Wang, Huan

Abstract Emerging research on the long-term impact of concussions on athletes has allowed public recognition of the potentially devastating effects of these and other mild head injuries. Mild traumatic brain injury (mTBI) is a multifaceted disease for which management remains a clinical challenge. Recent pre-clinical and clinical data strongly suggest a destructive synergism between brain temperature elevation and mTBI; conversely, brain hypothermia, with its broader, pleiotropic effects, represents the most potent neuro-protectant in laboratory studies to date. Although well-established in selected clinical conditions, a systemic approach to accomplish regional hypothermia has failed to yield an effective treatment strategy in traumatic brain injury (TBI). Furthermore, although systemic hypothermia remains a potentially valid treatment strategy for moderate to severe TBIs, it is neither practical nor safe for mTBIs. Therefore, selective head-neck cooling may represent an ideal strategy to provide therapeutic benefits to the brain. Optimizing brain temperature management using a National Aeronautics and Space Administration (NASA) spacesuit spinoff head-neck cooling technology before and/or after mTBI in contact sports may represent a sensible, practical, and effective method to potentially enhance recover and minimize post-injury deficits. In this paper, we discuss and summarize the anatomical, physiological, preclinical, and clinical data concerning NASA spinoff head-neck cooling technology as a potential treatment for mTBIs, particularly in the context of contact sports.

Traumatic brain injury (TBI) is a global public health epidemic. In the US alone, more than 3 million people sustain a TBI annually. It is one of the most disabling injuries as it may cause motor and sensory deficits and lead to severe cognitive, emotional, and psychosocial impairment, crippling vital areas of higher functioning. Fueled by the recognition of TBI as the “signature injury” in our wounded soldiers in Iraq and Afghanistan, and its often devastating impact on athletes playing contact sports, interest in TBI and TBI research has increased dramatically. Unfortunately, despite increased awareness of its detrimental consequences, there has been little progress in developing effective TBI interventions. Recent evidence, however, strongly indicates that nutritional intervention may provide a unique opportunity to enhance the neuronal repair process after TBI. To date, two omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), have the most promising laboratory evidence for their neuro-restorative capacities in TBI. Although both animal models and human studies of brain injuries suggest they may provide benefits, there has been no clinical trial evaluating the effects of n-3 fatty acids on resilience to, or treatment, of TBI. This article reviews the known functions of n-3 fatty acids in the brain and their specific role in the cellular and biochemical pathways underlying neurotraumatic injury. We also highlight recent studies on the therapeutic impact of enhanced omega 3 intake in vivo , and how this may be a particularly promising approach to improving functional outcome in patients with TBI.

Object The purpose of this study was to determine the incidence of shunt infection in patients with subarachnoid hemorrhage (SAH) after converting an external ventricular drain (EVD) to a ventriculoperitoneal (VP) shunt using the existing EVD site. The second purpose was to assess the risk of shunt malfunction after converting the EVD to a permanent shunt irrespective of the cerebrospinal fluid (CSF) protein and red blood cell (RBC) counts. Methods Data obtained in 80 consecutive adult patients (18 men and 62 women, mean age 60.8 years, range 33–85 years) who underwent direct conversion of an EVD to a VP shunt for post-SAH hydrocephalus between August 2002 and March 2007 were retrospectively reviewed. In each patient, the existing EVD site was used to pass the proximal shunt catheter. In no patient was VP shunt insertion delayed based on preoperative RBC or protein counts. Results The mean period of external ventricular drainage before VP shunt placement was 14.1 days (range 3–45 days). No patient suffered ventriculitis. The mean perioperative CSF protein level was 124 mg/dl (range 17–516 mg/dl). The mean and median perioperative RBC values in CSF were 14,203 RBCs/mm3 and 4600 RBCs/mm3 (range 119–290,000/mm3), respectively. No patient was lost to follow-up. The mean follow-up duration was 24 months (range 2–53 months). Three patients (3.8%) had shunt malfunction related to obstruction of the shunt system after 15 days, 2 months, and 18 months, respectively. There were no shunt-related infections. No patient suffered a clinically significant hemorrhage from ventricular catheter placement after VP shunt insertion. Conclusions In adult patients with aneurysmal SAH, conversion of an EVD to a VP shunt can be safely done using the same EVD site. In this defined patient population, protein and RBC counts in the CSF do not seem to affect shunt survival adversely. Thus, conversion of an EVD to VP shunt should not be delayed because of an elevated protein or RBC count.