Articles: traumatic-brain-injuries.
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Appl Neuropsychol Adult · Jan 2015
Cognitive and self-reported psychological outcomes of blast-induced mild traumatic brain injury in veterans: a preliminary study.
The increased use of explosives in combat has resulted in a large number of returning veterans suffering from blast-related mild traumatic brain injury (mTBI) and self-reported complications. It remains unclear whether this increase in self-reported difficulties is unique to the blast mechanism or stressful preinjury environment and whether cognitive-functioning deficits correspond with these difficulties in the postacute phase. This study examined the relationship between cognitive performance and self-reported psychological and somatic symptoms of blast-related mTBI compared with civilian mTBI, independent of comorbid posttraumatic stress disorder (PTSD) symptoms. ⋯ Overall, preliminary results suggest that in the postacute phase, subjective complaints related to blast-related mTBI do not covary with objective cognitive performance. Additionally, cognitive outcomes from blast-related mTBI were similar to those of civilian forms of mTBI. Future studies should identify the cognitive and self-reported sequelae of blast-related mTBI independent of comorbid PTSD in a larger sample of veterans.
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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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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.