Leis A A, Kronenberg M F, Stĕtkárová I, Paske W C, Stokić D S
Department of Neurology, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Neurology. 1996 Jul;47(1):231-7. doi: 10.1212/wnl.47.1.231.
Few studies in humans have assessed the ability of Ia afferent and antidromic motor volleys to activate motoneurons during spinal shock. Hence, little is known about the excitability state of the spinal motoneuron pool after acute spinal cord injury (SCI) in humans.
In 14 patients with acute SCI involving anatomic levels T10 and above, we performed clinical and electrophysiologic studies early after injury (within 24 hours in seven subjects) and on day 10, 20, and 30 postinjury. Maximal H:M ratios, F-wave persistence, and tendon tap T-reflexes were recorded. Sixteen normal subjects and eight chronic SCI patients served as control subjects.
Ten of 14 patients had spinal shock (complete paralysis, loss of sensation, absent reflexes, and muscle hypotonia below the injury) at the time of initial evaluation. F-waves were absent in patients with spinal shock, reduced in persistence in patients with acute SCI without spinal shock, and normal in persistence in patients with chronic SCI. H-reflexes were absent or markedly suppressed in patients with spinal shock within 24 hours of injury but recovered to normal amplitudes within several days postinjury. This recovery occurred despite absence of F-waves that persisted for several weeks postinjury. Deep tendon reflexes were proportionally more depressed in spinal shock than were H-reflexes. All patients had elicitable H-reflexes for days or weeks before the development of clinical reflexes.
Rostral cord injury causes postsynaptic changes (hyperpolarization) in caudal motoneurons. This hyperpolarization is a major physiologic derangement in spinal shock. The rise in H-reflex amplitude despite evidence of persistent hyperpolarization is due to enhanced transmission at Ia fiber-motoneuron connections below the SCI. Finally, the observation that the stretch reflex is proportionally more depressed than the H-reflex is consistent with fusimotor drive also being depressed after SCI.
在人体中,很少有研究评估Ia类传入神经和逆向运动冲动在脊髓休克期间激活运动神经元的能力。因此,对于人类急性脊髓损伤(SCI)后脊髓运动神经元池的兴奋性状态知之甚少。
在14例解剖平面为T10及以上的急性SCI患者中,我们在损伤后早期(7例患者在24小时内)以及损伤后第10、20和30天进行了临床和电生理研究。记录最大H:M比值、F波持续时间和腱反射T波。16名正常受试者和8名慢性SCI患者作为对照。
14例患者中有10例在初次评估时出现脊髓休克(完全瘫痪、感觉丧失、反射消失和损伤平面以下肌肉张力减退)。脊髓休克患者F波消失,无脊髓休克的急性SCI患者F波持续时间缩短,慢性SCI患者F波持续时间正常。损伤后24小时内脊髓休克患者的H反射消失或明显抑制,但在损伤后数天内恢复到正常幅度。尽管损伤后数周F波持续存在,但仍出现这种恢复。脊髓休克时,深腱反射比H反射的抑制程度更大。所有患者在临床反射出现前数天或数周均可引出H反射。
脊髓上段损伤导致脊髓下段运动神经元发生突触后变化(超极化)。这种超极化是脊髓休克的主要生理紊乱。尽管有持续超极化的证据,但H反射幅度增加是由于SCI平面以下Ia纤维-运动神经元连接处的传递增强。最后,牵张反射比H反射抑制程度更大的观察结果与SCI后肌梭运动神经驱动也受到抑制一致。