Journal of neurosurgery
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Journal of neurosurgery · Oct 2002
Surgical treatment of spinal deformities associated with neurofibromatosis type 1. Report of 12 cases.
In 10 to 50% of cases with neurofibromatosis, skeletal disorders are present, mainly as various deformities of the spine. These deformities can be divided into dystrophic and nondystrophic groups depending on the absence or presence of bone dystrophy. The nondystrophic curves are highly similar to those in idiopathic scoliosis, whereas the dystrophic curves are manifested early and, by progressing inexorably, may lead to neurological symptoms. In this article the authors report on a series of 12 patients (11 with dystrophic and one with nondystrophic deformities) who underwent surgical treatment. ⋯ The surgical treatment of dystrophic curves always included 360 degrees fusion and the use of a tibial corticocancellous graft, which must be placed on the concave side of the curve in the frontal plane, the graft thereby providing biomechanical support.
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Journal of neurosurgery · Oct 2002
Successful and safe perfusion of the primate brainstem: in vivo magnetic resonance imaging of macromolecular distribution during infusion.
Intrinsic disease processes of the brainstem (gliomas, neurodegenerative disease, and others) have remained difficult or impossible to treat effectively because of limited drug penetration across the blood-brainstem barrier with conventional delivery methods. The authors used convection-enhanced delivery (CED) of a macromolecular tracer visible on magnetic resonance (MR) imaging to examine the utility of CED for safe perfusion of the brainstem. ⋯ First, CED can be used to perfuse the brainstem safely and effectively with macromolecules. Second, a large-molecular-weight imaging tracer can be used successfully to deliver, monitor in vivo, and control the distribution of small- and large-molecular-weight putative therapeutic agents for treatment of intrinsic brainstem processes.
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Journal of neurosurgery · Oct 2002
Reversal of attenuation of cerebrovascular reactivity to hypercapnia by a nitric oxide donor after controlled cortical impact in a rat model of traumatic brain injury.
Traumatic brain injury (TBI) attenuates the cerebral vasodilation to hypercapnia. Cortical spreading depression (CSD) also transiently reduces hypercapnic vasodilation. The authors sought to determine whether the CSD elicited by a controlled cortical impact (CCI) injury masks the true effect of TBI on hypercapnic vasodilation, and whether a nitric oxide (NO) donor can reverse the attenuation of hypercapnic vasodilation following CCI. ⋯ The authors conclude that CSD elicited by CCI can mask the true effect of TBI on hypercapnic vasodilation for at least 30 minutes. Exogenous NO, but not papaverine, can reverse the attenuation of cerebrovascular reactivity to CO2 caused by TBI. This result supports the hypothesis that NO production is reduced after TBI and that the NO donor has a potential beneficial role in the clinical management of head injury.