Activation of peripheral trigeminal fibers induces neurogenic inflammation in rat dura mater, as well as vascular and mat cell changes. These changes parallel an increase of vasodilating and permeability promoting peptides in venous effluent of the cephalic circulation. The experimental model of electrical trigeminal ganglion stimulation or systemic capsaicin administration has proven effective in detecting cellular activation in brainstem trigeminal nuclei. Animal experimental models of trigeminovascular activation and the effects of antimigraine drugs on functional and morphological consequences of such activation provide the background for further models and for developing pharmacological strategies in this field.

Our aim was to relate MRI findings in patients with severe traumatic brain injury (TBI) to clinical severity and long-term outcome. We studied 37 patients with severe TBI, who were submitted to clinical assessment for disability and cognition and to MRI 60-90 days after trauma. Clinical assessment was also performed 3, 6 and 12 months later. The number and volume of lesions in various cerebral structures were calculated semiautomatically from FLAIR and fast field-echo images. Possible correlations between total and regional lesion volume and clinical deficits were then investigated. The frontal and temporal lobes were most frequently involved. Total lesion volume on FLAIR images correlated significantly with clinical outcome, whereas that on FFE images did not. Regional analysis showed that FLAIR lesion volume in the corpus callosum correlated significantly with scores on disability and cognition scales at the first clinical assessment. FLAIR lesion volume in the frontal lobes correlated significantly with clinical scores 1 year later.

In a previous study, we found that the extent of necrosis was the only radiological feature which correlated significantly with survival in patients with glioblastoma. The aim of this paper was to evaluate the variability and prognostic value of the extent of the necrotic area as seen on contrast-enhanced MRI and CT in a larger series. We studied 72 patients who underwent surgical removal of supratentorial glioblastomas and had CT and/or MRI with contrast medium before surgery; 38, all undergoing the same treatment (surgery plus radiotherapy), were followed clinically. Necrosis within the tumour varied greatly, ranging from none (only 1 case) to involvement of 76% of the tumour. Survival data in the subgroup suggested that only patients with a small area of necrosis (less than 35% of the tumour) had a significantly longer survival time. When necrosis involved more than 35% of the mass, patients had a shorter survival time, without any further correlation with the extent of necrosis.

We report the MR imaging findings of three patients with eclampsia and PRES as well as a careful review of literature.

The aim of this study was to obtain an MRI severity-related classification of diffuse astrocytic tumours able to integrate the histological data in the grading of such tumours. We studied presurgical MR images of 91 patients with a histological diagnosis of astrocytoma, anaplastic astrocytoma and glioblastoma. A score ranging from 1 to 3 was assigned by two independent readers to each of the following MR features: oedema, mass effect, contrast enhancement, borders, signal homogeneity, necrosis, haemorrhage and flow void. Statistical analysis showed significant differences in the mean MRI scores between the three histological grades. Contrast enhancement was found to be the best predictor of the histological grade followed by necrosis, signal homogeneity and border scores. This classification represents a simple and reproducible means of carefully evaluating some macroscopic characteristics of these tumours. It could be used to integrate histological data especially in cases in which tissue sampling defects may affect the validity of this examination.