Research article
Conduction slowing without conduction block of compound muscle and nerve action potentials due to sodium channel block

https://doi.org/10.1016/0022-510X(94)90330-1Get rights and content

Abstract

We studied the effect of lidocaine on nerve conduction in vivo. Recovery of the compound muscle action potential (CMAP), sensory nerve action potential (SNAP), and single motor unit potential (MUP) of median nerve stimulation was recorded in four healthy volunteers after intravenous infusion of 20 ml of 0.5% lidocaine. During loading, CMAP and SNAP amplitudes rapidly decreased and their latencies increased. After recovery of the CMAP and SNAP amplitudes, nerve conduction velocity improved gradually over a period of 3–6 h, the amplitudes and configurations of CMAP and SNAP remaining unchanged. The conduction velocity of the single MUP markedly slowed before it is blocked. This indicates that maximum conduction velocity of CMAP and SNAP could be slowed by the partial inactivation of sodium channels without accompanying conduction block. Prolongation of the rise time of depolarization of the axonal membrane potential may be the active mechanism in this slowing because of sodium channel inactivation. Abnormalities in sodium channels at the nodes of Ranvier should be considered as a mechanism of conduction slowing even when there is no conduction block.

References (23)

  • O.K. Langley

    Histochemistry of polyanions in peripheral nerve

  • Cited by (36)

    • Acute peripheral neuropathy following animal envenomation: A case report and systematic review

      2022, Journal of the Neurological Sciences
      Citation Excerpt :

      It is known that, at the nodes of Ranvier, sodium and potassium channels are clustered for faster and efficient axonal action potential conduction. Antagonists of sodium channels in humans (by intravenous infusion of lidocaine or tetrodotoxin intoxication) reduces nerve conduction velocity [64,65]. The recent concept of ‘nodoparanodopathy’ was first and mainly introduce to describe immune-mediated peripheral neuropathy [66], but this categorization was extended to include peripheral neuropathies of various etiologies (autoimmune, inflammatory, ischemic, nutritional and toxic) in which the involvement of the nodal region is thought to be determinant in the pathogenesis [67].

    • The electrophysiology of axonal neuropathies: More than just evidence of axonal loss

      2020, Clinical Neurophysiology
      Citation Excerpt :

      Circumstantial evidence supporting this hypothesis comes from the following examples. Partial inactivation of the Na+ channel in humans, by intravenous infusion of lidocaine, reduces the CV of single motor unit potential by 20–30 m/s before failure of conduction occurs (Yokota et al., 1994). Lidocaine prolongs the closed- inactive state of Nav channel and slows CV possibly by increasing the time to reach the threshold for the action potential at the nodes.

    • The electrodiagnosis of Guillain-Barré syndrome subtypes: Where do we stand?

      2018, Clinical Neurophysiology
      Citation Excerpt :

      These findings may be confusing as, in the common belief, slow conduction velocity is assumed to be a characteristic of a demyelinating process. However, intravenous infusion of lidocaine or tetrodotoxin intoxication in humans, reducing the functioning voltage gated sodium channels at consecutive nodes of Ranvier, decrease conduction velocity conceivably by increasing the rise time of the action potential and the internodal conduction time (Oda et al., 1989; Yokota et al., 1994). From the above examples it is intuitive that only serial studies may provide a full understanding of the GBS pathophysiology and this is the reason why we eventually developed a criteria set based on the electrophysiological findings at two sequential studies (Table 1) (Uncini et al., 2017).

    • Neurophysiologic responses of peripheral nerve to anoxia: Effects of hypothermia and age

      2013, Clinical Neurophysiology
      Citation Excerpt :

      Additional studies using structural imaging may help identify the effects on amplitude as related to changes in the axon and the changes in velocity and duration as being related to changes in myelin or changes in channel kinetics. Disruption of myelin generally produces changes in NAP velocity initially and later reduction in amplitude as conduction block develops, although changes in velocity can also result from slowed activation or inactivation of sodium channels (Kiernan et al., 2001; Hardy, 1973a,b; Louis and Hotson, 1986; Delbeke et al., 1978; Yokota et al., 1994), or the preferential loss of rapidly conducting axons. The pattern of changes seen in the conditioned stimulus response is very different when hypothermia is continuous and when it is given only during anoxia.

    • Conduction block and axonal degeneration co-occurring in a patient with axonal Guillain-Barré syndrome

      2012, Journal of the Neurological Sciences
      Citation Excerpt :

      Although excessive temporal dispersion and conduction slowing are commonly associated with peripheral nerve demyelination, it is not exclusively due to demyelination. Conduction slowing can also occur in sodium channel block following tetrodotoxin intoxication or local anesthesia [19,20]. In our patient, temporal dispersion of proximal CMAPs in the median nerve resolved within 2 weeks after onset (Fig. 1).

    View all citing articles on Scopus
    View full text