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  • Author or Editor: Alfredo Conti x
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Roberto C. Heros

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Francesco Tomasello, Alfredo Conti, Salvatore Cardali and Filippo Flavio Angileri

Object

Surgical treatment of parasagittal meningiomas is challenging. Preserving the venous outflow is the key point, but this may preclude radical resection. Different surgical strategies have been proposed. To contribute to the debate on the optimal strategy for treating these tumors, a single-institutional, single-surgeon series of patients with parasagittal meningiomas was analyzed and the available literature reviewed.

Methods

Clinical charts of patients with parasagittal meningioma, managed at the University of Messina between 1988 and 2008, were retrospectively reviewed. A microsurgical resection, the goal of which was to preserve the venous outflow, was performed. Only if the superior sagittal sinus (SSS) was angiographically occluded, but if alternative venous outflow was clearly recognized, was the tumor resected, together with the sinus without further flow restoration. A MEDLINE review of the literature published between 1955 and 2011 was performed.

Results

Long-term follow-up (mean 80 months) data obtained in 67 patients with meningiomas involving the SSS were analyzed. The recurrence rate was 10.4%; the morbidity and mortality rates were 10.4% and 4.5%, respectively. The authors identified in the literature 19 relevant studies on this issue, and based on their review of the literature, there is no evidence that aggressive management offers an advantage in terms of recurrence rate.

Conclusions

Analysis of the data obtained in the 67 patients confirmed good outcome and long-term tumor control following a surgical strategy aimed to preserve venous outflow. These findings and the results of the authors' analysis of the literature emphasize that the goal of radical tumor resection should be balanced by an awareness of the increased surgical risk attendant on aggressive management of the SSS and bridging veins.

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Domenico G. Iacopino, Alfredo Conti, Calogero Battaglia, Clotilde Siliotti, Tullio Lucanto, Letterio B. Santamaria and Francesco Tomasello

Object. Nitrous oxide has an adverse effect on cerebrovascular hemodynamics. Increased intracranial pressure, cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and reduced autoregulation indices have been reported, but their magnitudes are still being debated.

This study was designed to evaluate the effect of N2O on CBF and autoregulatory indexes during N2O—sevoflurane anesthesia in a prospective randomized controlled series of patients.

Methods. Two groups of 20 patients were studied on the basis of the use of N2O in the anesthetic gas mixture. The transient hyperemic response test, which relies on transcranial Doppler ultrasound techniques, was used to assess cerebral hemodynamics.

The time-averaged mean flow velocity, considered to be an index of actual CBF, increased significantly (p < 0.001) after introduction of N2O. The hyperemic response, considered as the index of autoregulatory potential, decreased significantly after introduction of N2O into the gas mixture (p < 0.001).

Conclusions. The increase in CBF and the reduction in autoregulatory indices suggest caution in using N2O during sevoflurane anesthesia, especially in patients with reduced autoregulatory reserve and during neurosurgical interventions. Transcranial Doppler ultrasonography is an efficacious method to evaluate the effects of anesthetic agents on CBF.

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Francesco Tomasello, Filippo F. Angileri, Salvatore Cardali and Alfredo Conti

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Alfredo Conti, M'Hammed Aguennouz, Domenico La Torre, Salvatore Cardali, Filippo Flavio Angileri, Catia Buemi, Chiara Tomasello, Domenico Gerardo Iacopino, Domenico D'Avella, Giuseppe Vita and Francesco Tomasello

Object. Tumor necrosis factor receptor (TNFR)—associated factors (TRAFs) are a recently established group of proteins involved in the intracellular signaling of the TNFR superfamily members. The TRAFs have been implicated in promoting cell survival through the activation of transcription factor nuclear factor (NF)—κB. The authors investigated the expression of NF-κB, caspase 3, TRAF1, TRAF2, and TRAF-associated NF-κB activator/TRAF—interacting protein (TANK/I-TRAF), a regulator of TRAF activity, in human gliomas.

Methods. Tumor samples were obtained in 27 adult patients harboring seven low-grade gliomas, nine anaplastic astrocytomas, and 11 glioblastomas multiforme. The NF-κB activation was analyzed using the electrophoresis mobility shift assay; TRAF1, TRAF2, TANK/I-TRAF, and caspase 3 expression were studied using Western blot analysis.

Upregulated NF-κB DNA—binding activity, compared with that in normal brain tissue, was detected in all tumor samples (p = 0.002). The level of NF-κB activity showed some correlation with World Health Organization tumor grades (p = 0.01), even though variable activity levels were demonstrated in relation to tissue heterogeneity, which resulted in a substantial number of outliers in the quantitative analysis. Increased levels of TRAF1, TRAF2, and TANK/I-TRAF were expressed in astrocytomas compared with levels in normal brain tissue (p = 0.02, 0.006, and 0.01, respectively).

Conclusions. Data in this study confirm the upregulation of NF-κB in gliomas and reveal a correlation between levels of this transcription factor and tumor grade. A constitutive expression of TRAF1, TRAF2, and TANK/I-TRAF in human gliomas was documented. These proteins are involved in the intracellular signal transduction of the TNFR superfamily and in the control of NF-κB expression and its antiapoptotic activity.

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Giovanni Grasso, Marcello Passalacqua, Alessandra Sfacteria, Alfredo Conti, Antonio Morabito, Giuseppe Mazzullo, Gionata De Vico, Michele Buemi, Battesimo Macrì and Francesco Tomasello

Object. Results of recent studies indicate that erythropoietin (EPO) produces a neuroprotective effect on experimental subarachnoid hemorrhage (SAH). It has been reported that S-100 protein levels increase in cerebrospinal fluid (CSF) after SAH, providing a highly prognostic indication of unfavorable outcome. This study was conducted to validate further the findings of S-100 protein as an index of brain damage and to assess whether treatment with recombinant human EPO (rhEPO) would limit the increase of S-100 protein level in CSF following experimental SAH.

Methods. Thirty-two rabbits were each assigned to one of four groups: Group 1, control; Group 2, SAH; Group 3, SAH plus placebo; and Group 4, SAH plus rhEPO (each group consisted of eight rabbits). The rhEPO and placebo were administered to the rabbits after SAH had been induced, and S-100 protein levels in the CSF of these animals were measured at 24, 48, and 72 hours after the experimental procedure. In each group of animals levels of S-100 protein were compared with the mortality rate, neurological outcome, and neuronal ischemic damage. High S-100 protein levels were found in rabbits in Groups 2 and 3, which exhibited poor neurological status and harbored a high number of damaged cortical neurons. Favorable neurological outcome and significant reductions in total numbers of damaged neurons were observed in animals in Group 4 in which there were significantly lower S-100 protein concentrations compared with animals in Groups 2 and 3 (p < 0.001).

Conclusions. The results of this study support the concept that determination of the S-100 protein level in CSF has prognostic value after SAH. The findings also confirm that rhEPO acts as a neuroprotective agent during experimental SAH.