Journal of neurosurgery
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Journal of neurosurgery · May 2003
ReviewSystematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage.
There is uncertainty about the efficacy of hypertension, hypervolemia, and hemodilution (triple-H) therapy in reducing the occurrence of delayed ischemic neurological deficits (DINDs) and death after subarachnoid hemorrhage. The authors therefore conducted a systematic review to evaluate the efficacy of triple-H prevention in decreasing the rate of clinical vasospasm, DINDs, and death. ⋯ The paucity of information and important limitations in the design of the studies analyzed preclude evaluation of the efficacy of triple-H prevention and formulation of any recommendations regarding its use for the prevention of cerebral vasospasm.
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Journal of neurosurgery · May 2003
Review Case ReportsRapid development of Chiari I malformation in an infant with Seckel syndrome and craniosynostosis. Case report and review of the literature.
To illustrate the rapidity with which a child can develop a severe, symptomatic Chiari I malformation, the authors present the case of a 3-month-old infant with Seckel syndrome (microcephaly, micrognathia, craniosynostosis, and multiple other abnormalities) and posterior sagittal and bilateral lambdoid synostosis. The infant underwent magnetic resonance (MR) imaging shortly after birth; the initial image demonstrated the cerebellar tonsils in the posterior fossa, with no herniation. He subsequently developed severe apneic episodes and bradycardia; repeated MR imaging at 3 months demonstrated severe tonsillar herniation with compression of the brainstem. ⋯ In most cases, a lumbar cerebrospinal fluid (CSF) diversion had been performed. This patient developed a severely symptomatic Chiari I malformation during a 3-month period. These reports illustrate that the Chiari I malformation can develop rapidly in the face of increased intracranial pressure, craniosynostosis, and spinal CSF diversion.
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Journal of neurosurgery · May 2003
Lack of improvement in cerebral metabolism after hyperoxia in severe head injury: a microdialysis study.
The authors investigated the effects of hyperoxia on brain tissue PO2 and on glucose metabolism in cerebral and adipose tissue after traumatic brain injury (TBI). ⋯ Hyperoxia slightly reduced lactate levels in brain tissue after TBI. The estimated redox status of the cells, however, did not change and cerebral O2 extraction seemed to be reduced. These data indicate that oxidation of glucose was not improved by hyperoxia in cerebral and adipose tissue, and might even be impaired.
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Journal of neurosurgery · May 2003
Case Reports Comparative StudyMethionine positron emission tomography of recurrent metastatic brain tumor and radiation necrosis after stereotactic radiosurgery: is a differential diagnosis possible?
In this study the authors examined how to differentiate radiation necrosis from recurrent metastatic brain tumor following stereotactic radiosurgery by using positron emission tomography (PET) with L-[methyl-11C]methionine (MET). ⋯ The use of MET-PET scanning is a sensitive and accurate technique for differentiating between metastatic brain tumor recurrence and radiation necrosis following stereotactic radiosurgery. This study reveals important information for creating strategies to treat postradiation reactions.
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Journal of neurosurgery · May 2003
Edema after intracerebral hemorrhage: correlations with coagulation parameters and treatment.
Development of edema is known to contribute to poor outcome after spontaneous intracerebral hemorrhage (ICH). Recent research has identified thrombin as a key mediator in the development of edema in animal models; however, little has been published correlating the coagulation cascade and edema in humans. ⋯ The authors propose that factors released from activated platelets at the site of hemorrhage, for example vascular endothelial growth factor, may interact with thrombin to increase vascular permeability and contribute to the development of edema.