Strength-duration properties of human peripheral nerve.

The strength-duration time constant (tau SD) is a property of nodal membrane and, while it depends on a number of factors, its measurement may shed light on axonal properties when taken in conjunction with measurements of axonal excitability. For example, tau SD increases with demyelination as the exposed membrane is enlarged by inclusion of paranodal and internodal membrane, it decreases with hyperpolarization and it increases with depolarization. The present study was undertaken in 20 normal volunteers to compare strength-duration curves for compound sensory and muscle action potentials, to determine the most appropriate curve fitting equation for the data, and to examine the reproducibility of the calculated time constant on different days, for potentials of different amplitude and at different sites along the nerve. Using a computerized threshold-tracking system, stimulus intensity was adjusted to produce an antidromic compound sensory action potential (CSAP) or an orthodromic muscle action potential of 30% of maximum. Stimulus duration was increased every minute in 20 microseconds steps from 20 microseconds to 1 ms. The time constant for compound sensory potentials (665 +/- 182 microsecond) was longer than that for compound EMG potentials (459 +/- 126 microseconds). Weiss's formula, which relates threshold charge to stimulus duration, provided an accurate fit for the experimental data, and the study validated that, using it, relatively few experimental measurements were required to calculate the time constant. In repeated studies on the same subject, time constants usually differed by < 400 microseconds for sensory axons and < 250 microseconds for motor axons. They were identical at different sites along the nerve and did not alter with the size of the compound action potential. These characteristics suggest that the determinations of strength-duration time constant could be suitable for clinical usage.

[1]  S G Waxman,et al.  Delayed depolarization and slow sodium currents in cutaneous afferents. , 1994, Journal of neurophysiology.

[2]  S. Waxman,et al.  Activity‐dependent modulation of excitability: Implications for axonal physiology and pathophysiology , 1994, Muscle & nerve.

[3]  J. L. Taylor,et al.  Physiological evidence for a slow K+ conductance in human cutaneous afferents. , 1992, The Journal of physiology.

[4]  H. Bostock,et al.  Post-tetanic excitability changes and ectopic discharges in a human motor axon. , 1994, Brain : a journal of neurology.

[5]  H Bostock,et al.  The strength‐duration relationship for excitation of myelinated nerve: computed dependence on membrane parameters. , 1983, The Journal of physiology.

[6]  T Brismar,et al.  Electrical properties of isolated demyelinated rat nerve fibres. , 1981, Acta physiologica Scandinavica.

[7]  P. Grafe,et al.  Threshold tracking provides a rapid indication of ischaemic resistance in motor axons of diabetic subjects. , 1989, Electroencephalography and clinical neurophysiology.

[8]  T Brismar,et al.  Potential clamp analysis of membrane currents in rat myelinated nerve fibres. , 1980, The Journal of physiology.

[9]  J. Rothwell,et al.  THE TIME CONSTANTS OF MOTOR AND SENSORY AXONS IN HUMAN PERIPHERAL-NERVE , 1995 .

[10]  J Nilsson,et al.  The time constants of motor and sensory peripheral nerve fibers measured with the method of latent addition. , 1994, Electroencephalography and clinical neurophysiology.

[11]  D Burke,et al.  Hyperexcitability of cutaneous afferents during the supernormal period. Relevance to paraesthesiae. , 1987, Brain : a journal of neurology.

[12]  D. Burke,et al.  Activity-dependent changes in impulse conduction in normal human cutaneous axons. , 1995, Brain : a journal of neurology.

[13]  H Bostock,et al.  Depolarization changes the mechanism of accommodation in rat and human motor axons. , 1989, The Journal of physiology.

[14]  L. Geddes,et al.  The Strength-Duration Curve , 1985, IEEE Transactions on Biomedical Engineering.

[15]  J R Schwarz,et al.  Heterogeneous distribution of fast and slow potassium channels in myelinated rat nerve fibres. , 1989, The Journal of physiology.

[16]  H Bostock,et al.  Changes in excitability of human motor axons underlying post‐ischaemic fasciculations: evidence for two stable states. , 1991, The Journal of physiology.

[17]  D Burke,et al.  Changes in excitability of human cutaneous afferents following prolonged high-frequency stimulation. , 1989, Brain : a journal of neurology.

[18]  H Bostock,et al.  Differences in behaviour of sensory and motor axons following release of ischaemia. , 1994, Brain : a journal of neurology.

[19]  D. Burke Microneurography, impulse conduction, and paresthesias , 1993, Muscle & nerve.

[20]  Werner Vogel,et al.  Voltage-clamp studies in axons: Macroscopic and single-channel currents , 1995 .

[21]  M. Hallett,et al.  Relevance of stimulus duration for activation of motor and sensory fibers: implications for the study of H-reflexes and magnetic stimulation. , 1988, Electroencephalography and clinical neurophysiology.

[22]  T A Sears,et al.  The spatial distribution of excitability and membrane current in normal and demyelinated mammalian nerve fibres. , 1983, The Journal of physiology.

[23]  W Vogel,et al.  Ion channels in human axons. , 1993, Journal of neurophysiology.

[24]  G. Weiss Sur la possibilite de rendre comparables entre eux les appareils servant a l'excitation electrique. , 1990 .

[25]  J. M. Ritchie,et al.  A quantitative description of membrane currents in rabbit myelinated nerve. , 1979, The Journal of physiology.

[26]  J. M. Ritchie,et al.  Molecular dissection of the myelinated axon , 1993, Annals of neurology.

[27]  H. Bostock,et al.  Evidence for two types of potassium channel in human motor axons in vivo , 1988, Brain Research.

[28]  P. Grafe,et al.  Function and distribution of three types of rectifying channel in rat spinal root myelinated axons. , 1987, The Journal of physiology.