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1 in the neuronal GlyR alpha or beta subunits (spasmodic and spastic) were shown to be deficient in the
7 to the clinical and subclinical features of spasmodic dysphonia and may represent the neurochemical
8 YT4 dystonia, a dominantly inherited form of spasmodic dysphonia combined with other focal or general
12 re is insufficient research on the effect of spasmodic dysphonia or its treatment with botulinum neur
13 the corticobulbar/corticospinal tract in 20 spasmodic dysphonia patients compared to 20 healthy subj
15 ries study found that employed patients with spasmodic dysphonia reported voice-related work producti
17 C DeltaBP measures, while longer duration of spasmodic dysphonia was associated with a decrease in ta
22 capacitation, but capacitation of sperm from spasmodic mice for up to 3 h did not result in significa
27 ine at amino acid 52, is responsible for the spasmodic phenotype in mice and alters the ability of gl
31 disease duration >/=3 years, Toronto Western Spasmodic Torticollis Rating Scale [TWSTRS] severity sco
32 muscles was investigated in 24 patients with spasmodic torticollis using small, abrupt 'drops' of the
35 -collic reflex is disrupted in patients with spasmodic torticollis, a finding which corroborates the