case of diffuse axonal injury (DAI) emphasizes features that help to separate focal outer head trauma owing to blows and/or falls from angular acceleration head injuries associated with diffuse inner brain lesions. In the past, explaining significant neurological deficits and death as the result of diffuse closed head trauma received from high-speed automobile accidents has been difficult as well as confusing. The long-term consequences from such diffuse inner cerebral trauma are still poorly defined. Head injuries sustained in automobile accidents have been associated with diffuse brain damage characterized by axonal injury at the moment of impact. The reported victim of a motor vehicle accident showed post-mortem findings for both inner cerebral trauma and focal outer cerebral damage. The diffuse degeneration of cerebral white matter is associated with sagittal and lateral acceleration with centroaxial trauma and has a different pathogenesis from outer focal head trauma, typified by subdural hematomas and coup injuries. Unlike outer cerebral injury, over 50 percent of victims with diffuse axonal injury die within two weeks. These individuals characteristically have no lucid interval and remain unconscious, vegetative, or severely disabled until death. Compared to head trauma victims without diffuse axonal injury, there is a lower incidence of skull fractures, subdural hemorrhages, or other intracranial mass effect as well as outer brain contusions. Primary brainstem injuries often demonstrated at autopsy are seen in the reported victim. Diffuse axonal injury is produced by various angles of acceleration with prolonged acceleration/deceleration usually accompanying traffic accidents. Less severe diffuse axonal injury causes concussion.     

Necropsy study of mountaineering accidents in Scotland.

One hundred and twenty one people died in mountaineering accidents in Scotland between July 1978 and December 1983. Necropsies were carried out on 42, which form the basis of this report. In 21 cases head injury was major fatality factor, but in 11 of these there were also serious chest injuries. Focal brain damage (haematomas, contusions, or lacerations) was more common (n = 21) than diffuse brain damage (n = 18). Over half of the victims with severe head injury had few other injuries and would probably have survived had the head injury been prevented. Spinal injuries usually occurred with other major injuries. Chest injuries were common, being serious in 18 cases, but abdominal injuries were uncommon. Four climbers with only minor injuries died of hypothermia.     

Classification of Sport-Related Head Trauma: A Spectrum of Mild to Severe Injury

OBJECTIVE: To identify the types of injuries the human brain incurs as a result of traumatic forces applied to the cranium. In athletic events and endeavors, the full spectrum of intracranial hemorrhages in various compartments, raised intracranial pressure, and diffuse nonhemorrhagic damage may be seen. In this review, we describe these serious injuries and the more common mild traumatic brain injury in their clinical presentations and relate concussion classification to the overall picture of traumatic brain injury. METHODS: Our cumulative experience with athletic injuries, both at the catastrophic and mild traumatic brain injury levels, has led us to a management paradigm that serves to guide us in the classification and treatment of these athletes. DISCUSSION: The occurrence of intracranial injuries in sports has now been well documented. Intracranial hematomas (epidural, subdural, and parenchymal) and cerebral contusions can result from head injury. Many patients sustain a diffuse brain injury, resulting in elevated intracranial pressures, without a blood clot or mass lesion. The classification of concussion and the use of concussion guidelines are not uniform. However, the major emphases are agreed upon: the close and careful scrutiny of the athlete, an expeditious but reliable neurologic examination, and proper on-field management. Return-to-play decisions are based on many factors that affect normal functioning, both on and off the playing field. CONCLUSIONS: Sufficient knowledge now exists to allow us to carefully evaluate the injured athlete, to place him or her in the management scheme to minimize the potential for permanent cerebral dysfunction, and to know when the athlete can safely return to contact sport participation.     

Assessment of cognitive function following magnesium therapy in the traumatically injured brain.

Many studies have examined the preclinical efficacy of Mg2+ therapy in models of traumatic brain injury. However, more of these studies have examined sensorimotor and motor performance than cognitive performance following injury. The present paper reviews the use of Mg2+ therapy to facilitate cognitive recovery in several models of cortical injury in the rodent. The first study examined the ability of daily injections of MgCl2 (1 or 2 mmol) to impair acquisition of a reference memory task in the Morris Water Maze. Additional studies examined the ability of MgCl2 to improve cognitive function following bilateral anterior medial cortex ablations, bilateral frontal cortex contusions, and unilateral frontal contusions. The results from these studies indicate that MgCl2 therapy is biologically active and readily crosses the blood-brain barrier because daily injections of MgCl2 impaired learning of a reference memory task in intact rats. Mg2+ therapy for brain injury revealed that administration of post-injury MgCl2 effectively improved recovery of cognitive deficits following injury. These results suggest that Mg2+ therapy is effective in facilitating cognitive recovery of function following brain injury; however, there are task and dose-dependent aspects to this recovery.     

Blunt Trauma to the Chest

Pulmonary contusions following blunt trauma often are visible roentgenographically immediately after injury. The case presented illustrates the need for prompt x-ray studies of the chest following blunt injury.     

The contrecoup phenomenon: Reappraisal of a classic problem

We describe briefly and comment upon the salient strengths and limitations of the major published theories that purport to explain the mechanism of contrecoup cerebrocortical contusions. Through the application of mechanical principles, we then present a modification, clarification, and expansion of selected aspects of several theories. Our final formulation emphasizes the injurious potential of nonuniform compressive stress and the relationship between brain lag and rotationally induced injury. The resulting theory remains faithful to the laws of physics while explaining the location and distribution of cerebrocortical contusions opposite the site of a moving head impact.     

Accidental traumatic head injury in infants and young children

Abstract This article will discuss accidental head injuries in infants and young children. The first category of injury is the crushing head injury. Static forces applied slowly to the head result in multiple fractures of the skull and contusions and lacerations of the brain resulting from the bone fragments striking the brain. This article will discuss the subject of short falls in young children and the resulting head injuries. Because falls are frequent events in early life, many cases have been collected and many papers written on the subject. Study of these cases is informative about the injuries likely to occur in these falls. Most often, only a minor contact injury such as scalp bruise or laceration results. In a 2 to 3% of falls, a simple linear skull fracture occurs and the majority of these are uneventful in terms of neurological deficit or intracranial bleeding. In about 1% of the fractures, an epidural or subdural hemorrhage occurs. Each of these forms of contact hemorrhages will be discussed and illustrated. While these are relatively rare injuries, it is essential that they can be identified as consistent with an accidental mechanism so that an erroneous diagnosis of inflicted injury is not made.     

Postinfectious glomerulonephritis

Postinfectious glomerulonephritis (PIGN) is an immunologically mediated glomerular injury triggered by an infection. Poststreptococcal glomerulonephritis (PSGN) is a classic example of PIGN with diffuse proliferative and exudative glomerular histology, dominant C3 staining and subepithelial "humps." Only the nephritogenic streptococcal infections cause PSGN and susceptibility to develop PSGN depends on both host and microbial factors. Over the last decade, two nephritogenic antigens, "nephritis-associated plasmin receptor" and "streptococcal pyrogenic exotoxin B" have been identified. PSGN is a self-limited disease, especially in children, but long-term follow-up studies indicate persistent low-grade renal abnormalities in a significant proportion of patients. PSGN continues to be a serious public health concern in third world countries, but the incidence of streptococcal infections has steadily declined in industrialized nations. PIGN in the western world is now primarily because of nonstreptococcal infections, often affecting older individuals with comorbidities such as diabetes mellitus or alcoholism, and is associated with poor outcomes. Although the acute PIGN has diffuse proliferative, focal segmental proliferative or mesangioproliferative patterns of glomerular injury, chronic or subacute infection-associated glomerulonephritis typically results in membranoproliferative appearance. PIGN has dominant C3 staining with frequent occurrence of subepithelial "humps" as well as subendothelial deposits. The immunoglobulin staining on immunofluorescence is typically weak, but immunoglobulin A-dominant PIGN is a recently defined entity often associated with staphylococcal infections. The wide spectrum of morphologic changes seen in PIGN poses a diagnostic challenge, especially if adequate clinical and serological data are lacking.     

The use of black and white infrared photography for recording blunt force injury

Infrared (IR) wavelengths penetrate skin and can selectively image volumes of subsurface blood. Twenty‐eight blunt force injuries on nine decedents were photographed with color and IR film to compare the ability of each to image the injury. Of the 28 injuries, 10 were clinically interpreted as contusions, 4 as abrasions, 10 as abraded contusions, and 4 as erythematous discolorations, nos. Twenty‐four of these injuries were incised to determine the presence and extent of subsurface bleeding. It was found that contusion had been clinically missed in five cases, three because they were hidden by abrasion and two because they appeared only as a mild cutaneous erythema. All five cases were detected by IR and verified by incision. Melanin pigmentation contributed to masking of contusion in one case and postmortem lividity confounded interpretation of contusion in one case. In all 14 injuries featuring abrasion as a component, IR de‐emphasized or eliminated the visibility of abrasion. A single false negative was reported in which a visible contusion, verified by incision, was not seen with IR. In comparing injury patterns, color and IR renditions were dissimilar in a number of cases reflecting the difference between the manner in which light and IR photography imaged the depth and volume of blood within an injury. In summary, IR imaging of wounds can discover hidden bruises, verify clinical diagnosis of bruises, and augment interpretation of wound patterns. Clin. Anat. 2013. © 2012 Wiley Periodicals, Inc.     

The Nature, Distribution and Causes of Traumatic Brain Injury

The identification and interpretation of brain damage resulting from a non-missile head injury is often not easy with the result that the most obvious structural damage identified postmortem may not be the most important in trying to establish clinico-pathological correlations. For example patients with a fracture of the skull, quite severe cerebral contusions or a large intracranial haematoma that is successfully treated can make an uneventful and complete recovery if no other types of brain damage are present. However, not infrequently more subtle forms of pathology are present and ones that can only be identified microscopically. A systematic and pragmatic approach through the autopsy is therefore required and one that recognises the need for tissue to be retained in ways that are appropriate for cellular and molecular studies.     

Intercollegiate ice hockey injuries: a three-year analysis

The purpose of this study was to investigate the type, nature, and frequency of injuries sustained in intercollegiate ice hockey. Seven schools from the Eastern Collegiate Athletic Conference and Hockey East Conference participated from 1987 through 1990. There were 280 injuries reported with a total injury rate of 10.22/1000 athlete exposures (AE). The contest injury rate (14.73/1000 AE) was higher than practice (2.52/1000 AE). Forwards (11.40/1000 AE) had the highest rate of injury followed by the defense (9.90/1000 AE). Eighty-six percent of all injuries were sustained by a direct impact mechanism, of which person/ice contact had an injury rate of 4.20/1000 AE. The shoulder (1.86/1000 AE) and knee (1.61/1000 AE) were the most frequently injured body parts. The data reported are consistent with other studies, with contusions as the most common type of injury and a higher incidence of injury reported during competition. There was a low rate of head/face/neck injuries (1.13/1000 AE), which may be a result of the required use of helmets and face guards in this population.     

Ultrastructural localization of immunoglobulin G and complement C9 in the brain stem and spinal cord following peripheral nerve injury: an immunoelectron microscopic study

SummaryThe ultrastructural localization of immunoreactivity for immunoglobulin G (IgG), F(ab)2 and complement C9 was examined with preembedding immunoelectron microscopy in the hypoglossal nucleus and gracile nucleus as well as in the L4 spinal cord dorsal horn 1 week following hypoglossal or sciatic nerve transection, respectively. Only a few scattered immunoreactive profiles were observed on the unoperated side. On the operated side, IgG and F(ab)2 immunoreactivity was present in the membranes of all reactive microglial cells observed. In addition, the cell membrane of some hypoglossal motoneurons showed IgG immunoreactivity. Complement C9 immunoreactivity was present in the cytoplasm of all reactive microglial cells examined. In addition, there was diffuse C9 immunoreactivity in motoneuron perikarya ipsilateral to nerve injury as well as in cell membranes in the neuropil, some of which could be identified as neuronal. Our interpretation of these findings is (1) that peripheral nerve injury results in binding of IgG to reactive microglia, as well as to some axotomized neurons, and (2) that C9 is synthesized by reactive microglia in response to axon injury and is also associated with axotomized motoneurons. These findings suggest that IgG and complement C9 are involved in microglia-neuron interactions after peripheral nerve injury.     

Axonal cytoskeletal changes after non-disruptive axonal injury

In animal models of human diffuse axonal injury, axonal swellings leading to secondary axotomy occur between 2 and 6 h after injury. But, analysis of cytoskeletal changes associated with secondary axotomy has not been undertaken. We have carried out a quantitative analysis of cytoskeletal changes in a model of diffuse axonal injury 4 h after stretch-injury to adult guinea-pig optic nerves. The major site of axonal damage was the middle portion of the nerve. There was a statistically significant increase in the proportion of small axons with a diameter of 0.5 m and smaller in which there was compaction of neurofilaments. Axons with a diameter greater than 2.0 m demonstrated an increased spacing between cytoskeletal elements throughout the length of the nerve. However, in the middle segment of the nerve these larger axons demonstrated two different types of response. Either, where periaxonal spaces occurred, there was a reduction in axonal calibre, compaction of neurofilaments but no change in their number, and a loss of microtubules. Or, where intramyelinic spaces occurred there was an increased spacing between neurofilaments and microtubules with a significant loss in the number of both. Longitudinal sections showed foci of compaction of neurofilaments interspersed between regions where axonal structure was apparently normal. Neurofilament compaction was correlated with disruption of the axolemma at these foci present some hours after injury. We suggest that the time course of these axonal cytoskeletal changes after stretch-injury to central axons is shorter than those changes documented to occur during Wallerian degeneration.     

Focal axonal injury: the early axonal response to stretch

Summary 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 nodal 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.     

Epidemiology of Injuries in National Collegiate Athletic Association Men's Basketball: 2014–2015 Through 2018–2019

ContextBasketball has remained a popular sport for players and spectators in the United States since before the first National Collegiate Athletic Association men''s championship tournament in 1939.BackgroundRoutine examinations of men''s basketball injuries are important for identifying emerging temporal patterns.MethodsExposure and injury data collected in the National Collegiate Athletic Association Injury Surveillance Program during 2014–2015 through 2018–2019 athletic seasons were analyzed. Injury counts, rates, and proportions were used to describe injury characteristics, and injury rate ratios were used to examine differences in injury rates.ResultsThe overall injury rate was 7.28 per 1000 athlete exposures, with competition rates twice those of practices (injury rate ratio = 2.07; 95% CI = 1.93, 2.22). Injuries to the ankle (22.2%), knee (13.0%), head/face (11.3%), and hand/wrist (10.1%) accounted for most reported injuries, with sprains (30.4%), contusions (14.3%), and strains (13.9%) most commonly reported. Ankle sprain rates initially trended upward and decreased between 2017–2018 and 2018–2019; concussion rates remained relatively stable during 2014–2015 through 2018–2019.ConclusionsFindings suggest that common injury rates are trending downward relative to previous study findings.     

Effects of diffuse axonal injury on speed of information processing following severe traumatic brain injury

To test the hypothesis that slowed information processing in traumatic brain injury is related to diffuse axonal injury (DAI), the authors compared 10 patients with predominant DAI (diffuse group) and minimal DAI (mixed injury group) on the Symbol Digit Modalities Test, simple and choice reaction time, Trail Making Tests A and B, and the Stroop Neuropsychological Screening Test. The diffuse group was slower than the mixed injury and control groups on basic speed of processing tasks. This difference was not apparent on complex speeded tasks once basic speed of processing was controlled for. The diffuse group's slower speed of processing was not accounted for by differences in injury severity, age, or time postinjury. The diffuse group showed greater recovery over time.     

Early brain injury in children: development and reorganization of cognitive function

Children who sustain congenital or acquired brain injury typically experience a diffuse insult that impacts many areas of the brain. Yet research has only recently begun to examine the development of these children, who often provide excellent examples of the presence or absence of neural plasticity. Development and recovery after such injuries reflects both restoration and reorganization of cognitive functions. To understand these processes, research should focus on questions and assessment paradigms oriented toward the acquisition (rather than the recovery) of cognitive functions. Outcomes may appear similar across types of insults, even when the sources of difficulties and their neural correlates are different. Comparisons of outcomes involving intellectual functions, memory and learning, reading, and language/discourse in children who sustain congenital injury (spina bifida meningomyelocele) and acquired injury (traumatic brain injury) illustrate these principles and the value of research on diffuse brain injury in children.