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1 imulation in restoring fine motor control in focal dystonia.
2 ere more likely tremulous than patients with focal dystonia.
3 s a fundamental disturbance in patients with focal dystonia.
4 ealthy subjects and in patients with primary focal dystonia.
5 s may explain the clinical symptomatology of focal dystonia.
6 ix of them had segmental dystonia and 59 had focal dystonia.
7 o the role of muscle spindle Ia afferents in focal dystonia.
8 (ICD) is the most common form of adult-onset focal dystonia.
9 lvement in the pathophysiology of idiopathic focal dystonia.
10 across different phenotypes and genotypes of focal dystonia.
11 (linked or not linked to 9q34) and sporadic focal dystonia.
12 motor manifestations of isolated adult-onset focal dystonias.
13 ortex are differentially affected in primary focal dystonias.
14 may play a central role in these particular focal dystonias.
15 r blepharospasm, hemifacial spasm, and other focal dystonias.
16 he possibility of DDP mutation in women with focal dystonias.
17 o further investigate genetic factors in the focal dystonias.
18 teral motor cortices of 20 pianists (10 with focal dystonia, 10 healthy controls) were electrically s
19 athophysiological role for the phenomenon in focal dystonia and divergent pathophysiological processe
20 g deficits in neurological diseases, such as focal dystonia and Parkinson's disease, and possibly pro
21 ce of a mitochondrial deficiency in sporadic focal dystonia and provide a biochemical dimension to th
22 one in putamen in 21 patients with these two focal dystonias and compared the findings with those fro
23 t is often genetic in origin, to adult-onset focal dystonias and rarer forms of secondary dystonias,
24 ocial anxiety severity vary by onset site of focal dystonia, and this variation is not explained by d
25 e best treatment option for the treatment of focal dystonias: blepharospasm, hemifacial spasm, and ap
26 tients from northern Germany who had primary focal dystonia, both for the GAG deletion in the DYT1 ge
27 um between several chromosome 18 markers and focal dystonia, both in sporadic patients from northern
28 c complex I defect in patients with sporadic focal dystonia but could not find any abnormality in pat
30 nical phenotype of genetically proven DRD to focal dystonia, dystonia with relapsing and remitting co
31 two new dystonia genes, one for adult-onset focal dystonia (DYT7) and one for a mixed dystonia pheno
32 include idiopathic torsion dystonia (DYT1), focal dystonias (DYT7) and mixed dystonias (DYT6 and DYT
33 features that can be seen in parkin disease: focal dystonia; early instability; freezing; festination
36 significantly increased in both hands in the focal dystonia groups (thresholds were similar for each
37 ion included the Fahn dystonia scale for the focal dystonia groups and the Marsden-Burke-Fahn scale f
38 igated the pathophysiology of two idiopathic focal dystonias: hand cramp with excessive cocontraction
40 er, these results suggest that most cases of focal dystonia in patients of northern German or central
44 l hand somatosensory area of 6 patients with focal dystonia of the hand, we found an abnormality of t
45 e decreased in specific brain regions of the focal dystonia patients compared to normal controls.
46 own about its origins; it is classified as a focal dystonia secondary to an unknown neurobiological m
47 ed has increased greatly to include numerous focal dystonias, spasticity, tremors, cosmetic applicati
48 ncy in platelets from patients with sporadic focal dystonia suggests that a defect of energy metaboli
49 ction of linkage for one form of adult-onset focal dystonia to chromosome 18p (DYT7) in a family from
50 architecture of the functional connectome in focal dystonia was analyzed in a large population of pat
52 Task-specific dystonia is a form of isolated focal dystonia with the peculiarity of being displayed o
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