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a Department of Neurology A, b Department
of Neuroradiology, c Department of Neurology B, CHRU de Lille, France
Correspondence to: Professor A Destée, Service de Neurologie A, Hôpital R Salengro CHRU, 59037 Lille Cedex, France. Telephone 0033 3 20 44 67 52; fax 0033 3 20 44 66 80.
Received 18 August 1997 and in revised form 23
March 1998;
Accepted 31 March 1998
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
cort ico - striat o - pallido - thalamo - cort ica l loop.
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