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Motor Prostheses

J. Thomas Mortimer

10.1002/cphy.cp010205

Source: Supplement 2: Handbook of Physiology, The Nervous System, Motor Control

Originally published: 1981

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 History
2 Perspective
3 Electrochemical Aspects of Stimulation
3.1 Metal‐Tissue Interface Without Applied Field
3.2 System for Electrical Excitation
3.3 Relationship Between Electrode Potential and Charge Density
3.4 Regulated Voltage vs. Regulated Current
3.5 Monophasic Stimulation
3.6 Biphasic Stimulation
3.7 Summary
4 Tissue Damage
4.1 Electrode Materials
4.2 Brain (Surface Electrodes)
4.3 Nerve (Cuff Electrode)
4.4 Muscle (Coiled Wire Electrode)
4.5 Summary
5 Nerve Excitation
5.1 Membrane Response to Applied Electrical Field
5.2 Excitation of Myelinated Nerve
5.3 Threshold Relationship Between Nerve and Muscle
5.4 Effects of Electrode Configuration on Threshold and Excitation Site
5.5 Neural Fatigue
5.6 Summary
6 Electrical Activation of Skeletal Muscle
6.1 Brief Review of Muscle Physiology
6.2 Electrical Excitation of Normal Muscle
6.3 Muscle Alterations Induced by Electrical Activation
6.4 Force Modulation
6.5 Summary
7 Clinical Applications
7.1 Paralyzed Muscle
7.2 Scoliosis
7.3 Summary
8 Summary
Figure 1. Figure 1.

Cross‐sectional representation of metal‐electrolyte interface. Charge in inner layer is more highly organized than in outer or diffuse layer, but because of inhomogeneities in surface conditions, it is not necessarily uniformly distributed. Surface deformations and coatings or contaminants on surface produce local potential differences that can support current flow or modify charge transfer properties of electrode under active conditions.

From Dymond 19
Figure 2. Figure 2.

Schematic representation of electrode test configuration. The potential VS represents system potential and includes surface potential of both test and indifferent (INDF.) electrodes. The potential V′E is electrode potential VE plus ohmic potential of electrode and component of the ohmic potential of electrolyte medium. Value of resistor can be adjusted to yield value of VR that equals ohmic component of V′E. Subtracting VR from V′E approximates VE, electrode potential. REF, reference electrode.
Figure 3. Figure 3.

Idealized representation of relationship between electrode potential VE and charge density (charge per unit of real electrode area, Q/A). Charge injection in reversible region involves processes that are completely reversible and do not result in net change in chemical species. Charge injection in irreversible regions (to right of point I or left of point II) involves electrochemical reactions that cannot be reversed by driving current in opposite direction.
Figure 4. Figure 4.

Voltage waveform observed between test electrode and reference electrode in response to regulated‐current pulse. See text for explanation.
Figure 5. Figure 5.

Electrode response to monophasic regulated‐current stimulation. Current waveform is shown in upper part of figure, and voltage waveform is shown in middle. Points 1–8 shown in electrode potential‐charge density plot correspond to points listed on time axis of current waveform. See text for details.
Figure 6. Figure 6.

Balanced‐charge biphasic stimulation. A: stimulus waveform with zero net charge transfer per cycle. B: variation in electrode potential, for conditions where charge is accommodated entirely within reversible region. I and D refer to current pulse amplitude and pulse duration. Subscripts P and S refer to primary and secondary stimulus pulses, respectively. Parameter τ is time delay between end of primary pulse and beginning of secondary pulse. Points 1–7 in A correspond to points in B.
Figure 7. Figure 7.

Electrode‐potential behavior for biphasic stimulation under conditions of charge imbalance. In case illustrated, anodic charge injected per unit area in primary pulse is 1 unit greater than that injected during secondary cathodic pulse. Numbers appearing on current waveform correspond to numbers appearing on plot of VE vs. Q/A.
Figure 8. Figure 8.

Electrode‐potential variation for relatively large stimulus pulses under balanced charge conditions. See text for details.
Figure 9. Figure 9.

Schematic diagram for practical balanced‐charge triphasic stimulator with timing diagrams. I, stimulator current; S, switch, closed during indicated period; VC, voltage developed across capacitor C; i, electrode current. Circuit operation is described in text.
Figure 10. Figure 10.

Coiled wire stimulating electrode. Right: electrode formed from stranded wire loaded in 19‐gauge hypodermic needle. Left: electrode formed from insulated stainless steel wire (45‐μm diam) loaded in 23‐gauge hypodermic needle. Light‐colored areas of coil are deinsulated. These electrodes are similar to those described by Caldwell and Reswick 13.
Figure 11. Figure 11.

Typical muscle‐tissue reaction to passive implant of single‐strand coiled wire electrode. Section was taken from cat triceps brachii muscle 5 days after electrode insertion. Implanted electrode was identical to electrode formed from 45‐μm stainless steel wire shown in Figure 10. Section shown is stained with hematoxylin and eosin. Vertical bar, 100 μm long. (J. T. Mortimer, D. Kaufman, and U. Roessmann, unpublished data.)
Figure 12. Figure 12.

Tissue reaction to active implant as function of stimulus parameters. Closed circles represent data taken from muscle stimulated with monophasic current pulses. Open circles indicate data based on balanced‐charge biphasic stimulation. Tissue reaction is measured in terms of area occupied by abnormally staining tissue (damaged area). Dotted line indicates average reaction area for passive coiled wire electrode implant of single‐strand type. Stimulus amplitude was fixed at 20 mA and frequency was 50 Hz for all tests. Horizontal axis is given in units of pulse duration, charge density in the primary pulse, and average current density (for monophasic stimulation). (J. T. Mortimer, D. Kaufman, and U. Roessmann, unpublished data.)
Figure 13. Figure 13.

Ladder‐network model for nerve‐fiber excitation. In upper part of figure is axon model; RO is extracellular internodal impedance, ZM is transmembrane impedance, and R1 is the intracellular internodal impedance. VM is transmembrane potential; under conditions of rest, inside is negative relative to outside. Membrane response to 3 current pulses of different magnitude (I1, I2, and I3), at anode in lower left and at cathode in lower right. See text for details.
Figure 14. Figure 14.

Charge injected to reach membrane threshold in excess of theoretical minimum as function of pulse duration. Pulse duration (t) has been normalized to the chronaxie value (tc).
Figure 15. Figure 15.

Transmembrane voltage response of myelinated nerve to short pulse stimuli. A: effect of increasing primary pulse amplitude. B: effect of increasing secondary pulse amplitude. C: transmembrane voltage response of myelinated nerve to increasing delay between primary and secondary pulses. Vertical calibration bar is 20 mV, and horizontal bars are 50 μs.

From van den Honert and Mortimer 76
Figure 16. Figure 16.

Reduction in evoked muscle force resulting from effects of secondary stimulus pulse. Force is shown as function of increasing delay between end of primary pulse and onset of secondary pulse. Secondary pulse in this experiment was insufficient to effect a measurable force.

From van den Honert and Mortimer 76
Figure 17. Figure 17.

Effect of altering amplitude of secondary pulse on evoked muscle force. Circuit used to generate balanced‐charge biphasic waveform is shown in Figure 9. See text for explanation.

From van den Honert and Mortimer 76
Figure 18. Figure 18.

Relationship among stimulus amplitude, pulse width, and fiber diameter derived from Frankenhaeuser‐Huxley equations of myelinated axon. A: strength‐duration curves for nerve fibers with diameters ranging from 2 μm to 20 μm. B: stimulus threshold as function of nerve diameter and stimulus pulse width.

Curves were generated in our laboratory using mathematical model described by McNeal 44
Figure 19. Figure 19.

Effect of increasing separation between electrode and axon on stimulus threshold. In these calculations stimulus pulse width was fixed at 100 μs.

Curves were generated in our laboratory using mathematical model described by McNeal 44
Figure 20. Figure 20.

Strength‐duration relationship for nerve excitation (indirect muscle excitation) and direct muscle excitation. During these experiments evoked muscle response was held constant at small fraction of total possible muscle force. Stimulus was delivered through intramuscular electrode before and after administration of curare.

(Data are representative of data collected from many experiments in our laboratory and are, in principle, identical to type of curves classically presented for innervated and denervated muscle
Figure 21. Figure 21.

Bipolar nerve cuff electrode. A: electrode in longitudinal section. Nerve courses from right to left through center of electrode; possible stimulus current pathways are indicated by arrows. B: ladder‐network model of system, including current pathways external to electrode cuff. See Figure 13 for details of model. Arrows indicate direction of local current flow.
Figure 22. Figure 22.

Transmembrane current distribution for axon in cuff‐type electrode. Negative current results in local depolarization of axon. Shaded region represents insulator portion of electrode with axon located along horizontal axis of graph. Nodes of Ranvier, for ladder‐network model, are located at tic marks along horizontal axis. Node separation in model was 2.5 mm. Anode electrode was located at point indicated by A, and for closely spaced case (2.5 mm), cathode was located at point C1. Cathode was located at C2 for 20‐mm separation case. Solid line, current distribution for case C1. Dashed line, current distribution for case C2.

Adapted from Karkar 37
Figure 23. Figure 23.

Electrical field map (dashed lines) and resultant current flow (solid lines) for tripolar cuff electrode. Electrode shown in longitudinal section.

Adapted from Testerman et al. 75
Figure 24. Figure 24.

Transmembrane potential change along nerve cell. Stimulating electrode is located at zero, and indifferent electrode is located a great distance to right. Note that change in transmembrane potential reverses sign at distance r to right of stimulating electrode.

Adapted from Marks 42
Figure 25. Figure 25.

Cross section of rat tibialis anterior muscle. Fibers have been stained for NAD diaphorase. Dark‐staining fibers are classified as oxidative. Superficial portion of muscle is in upper part of figure. Calibration, 1 mm. (Compare with Fig. 2 in ref. 51).
Figure 26. Figure 26.

Fatigue characteristics of 3 motor unit types: FG, fast twitch, glycolytic; FO, fast twitch, oxidative; and SO, slow twitch, oxidative.

Adapted from Edström and Kugelberg 20
Figure 27. Figure 27.

Cross section of muscle A: innervation pattern and electrode location. Circular area around electrode represents region of muscle subjected to threshold or suprathreshold stimulus pulse. Shaded area represents region of muscle activated. B: cross section of rat tibialis anterior muscle stained for glycogen (PAS, periodic acid Schiff). Light‐staining area has been depleted of glycogen by stimulation at 10 Hz for 10 min. (Compare with ref. 51.) Calibration bar is 1 mm long.
Figure 28. Figure 28.

Changes in duration of twitch contraction as function of daily period of stimulation, measured after 4 wk of stimulation. Assuming fusion frequency in unstimulated control muscle is 40 Hz, new fusion frequency can be estimated by change in twitch duration. (J. T. Mortimer and U. Roessmann, unpublished data.)
Figure 29. Figure 29.

Histochemical changes seen in electrically stimulated muscle. Muscle had been stimulated at 10 Hz, 24 h/day, for 28 days. A: section stained for NADH. Darker area is stimulated region. B: section stained for myofibrillar ATPase; light‐staining fibers are classified as slow twitch, oxidative. Calibration bar is 100 μm long. (J. T. Mortimer and U. Roessmann, unpublished data.)
Figure 30. Figure 30.

Blood flow (left) and oxygen consumption (right) in rabbit muscles stimulated for 28 days (broken lines) and in contralateral control muscles (solid lines), at rest (time 0) and during a 10‐min period of isometric contractions

From Hudlická et al. 35
Figure 31. Figure 31.

Rise time of twitch contraction recorded from 6 cats. Each curve represents 1 animal, and each animal was stimulated at 10 Hz, 24 h/day.

From Murphy 52
Figure 32. Figure 32.

Fatigue characteristics of stimulated cat tibialis anterior muscle. Stimulus frequency was 10 Hz. Shaded region of control indicates muscle force returned to resting level between successive stimuli. Stimulated muscle was virtually fused at 10 Hz. Muscle force is given in newtons.

Data were obtained in our laboratory from normal muscle and muscle that had been stimulated at 10 Hz, for 24 h/day, for 250 days 49
Figure 33. Figure 33.

Muscle force as function of charge injected during monophasic stimulation in cat tibialis anterior muscle. Each curve was obtained at fixed pulse width.

Unpublished data from our laboratory. They convey essentially the same information presented by Crago, Mortimer, et al. 15
Figure 34. Figure 34.

Force‐frequency characteristics. A: fast muscle (cat tibialis anterior). B: slow muscle (cat soleus). Horizontal axis is shown as natural log frequency. Force is in arbitrary units.
Figure 35. Figure 35.

Sequential stimulation. A: force contribution of 3 compartments of muscle, each stimulated 120° out of phase with the others. B: summed force as seen by common muscle tendon.

Adapted from Peckham et al. 59
Figure 36. Figure 36.

Idealized representation of compartment overlap. F1 and F2, forces measured as functions of stimulus strength; F12, force effected by I1 or I2 and common to both (see text).
Figure 37. Figure 37.

Force characteristics of muscle controlled by stimulus‐amplitude modulation and pulse‐rate modulation. Numbers shown in brackets indicate pulse width, in μs, for each of 3 electrodes at that particular force level.

From Peckham and Mortimer 55
Figure 38. Figure 38.

Force and fatigue characteristics for patients with spinal cord injury before and after program of electrically induced exercise. A: force before exercise (solid bar) and after exercise (open bar). Dotted line indicates minimum force level generally considered necessary for performing functions of daily living. B: fatigue resistance is indicated by percent of maximum force remaining after 10 min of 10‐Hz stimulation. Solid bar indicates fatigue before exercise and open bar shows fatigue after exercise.

From Peckham, Mortimer, and Marsolais 56
Figure 39. Figure 39.

Three types of stimulus waveforms applied to phrenic nerve through bipolar electrodes.

From Tanae et al. 74
Figure 40. Figure 40.

Average tidal‐volume changes during 2 h of stimulation using the stimulus waveform shown in Figure 39.

From Tanae et al. 74


Figure 1.

Cross‐sectional representation of metal‐electrolyte interface. Charge in inner layer is more highly organized than in outer or diffuse layer, but because of inhomogeneities in surface conditions, it is not necessarily uniformly distributed. Surface deformations and coatings or contaminants on surface produce local potential differences that can support current flow or modify charge transfer properties of electrode under active conditions.

From Dymond 19


Figure 2.

Schematic representation of electrode test configuration. The potential VS represents system potential and includes surface potential of both test and indifferent (INDF.) electrodes. The potential V′E is electrode potential VE plus ohmic potential of electrode and component of the ohmic potential of electrolyte medium. Value of resistor can be adjusted to yield value of VR that equals ohmic component of V′E. Subtracting VR from V′E approximates VE, electrode potential. REF, reference electrode.



Figure 3.

Idealized representation of relationship between electrode potential VE and charge density (charge per unit of real electrode area, Q/A). Charge injection in reversible region involves processes that are completely reversible and do not result in net change in chemical species. Charge injection in irreversible regions (to right of point I or left of point II) involves electrochemical reactions that cannot be reversed by driving current in opposite direction.



Figure 4.

Voltage waveform observed between test electrode and reference electrode in response to regulated‐current pulse. See text for explanation.



Figure 5.

Electrode response to monophasic regulated‐current stimulation. Current waveform is shown in upper part of figure, and voltage waveform is shown in middle. Points 1–8 shown in electrode potential‐charge density plot correspond to points listed on time axis of current waveform. See text for details.



Figure 6.

Balanced‐charge biphasic stimulation. A: stimulus waveform with zero net charge transfer per cycle. B: variation in electrode potential, for conditions where charge is accommodated entirely within reversible region. I and D refer to current pulse amplitude and pulse duration. Subscripts P and S refer to primary and secondary stimulus pulses, respectively. Parameter τ is time delay between end of primary pulse and beginning of secondary pulse. Points 1–7 in A correspond to points in B.



Figure 7.

Electrode‐potential behavior for biphasic stimulation under conditions of charge imbalance. In case illustrated, anodic charge injected per unit area in primary pulse is 1 unit greater than that injected during secondary cathodic pulse. Numbers appearing on current waveform correspond to numbers appearing on plot of VE vs. Q/A.



Figure 8.

Electrode‐potential variation for relatively large stimulus pulses under balanced charge conditions. See text for details.



Figure 9.

Schematic diagram for practical balanced‐charge triphasic stimulator with timing diagrams. I, stimulator current; S, switch, closed during indicated period; VC, voltage developed across capacitor C; i, electrode current. Circuit operation is described in text.



Figure 10.

Coiled wire stimulating electrode. Right: electrode formed from stranded wire loaded in 19‐gauge hypodermic needle. Left: electrode formed from insulated stainless steel wire (45‐μm diam) loaded in 23‐gauge hypodermic needle. Light‐colored areas of coil are deinsulated. These electrodes are similar to those described by Caldwell and Reswick 13.



Figure 11.

Typical muscle‐tissue reaction to passive implant of single‐strand coiled wire electrode. Section was taken from cat triceps brachii muscle 5 days after electrode insertion. Implanted electrode was identical to electrode formed from 45‐μm stainless steel wire shown in Figure 10. Section shown is stained with hematoxylin and eosin. Vertical bar, 100 μm long. (J. T. Mortimer, D. Kaufman, and U. Roessmann, unpublished data.)



Figure 12.

Tissue reaction to active implant as function of stimulus parameters. Closed circles represent data taken from muscle stimulated with monophasic current pulses. Open circles indicate data based on balanced‐charge biphasic stimulation. Tissue reaction is measured in terms of area occupied by abnormally staining tissue (damaged area). Dotted line indicates average reaction area for passive coiled wire electrode implant of single‐strand type. Stimulus amplitude was fixed at 20 mA and frequency was 50 Hz for all tests. Horizontal axis is given in units of pulse duration, charge density in the primary pulse, and average current density (for monophasic stimulation). (J. T. Mortimer, D. Kaufman, and U. Roessmann, unpublished data.)



Figure 13.

Ladder‐network model for nerve‐fiber excitation. In upper part of figure is axon model; RO is extracellular internodal impedance, ZM is transmembrane impedance, and R1 is the intracellular internodal impedance. VM is transmembrane potential; under conditions of rest, inside is negative relative to outside. Membrane response to 3 current pulses of different magnitude (I1, I2, and I3), at anode in lower left and at cathode in lower right. See text for details.



Figure 14.

Charge injected to reach membrane threshold in excess of theoretical minimum as function of pulse duration. Pulse duration (t) has been normalized to the chronaxie value (tc).



Figure 15.

Transmembrane voltage response of myelinated nerve to short pulse stimuli. A: effect of increasing primary pulse amplitude. B: effect of increasing secondary pulse amplitude. C: transmembrane voltage response of myelinated nerve to increasing delay between primary and secondary pulses. Vertical calibration bar is 20 mV, and horizontal bars are 50 μs.

From van den Honert and Mortimer 76


Figure 16.

Reduction in evoked muscle force resulting from effects of secondary stimulus pulse. Force is shown as function of increasing delay between end of primary pulse and onset of secondary pulse. Secondary pulse in this experiment was insufficient to effect a measurable force.

From van den Honert and Mortimer 76


Figure 17.

Effect of altering amplitude of secondary pulse on evoked muscle force. Circuit used to generate balanced‐charge biphasic waveform is shown in Figure 9. See text for explanation.

From van den Honert and Mortimer 76


Figure 18.

Relationship among stimulus amplitude, pulse width, and fiber diameter derived from Frankenhaeuser‐Huxley equations of myelinated axon. A: strength‐duration curves for nerve fibers with diameters ranging from 2 μm to 20 μm. B: stimulus threshold as function of nerve diameter and stimulus pulse width.

Curves were generated in our laboratory using mathematical model described by McNeal 44


Figure 19.

Effect of increasing separation between electrode and axon on stimulus threshold. In these calculations stimulus pulse width was fixed at 100 μs.

Curves were generated in our laboratory using mathematical model described by McNeal 44


Figure 20.

Strength‐duration relationship for nerve excitation (indirect muscle excitation) and direct muscle excitation. During these experiments evoked muscle response was held constant at small fraction of total possible muscle force. Stimulus was delivered through intramuscular electrode before and after administration of curare.

(Data are representative of data collected from many experiments in our laboratory and are, in principle, identical to type of curves classically presented for innervated and denervated muscle


Figure 21.

Bipolar nerve cuff electrode. A: electrode in longitudinal section. Nerve courses from right to left through center of electrode; possible stimulus current pathways are indicated by arrows. B: ladder‐network model of system, including current pathways external to electrode cuff. See Figure 13 for details of model. Arrows indicate direction of local current flow.



Figure 22.

Transmembrane current distribution for axon in cuff‐type electrode. Negative current results in local depolarization of axon. Shaded region represents insulator portion of electrode with axon located along horizontal axis of graph. Nodes of Ranvier, for ladder‐network model, are located at tic marks along horizontal axis. Node separation in model was 2.5 mm. Anode electrode was located at point indicated by A, and for closely spaced case (2.5 mm), cathode was located at point C1. Cathode was located at C2 for 20‐mm separation case. Solid line, current distribution for case C1. Dashed line, current distribution for case C2.

Adapted from Karkar 37


Figure 23.

Electrical field map (dashed lines) and resultant current flow (solid lines) for tripolar cuff electrode. Electrode shown in longitudinal section.

Adapted from Testerman et al. 75


Figure 24.

Transmembrane potential change along nerve cell. Stimulating electrode is located at zero, and indifferent electrode is located a great distance to right. Note that change in transmembrane potential reverses sign at distance r to right of stimulating electrode.

Adapted from Marks 42


Figure 25.

Cross section of rat tibialis anterior muscle. Fibers have been stained for NAD diaphorase. Dark‐staining fibers are classified as oxidative. Superficial portion of muscle is in upper part of figure. Calibration, 1 mm. (Compare with Fig. 2 in ref. 51).



Figure 26.

Fatigue characteristics of 3 motor unit types: FG, fast twitch, glycolytic; FO, fast twitch, oxidative; and SO, slow twitch, oxidative.

Adapted from Edström and Kugelberg 20


Figure 27.

Cross section of muscle A: innervation pattern and electrode location. Circular area around electrode represents region of muscle subjected to threshold or suprathreshold stimulus pulse. Shaded area represents region of muscle activated. B: cross section of rat tibialis anterior muscle stained for glycogen (PAS, periodic acid Schiff). Light‐staining area has been depleted of glycogen by stimulation at 10 Hz for 10 min. (Compare with ref. 51.) Calibration bar is 1 mm long.



Figure 28.

Changes in duration of twitch contraction as function of daily period of stimulation, measured after 4 wk of stimulation. Assuming fusion frequency in unstimulated control muscle is 40 Hz, new fusion frequency can be estimated by change in twitch duration. (J. T. Mortimer and U. Roessmann, unpublished data.)



Figure 29.

Histochemical changes seen in electrically stimulated muscle. Muscle had been stimulated at 10 Hz, 24 h/day, for 28 days. A: section stained for NADH. Darker area is stimulated region. B: section stained for myofibrillar ATPase; light‐staining fibers are classified as slow twitch, oxidative. Calibration bar is 100 μm long. (J. T. Mortimer and U. Roessmann, unpublished data.)



Figure 30.

Blood flow (left) and oxygen consumption (right) in rabbit muscles stimulated for 28 days (broken lines) and in contralateral control muscles (solid lines), at rest (time 0) and during a 10‐min period of isometric contractions

From Hudlická et al. 35


Figure 31.

Rise time of twitch contraction recorded from 6 cats. Each curve represents 1 animal, and each animal was stimulated at 10 Hz, 24 h/day.

From Murphy 52


Figure 32.

Fatigue characteristics of stimulated cat tibialis anterior muscle. Stimulus frequency was 10 Hz. Shaded region of control indicates muscle force returned to resting level between successive stimuli. Stimulated muscle was virtually fused at 10 Hz. Muscle force is given in newtons.

Data were obtained in our laboratory from normal muscle and muscle that had been stimulated at 10 Hz, for 24 h/day, for 250 days 49


Figure 33.

Muscle force as function of charge injected during monophasic stimulation in cat tibialis anterior muscle. Each curve was obtained at fixed pulse width.

Unpublished data from our laboratory. They convey essentially the same information presented by Crago, Mortimer, et al. 15


Figure 34.

Force‐frequency characteristics. A: fast muscle (cat tibialis anterior). B: slow muscle (cat soleus). Horizontal axis is shown as natural log frequency. Force is in arbitrary units.



Figure 35.

Sequential stimulation. A: force contribution of 3 compartments of muscle, each stimulated 120° out of phase with the others. B: summed force as seen by common muscle tendon.

Adapted from Peckham et al. 59


Figure 36.

Idealized representation of compartment overlap. F1 and F2, forces measured as functions of stimulus strength; F12, force effected by I1 or I2 and common to both (see text).



Figure 37.

Force characteristics of muscle controlled by stimulus‐amplitude modulation and pulse‐rate modulation. Numbers shown in brackets indicate pulse width, in μs, for each of 3 electrodes at that particular force level.

From Peckham and Mortimer 55


Figure 38.

Force and fatigue characteristics for patients with spinal cord injury before and after program of electrically induced exercise. A: force before exercise (solid bar) and after exercise (open bar). Dotted line indicates minimum force level generally considered necessary for performing functions of daily living. B: fatigue resistance is indicated by percent of maximum force remaining after 10 min of 10‐Hz stimulation. Solid bar indicates fatigue before exercise and open bar shows fatigue after exercise.

From Peckham, Mortimer, and Marsolais 56


Figure 39.

Three types of stimulus waveforms applied to phrenic nerve through bipolar electrodes.

From Tanae et al. 74


Figure 40.

Average tidal‐volume changes during 2 h of stimulation using the stimulus waveform shown in Figure 39.

From Tanae et al. 74
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Article Title: Motor Prostheses
 

How to Cite

J. Thomas Mortimer. Motor Prostheses. Compr Physiol 2011, Supplement 2: Handbook of Physiology, The Nervous System, Motor Control: 155-187. First published in print 1981. doi: 10.1002/cphy.cp010205