Intraventricular and subarachnoid basal cisterns neurocysticercosis: a comparative study between traditional treatment versus neuroendoscopic surgery.

OBJECTIVE: The purpose of this study was to evaluate the efficacy of traditional treatment and minimal invasive flexible endoscopy surgery (MIFNES) in the treatment of intraventricular and subarachnoid basal cisterns neurocysticercosis (NCC). METHODS: This was an observational comparative study of two independent series with a total of 140 patients with extremely severe forms of NCC from two different institutions. All 83 patients submitted for traditional treatment series received albendazole, and some of them received additionally praziquantel. Each cycle of both regimens lasted 4 weeks. The majority of these patients had at least one ventriculoperitoneal (VP) shunt. The rest 57 patients were submitted to the MIFNES treatment. The follow-up period was at least 6 months. RESULTS: In all patients of both series cysticercal cysts disappeared, became calcified, or were removed. Symptoms of 136 patients improved. Four patients died. The average in the quality of life measured using the Karnofsky scale improved from a mean of 52.22 and 52.44 at the beginning to 85.48 and 90.37 at 6 months (p < 0.003), in the traditional treatment and MIFNES series, respectively. From traditional treatment, almost all patients remained with at least one VP shunt, and from the MIFNES series only 12 patients. CONCLUSIONS: The authors postulate that MIFNES is a good alternative for the management of intraventricular and subarachnoid basal cisterns NCC because it allows removal of most of the parasites, rapid recovery of the patients, and removal and placement of shunt under direct vision when necessary. Traditional treatment is a second option where the MIFNES procedure is not available.

L-arginine reverses alterations in drug disposition induced by spinal cord injury by increasing hepatic blood flow.

High hepatic extraction drugs--such as phenacetin, methylprednisolone, and cyclosporine--exhibit an increased bioavailability after acute spinal cord injury (SCI) due to an impaired clearance. For these drugs, metabolic clearance depends on hepatic blood flow. Thus, it is possible that pharmacokinetic alterations can be reversed by increasing liver perfusion. Therefore, we evaluated the effect of L-arginine, a nitric oxide precursor, on the pharmacokinetics of a prototype drug with high hepatic extraction, and on hepatic microvascular blood flow (MVBF) after acute SCI. Pharmacokinetics of i.v. phenacetin was studied in rats 24 h after a severe T-5 spinal cord contusion; animals being pretreated with L-arginine 100 mg/kg i.v. or vehicle. MVBF was assessed under similar experimental conditions using laser Doppler flowmetry. SCI significantly altered phenacetin pharmacokinetics. Clearance was significantly reduced, resulting in a prolonged half-life and an increase in bioavailability, while volume of distribution was decreased. Pharmacokinetic alterations were reversed when injured rats were pretreated with L -arginine. It was also observed that L-arginine significantly increased hepatic MVBF in injured rats, notwithstanding it exhibited a limited effect on sham-injured animals. Our data hence suggest that L-arginine is able to reverse SCI-induced alterations in phenacetin pharmacokinetics due to an impaired hepatic MVBF, likely by increased nitric oxide synthesis leading to vasodilation. Further studies are warranted to examine the potential usefulness of nitric oxide supplementation in a clinical setting.

Lipid peroxidation by nitric oxide supplements after spinal cord injury: effect of antioxidants in rats.

To determine the extent to which exogenous nitric oxide (NO) might affect hemodynamics and/or increase oxidative damage after acute spinal cord (SC) injury, rats were submitted to SC contusion, and given a NO donor or NO precursor. Intravenous isosorbide dinitrate (10 microg/kg per min) or L-arginine (300 mg/kg per 23 h) showed a tendency to increase lipid peroxidation (LP), although without reaching significance compared to non-treated injured rats 24 h post-injury, and without affecting mean arterial pressure and heart rate importantly. LP due to injury and exogenous NO was significantly inhibited by the co-administration of a cocktail of antioxidants (12 mg/kg superoxide dismutase mimetic, 27000 U/kg catalase, and 12 mg/kg glutathione), but less effectively for the injury-L-arginine condition. These results demonstrate that in order to further test the potential neuroprotective effect of NO enhancing reagents after SC injury, antioxidants must be included in the treatment scheme.