Reactive oxygen species (ROS) represent reactive products belonging to the partial reduction of oxygen. It has been reported that ROS are involved in different signaling pathways to control cellular stability. Under normal conditions, the correct function of redox systems leads to the prevention of cell oxidative damage. When ROS exceed the antioxidant defense system, cellular stress occurs. The cellular redox impairment is strictly related to tumorigenesis. Tumor cells, through the generation of hydrogen peroxide, tend to the alteration of cell cycle phases and, finally to cancer progression. In adults, the most common form of primary malignant brain tumors is represented by gliomas. The gliomagenesis is characterized by numerous molecular processes all characterized by an altered production of growth factor receptors. The difficulty to treat brain cancer depends on several biological mechanisms such as failure of drug delivery through the blood-brain barrier, tumor response to chemotherapy, and intrinsic resistance of tumor cells. Understanding the mechanisms of ROS action could allow the formulation of new therapeutic protocols to treat brain gliomas.

An increase in blood-brain barrier (BBB) permeability after subarachnoid haemorrhage (SAH) has been described in humans and has been correlated with delayed cerebral ischemia and poor clinical outcome. Few studies examined in the laboratory the relationship between SAH and BBB, with contrasting results due to limitations in experimental probes adopted and in timing of observation. The aim of this study was to quantify the time-course of BBB changes after experimental SAH. Groups of eight rats received injections of 400 microl of autologous arterial blood into the cisterna magna. BBB was assessed 6, 12, 24, 36, 48, 60, and 72 hours after SAH and in sham-operated animals separately for cerebral cortex, i.e. frontal, temporal, parietal, occipital, subcortical gray matter (Caudate-Putamen-Thalamus), cerebellar cortex and nuclei, and brain stem by a spectrophotofluorimetric evaluation of Evans Blue dye extravasation. As compared to sham-operated controls, SAH determined a significant BBB permeability change beginning 36 hours after SAH, peaking at 48 hours, and normalizing on day 3. This study provides a quantitative description of the temporal progression and recovery of BBB dysfunction after SAH. These results have implications for the management of aneurysm patients and for assessing the rationale and the therapeutic window of new pharmacological approaches.

No abstract

No abstract

Mutism is an infrequent and transitory complication observed following posterior fossa surgery. Patients become mute in the immediate postoperative period, with restoration of speech within a few weeks in the absence of additional neurological alterations. The anatomical structures thought to be involved are the connections between the cerebellar dentate nucleus, the ventrolateral nucleus of the contralateral thalamus and the supplementary motor area. In an attempt to understand the pathophysiology of this syndrome, and to depict the perfusion of different brain areas semiquantitatively, in two children who had become mute after posterior fossa surgery we performed a Tc99M-HM-PAO SPECT study during the period of mutism and again when normal speech had returned. In one patient, who had a left cerebellar astrocytoma, the SPECT study showed a marked reduction of cerebral perfusion in the right fronto-parietal region, and in the other, who had a medulloblastoma, a left fronto-temporo-parietal perfusion alteration was observed. When the patients regained normal speech, the follow-up SPECT studies revealed normalization of the cerebral perfusion. This study demonstrates the occurrence of a focal dysfunction of cerebral perfusion in children with cerebellar mutism after posterior fossa surgery. These observations are useful in extending our understanding of the pathophysiology of this postoperative clinical syndrome.