Brain parenchymal abnormalities were associated with DVAs in close to two thirds of the cases evaluated. These abnormalities are thought to occur secondarily, likely during post-natal life, as a result of chronic venous hypertension. Outflow obstruction, progressive thickening of the walls of the DVA and their morphological organization into a venous convergence zone are thought to contribute to the development of venous hypertension in DVA.

Volumetric measurements of subcortical nuclei reveal atrophy of distinct subcortical nuclei in the patient group, predominantly ipsilateral to the focus. This finding probably reflects persistent abnormalities and not secondary change. In addition, the structural differences between patients with and patients without previous febrile convulsions suggest that these conditions may have different causes.

We present a new approach for non-invasive localization of focal epileptogenic discharges in patients considered for surgical treatment. EEG-triggered functional MR imaging (fMRI) and 3D EEG source localization were combined to map the primary electrical source with high spatial resolution. The method is illustrated by the case of a patient with medically intractable frontal lobe epilepsy. EEG obtained in the MRI system allowed triggering of the fMRI acquisition by the patient's habitual epileptogenic discharges. fMRI revealed multiple areas of signal enhancement. Three-dimensional EEG source localization identified the same active areas and provided evidence of onset in the left frontal lobe. Subsequent electrocorticography from subdural electrodes confirmed spike and seizure onset over this region. This approach, i.e. the combination of EEG-triggered fMRI and 3D EEG source analysis, represents a promising additional tool for presurgical epilepsy evaluation allowing precise non-invasive identification of the epileptic foci.

Detection of neoplastic cartilage invasion with CT greatly depended on the appropriate use of individual and combined CT criteria.

The four symptoms composing Gerstmann's syndrome were postulated to result from a common cognitive denominator (Grundstörung) by Gerstmann himself. He suggested that it is a disorder of the body schema restricted to the hand and fingers. The existence of a Grundstörung has since been contested. Here we suggest that a common psychoneurological factor does exist, but should be related to transformations of mental images rather than to the body schema. A patient (H.P.) was studied, who presented the four symptoms of Gerstmann's syndrome in the absence of any other neuropsychological disorders. MRI showed a focal ischaemic lesion, situated subcortically in the inferior part of the left angular gyrus and reaching the superior posterior region of T1. The cortical layers were spared and the lesion was seen to extend to the callosal fibres. On the basis of an extensive cognitive investigation, language, praxis, memory and intelligence disorders were excluded. The four remaining symptoms (finger agnosia, agraphia, right-left disorientation and dyscalculia) were investigated thoroughly with the aim of determining any characteristics that they might share. Detailed analyses of the tetrad showed that the impairment was consistently attributable to disorders of a spatial nature. Furthermore, cognitive tests necessitating mental rotation were equally shown to be impaired, confirming the essentially visuospatial origin of the disturbance. In the light of this report, the common cognitive denominator is hypothesized to be an impairment in mental manipulation of images and not in body schema.