Tsur Atzmon, Ring Haim
Rehabilitation Department, Western Galilee Hospital, Nahariya, Israel.
J Brachial Plex Peripher Nerve Inj. 2008 Dec 17;3:26. doi: 10.1186/1749-7221-3-26.
To prove the possibility of axillary nerve conduction changes following shoulder subluxation due to hemiplegia, in order to investigate the usefulness of screening nerve conduction studies in patients with hemiplegia for finding peripheral neuropathy.
Forty-four shoulders of twenty-two patients with a first-time stroke having flaccid hemiplegia were tested, 43 +/- 12 days after stroke onset. Wasting and weakness of the deltoid were present in the involved side. Motor nerve conduction latency and compound muscle action potential (CMAP) amplitude were measured along the axillary nerve, comparing the paralyzed to the sound shoulder. The stimulation was done at the Erb's point whilst the recording needle electrode was inserted into the deltoid muscle 4 cm directly beneath the lateral border of the acromion. Wilcoxon signed rank test was used to compare the motor conduction between the sound and the paralytic shoulder. Mann-Whitney test was used to compare between plegic and sound shoulder in each side.
Mean motor nerve conduction latency time to the deltoid muscle was 8.49, SD 4.36 ms in the paralyzed shoulder and 5.17, SD 1.35 ms in the sound shoulder (p < 0.001). Mean compound muscle action potential (CMAP) amplitude was 2.83, SD 2.50 mV in the paralyzed shoulder and was 7.44, SD 5.47 mV in the sound shoulder (p < 0.001). Patients with right paralyzed shoulder compared to patients with right sound shoulder (p < 0.001, 1-sided for latency; p = 0.003, 1-sided for amplitude), and patients with left paralyzed shoulder compared to patients with left sound shoulder (p = 0.011, 1-sided for latency, p = 0.001, 1-sided for amplitude), support the same outcomes. The electro-physiological changes in the axillary nerve may appear during the first six weeks after stroke breakout.
Continuous traction of the axillary nerve, as in hypotonic shoulder, may affect the electro-physiological properties of the nerve. It most probably results from subluxation of the head of the humerus, causing demyelinization and even axonopathy. Slowing of the conduction velocities of the axillary nerve in the paralyzed shoulders may be related also to the lowering of the skin temperature and muscular atrophy in the same limb. The usefulness of routine screening nerve conduction studies in the shoulder of hemiplegic patients seems to be advocated.
证明偏瘫所致肩关节半脱位后腋神经传导改变的可能性，以研究对偏瘫患者进行神经传导检查以发现周围神经病变的实用性。
对22例首次发生中风且伴有弛缓性偏瘫的患者的44个肩部进行检测，检测时间为中风发作后43±12天。患侧三角肌存在萎缩和无力。沿腋神经测量运动神经传导潜伏期和复合肌肉动作电位（CMAP）波幅，将瘫痪侧肩部与健侧肩部进行比较。刺激在Erb点进行，同时将记录针电极插入肩峰外侧缘正下方4 cm处的三角肌中。采用Wilcoxon符号秩检验比较健侧和瘫痪侧肩部的运动传导情况。采用Mann-Whitney检验比较每侧瘫痪肩部和健侧肩部的情况。
瘫痪侧肩部至三角肌的平均运动神经传导潜伏期为8.49，标准差4.36 ms，健侧肩部为5.17，标准差1.35 ms（p<0.001）。瘫痪侧肩部的平均复合肌肉动作电位（CMAP）波幅为2.83，标准差2.50 mV，健侧肩部为7.44，标准差5.47 mV（p<0.001）。右侧瘫痪肩部患者与右侧健侧肩部患者相比（潜伏期p<0.001，单侧；波幅p=0.003，单侧），左侧瘫痪肩部患者与左侧健侧肩部患者相比（潜伏期p=0.011，单侧；波幅p=0.001，单侧），结果相同。腋神经的电生理变化可能在中风发作后的前六周内出现。
如在低张性肩部中那样，腋神经的持续牵拉可能会影响神经的电生理特性。这很可能是由于肱骨头半脱位导致脱髓鞘甚至轴索性病变。瘫痪侧肩部腋神经传导速度减慢也可能与同一肢体皮肤温度降低和肌肉萎缩有关。似乎提倡对偏瘫患者肩部进行常规筛查神经传导检查。
