Peroneal nerve reconstruction by using glycerol-preserved veins: histological and functional assessment in rats

PURPOSE: To compare the degree of neural regeneration in rats upon interposition of autologous nerve graft, autogenous vein, glycerol-preserved autogenous vein, and glycerol-preserved allogeneic vein using qualitative and quantitative histological analyses as well as functional assessments. METHODS: Peroneal nerves were reconstructed differently in four groups of animals. Functional assessments were performed pre- and postoperatively for a period of six weeks. After six weeks, the animals were sacrificed and histological evaluations were performed. RESULTS: Histological patterns of autogenous veins without preservation showed pronounced neoangiogenesis and extensive axonal rarefaction, as confirmed by axonal counting and functional assessments. Glycerol-preserved veins had results similar to the control. CONCLUSIONS: Glycerol-preserved autogenous or allogeneic veins showed similar results to autograft results. The autogenous vein (without preservation in glycerol) presented histological and functional outcomes statistically lower than other groups.(AU)

Endovascular treatment: balloon angioplasty versus nimodipine intra-arterial for medically refractory cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Cerebral vasospasm (CV) accounts significant morbimortality after aneurysmal subarachnoid hemorrhage. The objective of this study was to compare the clinical outcome of patients with CV treated by 2 endovascular procedures: intra-arterial nimodipine angioplasty (IANA) and balloon angioplasty (BA). Between 2008 and June 2011, we performed 22 IANA and 8 BA in 30 patients. The mean age was 44 years and 60% was female. In 17 patients, the treatment was clipping, whereas 13 underwent coil treatment. The CV was severe in 63%, moderate in 30%, and mild in 7%. Good outcome between 2 groups was similar (P = .36). The clinical outcome according to the subgroups of CV severity and modality treatment was equivalent (P = .22). Mortality at 3 months was 16% and 20% at 1 year. We did not find differences in the clinical outcome despite the fact that both techniques produce adequate angiographic resolution of CV.

Depresiones corticales propagadas y su posible rol en la fisiopatología del daño neuronal subsecuente a la hemorragia subaracnoidea / Cortical spreading depressions and their role in the pathophysiology of neuronal damage subsequent to aneurysmal subarachnoid hemorrhage

El vasoespasmo cerebral es la principal causa potencialmente tratable de mortalidad e incapacidad en pacientes que sufren hemorragia subaracnoidea aneurismática (HSA). Sin embargo, a la fecha no existe un tratamiento eficaz para el mismo. La reciente demostración de la falta de respuesta clínica a la reversión farmacológica del espasmo arterial a consecuencia de HSA ha obligado un replanteo de los fundamentos fisiopatológicos de los déficits neurológicos isquémicos tardíos (“delayed ischemic neurologic déficit”, DIND) a consecuencia de HSA, los cuales se creían en relación al espasmo arterial observado en pacientes con HSA. Desde la demostración de hallazgos electrocorticográficos de depresión cortical propagada (“cortical spreading depression”, CSD) en pacientes con HSA, un interés creciente se ha despertado respecto del rol de estos fenómenos en la fisiopatología de los DIND observados en pacientes con HSA. Cuando inducidas en un cerebro saludable, las CSD se asocian con un aumento del flujo sanguíneo cerebral, facilitando la entrega del cerebro de los sustratos energéticos necesarios. En un cerebro que ha sido lesionado, sin embargo, la CSD se asocia con una reducción en flujo sanguíneo cerebral, lo cual, en el contexto de un aumento de las necesidades de energía, conduce a la insuficiencia energética y la hipoxia, empeorando así el daño cerebral. Estas observaciones sugieren que el déficit de energía producida por la CSD es un factor clave en la patogénesis de los DIND observados a consecuencia de HSA. Este resumen detalla características sobresalientes de las CSD y su potencial relevancia en la fisiopatología del vasoespasmo.

Cerebral vasospasm is the leading potentially treatable cause of mortality and disability in patients with aneurysmatic subarachnoid hemorrhage (SAH). However, to date there is no effective treatment for this entity. The recently demonstrated lack of clinical response to pharmacologic reversal of arterial spasm as a result of SAH has spurred a reassessment of the pathophysiological concepts on delayed ischemic neurologic deficits (DIND) that follow SAH, which were long believed the effect of the arterial spasm observed in patients with SAH. Since the discovery of electrocorticographic cortical spreading depressions (CSD) in patients with SAH, increasing interest has been shown on the role of these phenomena in the pathophysiology of DIND observed in patients with HSA. When induced in a healthy brain, CSD are associated with an increase in cerebral blood flow by facilitating the delivery of the necessary energy substrates. In a brain that has been injured, however, CSD are associated with a reduction in cerebral blood flow, which, in the context of increased energy requirements leads to energy shortage and hypoxia, thus worsening brain damage. These observations suggest that the energetic deficit produced by the CSD is a key factor in the pathogenesis of DIND observed as a result of HSA. This review details striking characteristics of CSD and their potential relevance in the pathophysiology of vasospasm.

Magnesium sulfate: role as possible attenuating factor in vasospasm morbidity.

BACKGROUND: Among the many complications of SAH, one of the most important is vasospasm. Several treatment alternatives have been proposed for this condition, with far-from-ideal results being obtained. Magnesium sulfate recently returned to the scene (with still unproven benefit) as an adjuvant in the treatment of vasospasm. METHODS: Seventy-two patients diagnosed with SAH by aneurysm rupture were submitted to microsurgery craniotomy and subdivided in 2 groups. Group 1, formed by 48 patients, received prophylactic hypervolemic and hemodilution therapy in addition to nimodipine. Group 2, composed of 24 patients, received the same treatment of group 1 with the addition of magnesium sulfate in continuous infusion from 120 to 150 mg a day, keeping serum magnesium levels close to double normal values. RESULTS: Age was 49 +/- 12.6 years. Ratio of female to male was 3.16:1. Most patients were admitted in a Hunt-Hess grade 2 (46.4%) and Fisher grade 3 (52.8%). Anterior communicating artery aneurysms were the most common in location (38.8%). Both groups were compared, and there was no statistical difference related to age, sex, and Glasgow, Fisher, or Hunt-Hess admission grades. No statistical difference in vasospasm incidence was found between the two groups. However, in group 1, vasospasm was correlated with a longer hospitalization time (P = .0003), different from group 2, in which patients with vasospasm receiving magnesium sulfate required less hospitalization time. CONCLUSION: Magnesium did not seem to interfere in vasospasm frequency but apparently acted favorably in decreasing morbidity and length of hospital stay.