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1 e major dose-limiting side-effect is a mixed sensorimotor neuropathy.
2 ction study corroborated a peripheral axonal sensorimotor neuropathy.
3 splayed mild and quiescent lower-limb axonal sensorimotor neuropathy.
4 erve conduction studies showed severe axonal sensorimotor neuropathy.
5 ccur almost exclusively in patients with HL, sensorimotor neuropathies and dermatomyositis are more f
6 childhood onset that presents as a prominent sensorimotor neuropathy and commonly progresses to affec
8 the molecular defect could explain both the sensorimotor neuropathy and the saccadic disorder, which
9 and global brain atrophy, axonal sensory and sensorimotor neuropathies, and sensorineural hearing los
10 gressive ataxia, corticospinal signs, axonal sensorimotor neuropathy, and disruption of visual fixati
11 ristine alone, there was evidence of a mixed sensorimotor neuropathy as indicated by changes in behav
12 = 0.80 [95% CI, 0.50 to 0.93]; P < .001) and sensorimotor neuropathy assessed using the Neuropathy Im
13 ute and usually multifocal, included sensory/sensorimotor neuropathies, cerebellar ataxia, myelopathy
14 malignancies, but it causes a dose-limiting sensorimotor neuropathy for which there is no effective
15 core phenotype of rapidly progressive axonal sensorimotor neuropathy (manifesting with sensory ataxia
17 y from predominantly cerebellar syndromes to sensorimotor neuropathy, ophthalmological disturbances,
18 the most common of which included peripheral sensorimotor neuropathy (two [2%] patients) and pyrexia
19 ssive, predominantly length dependent axonal sensorimotor neuropathy was the predominant phenotype.
22 nts presenting with cranial neuropathies and sensorimotor neuropathy with or without respiratory insu