Traumatic Brain Injury as Frequent Cause of Hypopituitarism and Growth Hormone Deficiency: Epidemiology, Diagnosis, and Treatment

Problem/Condition Traumatic brain injury (TBI) has short- and long-term adverse clinical outcomes, including death and disability. TBI can be caused by a number of principal mechanisms, including motor-vehicle crashes, falls, and assaults. This report describes the estimated incidence of TBI-related emergency department (ED) visits, hospitalizations, and deaths during 2013 and makes comparisons to similar estimates from 2007. Reporting Period 2007 and 2013. Description of System State-based administrative health care data were used to calculate estimates of TBI-related ED visits and hospitalizations by principal mechanism of injury, age group, sex, and injury intent. Categories of injury intent included unintentional (motor-vehicle crashes, falls, being struck by or against an object, mechanism unspecified), intentional (self-harm and assault/homicide), and undetermined intent. These health records come from the Healthcare Cost and Utilization Project’s National Emergency Department Sample and National Inpatient Sample. TBI-related death analyses used CDC multiple-cause-of-death public-use data files, which contain death certificate data from all 50 states and the District of Columbia. Results In 2013, a total of approximately 2.8 million TBI-related ED visits, hospitalizations, and deaths (TBI-EDHDs) occurred in the United States. This consisted of approximately 2.5 million TBI-related ED visits, approximately 282,000 TBI-related hospitalizations, and approximately 56,000 TBI-related deaths. TBIs were diagnosed in nearly 2.8 million (1.9%) of the approximately 149 million total injury- and noninjury-related EDHDs that occurred in the United States during 2013. Rates of TBI-EDHDs varied by age, with the highest rates observed among persons aged ≥75 years (2,232.2 per 100,000 population), 0–4 years (1,591.5), and 15–24 years (1,080.7). Overall, males had higher age-adjusted rates of TBI-EDHDs (959.0) compared with females (810.8) and the most common principal mechanisms of injury for all age groups included falls (413.2, age-adjusted), being struck by or against an object (142.1, age-adjusted), and motor-vehicle crashes (121.7, age-adjusted). The age-adjusted rate of ED visits was higher in 2013 (787.1) versus 2007 (534.4), with fall-related TBIs among persons aged ≥75 years accounting for 17.9% of the increase in the number of TBI-related ED visits. The number and rate of TBI-related hospitalizations also increased among persons aged ≥75 years (from 356.9 in 2007 to 454.4 in 2013), primarily because of falls. Whereas motor-vehicle crashes were the leading cause of TBI-related deaths in 2007 in both number and rate, in 2013, intentional self-harm was the leading cause in number and rate. The overall age-adjusted rate of TBI-related deaths for all ages decreased from 17.9 in 2007 to 17.0 in 2013; however, age-adjusted TBI-related death rates attributable to falls increased from 3.8 in 2007 to 4.5 in 2013, primarily among older adults. Although the age-adjusted rate of TBI-related deaths attributable to motor-vehicle crashes decreased from 5.0 in 2007 to 3.4 in 2013, the age-adjusted rate of TBI-related ED visits attributable to motor-vehicle crashes increased from 83.8 in 2007 to 99.5 in 2013. The age-adjusted rate of TBI-related hospitalizations attributable to motor-vehicle crashes decreased from 23.5 in 2007 to 18.8 in 2013. Interpretation Progress has been made to prevent motor-vehicle crashes, resulting in a decrease in the number of TBI-related hospitalizations and deaths from 2007 to 2013. However, during the same time, the number and rate of older adult fall-related TBIs have increased substantially. Although considerable public interest has focused on sports-related concussion in youth, the findings in this report suggest that TBIs attributable to older adult falls, many of which result in hospitalization and death, should receive public health attention. Public Health Actions The increase in the number of fall-related TBIs in older adults suggests an urgent need to enhance fall-prevention efforts in that population. Multiple effective interventions have been identified, and CDC has developed the STEADI initiative (Stopping Elderly Accidents Deaths and Injuries) as a comprehensive strategy that incorporates empirically supported clinical guidelines and scientifically tested interventions to help primary care providers address their patients’ fall risk through the identification of modifiable risk factors and implementation of effective interventions (e.g., exercise, medication management, and Vitamin D supplementation).

Traumatic brain injury (TBI) is a leading cause of morbidity and disability, with a considerable socioeconomic burden. Heterogeneity of pathoanatomical subtypes and diversity in the pathogenesis and extent of injury contribute to differences in the course and outcome of TBI. Following the primary injury, extensive and lasting damage is sustained through a complex cascade of events referred to as "secondary injury." Neuroinflammation is proposed as an important manipulable aspect of secondary injury in animal and human studies. Because neuroinflammation can be detrimental or beneficial, before developing immunomodulatory therapies, it is necessary to better understand the timing and complexity of the immune responses that follow TBI. With a rapidly increasing body of literature, there is a need for a clear summary of TBI neuroimmunology. This review presents our current understanding of the immune response to TBI in a chronological and compartment-based manner, highlighting early changes in gene expression and initial signaling pathways that lead to activation of innate and adaptive immunity. Based on recent advances in our understanding of innate immune cell activation, we propose a new paradigm to study innate immune cells following TBI that moves away from the existing M1/M2 classification of activation states toward a stimulus- and disease-specific understanding of polarization state based on transcriptomic and proteomic profiling.