Fatal Head Injuries Research Articles

Fatal child abuse-maltreatment syndrome: A retrospective study in Ontario, Canada, 1990–1995

Child death due to repeated episodes of physical assault or neglect has been termed the child abuse-maltreatment syndrome (CAMS). We characterized the injuries in a series of fatally abused or maltreated child to delineate objective diagnostic criteria for the CAMS for use by clinicians and pathologists. All deaths (age <17 years) investigated by the Office of the Chief Coroner for Ontario, Canada during the time period 1990–1995 were reviewed. Cases of CAMS were defined as death due to lethal recent injury or malnutrition in the presence of significant old (healing or healed) injuries indicative of repeated episode of inflicted trauma. The nature and frequency of the various injuries was determined. The frequency of the shaken baby syndrome, and the types and frequency of ano-genital injuries were also studied. Twenty-one cases of fatal CAMS were found in the study period. Most cases had significant recent head injury with intra-cranial hemorrhage (71%). Other significant recent injuries commonly observed included blunt injuries of the skin and soft tissues (67%), blunt abdominal trauma with visceral injuries (14%), and fractures (18%). Eight cases (38%) fulfilled accepted criteria for the shaken baby syndrome. Many children with fatal head injuries had evidence of older head trauma (38% of all cases). A significant minority of cases had evidence of malnutrition due to neglect (10%) or ongoing ano-genital injuries (10%). Most cases of child homicides due to repeated episodes of abuse or maltreatment involve head trauma including shaken baby syndrome. Fractures of long bone and ribs, the classical markers of child abuse, were relatively infrequent compared with head injury. A proportion of cases had ano-genital injuries due to repeated sexual abuse or punitive maltreatment. All clinicians and pathologists must recognize the wide spectrum of injuries in child abuse to ultimate protect the victim or other children in an at-risk situation.

Fatal Pediatric Head Injuries Caused by Short Distance Falls

Schaber, Bethann M.D.; Hart, Amy P. M.D.; Armbrustmacher, Vernon M.D.; Hirsch, Charles S. M.D. Author Information

Author’s Response to Fatal Pediatric Head Injuries Caused by Short Distance Falls

Author’s Response to Fatal Pediatric Head Injuries Caused by Short Distance Falls

Nucleus basalis of Meynert pathology in the human brain after fatal head injury.

Dysfunction of the basal forebrain cholinergic system has been hypothesized to contribute to deficits of memory and cognition after head injury. We have previously reported reduced levels of choline acetyltransferase activity in the cerebral cortex of patients who died after a head injury, demonstrating that there is a loss of cortical cholinergic innervation. In the present study, we examined the nucleus basalis of Meynert (NBM), which provides cortical cholinergic innervation, in fatally head-injured patients and in controls. The majority of head-injured patients had histological evidence of neuronal damage in the NBM, which was due to mechanical distortion of the tissue and/or ischemic damage. The findings demonstrate that the NBM is vulnerable after severe head injury and that secondary insults play an important role in the damage. Thus, both neuronal perikarya and terminals of the basal forebrain cholinergic system are damaged after human fatal head injury. This damage may contribute to persisting dysfunction of memory and cognition in head-injured patients who survive.

Head injury-related road crash mortality in rural Western Australia.

The aim of the present paper was to assess the incidence of, and identify factors associated with road crash (RC)-related fatal head injuries in rural and metropolitan Western Australia. Examination of demographics, driving behaviour and RC characteristics for RC fatalities involving a head injury (Abbreviated Injury Scale (AIS) > or = 2) between 1 January 1998 and 31 December 1999 was carried out using the State Coronial Database. There were 328 deaths. The median age was 28 years and 74.1% of cases were male. Seventy per cent died at the scene. Of scene survivors, 89% were transferred to a metropolitan hospital before dying. Sixty per cent of total RC and 65% of at-scene deaths occurred in rural areas. Single-vehicle crashes comprised 45% of total crashes, of which 72.8% occurred in rural locations. Poor driver behaviour was identified in 53% of deaths. Ethanol was implicated in 29.8% of deaths, other intoxicating drugs were implicated in 19.2%, speeding was implicated in 19.5%, and lack of safety restraints/devices was implicated in 22%. Poor driver behaviour was identified in 72% of single-vehicle deaths, compared with 38% of multivehicle crashes (P < 0.001). Rural people comprised 61% of rural crash victims. Ninety-one per cent of rural victims died in rural crashes. The incidence of RC death associated with head injury in the rural population is 13.4 deaths/100 000 per year, more than double that for the metropolitan population (6.4 deaths/100 000 per year; P < 0.001). The rural population of Western Australia is overrepresented in head injury-related RC deaths. Single-vehicle crashes where unsafe driving behaviour is implicated comprise a large proportion of these. Strategies to reduce unsafe driving practices aimed at rural drivers are necessary.

TUNEL-positive staining of surface contusions after fatal head injury in man

In frontal lobe contusions obtained post mortem from 18 patients who survived between 6 h and 10 days after head injury, DNA fragmentation associated with either apoptotic and/or necrotic cell death was identified by the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labelling (TUNEL) histochemical technique. Additional histological techniques were also used to identify regional and temporal patterns of tissue damage. TUNEL-positive cells were present in both the grey and white matter of the contusion, where they peaked in number between 25 and 48 h, and were still identifiable at 10 days post injury. Fewer TUNEL-positive cells were observed in grey than in white matter; and most TUNEL-positive neurons in the grey matter demonstrated the morphological features of necrosis. However, the morphology of some TUNEL-stained neurons, and of TUNEL-stained oligodendroglia and macrophages in white matter was suggestive of apoptosis. Apoptosis was not seen in age- and sex-matched controls, none of whom had died from intracranial pathology or had pre-existing neurological disease. These findings suggest that multiple cell types in frontal lobe contusions exhibit DNA fragmentation and that both necrosis and apoptosis are likely to contribute to post-traumatic pathology. These findings provide further evidence that the observations made in animal models of traumatic brain injury have fidelity with clinical head injury.

Global hypoxia per se is an unusual cause of axonal injury.

Irreversible hypoxic brain damage and axonal injury are present in over 90% of fatal blunt head injuries. Given the frequency of each, difficulties arise as to whether or not they are due to different mechanisms and, as such, can be separately recognised and quantified. Recent literature has raised the possible role of hypoxia in the formation of axonal bulbs. The present study of 17 cases of cardio-respiratory arrest, 12 of status epilepticus, 3 of carbon monoxide poisoning and 12 controls was designed to test the relationship between hypoxia and axonal injury and to test the hypothesis whether or not the two entities can be separated into primary and secondary forms of traumatic brain injury. Axonal damage was seen in 9/17 and 7/12 of the cases with cardiac arrest and status epilepticus, respectively, in most of whom there was also evidence of raised intracranial pressure (ICP). All 3 cases of carbon monoxide poisoning had evidence of white matter damage in keeping with the classical pattern of selective vulnerability. It is concluded that the great majority of axonal damage identified in cases dying after cardiac arrest and status epilepticus can be attributed to raised ICP and the vascular complications of internal herniation. However, in some cases, axonal damage was seen in the absence of an elevated ICP, although its amount and distribution were different from diffuse axonal injury. In many cases there was an increase in expression of neuronal beta amyloid precursor protein.

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

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

Trends in bicycling-related head injuries in children after implementation of a community-based bike helmet campaign

Background/Purpose: The aim of this study was to determine the effect of a community-based bike helmet promotion campaign on bike helmet use and related head injuries in children (0 to 14 years of age) in a large North American city. Methods: The authors established a multifaceted, multidisciplined, community-based campaign to promote bike helmet use by children in 1989. The goals were to increase helmet use by 100% per year, to reduce fatal bike-related head injuries by 50% overall, and to explore the feasibility of legislation mandating helmet use. Helmet use was measured by standardized field observations repeated annually in a single borough within the metropolitan area. To estimate head injury incidence, the number of admissions to hospital for the treatment of bike-related head injuries in a regional trauma registry, which included all residents in the target population was used. The authors were unable to control for changes in exposure to bicycling or in the criteria for admissions to hospital for the treatment of head injuries during the study period. Results: The bike helmet use rate rose from 4% in 1990 to 67% in 1996. The number of head injury admissions fell from 46 in 1990 to 24 in 1996. Legislation requiring helmet use by all children went into effect in October 1995. Conclusions:Bike helmet use increased significantly during the first 4 years of the campaign and again after the helmet law was implemented. The total number of bike-related head injury admissions declined by more than 50%. The campaign achieved all of its goals except for a 50% reduction in fatal head injuries, which were too infrequent for analysis. J Pediatr Surg 35:688-689. Copyright © 2000 by W.B. Saunders Company.

Beta-amyloid (Abeta)42(43), abeta42, abeta40 and apoE immunostaining of plaques in fatal head injury.

beta-Amyloid (Abeta) deposits are found in the brains of approximately one-third of patients who die within days after a severe head injury; their presence correlating strongly with possession of an apolipoprotein E (apoE)-epsilon4 allele. The aim of the study was to investigate the relationship between Abeta42, Abeta40 and apoE immunostaining of Abeta plaques in the cerebral cortex and the relevance of apoE genotype in 23 fatally head-injured patients. These cases were known to have Abeta deposits from a previous study in which they were examined and semiquantified and related to apoE genotype. In the present study, the temporal cortex was probed using four different antibodies that recognize Abeta42(43), Abeta40 and an antibody to apoE. Abeta42(43)-positive plaques were observed in all of the 23 cases and Abeta40 immunoreactivity in only 11 of the 23 cases. In addition, semiquantitative analysis showed that relatively fewer plaques were detected with anti-Abeta40 than anti-Abeta42(43). ApoE-immunoreactive plaques were identified in 18 of the 23 cases. The number of plaques stained for apoE was relatively less than for Abeta42(43) but greater than for Abeta40. Furthermore, the density of Abeta plaques detected using either Abeta42(43), Abeta40 or apoE antibodies was associated with possession of apoE-epsilon4 in an allele dose-dependent manner. The results are consistent with Abeta42(43) as the initially deposited species in brain parenchyma and provide evidence that apoE is involved in the early stages of amyloid deposition. Further, the findings may be of relevance to the role of apoE genotype in influencing outcome after acute brain injury.

The shaking trauma in infants – kinetic chains

The findings in three children who died as a consequence of shaking and those in another child who survived are presented. In the three fatal cases, a combination of anatomical lesions were identified at autopsy which appear to indicate the sites where kinetic energy related to the shaking episodes had been applied thus enabling the sequence of events resulting in the fatal head injury to be elucidated. Such patterns of injuries involved the upper limb, the shoulder, the brachial nerve plexus and the muscles close to the scapula; hemorrhages were present at the insertions of the sternocleidomastoid muscles due to hyperextension trauma (the so-called periosteal sign) and in the transition zone between the cervical and thoracic spine and extradural hematomas. Characteristic lesions due to traction were also found in the legs. All three children with lethal shaking trauma died from a subdural hematoma only a few hours after the event. The surviving child had persistant hypoxic damage of the brain following on massive cerebral edema. All the children showed a discrepancy between the lack of identifiable external lesions and severe internal ones.

Hazards of bicycling: from handlebars to lightning.

The bicycle, an invention that provides joy and transportation to millions of people, can also be a source of disabling injuries and death. The victims of bicycle accidents are usually in good health and often young. Most of the fatal head injury cases are teenagers. In this article, I have chosen four areas of bicycle trauma that frequently brings the bicycle patient to the attention of a neurologist. These areas are (1) head trauma as a consequence of road collisions; (2) compressive ulnar neuropathy; (3) impotence, probably due to compression of the pudendal nerve or its branches; and (4) lightning-related bicycle injuries. The one thing that all four categories have in common is that they are often preventable. Helmet usage and common sense would lower the number of serious head trauma cases by 50%. Compressive ulnar and pudendal neuropathies can be prevented or reduced if the cyclist would frequently change his or her position in relation to the handlebar and saddle. In the majority of cases of compressive neuropathies, the symptoms improve if the patient takes a holiday from bike riding. Lightning injuries can be avoided or lessened if the cyclist takes proactive measures to limit his or her exposure during thunderstorms. These proactive measures include knowing the climate patterns of the area and knowing where the nearest safe shelter is located.

APOE epsilon4 allele and amyloid beta-protein deposition in long term survivors of head injury.

Head injury and APOE epsilon4 are risk factors for Alzheimer's disease (AD). We previously found that deposits of amyloid beta-protein (Abeta) occur in fatal head injury, more frequently in patients with APOE epsilon4. We postulated that Abeta deposits triggered by injury could, in survivors, lead to AD-like pathology later in life. Here, we compared Abeta deposits in 21 long term survivors of head injury (up to 20 years) with age and APOE genotype matched controls. In both groups Abeta deposits were more common among patients with APOE epsilon4. However, Abeta deposits were not more common among survivors of head injury than controls. The findings support previous studies associating APOE epsilon4 with deposition of Abeta. However pathogenetic mechanisms other than Abeta deposition may explain the association of head injury with AD.

The neuropathology of the vegetative state after head injury.

The technologies of resuscitation and intensive care have reduced mortality after acute brain damage, but some of those rescued are left with permanent brain damage, the most severely aVected being...

Bruising in non-accidental head injured children; a retrospective study of the prevalence, distribution and pathological associations in 24 cases

Non-accidental head injury, be it shaking, impact(s) or a combination of the two, is characterised by subdural and/or subarachnoid haemorrhages with retinal haemorrhages, but minimal or absent external cranio-facial trauma. The classical assault scenario depicts the infant being gripped around the head, face, chest and abdomen and shaken or being gripped by a limb and swung. This gripping might be expected to leave physical evidence in the form of bruising. A study was undertaken to establish the prevalence, distribution and pathological association of external bruising in 24 cases of fatal non-accidental head injury in children. At autopsy, 17 cases had new external bruises, 15 old external bruises and 13, a combination of both. However, seven (29%) cases showed no fresh external bruising and five (21%) showed no external bruising at all. Thus, external bruising may be absent in children with fatal intracranial injury. The face was shown to be the commonest site of bruising followed by the forehead and buttocks. Limb, chest and abdominal bruising were found to be uncommon. Retinal haemorrhages were confirmed in 23 (96%) cases. It is hypothesised that bruising, when present, may be a result of abuse in the form of punches and slaps rather than due to gripping during the assault. We discuss why gripping does not necessarily result in external bruising.

Is there a genetic basis for the deposition of beta-amyloid after fatal head injury?

1. Alzheimer's disease is a heterogeneous disorder that may be caused by genetic or environmental factors or by a combination of both. Abnormalities in chromosomes 1, 14, and 21 have all been implicated in the pathogenesis of the early-onset form of the disease, while the epsilon 4 allele of the apolipoprotein E gene (on chromosome 19) is now recognized as a risk factor for early- and late-onset sporadic and familial Alzheimer's disease. 2. The best-established environmental trigger for the disease is a head injury, based on epidemiological and neuropathological evidence. Approximately 30% of patients who die after a single episode of severe head injury show intracerebral deposition of beta-amyloid protein (A beta), a protein that is thought to be central to the pathogenesis of Alzheimer's disease. 3. Recent studies have revealed an over-representation of the apoE epsilon 4 allele in those head-injured patients displaying A beta pathology, thus providing the first evidence for a link between a genetic susceptibility (apoE epsilon 4) and an environmental trigger (head injury) in the development of Alzheimer-type pathology.

Fatal Head Injuries among Hispanic Farmworkers and Farmers in Colorado, 1983-1992

The purpose of this cross-sectional study was to determine the risk of head injury deaths among Hispanic Coloradoans employed in agriculture. Hispanic farmworkers and farmer deaths from head injury were compared to non-Hispanic farmworkers and farmers. Colorado death certificates were obtained for the years 1983-1992. Head injuries were defined using the contributing and external causes of death based on the Ninth Revision of the International Classification of Diseases (ICD) codes. Occupational categories were based on 1980 Standard Occupational code equivalents. Denominators for risk estimates were based on 1990 United States Census of the Population for Colorado. Rates for head injury were calculated for each occupational category for Hispanics and non-Hispanics. Risk estimates comparing rates for Hispanic farmers and farm workers to non-Hispanics were: 1.79 (1.04, 3.11) and 2.5 (1.73, 3.60). Although there were no significant differences found comparing head injury rates of Hispanics and non-Hispanics among all Colorado residents, farmers and farmworkers of Hispanic origin were at significantly increased risk of head injury death compared to non-Hispanics in the same job categories.

A comparison of manual and semi‐automated methods in the assessment of axonal injury

Diffuse axonal injury (DAI) in the central nervous system is a common cause of post-traumatic coma and may result in varying degrees of disability up to and including the vegetative state. Experimental studies in man and animals have previously relied upon semi-quantitative grading systems for determining the relationship between the extent of DAI and the clinical features of patients. Using beta-amyloid precursor protein immunocytochemistry for the detection of DAI in sections of corpus callosum from 15 cases of fatal head injury, we have developed a quantitative image analysis technique for the assessment of axonal injury. This new method is objective and reproducible and should allow better correlation with biomechanical, radiological, and clinical parameters to increase our understanding of DAI.

Bruising in non-accidental head injured children; a retrospective study of the prevalence, distribution and pathological associations in 24 cases

Non-accidental head injury, be it shaking, impact(s) or a combination of the two, is characterised by subdural and/or subarachnoid haemorrhages with retinal haemorrhages, but minimal or absent external cranio–facial trauma. The classical assault scenario depicts the infant being gripped around the head, face, chest and abdomen and shaken or being gripped by a limb and swung. This gripping might be expected to leave physical evidence in the form of bruising. A study was undertaken to establish the prevalence, distribution and pathological associations of external bruising in 24 cases of fatal non-accidental head injury in children. At autopsy, 17 cases had new external bruises, 15 old external bruises and 13, a combination of both. However, seven (29%) cases showed no fresh external bruising and five (21%) showed no external bruising at all. Thus, external bruising may be absent in children with fatal intracranial injury. The face was shown to be the commonest site of bruising followed by the forehead and buttocks. Limb, chest and abdominal bruising were found to be uncommon. Retinal haemorrhages were confirmed in 23 (96%) cases. It is hypothesised that bruising, when present, may be a result of abuse in the form of punches and slaps rather than due to gripping during the assault. We discuss why gripping does not necessarily result in external bruising.

Immunohistochemical indicators of early brain injury: an experimental study using the fluid-percussion model in cats.

To detect early changes in neurons and astrocytes by immunohistochemical methods using antibodies against the neuron-specific enolase (NSE), neurofilament, glial fibrillary acid protein (GFAP), and S-100 protein, a fluid-percussion injury model in cats was chosen, in which a severe grade of injury (3.5-5.5 atm) was produced. Neuropathologic changes were produced through brain deformation by pressure gradients at the time of injury. The neuronal NSE immunoreactivity in the parietal cortex and the brain stem began to decrease at 1 to 2 hours after injury and were reduced markedly or even lost 4 hours after injury. Axons in the cerebral white matter and corpus callosum and in the hemorrhage regions at the brain stem were waved and enlarged <4 hours after injury. From 4 hours after injury, retraction balls were found after staining by antibody for the neurofilament. The GFAP-positive astrocytes appeared in the impact site in the parietal cortex and in the brain stem from 4 hours after injury, whereas S-100-positive astrocytes were not markedly changed, indicating that early after the injury, astrocytes manifested reactive hypertrophy without proliferation. These results suggest that immunochemical studies on NSE, neurofilament, GFAP, and S-100 are useful in pathologic and forensic practice in a patient who survives for a short time after a fatal head injury but without obvious focal damage.