Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2011
Anatomic study in cadaver of the motor branch of the musculocutaneous nerve.
This study of 80 cadavers demonstrates that the anatomic position of the motor branch of the musculocutaneous nerve with respect to that of the sensitive branch of the same nerve is lateral in more than 88% of cases in humans.The distance from plexus to the separation into the motor and sensitive fascicles was 8-9 cm long.Given the lateral position of the motor component of the musculocutaneous nerve, the nerves that are going to be used to neurotize this area can be directed so as to increase the efficacy of the results for the flexor function of the arm. ⋯ If the nerves that are to be used for neurotization of the musculacutaneous nerve are directly taken to the lateral fascicle of that nerve, which is generally the motor component, the treatment should be effective and should avoid the loss of motor axons resulting from anastomosing to the sensitive fascicle.
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Acta Neurochir. Suppl. · Jan 2011
The gamut of blood flow responses coupled to spreading depolarization in rat and human brain: from hyperemia to prolonged ischemia.
Cortical spreading depolarizations (SD) have been shown to occur frequently in patients with aneurysmal subarachnoid hemorrhage (SAH) and are associated with delayed ischemic brain damage. In animal models the link between SD and cell damage is the microvascular spasm coupled to the passage of SDs, resulting in spreading ischemia. Here we compared the hemodynamic changes induced by SD between human and rat cerebral cortex. ⋯ The spectrum ranged from normal hyperemic responses to prolonged cortical spreading ischemia with intermediate forms characterized by biphasic (hypoemic-hyperemic) responses. The bandwidths of rCBF responses were comparable and the relative response magnitudes of hypo- and hyperperfusion phases did not differ significantly between rats and humans. The correspondence of the rCBF response spectrum to SD between human and animal brain underscores the importance of animal models to learn more about the mechanisms underlying the early and delayed pathological sequelae of SAH.
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Acta Neurochir. Suppl. · Jan 2011
Isoflurane preconditioning affords functional neuroprotection in a murine model of intracerebral hemorrhage.
Exposure to isoflurane gas prior to neurological injury, known as anesthetic preconditioning, has been shown to provide neuroprotective benefits in animal models of ischemic stroke. Given the common mediators of cellular injury in ischemic and hemorrhagic stroke, we hypothesize that isoflurane preconditioning will provide neurological protection in intracerebral hemorrhage (ICH). ⋯ These results demonstrate the early functional neuroprotective effects of anesthetic preconditioning in ICH and suggest that methods of preconditioning that afford protection in ischemia may also provide protection in ICH.
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Acta Neurochir. Suppl. · Jan 2011
Matrix metalloproteinase 9 inhibition reduces early brain injury in cortex after subarachnoid hemorrhage.
This study investigated the role of matrix metalloproteinase-9 (MMP-9) in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Sprague-Dawley male rats (n=30) between 250 and 300 g were used. SAH was produced by injecting autologous arterial blood into the prechiasmatic cistern. ⋯ Laminin, the substrate of MMP-9, was decreased at 24h after SAH, and SB-3CT prevented laminin degradation. The number of TUNEL-positive neurons in cerebral cortex was increased after SAH and decreased by SB-3CT (P<0.01). MMP-9 may be involved in EBI after SAH and inhibition of MMP-9 may reduce EBI in cerebral cortex.
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Acta Neurochir. Suppl. · Jan 2011
Treatment with ginsenoside rb1, a component of panax ginseng, provides neuroprotection in rats subjected to subarachnoid hemorrhage-induced brain injury.
recent trials have shown Ginsenoside Rb1 (GRb1), an active component of a well known Chinese medicine Panax Ginseng, plays a significant role in improving the complications seen after an ischemic brain event. In the present study, we investigated the use of GRb1 as a treatment modality to reduce brain edema, reduce arterial vasospasm, and improve neurobehavioral function after subarachnoid hemorrhage-induced brain injury (SAH) in rats. ⋯ the results of the study suggest that GRb1 treatment reduces brain edema, improves neurobehavioral function, and blocks vasculature thickening and spasm after SAH in rats. Given the novelty of the study, further research will be needed to confirm the benefits of treatment and mechanisms behind neuroprotection.