Articles: traumatic-brain-injuries.
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Barbiturate coma therapy (BCT) is a choice treatment for refractory intracranial hypertension after all surgical or medical managements have failed to control the intracranial pressure (ICP). It helps to reduce cerebral blood flow, cerebral metabolic rate of oxygen consumption and ICP. ⋯ One of the underreported, but life-threatening complications is refractory hypokalemia, which can lead to subsequent rebound hyperkalemia after sudden cessation. We report our experience of managing unusual complication of refractory hypokalemia during BCT with thiopentone in postdecompressive craniectomy patient.
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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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Despite the debilitating consequences and the widespread prevalence of brain trauma insults including spinal cord injury (SCI) and traumatic brain injury (TBI), there are currently few effective therapies for most of brain trauma sequelae. As a consequence, there has been a major quest for identifying better diagnostic tools, predictive models, and directed neurotherapeutic strategies in assessing brain trauma. Among the hallmark features of brain injury pathology is the central nervous systems' (CNS) abnormal activation of the immune response post-injury. ⋯ It is being suggested that there may be an analogy of CNS autoantibodies secretion with the pathophysiology of autoimmune diseases, in which case, understanding and defining the role of autoantibodies in brain injury paradigm (SCI and TBI) may provide a realistic prospect for the development of effective neurotherapy. In this work, we will discuss the accumulating evidence about the appearance of autoantibodies following brain injury insults. Furthermore, we will provide perspectives on their potential roles as pathological components and as candidate markers for detecting and assessing CNS injury.
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Comparative Study
In vivo leukocyte-mediated brain microcirculatory inflammation: a comparison of osmotherapies and progesterone in severe traumatic brain injury.
Mannitol, hypertonic saline, and progesterone may blunt leukocyte recruitment after traumatic brain injury (TBI). We hypothesized that progesterone reduces pericontusional recruitment of leukocytes to a greater extent than either osmotherapy a day after TBI. ⋯ Leukocyte recruitment to injured brain is lowest with mannitol administration. How different agents alter progression of secondary brain injury will require further evaluation in humans.