Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Jan 2018
ReviewMedusa's Head: The Complement System in Traumatic Brain and Spinal Cord Injury.
Traumatic brain injury (TBI) and spinal cord injury (SCI) are critical medical conditions and a public health problem for which limited therapeutic options are available. The complement cascade is activated after TBI and SCI, and the resulting effects have been investigated in gene-knockout and pharmacological models. ⋯ The role of upstream classical, alternative, or extrinsic complement activation cascades remains unclear. Although several issues remain to be investigated, current evidence supports the investigation of a number of complement-targeting agents targeting C3 or C5, such as eculizumab, for repurposing in TBI and SCI treatment.
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We aim to formulate evidence-based recommendations to assist physicians decision-making in the assessment and management of children younger than 16 years presenting to the emergency department (ED) following a blunt head trauma with no suspicion of non-accidental injury. ⋯ Recommendations to guide physicians practice when assessing children presenting to the ED following blunt head trauma are reported in both summary and extensive format in the guideline document.
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The high rates of traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) diagnoses encountered in recent years by the United States Veterans Affairs Healthcare System have increased public awareness and research investigation into these conditions. In this review, we analyze the neural mechanisms underlying the TBI/PTSD comorbidity. TBI and PTSD present with common neuropsychiatric symptoms including anxiety, irritability, insomnia, personality changes, and memory problems, and this overlap complicates diagnostic differentiation. ⋯ These disturbances produce neuronal death and degeneration, axonal injury, and dendritic spine dysregulation and changes in neuronal morphology. In laboratory studies, various forms of pharmacological or psychological treatments are capable of reversing these detrimental processes and promoting axonal repair, dendritic remodeling, and neurocircuitry reorganization, resulting in behavioral and cognitive functional enhancements. Based on these mechanisms, novel neurorestorative therapeutics using anti-inflammatory, antioxidant, and anticonvulsant agents may promote better outcomes for comorbid TBI and PTSD.
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Brain injury : [BI] · Jan 2018
ReviewPrognostic value of neuron-specific enolase (NSE) for prediction of post-concussion symptoms following a mild traumatic brain injury: a systematic review.
This systematic review aimed to determine the prognostic value of neuron-specific enolase (NSE) to predict post-concussion symptoms following mild traumatic brain injury (TBI). ⋯ Early NSE serum level is not a strong independent predictor of post-concussion symptoms following mild TBI.
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Neurosci Biobehav Rev · Jan 2018
ReviewGlymphatic system disruption as a mediator of brain trauma and chronic traumatic encephalopathy.
Traumatic brain injury (TBI) is an increasingly important issue among veterans, athletes and the general public. Difficulties with sleep onset and maintenance are among the most commonly reported symptoms following injury, and sleep debt is associated with increased accumulation of beta amyloid (Aβ) and phosphorylated tau (p-tau) in the interstitial space. Recent research into the glymphatic system, a lymphatic-like metabolic clearance mechanism in the central nervous system (CNS) which relies on cerebrospinal fluid (CSF), interstitial fluid (ISF), and astrocytic processes, shows that clearance is potentiated during sleep. ⋯ Long-term consequences of chronic dysfunction within this system in the context of repetitive brain trauma and insomnia have not been established, but potentially provide one link in the explanatory chain connecting repetitive TBI with later neurodegeneration. Current research has shown p-tau deposition in perivascular spaces and along interstitial pathways in chronic traumatic encephalopathy (CTE), pathways related to glymphatic flow; these are the main channels by which metabolic waste is cleared. This review addresses possible links between mTBI-related damage to glymphatic functioning and physiological changes found in CTE, and proposes a model for the mediating role of sleep disruption in increasing the risk for developing CTE-related pathology and subsequent clinical symptoms following repetitive brain trauma.