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See detailExercise-induced dystonia as a preceding symptom of familial Parkinson's disease
Bruno, Michiko K; Ravina, Bernard; Garraux, Gaëtan ULg et al

in Movement Disorders (2004), 19(2), 228-230

Paroxysmal exercise-induced dystonia can occur with Parkinson's disease (PD), and in rare cases, this can also be the presenting symptom. We report on 2 second cousins (no known consanguinity) who ... [more ▼]

Paroxysmal exercise-induced dystonia can occur with Parkinson's disease (PD), and in rare cases, this can also be the presenting symptom. We report on 2 second cousins (no known consanguinity) who presented with paroxysmal exercise-induced dystonia who later developed clinical features of PD. Although autosomal recessive inheritance was suggested, and the dystonic features further suggest parkin as a possible cause, ssequencing for parkin mutations was negative and this family may represent a genetic variant of PD. Further genotype-phenotype studies in this and similar families may give clues to pre-symptomatic symptoms in PD and may reflect a particular phenotype of interest for genetics studies in the future. [less ▲]

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See detailVoxel-based distribution of metabolic impairment in corticobasal degeneration
Garraux, Gaëtan ULg; Salmon, Eric ULg; Peigneux, Philippe ULg et al

in Movement Disorders (2000), 15(5), 894-904

This report emphasizes the precise topographic distribution of cerebral metabolic impairment in corticobasal degeneration (CBD) and the pathophysiological differences between CBD and progressive ... [more ▼]

This report emphasizes the precise topographic distribution of cerebral metabolic impairment in corticobasal degeneration (CBD) and the pathophysiological differences between CBD and progressive supranuclear palsy (PSP). Statistical parametric mapping (SPM96) analysis of 18FDG positron emission tomography (PET) data was performed in 22 patients with CBD compared with 46 healthy subjects (HS) and 21 patients with PSP who were studied at rest. A statistical threshold of p <0.001 was fixed, further corrected for multiple or independent comparisons (p <0.05). In comparison with HS, the metabolic impairment in CBD was asymmetrically distributed in the putamen, thalamus, precentral (Brodmann's area, BA 4), lateral premotor (BA 6/44) and supplementary motor areas (SMA, BA 6), dorsolateral prefrontal (8/9/46) cortex, and the anterior part of the inferior parietal lobe (BA 40) including the intraparietal sulcus (BA 7/40). A similar hypometabolic pattern was observed for most individual analyses. When PSP was compared with CBD, metabolic impairment predominated in the midbrain, anterior cingulate (BA 24/32), and orbitofrontal regions (BA 10). The reverse contrast showed more posterior involvement in CBD (BA 6 and 5/7/40) including SMA. Our data suggest that multiple components of neural networks related to both movement execution and production of skilled movements are functionally disturbed in CBD compared with both HS and PSP. [less ▲]

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See detailPostencephalitic stereotyped involuntary movements responsive to L-Dopa
Picard, F.; deSaintMartin, A.; Salmon, Eric ULg et al

in Movement Disorders (1996), 11(5), 567-570

In 1954, at the age of 5 years, our patient had an encephalitic syndrome associated with a prolonged lethargic state. After this episode, he developed a severe parkinsonian syndrome that, after a few ... [more ▼]

In 1954, at the age of 5 years, our patient had an encephalitic syndrome associated with a prolonged lethargic state. After this episode, he developed a severe parkinsonian syndrome that, after a few years, was associated with axial dystonia and stereotyped abnormal movements of the upper limbs. This complex and progressive extrapyramidal syndrome had many similarities to the encephalitis lethargica as described by von Economo. Results of cerebral computed tomography and magnetic resonance imaging were normal. Fluorodopa positron emission tomography showed a significant bilateral reduction of tracer accumulation in both putamen, similar to that observed in patients with idiopathic Parkinson's disease. However, in this patient, treatment with L-Dopa suppressed all akinetic, dystonic and dyskinetic symptoms. The effectiveness of L-Dopa was abolished by administration of a D2 antagonist and was fully reproduced by a D2 agonist. In conclusion, this patient presented a complex postencephalitic, extrapyramidal syndrome, with akinetic symptoms and involuntary movements. These symptoms appeared to be related to a limited lesion of the dopaminergic neurons of the zona compacta of the substantia nigra. [less ▲]

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