Stendel Ruediger, Jahnke Uwe, Straschill Max
Department of Neurosurgery, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
J Brachial Plex Peripher Nerve Inj. 2006 Oct 20;1:4. doi: 10.1186/1749-7221-1-4.
Animal studies have demonstrated complex cortical reorganization following peripheral nerve lesion. Central projection fields of intact nerves supplying skin areas which border denervated skin, extended into the deafferentiated cortical representation area. As a consequence of nerve lesions and subsequent reorganization an increase of the somatosensory evoked potentials (SEPs) was observed in cats when intact neighbouring nerves were stimulated. An increase of SEP-components of patients with nerve lesions may indicate a similar process of posttraumatic plastic cortical reorganization.
To test if a similar process of post-traumatic plastic cortical reorganization does occur in humans, the SEP of intact neighbouring hand nerves were recorded in 29 patients with hand nerve lesions. To hypothetically explain the observed changes of SEP-components, SEP recording following paired stimulation of the median nerve was performed in 12 healthy subjects.
Surprisingly 16 of the 29 patients (55.2%) showed a reduction or elimination of N35, P45 and N60. Patients with lesions of two nerves showed more SEP-changes than patients with a single nerve lesion (85.7%; 6/7 nerves; vs. 34.2%; 13/38 nerves; Fisher's exact test, p < 0.05). With paired stimulation a suppression of the amplitude of N20, P25 and P45 (p < 0.05; sign test), and a marked increment of N35 (p < 0.05; sign test) and N60 (not significant; sign test) of the second response could be observed.
The results of the present investigation do not provide evidence of collateral innervation of peripherally denervated cortical neurons by neurons of adjacent cortical representation areas. They rather suggest that secondary components of the excitatory response to nerve stimulation are lost in cortical areas, which surround the denervated region.
动物研究表明,周围神经损伤后会发生复杂的皮质重组。供应与失神经皮肤相邻皮肤区域的完整神经的中枢投射场,会延伸到去传入皮质代表区。由于神经损伤及随后的重组,当刺激完整的相邻神经时,在猫身上观察到体感诱发电位(SEP)增加。神经损伤患者SEP成分的增加可能表明创伤后皮质可塑性重组的过程类似。
为了测试创伤后皮质可塑性重组过程在人类中是否确实发生,对29例手部神经损伤患者记录了相邻完整手部神经的SEP。为了假设性地解释观察到的SEP成分变化,对12名健康受试者进行了正中神经配对刺激后的SEP记录。
令人惊讶的是,29例患者中有16例(55.2%)N35、P45和N60降低或消失。两条神经损伤的患者比单条神经损伤的患者表现出更多的SEP变化(85.7%;6/7条神经;对比34.2%;13/38条神经;Fisher精确检验,p<0.05)。通过配对刺激,可观察到第二次反应中N20、P25和P45波幅的抑制(p<0.05;符号检验),以及N35(p<0.05;符号检验)和N60(无显著性差异;符号检验)的显著增加。
本研究结果未提供相邻皮质代表区神经元对周围失神经皮质神经元进行侧支神经支配的证据。相反,它们表明在失神经区域周围的皮质区域,对神经刺激的兴奋性反应的次级成分丧失。