Lowndes H E, Baker T, Michelson L P, Vincent-Ablazey M
Ann Neurol. 1978 May;3(5):433-7. doi: 10.1002/ana.410030513.
Depressed or lost tendon reflexes commonly observed in patients with peripheral neuropathies may result partly from attenuation of the dynamic discharge from the primary endings of muscle spindles. This possibility was investigated in cats with an experimental neuropathy induced with acrylamide (30 mg/kg/day intramuscularly). Achilles tendon reflexes and the dynamic discharge from primary muscle spindles were evaluated after five or ten injections of acrylamide. After five injections the animals were moderately impaired neurologically, the Achilles tendon reflex was difficult to elicit in 2 of 5 animals, and the dynamic responses of primary endings of soleus muscle spindles to stretch were depressed. Following ten injections of acrylamide the cats were severely impaired neurologically; tendon responses were either absent or difficult to elicit, and the dynamic responses of their muscle spindles to stretch were reduced by 50% (p less than 0.01). Additionally, the spindels responded to stretch with only 20 to 30% the normal number of afferent impulses. These data suggest that lost tendon responses in acrylamide neuropathy result in part from inadequate activation of motoneurons by spindle afferent discharge.
周围神经病患者中常见的腱反射减弱或消失,可能部分是由于肌梭初级末梢动态放电的减弱所致。在通过丙烯酰胺(30毫克/千克/天,肌肉注射)诱发实验性神经病的猫身上研究了这种可能性。在注射五次或十次丙烯酰胺后,评估跟腱反射和来自初级肌梭的动态放电。注射五次后,动物出现中度神经功能障碍,5只动物中有2只难以引出跟腱反射,比目鱼肌梭初级末梢对牵张的动态反应减弱。注射十次丙烯酰胺后,猫出现严重神经功能障碍;腱反射要么消失,要么难以引出,其肌梭对牵张的动态反应降低了50%(P小于0.01)。此外,肌梭对牵张的反应仅为正常传入冲动数量的20%至30%。这些数据表明,丙烯酰胺神经病中腱反射消失部分是由于肌梭传入放电对运动神经元的激活不足所致。