Articles: traumatic-brain-injuries.
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Brain injury : [BI] · Jan 2015
Case ReportsInfluence of intrathecal baclofen on the level of consciousness and mental functions after extremely severe traumatic brain injury: brief report.
Whenever oral treatment or botulinum toxin injections fail to control severe spasticity, a trial with intrathecal baclofen is recommended no earlier than 1 year after brain injury. When irreversible contractures are to be avoided, such a trial might be done earlier. Some have briefly reported cognitive modifications with this treatment. ⋯ Intrathecal baclofen should be considered within the first year after brain injury whenever spasticity does not respond to medication. ITB lessens the degree of spasticity which in turn facilitates care and, thus, has the potential to limit contractures. After severe brain injury, this treatment might trigger recovery from altered states of consciousness, improve cognition and facilitate rehabilitation.
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Acta Radiol Short Rep · Jan 2015
Multimodal MR imaging of acute and subacute experimental traumatic brain injury: Time course and correlation with cerebral energy metabolites.
Traumatic brain injury (TBI) is one of the leading causes of death and permanent disability world-wide. The predominant cause of death after TBI is brain edema which can be quantified by non-invasive diffusion-weighted magnetic resonance imaging (DWI). ⋯ The partial ATP reduction was interpreted to be partially caused by a loss of neurons in parallel with transient dilution of the regional ATP concentration by pronounced vasogenic edema. The normalization of energy metabolism after 7 days was likely due to infiltrating glia and not to recovery. The MRI combined with metabolite measurement further improves the understanding and evaluation of brain damages after TBI.
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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.
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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.
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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.