摘要
Background： Motor dysfunction is common in stroke patients. Clinical electrophysiological studies suggest that transsynaptic degeneration occurred in the lower motor neurons, while pathological evidence is lacked. This study aimed to combine the electrophysiological and pathological results to prove the existence of transsynaptic degeneration in the motor system after stroke. Methods： Modified neurologic severity score, electrophysiological, and pathological assessments were evaluated in rats before middle cerebral artery occlusion （MCAO）, and at 24 hours, 7 days, and 14 days after MCAO. Paired and independent-sample t-tests were applied to assess the changes of electrophysiological and pathological data. Results： Compound motor action potential amplitude in the paretic side was significantly lower than the nonparetic side at both 24 hours （61.9 ± 10.4 vs. 66.6 ± 8.9, P 〈 0.05） and 7 days （60.9 ± 8.4 vs. 67.3 ±9.6, P 〈 0.05） after MCAO. Motor unit number estimation of the paretic side was significantly less than the nonparetic side （379.0 ± 84.6 vs. 445.0 ±9.5, P 〈 0.05） at 7 days after MCAO. Until 14 days after stroke, the pathological loss of motor neurons was detected. Motor neurons in 14-day MCAO group were significantly decreased, compared with control group （5.3 ± 0.7 vs. 7.3 ± 1.8, P 〈 0.05）. Conclusions： Both electrophysiological and pathological studies showed transsynaptic degeneration after stroke. This study identified the asynchronization in changes of electrophysiology and pathology. The abnormal physiological changes and function impairment can be detected in the early stage and recovered quickly, while the pathological loss of motor neuron can be detected only in a later stage.
Background： Motor dysfunction is common in stroke patients. Clinical electrophysiological studies suggest that transsynaptic degeneration occurred in the lower motor neurons, while pathological evidence is lacked. This study aimed to combine the electrophysiological and pathological results to prove the existence of transsynaptic degeneration in the motor system after stroke. Methods： Modified neurologic severity score, electrophysiological, and pathological assessments were evaluated in rats before middle cerebral artery occlusion （MCAO）, and at 24 hours, 7 days, and 14 days after MCAO. Paired and independent-sample t-tests were applied to assess the changes of electrophysiological and pathological data. Results： Compound motor action potential amplitude in the paretic side was significantly lower than the nonparetic side at both 24 hours （61.9 ± 10.4 vs. 66.6 ± 8.9, P 〈 0.05） and 7 days （60.9 ± 8.4 vs. 67.3 ±9.6, P 〈 0.05） after MCAO. Motor unit number estimation of the paretic side was significantly less than the nonparetic side （379.0 ± 84.6 vs. 445.0 ±9.5, P 〈 0.05） at 7 days after MCAO. Until 14 days after stroke, the pathological loss of motor neurons was detected. Motor neurons in 14-day MCAO group were significantly decreased, compared with control group （5.3 ± 0.7 vs. 7.3 ± 1.8, P 〈 0.05）. Conclusions： Both electrophysiological and pathological studies showed transsynaptic degeneration after stroke. This study identified the asynchronization in changes of electrophysiology and pathology. The abnormal physiological changes and function impairment can be detected in the early stage and recovered quickly, while the pathological loss of motor neuron can be detected only in a later stage.
基金
This study wasfunded by a grant of National Natural Science Foundation of China （No. 81241045）.
