Hydrocephalus following bilateral dumbbell-shaped c2 spinal neurofibromas resection and postoperative cervical pseudomeningocele in a patient with neurofibromatosis type 1: a case report.

Study Design Case report. Objective To present a rare case of hydrocephalus following bilateral dumbbell-shaped C2 spinal neurofibromas resection and postoperative cervical pseudomeningocele in a patient with neurofibromatosis type 1 (NF1). Methods The patient's clinical course is retrospectively reviewed. A 37-year-old man affected by NF1 referred to our department for progressive weakness of both lower extremities and gait disturbance. Radiological imaging showed bilateral dumbbell-shaped C2 spinal neurofibromas. After its resection, at the 1-month follow-up evaluation, the patient reported headache and nausea. A CT brain scan showed a postoperative cervical pseudomeningocele and an increase in the ventricular sizes, resulting in hydrocephalus. Results A ventriculoperitoneal shunting was performed using a programmable valve opening pressure set to 120 mmH20. After surgery, the patient's neurological status markedly improved. Conclusion Hydrocephalus must be considered a possible complication of cervical spine tumor resection.

Key role of uridine kinase and uridine phosphorylase in the homeostatic regulation of purine and pyrimidine salvage in brain.

Uridine, the major circulating pyrimidine nucleoside, participating in the regulation of a number of physiological processes, is readily uptaken into mammalian cells. The balance between anabolism and catabolism of intracellular uridine is maintained by uridine kinase, catalyzing the first step of UTP and CTP salvage synthesis, and uridine phosphorylase, catalyzing the first step of uridine degradation to beta-alanine in liver. In the present study we report that the two enzymes have an additional role in the homeostatic regulation of purine and pyrimidine metabolism in brain, which relies on the salvage synthesis of nucleotides from preformed nucleosides and nucleobases, rather than on the de novo synthesis from simple precursors. The experiments were performed in rat brain extracts and cultured human astrocytoma cells. The rationale of the reciprocal regulation of purine and pyrimidine salvage synthesis in brain stands (i) on the inhibition exerted by UTP and CTP, the final products of the pyrimidine salvage pathway, on uridine kinase and (ii) on the widely accepted idea that pyrimidine salvage occurs at the nucleoside level (mostly uridine), while purine salvage is a 5-phosphoribosyl-1-pyrophosphate (PRPP)-mediated process, occurring at the nucleobase level. Thus, at relatively low UTP and CTP level, uptaken uridine is mainly anabolized to uridine nucleotides. On the contrary, at relatively high UTP and CTP levels the inhibition of uridine kinase channels uridine towards phosphorolysis. The ribose-1-phosphate is then transformed into PRPP, which is used for purine salvage synthesis.

Analysis of RR variability in drug-resistant epilepsy patients chronically treated with vagus nerve stimulation.

Vagus nerve stimulation (VNS) has been suggested as an adjunctive treatment for drug-resistant epilepsy when surgery is inadvisable. The overall safety profile of VNS seems to be favorable as only minor adverse effects have been described. The purpose of this study was to determine if cardiac vagal tone is eventually modified by short- and long-term VNS. The effects of short- and long-term VNS were evaluated in seven subjects with intractable epilepsy. Autonomic cardiac function has been carried out by means of a 24-h analysis of RR variability at baseline (t(0)), 1 month (t(1), short-term VNS) and 36 months after VNS initiation (t(2), long-term VNS). Frequency- and time-domain parameters were calculated. Periodic cardiological and neurological evaluations were performed.Clinically relevant cardiac effects were not observed throughout the study. Despite the limited number of patients and the variety of data among them, for all the patients, a common trend towards a nocturnal decrease in the high-frequency (HF) component of the spectrum was observed after long-term VNS (mean+/-S.D.: 40+/-18 normalized units (nu) at t(0), 38+/-17 nu at t(1), 18+/-10 nu at t(2); p<0.05 of t(2) vs. either t(0) or t(1)). The day-to-night changes in the power of low-frequency (LF) and HF components were significantly blunted after long-term VNS (LF day-to-night change: +16+/-13 nu at t(0) and +15+/-8 nu at t(1) vs. +3+/-13 nu at t(2), p<0.02; HF day-to-night change: -18+/-13 nu at t(0) and -13+/-11 nu at t(1) vs. +3+/-12 nu at t(2), p<0.003). No significant changes were observed with regard to the time-domain parameters of the heart rate variability. Throughout the neurological follow-up, one subject became seizure-free, three experienced a seizure reduction of >50%, two patients of <50% and one had no changes in his seizure frequency. Our findings suggest that long-term VNS might slightly affect cardiac autonomic function with a reduction of the HF component of the spectrum during night and a flattening of sympathovagal circadian changes, not inducing, however, clinically relevant cardiac side effects.

Daytime vigilance and quality of life in epileptic patients treated with vagus nerve stimulation.

OBJECTIVES: The goal of this study was to determine if vagus nerve stimulation (VNS) has any effect on daytime vigilance and perceived sense of well-being. METHODS: Multiple Sleep Latency Tests (MSLTs) were performed and visual reaction times (VRTs) obtained in eight epileptic patients before and during treatment with VNS. Prior to VNS initiation patients' baseline MSLT and VRT scores were recorded. Six months after VNS was initiated, treatment MSLT and VRT scores were obtained. A group of 12 age-matched healthy subjects served as controls. In addition, there was a global evaluation of well-being at baseline and during a follow-up of 6 months. RESULTS: As expected, patients evaluated both at baseline and during VNS showed more sleepiness than controls. In this group, baseline sleep latencies on the MSLT were significantly shorter, while VRT latencies were significantly longer than those of controls. After 6 months of VNS, MSLT scores in the eight patients did not change significantly with respect to baseline. However, if the single patient treated with relatively high stimulus intensities (1.75 mA) was excluded from the group and only the seven patients treated with low stimulus intensities (

A simulation model for analysing brain structure deformations.

Recent developments of medical software applications--from the simulation to the planning of surgical operations--have revealed the need for modelling human tissues and organs, not only from a geometric point of view but also from a physical one, i.e. soft tissues, rigid body, viscoelasticity, etc. This has given rise to the term 'deformable objects', which refers to objects with a morphology, a physical and a mechanical behaviour of their own and that reflects their natural properties. In this paper, we propose a model, based upon physical laws, suitable for the realistic manipulation of geometric reconstructions of volumetric data taken from MR and CT scans. In particular, a physically based model of the brain is presented that is able to simulate the evolution of different nature pathological intra-cranial phenomena such as haemorrhages, neoplasm, haematoma, etc and to describe the consequences that are caused by their volume expansions and the influences they have on the anatomical and neuro-functional structures of the brain.