期刊
OPEN MEDICINE
卷 17, 期 1, 页码 397-402出版社
DE GRUYTER POLAND SP Z O O
DOI: 10.1515/med-2022-0444
关键词
amyotrophic lateral sclerosis; delayed onset muscle soreness; extraocular muscle; stretch reflex; blink reflex; Piezo2 ion channel
ALS is a fatal neurodegenerative disease that leads to motoneuron death, while DOMS causes delayed onset muscle soreness and stiffness. Both conditions share sensory deficits and impaired proprioception, but ALS spares extraocular muscles compared to limb skeletal muscles.
Amyotrophic lateral sclerosis (ALS) is a fatal, multisystem neurodegenerative disease that causes the death of motoneurons (MNs) progressively and eventually leads to paralysis. In contrast, delayed onset muscle soreness (DOMS) is defined as delayed onset soreness, muscle stiffness, loss of force-generating capacity, reduced joint range of motion, and decreased proprioceptive function. Sensory deficits and impaired proprioception are common symptoms of both ALS and DOMS, as impairment at the proprioceptive sensory terminals in the muscle spindle is theorized to occur in both. The important clinical distinction is that extraocular muscles (EOM) are relatively spared in ALS, in contrast to limb skeletal muscles; however, the blink reflex goes through a gradual impairment in a later stage of disease progression. Noteworthy is, that, the stretch of EOM induces the blink reflex. The current authors suggest that the impairment of proprioceptive sensory nerve terminals in the EOM muscle spindles are partially responsible for lower blink reflex, beyond central origin, and implies the critical role of Piezo2 ion channels and Wnt-PIP2 signaling in this pathomechanism. The proposed microinjury of Piezo2 on muscle spindle proprioceptive terminals could provide an explanation for the painless dying-back noncontact injury mechanism theory of ALS.
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