Complex impairment of IA muscle proprioceptors following traumatic or XXXX .

@entity1 @entity901 @entity4024 @entity1897 @entity35 @entity717 @entity2359
UNASSIGNED: The health of primary sensory afferents supplying muscle has to be a first consideration in assessing deficits in proprioception and related motor functions. Here we discuss the role of a particular proprioceptor, the IA muscle spindle proprioceptor in causing @entity717 in response to either regeneration of a sectioned peripheral nerve or damage from @entity2359 chemotherapy. For each condition, there is a single preferred and widely repeated explanation for disability of movements associated with proprioceptive function. We present a mix of published and preliminary findings from our laboratory, largely from in  vivo electrophysiological study of treated @entity35 to demonstrate newly discovered IA afferent defects that seem likely to make important contributions to @entity717 . First, we argue that reconnection of regenerated IA afferents with inappropriate targets, although often repeated as the reason for lost stretch-reflex contraction, is not a complete explanation. We present evidence that despite successful recovery of stretch-evoked sensory signaling, peripherally regenerated IA afferents retract synapses made with motoneurons in the spinal cord. Second, we point to evidence that @entity717 suffered by @entity1 subjects months after discontinuation of @entity901 (OX) chemotherapy for some is not accompanied by @entity1897 , which is the acknowledged primary cause of disability. Our studies of OX-treated @entity35 suggest a novel additional explanation in showing the loss of sustained repetitive firing of IA afferents during static muscle stretch. Newly extended investigation reproduces this effect in normal @entity35 with drugs that block @entity4024 channels apparently involved in encoding static IA afferent firing. Overall, these findings highlight multiplicity in IA afferent deficits that must be taken into account in understanding proprioceptive disability, and that present new avenues and possible advantages for developing effective treatment. Extending the study of IA afferent deficits yielded the additional benefit of elucidating normal processes in IA afferent mechanosensory function.
