Neurocritical care
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Recent advances in medicine, intensive care and diagnostic imaging modalities have led to a pronounced reduction in deaths and disability resulting from traumatic brain injury. However, there are not sufficient findings to evaluate and quantify the severity of the initial and secondary processes destructive and therefore there are not effective therapeutic measures to effectively predict the outcome. ⋯ Usually, the levels of these proteins increase following brain injury and are found in increasing concentrations in the cerebrospinal fluid depending on the injury magnitude, and can also be found in blood stream because of a compromised blood-brain barrier. In this review, we examine the various factors that must be taken into account in the search for a reliable non-invasive biomarkers in traumatic brain injury and their role in the diagnosis and outcome evaluation.
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Review Case Reports
Reversible obstructive hydrocephalus from hypertensive encephalopathy.
Diffuse edema involving the posterior fossa may be seen with hypertensive encephalopathy and has rarely been reported to cause hydrocephalus. We present three such cases and review the literature to better delineate this uniquely reversible syndrome. ⋯ It is imperative to recognize such cases where hypertension causes edema within the posterior fossa resulting in secondary hydrocephalus. Focusing management on lowering blood pressure avoids unnecessary or prolonged CSF diversion.
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Altered mental status and more subtle cognitive and personality changes after traumatic brain injury (TBI) are pervasive problems in patients who survive initial injury. MRI is not necessarily part of the diagnostic evaluation of these patients. ⋯ Injury to the splenium of the corpus callosum due to trauma may be extensive and can cause significant neurologic deficits. MRI is important in the diagnostic evaluation of patients with cognitive changes after TBI.
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Review
Cerebral blood flow, brain tissue oxygen, and metabolic effects of decompressive craniectomy.
Decompressive craniectomy (DC) is used for patients with traumatic brain injury (TBI), malignant edema from middle cerebral artery infarction, aneurysmal subarachnoid hemorrhage, and non-traumatic intracerebral or cerebellar hemorrhage. The objective of the procedure is to relieve intractable intracranial hypertension and/or to prevent or reverse cerebral herniation. Decompressive craniectomy has been shown to decrease mortality in selected patients with large hemispheric infarction and to control intracranial pressure in addition to improving pressure-volume compensatory reserve after TBI. ⋯ There are several unresolved controversies regarding optimal candidate selection, timing, technique, and post-operative management and complications. The nature and temporal progression of alterations in cerebral blood flow, brain tissue oxygen, and microdialysis markers have only recently been researched. Elucidating the pathophysiology of pressure-flow and cerebral hemodynamic consequences of DC could assist in optimizing clinical decision making and further defining the role of decompressive craniectomy.