Articles: traumatic-brain-injuries.
-
Experimental neurology · Jan 2015
Emergence of cognitive deficits after mild traumatic brain injury due to hyperthermia.
Mild elevations in core temperature can occur in individuals involved in strenuous activities that are risky for potentially sustaining a mild traumatic brain injury (mTBI) or concussion. Recently, we have discovered that mild elevations in brain temperature can significantly aggravate the histopathological consequences of mTBI. However, whether this exacerbation of brain pathology translates into behavioral deficits is unknown. ⋯ These results indicate that brain temperature is an important variable for mTBI outcome and that mildly elevated temperatures at the time of injury result in persistent cognitive deficits. Importantly, cooling to normothermia after mTBI prevents the development of long-term cognitive deficits caused by hyperthermia. Reducing temperature to normothermic levels soon after mTBI represents a rational approach to potentially mitigate the long-term consequences of mTBI.
-
Stud Health Technol Inform · Jan 2015
The Prognostic Scale CRASH in the Treatment of Children with Severe Traumatic Brain Injury.
The aim of the present study was to assess the effectiveness and validity of prognostic scale CRASH which is calculated using on-line resources and which may serve as a decision support for physicians in treating severe traumatic brain injury (TBI) in children. This retrospective study was conducted using clinical and physiological data of 168 hospitalized pediatric patients with severe traumatic brain injury (GCS score less than or equal to 8). CRASH scale was used for calculating the severity of patients' state and for prognosing death outcomes at 14 days and at 6 months using the on-line resource. ⋯ The study has also shown that the scale has a satisfactory calibration ability in the option of 14 days with CT (χ2 equal 8.7 and p-value equal to 0.368). Calibration ability for other options was unsatisfactory. Thus, CRASH scale with CT scan has turned to be useful for assessing death outcomes at 14 days in children with severe TBI.
-
Frontiers in neurology · Jan 2015
ReviewCathepsin B is a New Drug Target for Traumatic Brain Injury Therapeutics: Evidence for E64d as a Promising Lead Drug Candidate.
There is currently no therapeutic drug treatment for traumatic brain injury (TBI) despite decades of experimental clinical trials. This may be because the mechanistic pathways for improving TBI outcomes have yet to be identified and exploited. As such, there remains a need to seek out new molecular targets and their drug candidates to find new treatments for TBI. ⋯ Significantly, chemical inhibitors of cathepsin B are effective for improving deficits in TBI and related injuries including ischemia, cerebral bleeding, cerebral aneurysm, edema, pain, infection, rheumatoid arthritis, epilepsy, Huntington's disease, multiple sclerosis, and Alzheimer's disease. The inhibitor E64d is unique among cathepsin B inhibitors in being the only compound to have demonstrated oral efficacy in a TBI model and prior safe use in man and as such it is an excellent tool compound for preclinical testing and clinical compound development. These data support the conclusion that drug development of cathepsin B inhibitors for TBI treatment should be accelerated.
-
Brain injury : [BI] · Jan 2015
Multicenter Study Comparative StudyNeuroanatomical basis of paroxysmal sympathetic hyperactivity: a diffusion tensor imaging analysis.
Paroxysmal sympathetic hyperactivity (PSH) is observed in a sub-set of patients with moderate-to-severe traumatic brain injury (TBI). The neuroanatomical basis of PSH is poorly understood. It is hypothesized that PSH is linked to changes in connectivity within the central autonomic network. ⋯ Disconnection involving the posterior corpus callosum and of the posterior limb of the internal capsule may play a role in the pathogenesis or expression of PSH.
-
Frontiers in neurology · Jan 2015
ReviewThe Complexity of Biomechanics Causing Primary Blast-Induced Traumatic Brain Injury: A Review of Potential Mechanisms.
Primary blast-induced traumatic brain injury (bTBI) is a prevalent battlefield injury in recent conflicts, yet biomechanical mechanisms of bTBI remain unclear. Elucidating specific biomechanical mechanisms is essential to developing animal models for testing candidate therapies and for improving protective equipment. Three hypothetical mechanisms of primary bTBI have received the most attention. ⋯ These three mechanisms may not be mutually exclusive, and quantifying exposure thresholds (for blasts of a given duration) is essential for determining which mechanisms may be contributing for a level of blast exposure. Progress has been hindered by experimental designs, which do not effectively expose animal models to a single mechanism and by over-reliance on poorly validated computational models. The path forward should be predictive validation of computational models by quantitative confirmation with blast experiments in animal models, human cadavers, and biofidelic human surrogates over a range of relevant blast magnitudes and durations coupled with experimental designs, which isolate a single injury mechanism.