Fatal Traumatic Brain Injury Research Articles

Association between intravascular microthrombosis and cerebral ischemia in traumatic brain injury.

To determine the association between traumatic cerebral ischemia and intravascular thrombosis, a common finding after traumatic brain injury (TBI). We reviewed samples of the frontal cortex and hippocampus from individuals who had sustained a fatal TBI. Sections stained with hematoxylin and eosin were reviewed and rated for severity of selective neuronal necrosis (SNN). Because intravascular fibrin microthrombi may lyse within a few days of TBI, we restricted our analysis to patients who had died within 48 hours of injury. Medical records in all cases were reviewed to rule out severe or prolonged hypotension or hypoxemia. Eleven patients with severe or global SNN were compared with 11 patients in whom SNN was mild or absent. Slides adjacent to the hematoxylin and eosin sections were stained with an immunofluorescent antibody to antithrombin III and were reviewed for intravascular microthrombosis. The number of microthrombi on each slide was counted by an investigator blinded to the hematoxylin and eosin findings, and density of intravascular microthrombi was calculated. Intravascular microthrombi were noted in every section, excluding control (non-TBI) brain tissue. However, the density of microthrombi varied with the degree of SNN. We found a highly significant difference in the mean density of microthrombi between patients with severe SNN (7.74 +/- 3.7/cm(2)) and those with little or no SNN (2.58 +/- 1.0/cm(2)). Furthermore, a good correlation was noted between the location of intravascular microthrombi and that of SNN. These data support a strong link between intravascular microthrombosis and neuronal death after brain trauma in humans and may have important implications for new therapeutic approaches.

Estimating nonfatal traumatic brain injury hospitalizations using an urban/rural index.

To develop state-level estimates of the annual number of nonfatal cases of traumatic brain injury (TBI) resulting in hospitalization. The estimation process incorporates annual nonfatal TBI hospitalization case counts from 15 states funded by the Centers for Disease Control and Prevention to conduct TBI surveillance; annual fatal TBI case counts based on National Center for Health Statistics data for all 50 states; and an index reflecting the urban/rural character of each state. These data are used to develop a negative binomial regression model that yields estimates of the annual number of nonfatal TBI hospitalization cases for each state not funded to conduct TBI surveillance. Sensitivity analysis suggests that on average the estimates fall within +/- 15% of the case counts that would be obtained directly from surveillance. In combination, the TBI case count data and the urban/rural index support effective modeling and estimation of annual nonfatal TBI hospitalization case counts at the state level.

Trials and tribulations of using β-amyloid precursor protein immunohistochemistry to evaluate traumatic brain injury in adults

Axonal pathology is increasingly identified by β-amyloid precursor protein (βAPP) immunohistochemistry in the brains of patients who may or may not have a history of trauma. The presence of βAPP-IR + has been variously interpreted as either that diffuse traumatic axonal injury (TAI) is indeed a universal finding in cases of fatal traumatic brain injury (TBI) or there are other causes of βAPP-IR + axons which under certain circumstances may be sufficient to mimic TBI and therefore make the medico-legal interpretation of certain cases very difficult. To address some of the uncertainties we have undertaken a detailed analysis of the amount and distribution of βAPP immunohistochemistry in 63 cases of fatal TBI, 17 cases of patients dying after cardiac arrest, 12 cases dying in association with status epilepticus, 3 cases of carbon monoxide (CO) poisoning, 13 cases of hypoglycaemia and in 60 controls. Three patterns of βAPP-IR + were identified. First, diffuse multi-focal, second, corresponding to the outline of an infarct or haematoma, and thirdly a mixture of the two. The first pattern was seen in cases of the lesser grades of TAI, CO poisoning, and hypoglycaemia, the second pattern in cases in which there was evidence of raised intracranial pressure and the third in cases of severe TAI. It is concluded that the proper interpretation of cases requires the examination of a sufficient number of blocks ( n=15), processing using standardised protocols including βAPP immunohistochemistry and in some cases the mapping of any IR + on anatomical line diagrams. βAPP carried out on a small number of randomly taken blocks is likely to lead to misinterpretation of the clinico-pathological correlations and possibly to a miscarriage of justice.

A population-based study of inflicted traumatic brain injury in young children.

Physical abuse is a leading cause of serious head injury and death in children aged 2 years or younger. The incidence of inflicted traumatic brain injury (TBI) in US children is unknown. To determine the incidence of serious or fatal inflicted TBI in a defined US population of approximately 230 000 children aged 2 years or younger. All North Carolina children aged 2 years or younger who were admitted to a pediatric intensive care unit or who died with a TBI in 2000 and 2001 were identified prospectively. Injuries were considered inflicted if accompanied by a confession or a medical and social service agency determination of abuse. Incidence of inflicted TBI. Multivariate logistic regression models were used to compare children with inflicted injuries with those with noninflicted injuries and with the general state population aged 2 years or younger. A total of 152 cases of serious or fatal TBI were identified, with 80 (53%) incurring inflicted TBI. The incidence of inflicted traumatic brain injury in the first 2 years of life was 17.0 (95% confidence interval [CI], 13.3-20.7) per 100 000 person-years. Infants had a higher incidence than children in the second year of life (29.7 [95% CI, 22.9-36.7] vs 3.8 [95% CI, 1.3-6.4] per 100 000 person-years). Boys had a higher incidence than girls (21.0 [95% CI, 15.1-26.6] vs 13.0 [95% CI, 8.4-17.7] per 100 000 person-years). Relative to the general population, children who incurred an increased risk of inflicted injury were born to young mothers (< or =21 years), non-European American, or products of multiple births. In this population of North Carolina children, the incidence of inflicted TBI varied by characteristics of the injured children and their mothers. These data may be helpful for informing preventive interventions.

Traumatic brain injury in Denmark 1979-1996. A national study of incidence and mortality.

In order to describe and analyse the development of the incidence of traumatic brain injury (TBI) in Denmark for different age groups of the two genders from 1979 through 1993 (for fatal injuries through 1996), a computerised search corresponding to diagnoses ICD 8th ed., 800, 801, 803, 850-854 from 1979 through 1993 was carried through in the national hospital register. Each person was counted only once, according to the most serious injury during the study period. For fatal cases, the search was extended till 1996. From 1979-1981 to 1991-1993, the total age-adjusted incidence of persons hospitalised under diagnoses ICD 800, 801, 803, 850-854 decreased 41% from 265 to 157 per 100,000 of the population per year. Decreases were 42% for ICD 850, brain concussion, 56% for ICD 800, 801, 803, cranial fractures, and 16% for ICD 851 854, structural brain injury. The percentage of cases with ICD 851-854 increased from 8.4 to 11.7% of the total. From 1979-1981 to 1985-1987 there was a 2% decrease in fatal TBI in and outside hospital (from 14.68 to 14.35 per 100,000), against a total 27% decrease to 10.67 in 1994-1996. For diagnoses ICD 851-854 and for fatal cases, significantly accelerating decreases from 1985-1987 were found only for the younger age groups. Consequently, in the period from 1979 to 1993, the mean age at injury increased by 10 years for persons hospitalised under diagnoses ICD 851-854. Decreases may be explained partly by changing admission and other hospital practices, and partly by the effect of comprehensive national preventive programs launched at the middle of the study period, the effect of which seemed to vary by age group and gender.

Urban and rural traumatic brain injuries in Colorado

PURPOSE: The purpose of this study was to compare and contrast the epidemiology of traumatic brain injury among urban and rural residents of Colorado. METHODS: Cases of traumatic brain injury (ICD 800, 801, 803, 804, 850–854) for 1991 and 1992 from the Colorado surveillance system of hospitalized and fatal traumatic brain injuries were used. Urban cases resided in counties designated by the U.S. Census Bureau as metropolitan statistical areas (MSA). Rural cases were divided into two groups: “rural, nonremote,” if the country of residence was adjacent to an MSA county or if it had a population of 2500, and “rural, remote,” if not. RESULTS: Average annual age-adjusted rates of hospitalized and fatal traumatic brain injury varied significantly from 97.8 per 100,000 population for the most urban group to 172.1 per 100,000 population for the residents of rural, remote counties. Similarly, total mortality ranged from 18.1 per 100,000 population among residents of the most urban counties to 33.8 among residents of rural, remote counties. Prehospital mortality ranged from 10.0 to 27.7 traumatic brain injuries per 100,000 population. CONCLUSIONS: These results provide justification for expanding efforts to prevent traumatic brain injury to include the small, but high-risk group of residents in rural areas.

Epidemiology of traumatic brain injury in Johannesburg—II. Morbidity, mortality and etiology

Using the method described in Part I (p. 283), data on the epidemiology of traumatic brain injury (TBI) in Johannesburg are presented. The overall annual incidence of TBI is 316 per 100,000. Data for Africans and Whites show marked contrasts. Among Africans, incidence is 355/100,000, with a male-female ratio of 4.4, and 763/100.000 for males aged 25–44; for Whites, it is 109/100,000 overall, with a male-female ratio of 40.1, and 419/100,000 for men aged 15–24. The overall incidence of fatal TBI is 80/100,000, with a case fatality ratio of 0.20. Interpersonal violence accounts for 51% of nonfatal TBI among Africans, as against 10% for Whites, while motor vehicle accidents cause 27% of African nonfatal TBI and 63% among Whites. Some explanatory hypotheses for this race- and sex-specific skewing of the incidence and causes of TBI are developed.