1 e major dose-limiting side-effect is a mixed sensorimotor neuropathy.

2 splayed mild and quiescent lower-limb axonal sensorimotor neuropathy.

3 erve conduction studies showed severe axonal sensorimotor neuropathy.

4 ccur almost exclusively in patients with HL, sensorimotor neuropathies and dermatomyositis are more f

5 neuropathy phenotype characterized by axonal sensorimotor neuropathy and microcephaly.

6  the molecular defect could explain both the sensorimotor neuropathy and the saccadic disorder, which

7 gressive ataxia, corticospinal signs, axonal sensorimotor neuropathy, and disruption of visual fixati

8 ristine alone, there was evidence of a mixed sensorimotor neuropathy as indicated by changes in behav

9 = 0.80 [95% CI, 0.50 to 0.93]; P < .001) and sensorimotor neuropathy assessed using the Neuropathy Im

10 ute and usually multifocal, included sensory/sensorimotor neuropathies, cerebellar ataxia, myelopathy

11 core phenotype of rapidly progressive axonal sensorimotor neuropathy (manifesting with sensory ataxia

12 y from predominantly cerebellar syndromes to sensorimotor neuropathy, ophthalmological disturbances,

13 ssive, predominantly length dependent axonal sensorimotor neuropathy was the predominant phenotype.

14                                              Sensorimotor neuropathy was the principal nonhematologic

15                                  Peripheral (sensorimotor) neuropathy was found in 71% and autonomic

16 nts presenting with cranial neuropathies and sensorimotor neuropathy with or without respiratory insu