Military personnel with chronic symptoms following blast traumatic brain injury have differential expression of neuronal recovery and epidermal growth factor receptor genes.

The objective of this article is to report the proportion of soldiers in a Brigade Combat Team (BCT) with at least 1 clinician-confirmed deployment-acquired traumatic brain injury (TBI) and to describe the nature of sequelae associated with such injuries. Members of an Army unit (n = 3973) that served in Iraq were screened for history of TBI. Those reporting an injury (n = 1292) were further evaluated regarding sequelae. Of the injuries suffered, 907 were TBIs and 385 were other types of injury. The majority of TBIs sustained were mild. Postdeployment, responses to the Warrior Administered Retrospective Casualty Assessment Tool (WARCAT) facilitated clinical interviews regarding injury history and associated somatic (ie, headache, dizziness, balance) and neuropsychiatric symptoms (ie, irritability, memory). Traumatic brain injury diagnosis was based on the American Congress of Rehabilitation Medicine mild TBI criteria, which requires an injury event followed by an alteration in consciousness. A total of 22.8% of soldiers in a BCT returning from Iraq had clinician-confirmed TBI. Those with TBI were significantly more likely to recall somatic and/or neuropsychiatric symptoms immediately postinjury and endorse symptoms at follow-up than were soldiers without a history of deployment-related TBI. A total of 33.4% of soldiers with TBI reported 3 or more symptoms immediately postinjury compared with 7.5% at postdeployment. For soldiers injured without TBI, rates of 3 or more symptoms postinjury and postdeployment were 2.9% and 2.3%, respectively. In those with TBI, headache and dizziness were most frequently reported postinjury, with irritability and memory problems persisting and presenting over time. Following deployment to Iraq, a clinician-confirmed TBI history was identified in 22.8% of soldiers from a BCT. Those with TBI were significantly more likely to report postinjury and postdeployment somatic and/or neuropsychiatric symptoms than those without this injury history. Overall, symptom endorsement decreased over time.

The present study provides additional data on the psychometric properties of the 30-item Inventory of Depressive Symptomatology (IDS) and of the recently developed Quick Inventory of Depressive Symptomatology (QIDS), a brief 16-item symptom severity rating scale that was derived from the longer form. Both the IDS and QIDS are available in matched clinician-rated (IDS-C30; QIDS-C16) and self-report (IDS-SR30; QIDS-SR16) formats. The patient samples included 544 out-patients with major depressive disorder (MDD) and 402 out-patients with bipolar disorder (BD) drawn from 19 regionally and ethnicically diverse clinics as part of the Texas Medication Algorithm Project (TMAP). Psychometric analyses including sensitivity to change with treatment were conducted. Internal consistencies (Cronbach's alpha) ranged from 0.81 to 0.94 for all four scales (QIDS-C16, QIDS-SR16, IDS-C30 and IDS-SR30) in both MDD and BD patients. Sad mood, involvement, energy, concentration and self-outlook had the highest item-total correlations among patients with MDD and BD across all four scales. QIDS-SR16 and IDS-SR30 total scores were highly correlated among patients with MDD at exit (c = 0.83). QIDS-C16 and IDS-C30 total scores were also highly correlated among patients with MDD (c = 0.82) and patients with BD (c = 0.81). The IDS-SR30, IDS-C30, QIDS-SR16, and QIDS-C16 were equivalently sensitive to symptom change, indicating high concurrent validity for all four scales. High concurrent validity was also documented based on the SF-12 Mental Health Summary score for the population divided in quintiles based on their IDS or QIDS score. The QIDS-SR16 and QIDS-C16, as well as the longer 30-item versions, have highly acceptable psychometric properties and are treatment sensitive measures of symptom severity in depression.

Traumatic brain injury (TBI) has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inflammatory responses accompany TBI. A series of inflammatory cytokines and chemokines spreads to normal brain areas juxtaposed to the core impacted tissue. Among the repertoire of immune cells involved, microglia is a key player in propagating inflammation to tissues neighboring the core site of injury. Neuroprotective drug trials in TBI have failed, likely due to their sole focus on abrogating neuronal cell death and ignoring the microglia response despite these inflammatory cells’ detrimental effects on the brain. Another relevant point to consider is the veracity of results of animal experiments due to deficiencies in experimental design, such as incomplete or inadequate method description, data misinterpretation, and reporting may introduce bias and give false-positive results. Thus, scientific publications should follow strict guidelines that include randomization, blinding, sample-size estimation, and accurate handling of all data (Landis et al., 2012). A prolonged state of inflammation after brain injury may linger for years and predispose patients to develop other neurological disorders, such as Alzheimer’s disease. TBI patients display progressive and long-lasting impairments in their physical, cognitive, behavioral, and social performance. Here, we discuss inflammatory mechanisms that accompany TBI in an effort to increase our understanding of the dynamic pathological condition as the disease evolves over time and begin to translate these findings for defining new and existing inflammation-based biomarkers and treatments for TBI.