Articles: traumatic-brain-injuries.
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Frontiers in neurology · Jan 2015
ReviewVascular and inflammatory factors in the pathophysiology of blast-induced brain injury.
Blast-related traumatic brain injury (TBI) has received much recent attention because of its frequency in the conflicts in Iraq and Afghanistan. This renewed interest has led to a rapid expansion of clinical and animal studies related to blast. In humans, high-level blast exposure is associated with a prominent hemorrhagic component. ⋯ At low levels of blast exposure, a microvascular pathology has been observed in the presence of an otherwise normal brain parenchyma, suggesting that the vasculature may be selectively vulnerable to blast injury. Chronic immune activation in brain following vascular injury may lead to neurobehavioral changes in the absence of direct neuronal pathology. Strategies aimed at preventing or reversing vascular damage or modulating the immune response may improve the chronic neuropsychiatric symptoms associated with blast-related TBI.
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The central autonomic nervous system (CAN) is a multifaceted, richly connected neural network incorporating the hypothalamus, its descending tracts through the brainstem, the insular cortex and down into the spinal cord. All levels of the CAN are susceptible to injury following traumatic brain injury (TBI), whether from focal or diffuse injury. ⋯ Subarachnoid hemorrhage (SAH), a common complication following TBI, also has predictable effects on autonomic control that can be understood with reference to spontaneous SAH literature. Finally, paroxysmal sympathetic hyperactivity (PSH), a syndrome incorporating episodes of heightened sympathetic drive and motor overactivity following minor stimulation, is discussed as an example of what happens when central inhibitory control of spinal cord autonomics is impaired.
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Neuropsych Dis Treat · Jan 2015
ReviewTreatments for traumatic brain injury with emphasis on transcranial near-infrared laser phototherapy.
Traumatic brain injury (TBI) is a growing health concern affecting civilians and military personnel. In this review, treatments for the chronic TBI patient are discussed, including pharmaceuticals, nutraceuticals, cognitive therapy, and hyperbaric oxygen therapy. All available literature suggests a marginal benefit with prolonged treatment courses. ⋯ Symptoms were monitored by depression scales and a novel patient diary system specifically designed for this study. NIR light in the power range of 10-15 W at 810 nm and 980 nm can safely and effectively treat chronic symptoms of TBI. The clinical benefit and effects of infrared phototherapy on mitochondrial function and secondary molecular events are discussed in the context of adequate radiant energy penetration.
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Brain injury : [BI] · Jan 2015
ReviewOutcomes from mild and moderate traumatic brain injuries among children and adolescents: A systematic review of studies from 2008-2013.
To systematically review existing empirical evidence concerning neuropsychological, psychosocial and academic outcomes following mild and moderate TBI during childhood and adolescence. ⋯ The results suggest that not all children with mild or moderate TBI recover without long-term problems. Few studies followed children and adolescents with mild TBIs for extended periods of time, although it is clinically important to monitor patients over time.
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Neuropsych Dis Treat · Jan 2015
ReviewPituitary dysfunction following traumatic brain injury: clinical perspectives.
Traumatic brain injury (TBI) is a well recognized public health problem worldwide. TBI has previously been considered as a rare cause of hypopituitarism, but an increased prevalence of neuroendocrine dysfunction in patients with TBI has been reported during the last 15 years in most of the retrospective and prospective studies. Based on data in the current literature, approximately 15%-20% of TBI patients develop chronic hypopituitarism, which clearly suggests that TBI-induced hypopituitarism is frequent in contrast with previous assumptions. This review summarizes the current data on TBI-induced hypopituitarism and briefly discusses some clinical perspectives on post-traumatic anterior pituitary hormone deficiency.