Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2007
Intrathecal baclofen therapy: indications, pharmacology, surgical implant, and efficacy.
Intrathecal baclofen (ITB) therapy is an option for those in whom predominantly lower extremity spasticity is severe, problematic, and intractable to oral doses of medications and/or focal treatment. When delivered to the lumbar area, ITB avoids high concentrations from reaching the brain (4:1 ratio lumbar to brain cisterns). A screening test dose is done prior to implanting the pump via a lumbar puncture with 50 microg baclofen, working up to 100 microg if necessary. ⋯ Catheter complications are reduced by using a shallow-angle paramedian oblique insertion to the spine, and meticulous anchoring of the catheter. Threading the catheter to T6/7 rather than the traditional T10/11 can allow upper limb relief also. Long term efficacy is excellent, although catheter complications are frequent. and if not recognized and treated, can lead to significant effects of withdrawal of baclofen.
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Nerve tubes seeded with cultured Schwann cells have become a promising alternative to nerve autografts. However, the functional results of these bioartificial cellular grafts remain to be improved. To imitate the three-dimensional structure of peripheral nerves, we designed a Schwann cell-seeded intrinsic framework within a semipermeable biodegradable collagen nerve tube (Integra). ⋯ We conclude that the unique three-dimensional net allowed the settlement of Schwann cells onto the biodegradable filaments, which can be used as "artificial Bünger bands". With further refinements of the "artificial Bünger bands" and Schwann cell cultures there should be improved functional and histological results in the "bioartificial nerve graft" group.
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Acta Neurochir. Suppl. · Jan 2006
Randomized Controlled Trial Multicenter StudyDecompressive craniectomy in traumatic brain injury: the randomized multicenter RESCUEicp study (www.RESCUEicp.com).
The RESCUEicp (Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of intracranial pressure) study has been established to determine whether decompressive craniectomy has a role in the management of patients with traumatic brain injury and raised intracranial pressure that does not respond to initial treatment measures. We describe the concept of decompressive craniectomy in traumatic brain injury and the rationale and protocol of the RESCUEicp study.
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Acta Neurochir. Suppl. · Jan 2006
Modulation of AQP4 expression by the protein kinase C activator, phorbol myristate acetate, decreases ischemia-induced brain edema.
The protein kinase C activator, phorbol 12-myristate 13-acetate (PMA), is known to interact with aquaporin-4 (AQP4), a water-selective transporting protein abundant in astrocytes and ependymal cells, that has been found to decrease osmotically-induced swelling. The purpose of this study was to examine whether PMA given at different time points following focal ischemia induced by middle cerebral artery occlusion (MCAO) reduces brain edema by AQP4 modulation. Male Sprague-Dawley rats were randomly assigned to sham procedure, vehicle, or PMA infusion (230 microg/kg), starting either 60 minutes before, or 30 or 60 minutes after MCAO (each group n = 12). ⋯ PMA treatment significantly reduced brain water content concentration in the infarcted area when started before or 30 minutes post-occlusion (p < 0.001, p = 0.022) and prevented the subsequent sodium shift (p < 0.05). Furthermore, PMA reduced ischemia-induced AQP4 up-regulation (p < 0.05). Attenuation of the ischemia-induced AQP4 up-regulation by PMA suggests that the reduction in brain edema formation following PMA treatment was at least in part mediated by AQP4 modulation.
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Acta Neurochir. Suppl. · Jan 2006
Bolus tracer delivery measured by MRI confirms edema without blood-brain barrier permeability in diffuse traumatic brain injury.
Previous studies have shown that edema formation after diffuse traumatic brain injury (TBI) with secondary insult is cytotoxic and not vasogenic. This assumption is based on observations of reduced apparent diffusion coefficient (ADC) and lack of significant accumulation of intravascular tracer in brain tissue. However, ADC reduction does not exclude vasogenic edema, and intravascular tracer can only accumulate when it reaches the tissue and is not perfusion limited. This study aims to confirm tissue delivery of intravascular tracer and lack of BBB opening during a phase of rapid brain swelling after diffuse TBI. ⋯ Progressive cerebral edema formation after diffuse TBI occurred during ADC reduction and without continued BBB permeability. Tissue delivery of Gd-DTPA was confirmed, verifying that lack of tracer accumulation is due to an intact BBB and not to limited perfusion.