Traumatic brain injury clinical practice guidelines and best practices from the VA state of the art conference.

Management of symptoms following traumatic brain injury (TBI) can be complex and remains a high priority for Department of Defense (DoD) and Department of Veteran Affairs (VA). Concurrently, awareness of TBI in the public has increased. VA convened a State of the Art (SOTA) Conference to identify priorities for future research and promote best practices for TBI care. Scientific evidence of effective management of symptoms following TBI is expanding, and this evidence has been synthesized into Clinical Practice Guidelines (CPGs) and Clinical Practice Recommendations (CPRs). Knowledge gaps still exist and research efforts to address these gaps should include leveraging large administrative data sets and existing registries to determine effective treatments, investigate compliance of existing clinical care with CPGs and study limitations to determine modifiable vs. non-modifiable core tenants of the evidence-based treatments.

Neuralgic amyotrophy manifested by severe axillary mononeuropathy limited only to the anterior branch.

INTRODUCTION: In this study we describe a case demonstrating clinical, radiographic, electrophysiologic, and surgical evidence of a restricted but severe anterior branch axillary nerve mononeuropathy due to neuralgic amyotrophy (NA). METHODS: On each diagnostic modality there was severe involvement of the anterior and lateral deltoid muscle with sparing of the posterior deltoid and teres minor muscles and cutaneous innervation to the skin overlying the lateral shoulder. RESULTS: No structural etiologies were discovered during surgical exploration. CONCLUSIONS: This case provides another unique manifestation of NA and augments the theory of selective fascicular vulnerability.

Mild traumatic brain injury screening, diagnosis, and treatment.

The majority of combat-related traumatic brain injury (TBI) within the U.S. Armed Forces is mild TBI (mTBI). This article focuses specifically on the screening, diagnosis, and treatment aspects of mTBI within the military community. Aggressive screening measures were instituted in 2006 to ensure that the mTBI population is identified and treated. Screenings occur in-theater, outside the contiguous United States, and in-garrison. We discuss specific screening procedures at each screening setting. Current diagnosis of mTBI is based upon self-report or through witnesses to the event. TBI severity is determined by specific Department of Defense criteria. Abundant clinician resources are available for mTBI in the military health care setting. Education resources for both the patient and the clinician are discussed in detail. An evidence-based clinical practice guideline for the care of mTBI was created through collaborative efforts of the DoD and the U.S. Department of Veterans Affairs. Although symptoms following mTBI generally resolve with time, active treatment is centered on symptom management, supervised rest, recovery, and patient education. Medical specialty care, ancillary services, and other therapeutic services may be required.

Explosive-driven double-blast exposure: molecular, histopathological, and behavioral consequences.

Traumatic brain injury generated by blast may induce long-term neurological and psychiatric sequelae. We aimed to identify molecular, histopathological, and behavioral changes in rats 2 weeks after explosive-driven double-blast exposure. Rats received two 30-psi (~ 207-kPa) blasts 24 h apart or were handled identically without blast. All rats were behaviorally assessed over 2 weeks. At Day 15, rats were euthanized, and brains removed. Brains were dissected into frontal cortex, hippocampus, cerebellum, and brainstem. Western blotting was performed to measure levels of total-Tau, phosphorylated-Tau (pTau), amyloid precursor protein (APP), GFAP, Iba1, αII-spectrin, and spectrin breakdown products (SBDP). Kinases and phosphatases, correlated with tau phosphorylation were also measured. Immunohistochemistry for pTau, APP, GFAP, and Iba1 was performed. pTau protein level was greater in the hippocampus, cerebellum, and brainstem and APP protein level was greater in cerebellum of blast vs control rats (p < 0.05). GFAP, Iba1, αII-spectrin, and SBDP remained unchanged. No immunohistochemical or neurobehavioral changes were observed. The dissociation between increased pTau and APP in different regions in the absence of neurobehavioral changes 2 weeks after double blast exposure is a relevant finding, consistent with human data showing that battlefield blasts might be associated with molecular changes before signs of neurological and psychiatric disorders manifest.

MRI in Management of Mild TBI/Concussion in the Deployed Setting.

Magnetic resonance imaging (MRI) has specific limitations in theater and has unique requirements for its safe use with patients which require additional technician training and strict adherence to MRI-specific safety protocols. Neuroimaging is recommended for the evaluation of service members with clinical red flags new onset or persistent or worsening symptoms, and individuals whose recovery is not progressing as anticipated. This article is a brief discussion of when MRI is appropriate.

Blast-related traumatic brain injury.

A bomb blast may cause the full severity range of traumatic brain injury (TBI), from mild concussion to severe, penetrating injury. The pathophysiology of blast-related TBI is distinctive, with injury magnitude dependent on several factors, including blast energy and distance from the blast epicentre. The prevalence of blast-related mild TBI in modern war zones has varied widely, but detection is optimised by battlefield assessment of concussion and follow-up screening of all personnel with potential concussive events. There is substantial overlap between post-concussive syndrome and post-traumatic stress disorder, and blast-related mild TBI seems to increase the risk of post-traumatic stress disorder. Post-concussive syndrome, post-traumatic stress disorder, and chronic pain are a clinical triad in this patient group. Persistent impairment after blast-related mild TBI might be largely attributable to psychological factors, although a causative link between repeated mild TBIs caused by blasts and chronic traumatic encephalopathy has not been established. The application of advanced neuroimaging and the identification of specific molecular biomarkers in serum for diagnosis and prognosis are rapidly advancing, and might help to further categorise these injuries.