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In patients with cerebral ischemia, intravenous (i.v.) recombinant tissue plasminogen activator (rt-PA) increases survival without handicap or dependency despite an increased risk of bleeding. This study evaluated whether the results of randomized controlled trials are reproduced in clinical practice.

Les patients pris en charge à la phase aiguë d’un accident vasculaire cérébral (AVC) bénéficient des progrès de l’imagerie. L’Imagerie par Résonance Magnétique (IRM) permet de réaliser précocement, dès les premières minutes, le diagnostic de lésions ischémiques. Celles-ci sont susceptibles de régresser si un traitement adapté, visant à lever l’occlusion artérielle, est mis en route dans les premières heures. L’IRM évalue les possibilités de mise en route de ce traitement, écartant notamment l’éventualité d’un AVC hémorragique, détermine le pronostic et, enfin, participe au diagnostic étiologique. (J Mal Vasc 2006; 31: 252-259)

Objective To establish the pathophysiological mechanisms of striatopallidal and thalamic dystonia. Methods Five patients from among 26 who presented (between March 1987 and July 1996) with focal dystonia, segmental dystonia, or hemidystonia caused by a single localised vascular lesion, were selected. Patients with lesions with indefinite boundaries, and diffuse, or multiple, or large brain lesions were excluded. Three dimensional T1 weighted MRI (1.5 tesla) was performed to determine the topography of the lesions. The atlas of Hassler allowed the stereotactic localisation of the lesions to be specified exactly. Results Three patients had dystonic spasms associated with striatopallidal lesions and one with a thalamic and striatopallidal lesion. One other patient presented with a myoclonic dystonia related to a thalamic lesion. The striatopallidal lesions were located in the sensorimotor area with a somatotopical distribution. The pure thalamic lesion involved the centromedian nucleus, the sensory nuclei, and the pulvinar whereas the thalamic and striatopallidal lesion was located in the pallidonigral thalamic territory, which receives pallidonigral inputs. Conclusion The striatopallidal dystonia might be the consequence of the interruption of the cortico-striato-pallido-thalamo-cortical loop induced by lesions located within the sensorimotor part of the striatopallidal complex. By contrast, it is suggested that thalamic dystonia might be caused by lesions located in the centromedian or the ventral intermediate nuclei, outside the pallidonigral territory, but leading also to a dysfunction of the cortico-striato-pallido-thalamo-cortical loop.

In our memory clinic experience, memory impairment differs widely in patients with frontotemporal dementia (FTD). We searched for a correlation between explicit memory disturbance assessed with the Grober and Buschke test and medial temporal atrophy on CT scan in 22 consecutive patients with FTD. Five of the 22 patients had a medial temporal lobe (MTL) atrophy. There was no significant difference between the two groups for the demographic characteristics. Free recall, cued recall and the learning curve were significantly better in patients without MTL atrophy. The patients with MTL atrophy made more intrusions. We found a positive correlation between total recall and cued recall and the mean of medial temporal lobe measurement. These results are in agreement with the role of the hippocampal formation in the memory process. In our group, the ratio of patients with MTL atrophy is similar to the ratio of Pick’s disease in frontotemporal dementia. In histological series more severe hippocampal atrophy are reported in Pick’s disease. Therefore MTL atrophy on CT scan could be a marker of Pick’s disease in FTD.

L’épaisseur rétinienne est quantifiable de façon précise et reproductible en tomographie par cohérence optique (OCT). Une perte axonale rétinienne apparaît dans les 3 à 6 mois qui suivent un épisode clinique de névrite optique. Elle prédomine dans le quadrant temporal de la couche des fibres nerveuses de la rétine péripapillaire (T-pRNFL). En dehors de tout épisode de névrite optique, une atrophie de le T-pRNFL est aussi classiquement rapportée. La littérature actuelle suggère que cette atrophie rétinienne silencieuse soit la conséquence de lésions inflammatoires des radiations optiques et d’une dégénérescence rétrograde transsynaptique.