DYSTONIA AFTER STRIATOPALLIDAL AND THALAMIC STROKE - CLINICORADIOLOGICAL CORRELATIONS AND PATHOPHYSIOLOGICAL MECHANISMS

Objective-To establish the pathophysiological mechanisms of striatopal lidal and thalamic dystonia. Methods-Five patients from among 26 who p resented (between March 1987 and July 1996) with focal dystonia, segme ntal dystonia, or hemidystonia caused by a single localised vascular l esion, were selected. Patients with lesions with indefinite boundaries , and diffuse, or multiple, or large brain lesions were excluded. Thre e dimensional T1 weighted MRI (1.5 tesla) was performed to determine t he topography of the lesions, The atlas of Hassler allowed the stereot actic localisation of the lesions to be specified exactly. Results-Thr ee patients had dystonic spasms associated with striatopallidal lesion s and one with a thalamic and striatopallidal lesion. One other patien t presented with a myoclonic dystonia related to a thalamic lesion. Th e striatopallidal lesions were located in the sensorimotor area with a somatotopical distribution. The pure thalamic lesion involved the cen tromedian nucleus, the sensory nuclei, and the pulvinar whereas the th alamic and striatopallidal lesion was located in the pallidonigral tha lamic territory, which receives pallidonigral inputs. Conclusion-The s triatopallidal dystonia might be the consequence of the interruption o f 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 nucle i, outside the pallidonigral territory, but leading also to a dysfunct ion of the cortico-striato-pallido-thalamo-cortical loop.