Motor impairment is the most relevant clinical feature in Parkinson's disease (PD). Functional imaging studies on motor impairment in PD have revealed changes in the cortical motor circuits, with particular involvement of the fronto-striatal network. The aim of this study was to assess brain activations during the performance of three different motor exercises, characterized by progressive complexity, using a functional fMRI multiple block paradigm, in PD patients and matched control subjects. Unlike from single-task comparisons, multi-task comparisons between similar exercises allowed to analyse brain areas involved in motor complexity planning and execution. Our results showed that in the single-task comparisons the involvement of primary and secondary motor areas was observed, consistent with previous findings based on similar paradigms. Most notably, in the multi-task comparisons a greater activation of supplementary motor area and posterior parietal cortex in PD patients, compared with controls, was observed. Furthermore, PD patients, compared with controls, had a lower activation of the basal ganglia and limbic structures, presumably leading to the impairment in the higher levels of motor control, including complexity planning and execution. The findings suggest that in PD patients occur both compensatory mechanisms and loss of efficiency and provide further insight into the pathophysiological role of distinct cortical and subcortical areas in motor dysfunction.

Nimodipine (BAY e 9736), a new dihydropyridine derivative, has been shown to reduce neurological deficits and mortality induced by acute cerebral ischemia in experimental studies. We investigated the effects of this calcium antagonist in patients with acute ischemic stroke through a randomized, double-blind, parallel-designed trial in which nimodipine was compared with placebo. Forty-one of 54 screened cases were found to fulfil the inclusion criteria (sudden occurrence of a focal neurological deficit secondary to an acute ischemic event in the carotid area diagnosed after a complete neurological work-up) and entered the study. Nineteen of them were treated with nimodipine (40 mg t.i.d. administered for 28 days) and the remaining 22 with placebo, given in identical tablets. In all patients the treatment started within 12 h after the onset of the symptoms. Course and intensity of the neurological deficit were evaluated by the Mathew Scale (slightly modified). Forty patients concluded the trial. Nimodipine was withdrawn in one case following the occurrence of a skin rash whose causative relation with the test drug could not be clarified. Altogether, however, nimodipine was well tolerated and no severe cardiovascular adverse reactions were observed. In terms of efficacy, the scores obtained by the Mathew Scale showed a higher rate of improvement on nimodipine than on placebo, thus indicating that patients receiving the latter drug did not fare as well as those receiving the test medication. Our data suggest that nimodipine may be beneficial in the treatment of acute stroke.

Angiogenesis is a common characteristic of tumours, and it is reasonable to assume that it has an influence on tumour growth, depending on the grade of malignancy. We therefore studied angiogenesis in 25 patients: 14 with glioblastoma multiforme and 11 with grade I meningioma. Our aim was to assess how angiogenesis conditions growth and necrosis. The patients underwent MRI with standard and perfusion sequences. We calculated the volume of each tumour; for the glioblastomas the solid portion was taken as the difference between the overall volume and the volume of any necrotic portion. In the glioblastomas, we found an inverse relationship between blood volume and the size of the tumour, whereas in the meningiomas there was of a direct relationship. These correlations confirm in vivo the knowledge about necrosis in glioblastomas and its relationship to their inadequate vascular network. On the contrary, grade 1 meningiomas show an equilibrium between their microcirculation and the cellular component.

Topiramate (TPM) is a new antiepileptic drug approved for the prevention of migraine headache. However its use is limited by treatment-emergent adverse events; in particular, therapy can exert profound impact on language function. In this investigation, we used functional magnetic resonance imaging (fMRI) to study the anatomofunctional correlates of language disturbances in TPM patients experiencing subjective cognitive impairment. Ten right-handed individuals receiving therapy (five with and five without language disfluency) and five matched healthy control subjects took part in this study. During fMRI subjects alternately rested and performed a word-generating task. The task comprised the silent generation of words beginning with a different input letter visually presented. The activation paradigm consisted of six activation blocks alternating with six baseline rest blocks. The main fMRI measure was the pattern activation of the prefrontal regions (Brodmann's areas 44, 45, and 46) in both left and right hemispheres. Patients receiving TPM (50-100 mg/day) significantly reduced mean monthly migraine frequency. However several differences in fMRI activation were evident in the subject group comparison. Notably, changes in brain activity were observed during the phonemic task in patients with language disturbances. It is likely that TPM therapy is associated with a "remapping" of the language cerebral network.

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