Articles: traumatic-brain-injuries.
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J Anaesthesiol Clin Pharmacol · Jul 2014
ReviewCurrent concepts of optimal cerebral perfusion pressure in traumatic brain injury.
Traumatic brain injury (TBI) consists of varied pathophysiological consequences and alteration of intracranial dynamics, reduction of the cerebral blood flow and oxygenation. In the past decade more emphasis has been directed towards optimizing cerebral perfusion pressure (CPP) in patients who have suffered TBI. Injured brain may show signs of ischemia if CPP remains below 50 mmHg and raising the CPP above 60 mmHg may avoid cerebral oxygen desaturation. ⋯ Brain monitoring techniques such as jugular venous oximetry, monitoring of brain tissue oxygen tension (PbrO2), and cerebral microdialysis provide complementary and specific information that permits the selection of the optimal CPP. This review highlights the rationale for use CPP directed therapies and neuromonitoring to identify optimal CPP of head injured patients. The article also reviews the evidence provided by various clinical trials regarding optimal CPP and their application in the management of head injured patients.
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Experimental neurobiology · Jun 2014
ReviewDelayed and prolonged local brain hypothermia combined with decompressive craniectomy: a novel therapeutic strategy that modulates glial dynamics.
Hypothermia is considered a useful intervention for limiting pathophysiological changes after brain injury. Local hypothermia is a relatively safe and convenient intervention that circumvents many of the complications associated with systemic hypothermia. However, successful hypothermia treatment requires careful consideration of several factors including its practicality, feasibility, and associated risks. ⋯ The data show that the protective effects of therapeutic hypothermia, which mainly result from the modulation of inflammatory glial dynamics, are limited. We argue that decompressive craniectomy can be used to overcome the limitations of local brain hypothermia without causing histological abnormalities or other detrimental effects to the cooled area. Therefore, delayed and prolonged local brain hypothermia at the site of craniectomy is a promising intervention that may prove effective in the clinical setting.
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Traumatic brain injury (TBI) is recognized as an important risk factor for the long-term cognitive health of military personnel, particularly in light of growing evidence that TBI increases risk for Alzheimer's disease and other dementias. In this article, we review the neurocognitive and neuropathologic changes after TBI with particular focus on the potential risk for cognitive decline across the life span in military service members. Implications for monitoring and surveillance of cognition in the aging military population are discussed. Additional studies are needed to clarify the factors that increase risk for later life cognitive decline, define the mechanistic link between these factors and dementia, and provide empirically supported interventions to mitigate the impact of TBI on cognition across the life span.
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Traumatic brain injury (TBI) is a significant public health concern. On average, 1.7 million persons sustain a TBI annually, and about 5.3 million Americans are living with a TBI-related disability. As the leading cause of death and disability in persons under 45 years old, there is a need for developing evidence-based interventions to reduce morbidity from this injury. ⋯ The cascade of molecular and cellular changes after TBI involves plasticity in many different neurochemical systems, which represent putative targets for neurotherapeutic interventions. Accordingly, a successful TBI treatment may have to simultaneously attenuate many injury factors. The purpose of this review is to highlight four promising nutritional intervention options that have been identified-omega-3, zinc, vitamin D, and glutamine-and to provide an up-to-date summary regarding their apparent efficacy for affecting TBI.
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Mild traumatic brain injury (mTBI) includes concussion, subconcussion, and most exposures to explosive blast from improvised explosive devices. mTBI is the most common traumatic brain injury affecting military personnel; however, it is the most difficult to diagnose and the least well understood. It is also recognized that some mTBIs have persistent, and sometimes progressive, long-term debilitating effects. Increasing evidence suggests that a single traumatic brain injury can produce long-term gray and white matter atrophy, precipitate or accelerate age-related neurodegeneration, and increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease. ⋯ Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus; septal abnormalities; and abnormal deposits of hyperphosphorylated tau as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy has clinical and pathological features that overlap with postconcussion syndrome and posttraumatic stress disorder, suggesting that the three disorders might share some biological underpinnings.