EVIDENCE THAT ALTERATIONS IN PRESYNAPTIC INHIBITION CONTRIBUTE TO SEGMENTAL HYPOEXCITABILITY AND HYPEREXCITABILITY AFTER SPINAL-CORD INJURY IN MAN

EVIDENCE THAT ALTERATIONS IN PRESYNAPTIC INHIBITION CONTRIBUTE TO SEGMENTAL HYPOEXCITABILITY AND HYPEREXCITABILITY AFTER SPINAL-CORD INJURY IN MAN
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DOI:
10.1016/0168-5597(93)90131-8
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发表时间:
1993-06-01
期刊:
ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY
影响因子:
--
通讯作者:
AYYAR, DR
AYYAR, DR
中科院分区:
其他
文献类型:
--
作者:
CALANCIE, B;BROTON, JG;AYYAR, DR

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我们检测了3组成年受试者的Hoffmann(H)和Tenon(T)反射:急性脊髓损伤(损伤后2周)、对照组和慢性脊髓损伤(损伤后1年)。我们进一步研究了连续肌腱振动和不同刺激率对这些受试者群体中诱发的H反射大小的影响。所有的反射幅度都被表示为最大直接肌肉反应(M波)的函数,以便于在受试者之间进行比较。所有受试者都成功地诱发了H和T反射,包括那些患有脊椎休克的受试者。肌腱振动导致急性脊髓损伤受试者H反射显著减弱,对照组为中度减弱,而慢性脊髓损伤组影响相对较小。与对照组(中度衰减)或慢性SCI(有限衰减)受试者相比,急性SCI受试者在特定刺激率下H反射的衰减最大。频率敏感性和振动影响均与突触前抑制机制有关。我们认为,脊髓损伤破坏了脊髓上对节段性中间神经元介导的突触前抑制的影响,与脊髓休克相关的反射减退部分是由于突触前抑制的效果显著增加。相反,随着时间的推移,脊髓损伤受试者踝伸肌Ia输入的突触前抑制水平下降到比对照受试者更低的水平,有助于增强脊髓反射,与慢性脊髓损伤中所见的临床状态的痉挛相一致。
We examined Hoffmann (H) and tendon (T) reflexes in 3 populations of adult subjects: acute SCI ( < 2 weeks post injury), controls, and chronic SCI ( > 1 year post injury). We further investigated the effects of continuous tendon vibration and different stimulus rates on the size of evoked H reflexes in these,subject populations. All reflex amplitudes were expressed as a function of the maximum direct muscle response (M wave), to allow comparison between subjects.Both H and T reflexes were successfully-elicited from all subjects examined, including those in 'spinal shock.' Tendon vibration caused a marked attenuation of H reflexes in acute SCI subjects, intermediate attenuation in controls, and relatively little effect in the chronic SCI group. H reflexes showed greatest attenuation for a given stimulus rate in acute SCI subjects compared to controls (intermediate attenuation) or chronic SCI (limited attenuation) subjects.Both rate sensitivity and vibration influence have been linked to presynaptic inhibitory mechanisms. We suggest that spinal cord injury disrupts the supraspinal influence over segmental interneurons mediating presynaptic inhibition, and that the hyporeflexia associated with 'spinal shock' is due in part to a substantial increase in the efficacy of presynaptic inhibition. Conversely, over time the level of presynaptic inhibition of ankle extensor Ia input in SCI subjects declines to levels less than those of control subjects, contributing to the enhancement of spinal reflexes consistent with the clinical state of 'spasticity' seen in chronic SCI.