The incidence of ARDS and associated mortality in severe TBI using the Berlin definition.

BACKGROUND: The incidence of adult respiratory distress syndrome (ARDS) in severe traumatic brain injury (TBI) is poorly reported. Recently, a new definition for ARDS was proposed, the Berlin definition. The percentage of patients represented by TBI in the Berlin criteria study is limited. This study describes the incidence and associated mortality of ARDS in TBI patients. METHODS: The study was an analysis of the safety of erythropoietin administration and transfusion threshold on the incidence of ARDS in severe TBI patients. Three reviewers independently assessed all patients enrolled in the study for acute lung injury/ARDS using the Berlin and the American-European Consensus Conference (AECC) definitions. A Cox proportional hazards model was used to assess the relationship between ARDS and mortality and 6-month Glasgow Outcome Scale (GOS) score. RESULTS: Two hundred patients were enrolled in the study. Of the patients, 21% (41 of 200) and 26% (52 of 200) developed ARDS using the AECC and Berlin definitions, respectively, with a median time of 3 days (interquartile range, 3) after injury. ARDS by either definition was associated with increased mortality (p = 0.04) but not with differences in functional outcome as measured by the GOS score at 6 months. Adjusted analysis using the Berlin criteria showed an increased mortality associated with ADS (p = 0.01). CONCLUSION: Severe TBI is associated with an incidence of ARDS ranging from 20% to 25%. The incidence is comparable between the Berlin and AECC definitions. ARDS is associated with increased mortality in severe TBI patients, but further studies are needed to validate these findings. LEVEL OF EVIDENCE: Epidemiologic study, level II.

Human traumatic brain injury induces autoantibody response against glial fibrillary acidic protein and its breakdown products.

The role of systemic autoimmunity in human traumatic brain injury (TBI) and other forms of brain injuries is recognized but not well understood. In this study, a systematic investigation was performed to identify serum autoantibody responses to brain-specific proteins after TBI in humans. TBI autoantibodies showed predominant immunoreactivity against a cluster of bands from 38-50 kDa on human brain immunoblots, which were identified as GFAP and GFAP breakdown products. GFAP autoantibody levels increased by 7 days after injury, and were of the IgG subtype predominantly. Results from in vitro tests and rat TBI experiments also indicated that calpain was responsible for removing the amino and carboxyl termini of GFAP to yield a 38 kDa fragment. Additionally, TBI autoantibody staining co-localized with GFAP in injured rat brain and in primary rat astrocytes. These results suggest that GFAP breakdown products persist within degenerating astrocytes in the brain. Anti-GFAP autoantibody also can enter living astroglia cells in culture and its presence appears to compromise glial cell health. TBI patients showed an average 3.77 fold increase in anti-GFAP autoantibody levels from early (0-1 days) to late (7-10 days) times post injury. Changes in autoantibody levels were negatively correlated with outcome as measured by GOS-E score at 6 months, suggesting that TBI patients with greater anti-GFAP immune-responses had worse outcomes. Due to the long lasting nature of IgG, a test to detect anti-GFAP autoantibodies is likely to prolong the temporal window for assessment of brain damage in human patients.

Arthur L. Benton, Ph.D.: pioneer, colleague, mentor, and friend.

Arthur Benton, 97, died in Glenview, IL on December 27, 2006. He was born October 16, 1909 in New York City. He received his B.A. and M.A. degrees from Oberlin College, where Raymond Stetson was his mentor, and his Ph.D. in Psychology from Columbia University in 1935 under the mentorship of Carney Landis of the New York State Psychiatric Institute. Benton completed his training as a psychologist at the Payne Whitney Psychiatric Clinic of New York Hospital. Early in 1941, he volunteered for service in the United States Navy and was commissioned as a lieutenant in the medical department. His active duty lasted until 1945, followed by many years of service in the United States Navy Reserve, retiring at the rank of Captain. During his assignment at the San Diego Naval Hospital, Benton worked closely with neurologist Morris Bender and examined servicemen who had sustained penetrating brain wounds during combat. The experience of assessing servicemen with brain injury and Bender's influence led Benton to develop the Visual Retention Test, which still bears his name and continues to be widely used in clinical neuropsychological assessment.

Intelligence, parental depression, and behavior adaptability in deaf children being considered for cochlear implantation.

Cognitive ability and behavioral adaptability are distinct, yet related, constructs that can impact childhood development. Both are often reduced in deaf children of hearing parents who do not provide sufficient language and communication access. Additionally, parental depression is commonly observed due to parent-child communication difficulties that can lead to parents' feelings of inadequacy and frustration. We sought to assess whether adaptive behavior in deaf children was associated with nonverbal intelligence and parental depression. Parents of precochlear implant patients seen for neuropsychological assessment were administered the Parenting Stress Index and Vineland Behavior Adaptive Scales to obtain measures of parental distress and child's behavioral adaptability. Precochlear implant patients' cognitive functioning was assessed via the Mullen Scales of Early Learning or the Leiter International Performance Scale-Revised, depending on the child's age at the time of testing. Regardless of age or neurological status, the deaf child's adaptive behavior consistently showed a strong relationship with intelligence. Moderate correlation between parental depression and the child's adaptive behavior was observed only in the younger group. The relationship between parental depression and communication subscale was moderated by intelligence for deaf children without neurological complications. The findings provide important implications for promoting family-centered interventions with early communication and language development.