Brain, Vol. 122, No. 5, 933-941,
May 1999
© 1999 Oxford University Press
Conduction block in carpal tunnel syndrome
Prince of Wales Medical Research Institute and Department of Neurology, Prince of Wales Hospital, Randwick, Sydney, Australia
Correspondence to:
Dr Matthew Kiernan, Prince of Wales Medical Research Institute, High Street, Randwick, NSW 2031, Australia E-mail: Matthew.Kiernan{at}unsw.edu.au
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Abstract |
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Wrist extension was performed in six healthy subjects to establish, first, whether it would be sufficient to produce conduction block and, secondly, whether the excitability changes associated with this manoeuvre are similar to those produced by focal nerve compression. During maintained wrist extension to 90°, all subjects developed conduction block in cutaneous afferents distal to the wrist, with a marked reduction in amplitude of the maximal potential by >50%. This was associated with changes in axonal excitability at the wrist: a prolongation in latency, a decrease in supernormality and an increase in refractoriness. These changes indicate axonal depolarization. Similar studies were then performed in seven patients with carpal tunnel syndrome. The patients developed conduction block, again with evidence of axonal depolarization prior to block. Mild paraesthesiae were reported by all subjects (normals and patients) during wrist extension, and more intense paraesthesiae were reported following the release of wrist extension. In separate experiments, conduction block was produced by ischaemic compression, but its development could not be altered by hyperpolarizing currents. It is concluded that wrist extension produces a `depolarization' block in both normal subjects and patients with carpal tunnel syndrome, much as occurs with ischaemic compression, but that this block cannot be altered merely by compensating for the axonal depolarization. It is argued that conduction slowing need not always be attributed to disturbed myelination, and that ischaemic compression may be sufficient to explain some of the intermittent symptoms and electrodiagnostic findings in patients with carpal tunnel syndrome, particularly when it is of mild or moderate severity.
conduction block; cutaneous afferents; paraesthesiae; carpal tunnel syndrome
CMAP = compound muscle action potential; CNAP = compound nerve action potential; CSAP = compound sensory action potential
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Introduction |
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In human subjects, the commonest compression neuropathy is of the median nerve at the wrist (Stewart and Aguayo, 1984
), due to entrapment of the nerve beneath the transverse carpal ligament at the wrist (Brain et al., 1947; Phalen et al., 1950; Kremer et al., 1953). Patients suffering from carpal tunnel syndrome typically complain of nocturnal numbness, tingling and painful paraesthesiae in the fingers and hand, and pain that may be experienced proximally in the forearm, shoulder and neck (Brown, 1984; Kimura, 1989). Electrophysiological techniques commonly demonstrate slowing of impulse conduction localized to the carpal tunnel segment (Buchthal and Rosenfalck, 1971; Casey and Le Quesne, 1972; Kimura, 1979; Goadsby and Burke, 1994), usually maximal in the distal 1–2 cm of the tunnel (Brown et al., 1976; Kimura 1979), with normal conduction on either side of the tunnel (Buchthal and Rosenfalck, 1971; Kimura, 1979; Goadsby and Burke, 1994). This pattern of slowing suggests focal pathology at which the safety margin for impulse conduction is impaired.
The pathophysiology of carpal tunnel syndrome has not been completely resolved (Dawson et al., 1990). While carpal tunnel syndrome results from nerve compression, the relative importance of ischaemia on the one hand and mechanical deformation with associated myelin disturbance and other nerve fibre changes on the other has not been established. The focal conduction slowing in patients with carpal tunnel syndrome is often presumed to result from a focal disturbance to myelin and, indeed, paranodal demyelination has been documented pathologically (Ochoa and Marotte, 1973; Gilliatt, 1980; Brown, 1984). Gilliatt (1980) established that subjecting a peripheral nerve to acute compression results in conduction block which can be rapidly reversed. With more severe compression, demyelination occurs and, later, Wallerian degeneration. The validity of these experimental models of peripheral nerve compression is supported by postmortem examinations of patients with carpal tunnel syndrome in which there was loss of the myelin sheath and reduction in nerve fibre diameter (Thomas and Fullerton, 1963; Neary et al., 1975). However, despite these findings the focal slowing of conduction in cutaneous afferents is not associated with critical impairment of the safety margin for impulse conduction (Miller et al., 1996; Kiernan et al., 1996b), as might be expected in a demyelinated lesion that was sufficient to produce conduction block in some axons (Bostock and Grafe, 1985).
In the neutral position of the wrist, the pressure in the carpal tunnel is much greater in patients with carpal tunnel syndrome than in normal subjects (Gelberman et al., 1981), and it increases with flexion and extension of the wrist (Brain et al., 1947; Tanzer, 1959; Robbins, 1963; Gelberman et al., 1981). In patients, the pressure in the tunnel increases from 32 to 94 mmHg with wrist flexion to 90° and to 110 mmHg with wrist extension to 90° (Gelberman et al., 1981). Prolonged wrist flexion produces conduction block in patients with carpal tunnel syndrome (Hansson and Nilsson, 1995), and wrist extension should do so, at least as readily, if the mechanism was ischaemic compression. While extreme flexion of the wrist is an unusual movement, extension is common and is associated with many normal manual tasks that can precipitate the symptoms of carpal tunnel syndrome. The present study aimed to establish whether wrist extension would be sufficient to produce conduction block in both normal subjects and patients with carpal tunnel syndrome and, if so, whether the excitability changes associated with this manoeuvre were similar to those produced by focal nerve compression.
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Methods |
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Four series of experiments were conducted on six normal subjects (aged 21–51 years) without clinical or neurophysiological evidence of a peripheral nerve disorder. A further series of experiments was undertaken in seven patients with carpal tunnel syndrome (aged 23–62 years). Each patient had a clinical diagnosis of carpal tunnel syndrome with electrophysiological evidence of focal slowing of conduction in the median nerve at the wrist (Goadsby and Burke, 1994
). All patients complained of paraesthesiae or numbness in the appropriate upper limb, but none had objective evidence of a cutaneous sensory deficit or of weakness of the thenar muscles. No subject had a history of other medical conditions known to affect nerve function. All gave informed consent to the experimental procedures, which had the approval of the Committee on Experimental Procedures Involving Human Subjects of the University of New South Wales. In 12 experiments on six normal volunteers, the development of conduction block was documented following maintained extension of the wrist to 90°. Conduction block was demonstrated by the gradual reduction in the size of the maximal compound sensory action potential (CSAP) produced in digit II by supramaximal stimulation of the median nerve at the wrist. In some experiments, simultaneous changes in the compound muscle action potential (CMAP) of the thenar muscles were also followed. The median nerve was stimulated using bipolar self-adhesive surface electrodes (Red-Dot; 3M Canada, London, Ontario, Canada) 4 cm apart at the wrist, and the evoked CSAP was recorded using ring electrodes around the proximal phalanx. The compound nerve action potential (CNAP) was also recorded at the elbow, using bipolar electrodes with an interelectrode distance of 4 cm, to ensure that the site of conduction block was distal, presumably within the carpal tunnel. Two stimulus intensities were used, both intentionally supramaximal, to ensure that movement did not disturb the recording: if stimuli of different intensity produced potentials of identical amplitude the responses must have been maximal. This ensured that any decrease in amplitude could be attributed to conduction block affecting some axons or to increased temporal dispersion of the CSAP.
In six experiments on five normal subjects, the changes in axonal excitability produced by wrist extension were measured just proximal to the wrist. Changes in excitability were measured on-line, with the computer altering stimulus intensity to keep the amplitude of the CSAP constant at 30–40% of maximum (`threshold tracking'; Bostock and Baker, 1988). Supernormality was assessed using a supramaximal conditioning stimulus delivered 7 ms before the submaximal test stimulus, the interval at which it is normally maximal (Kiernan et al., 1996a). Refractoriness was measured similarly using a conditioning–test interval of 2 ms. The maximal potential produced by the supramaximal conditioning stimulus contaminated the test potential during refractoriness and, to a lesser extent, during supernormality. To overcome this, the test potential was measured after subtraction of the response to the conditioning stimulus, the subtraction being performed on-line by computer. The extent of supernormality and that of refractoriness were determined as the differences in the thresholds for the conditioned and unconditioned potentials, normalized by dividing by the unconditioned threshold. Accordingly, refractoriness was measured as the increase in current required to produce the target CSAP when the conditioning–test interval was 2 ms and supernormality as the decrease in current required to produce the target CSAP when the conditioning–test interval was 7 ms, both values being normalized to the threshold for the unconditioned CSAP.
Similar experiments were undertaken in seven patients with carpal tunnel syndrome who had undergone routine nerve conduction studies to establish the presence of focal slowing across the carpal tunnel (Goadsby and Burke, 1994). These studies included comparison of the digital sensory potentials from digit II to wrist and elbow and from digit V to wrist, the radial and median sensory potentials for digit I, and the median and ulnar potentials for digit IV (Table 1). Palmar stimulation was performed for the median nerve measuring orthodromic conduction from palm to wrist and antidromic conduction from palm to digit II, in order to demonstrate that the conduction slowing was maximal over the carpal tunnel segment. To be included in the study, the amplitude of the CSAP from digit II had to exceed 5 µV to be accurately tracked by computer and, as a result, patients with very small or absent potentials were excluded.
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To determine whether the development of conduction block associated with wrist extension could be altered by hyperpolarization, a further two sets of studies were undertaken in normal subjects. In the first series, eight experiments were performed on five subjects, in whom a sphygmomanometer cuff was inflated around the wrist to 200 mmHg to produce a progressive ischaemic block. The median nerve was stimulated using two supramaximal stimulus intensities, with the same rationale as discussed earlier. Comparison was made between these stimuli, one delivered alone and the other superimposed on a hyperpolarizing pulse of 15 ms duration, beginning 10 ms before the supramaximal stimulus. The strength of the hyperpolarizing current was set at ~20% of the threshold for a CSAP of 30–40% of maximum using test stimuli of 1 ms duration. To avoid ischaemia of the hand, a second set of studies was performed in four subjects using focal pressure on the median nerve. A 1.3 cm diameter button at the end of the main arm of a T-bar was pushed down over the nerve by a strap around the wrist. The arms of the T prevented the strap from contacting the volar aspect of the wrist and so prevented ischaemia of the hand. The nerve was stimulated through an electrode in the button, again using supramaximal stimuli, with or without a hyperpolarizing current, as described previously.
In all studies skin temperature was measured at the second metacarpophalangeal joint and the wrist, and was kept above 32°C (varying by less than ±0.5°C) at both sites by radiant heat and wrapping the limb in a blanket. The amplitude of the CSAP or CNAP was measured from the negative peak to the following positive peak (i.e. the falling phase of the potential). The latency of the CSAP or CNAP produced by the test stimulus was measured to negative peak. The changes in threshold, refractoriness and supernormality were measured when maximal for each experiment because the time to maximal change varied for each subject, rendering measurement at a fixed time inappropriate. All data are quoted as mean ± SEM.
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Results |
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Changes in impulse conduction in normal subjects
Extreme wrist extension produced conduction block in normal subjects (Figs 1 and 2
). Sometimes the wrist had to be repositioned and hyperextended, but ultimately conduction block developed between the wrist and digit II in all six subjects. The decrease in amplitude of the CSAP was associated with an increase in its latency by 0.31 ± 0.1 ms. The amplitude reduction began at 21.8 ± 5.8 min and was maximal at 49.3 ± 10.7 min. Overall, there was a reduction in amplitude of the maximal CSAP recorded at digit II by 61.5 ± 12.2% over this period.
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Figure 1
shows the earlier development of changes in the CSAP than the CMAP and, accordingly, subsequent studies were confined to the CSAP. These findings suggest that sensory axons are more sensitive than motor axons to this manoeuvre. However, the CSAP is more susceptible to amplitude changes due to temporal dispersion of the afferent volley, and there were prominent changes in latency as conduction block developed. This issue is considered further in the Discussion section, but it should be recognized that the decrease in amplitude of the CSAP probably involved both dispersion of the volley and conduction block.
In these experiments, the CNAP was recorded simultaneously at the elbow in addition to the digit, following stimulation at the wrist. The elbow potential was often contaminated by EMG activity from nearby muscles because the subjects had difficulty relaxing, but there was no decrease in the size of the nerve potential, and no increase in its latency as conduction block developed between the wrist and finger (Fig. 2A and B). This finding indicates that the changes in amplitude and latency of the CSAP occurred distal to the stimulus site, presumably within the carpal tunnel.
Excitability changes associated with wrist extension
Changes in axonal excitability were measured just proximal to the wrist during maintained wrist extension by tracking the changes in stimulus intensity required to produce a CSAP of 30–40% of maximum (Fig. 3). Extension of the wrist in five subjects was associated with a reduction in the required stimulus current by 16.1 ± 5.7%. The increase in excitability was associated with appropriate changes in other excitability indices that are sensitive to changes in membrane potential, and this indicates that it was due to axonal depolarization (Fig. 3B).
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Supernormality was measured as the decrease in current necessary to produce the target CSAP when a conditioning stimulus was delivered 7 ms before the test stimulus, i.e. the interval at which supernormality is normally maximal (Kiernan et al., 1996b
). Prior to wrist extension, the resting level of supernormality was –14.6 ± 1.1%. With extension, there was a gradual reduction in supernormality, until finally it was completely abolished at the 7-ms conditioning–test interval, replaced by refractoriness of 4.6%. The overall change in threshold of the conditioned potential was 19.2 ± 4.4%. Refractoriness was measured as the increased current required to produce the test potential when the conditioning–test interval was 2 ms, an interval that sampled the relatively refractory period. At rest, there was refractoriness of 17.8 ± 6.0%. Wrist extension was associated with a prominent increase in refractoriness by 85.2 ± 9.7%. Based on the appearance of refractoriness at the 7-ms conditioning–test interval (see above), the increase in refractoriness involved its duration as well as its extent.
Wrist extension resulted in prolongation of the latency of the unconditioned potential by 0.44 ± 0.07 ms (Fig. 3D). The above changes (increased axonal excitability, increased latency, decreased supernormality, increased refractoriness) are those previously reported to occur during the ischaemic compression produced by inflation of a sphygmomanometer cuff (Mogyoros et al., 1997). Presumably, therefore, wrist extension depolarizes axons and produces conduction block within the carpal tunnel, with spread of the excitability changes to the wrist. The relative importance of compression, ischaemia and traction on the nerve in these excitability changes is unknown (and any difference may only be semantic; see Discussion).
Changes in axonal excitability and conduction block in carpal tunnel syndrome
Each of the seven patients had evidence of focal conduction slowing across the carpal tunnel segment of the median nerve (Table 1). These findings and those of palmar stimulation (Goadsby and Burke, 1994) established that conduction was normal in the median nerve proximal and distal to the carpal tunnel segment. At the distal crease of the wrist, refractoriness (21.3 ± 5.6%) and supernormality (–13.3 ± 1.6%) at rest were not significantly different from those in the control subjects.
The development of conduction block was recorded in the patients using paired supramaximal test stimuli as previously described (Fig. 4C). In all subjects the maximal CSAP decreased with wrist extension, the change beginning at 12.8 ± 2.8 min and becoming maximal at 28.1 ± 3.3 min. Though the means were longer for the patients, these values were not significantly different from control values (onset, P < 0.1; peak, P < 0.09; unpaired t test). The amplitude of the maximal CSAP decreased by 77.7% over this 14–15 min period.
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Wrist extension produced changes in nerve excitability in the seven patients that were qualitatively similar to those in the control subjects (Fig. 4
). The threshold of the submaximal CSAP was reduced by 24.1 ± 4.6% (Fig. 4A). During wrist extension, supernormality was reduced by 19.2%, the test potential becoming refractory (+5.8%) at the 7-ms conditioning–test interval, much as in control subjects (Fig. 4B). This was associated with an increase in refractoriness by 115% and a prolongation in latency of the unconditioned test potential by 0.51 ± 0.05 ms (Fig. 4B). As in the studies on normal subjects, these findings indicate that axonal depolarization extended to the wrist level, the site of the stimulating electrodes.
Paraesthesiae during wrist extension and after its release
All subjects, both normals and patients with carpal tunnel syndrome, experienced paraesthesiae during the development of conduction block associated with wrist extension, but these were relatively mild. Paraesthesiae were experienced by all subjects—normal controls and patients—after the release of wrist extension, and were invariably reported to be more intense. The intensity of paraesthesiae was not formally quantified because comparisons between subjects of the intensity of a purely subjective phenomenon are difficult to make accurately. Nevertheless, there was no clear tendency for the patients to report greater or less paraesthesiae during wrist extension or following its release.
Can depolarization block be altered by hyperpolarization?
Two sets of experiments were performed on five normal subjects to test the hypothesis that depolarization block could be altered by hyperpolarizing axons at the site of nerve compression to counteract the compression-induced depolarization. In eight experiments a sphygmomanometer cuff was inflated around the wrist to 200 mmHg to produce a progressive ischaemic block. Comparison was made of the CSAPs produced by four supramaximal stimuli delivered to the median nerve under the cuff. Two stimuli of different intensity were delivered in isolation, and two identical stimuli were superimposed on a hyperpolarizing pulse of 15 ms duration, beginning 10 ms before the supramaximal stimulus. The strength of the hyperpolarizing current was set at 20% of the threshold for a CSAP of 30–40% of maximum in response to a 1-ms stimulus. Such polarizing currents have clear effects on membrane potential, increasing threshold, reducing refractoriness and increasing supernormality (Burke et al., 1998). The hyperpolarizing current produced no significant difference in the amplitude of the maximal CSAP.
To produce focal nerve compression without the distal ischaemia, presumably a situation more akin to carpal tunnel syndrome, focal pressure was applied to the median nerve in five experiments on four subjects. A button at the end of a T-bar was pushed down over the nerve at the wrist by a strap that could not tighten around the wrist and therefore did not make the rest of the hand ischaemic. The nerve was stimulated through an electrode in the button using supramaximal stimuli, with or without a hyperpolarizing current, as in the previous eight experiments. Again, the hyperpolarizing current did not alter the development of conduction block (Fig. 5).
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Discussion |
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The present study has documented that prolonged wrist extension induces conduction block both in normal subjects and in patients with carpal tunnel syndrome, and that the excitability changes recorded a few centimetres proximal to the site of block are similar to those observed with ischaemic compression (Stöhr et al., 1981
; Bostock et al., 1994; Mogyoros et al., 1997). The following discussion will focus, first, on the conclusion that, in both the patients and the normal subjects, the conduction block was a `depolarization' block, due to nerve compression, secondly on the implications of the present findings for the pathophysiology of carpal tunnel syndrome, and thirdly on the finding that hyperpolarizing currents did not alter the development of conduction block.
The nature of the conduction block
Reduction in the amplitude of a maximal compound nerve volley could be due to dispersion of the action potentials of the single fibres making up the volley, in addition to conduction block, and this may explain why changes in the CSAP preceded those in the CMAP. However, because ischaemic compression may initially involve predominantly the fastest axons contributing to the compound volley, there can be a small transient increase in amplitude of the CSAP (Kiernan et al., 1995), as seen in Figs 3C and 5. We cannot be certain of the extent to which dispersion contributed to the amplitude reductions seen in the present study, but when the reduction exceeded 50%, as in all subjects studied, it is likely that conduction block was the dominant factor in the amplitude reduction. The fact that the amplitude and latency of the CNAP recorded at the elbow remain unchanged (Figs 2 and 4) confirms that the block was restricted to the segment between the wrist and the finger, even if excitability changes extended more proximally.
It should be noted that the excitability changes were measured at the wrist, proximal to the site of maximal pressure and of developing block. Presumably qualitatively similar but quantitatively greater changes occurred within the carpal tunnel, but these would have been difficult to track as conduction block developed. The changes in axonal excitability just proximal to the wrist indicate that wrist extension depolarized axons. In addition to the reduction in threshold of the submaximal CSAP, there was an increase in its latency, an increase in refractoriness and abolition of supernormality, all consistent with axonal depolarization. These changes are both qualitatively and quantitatively similar to those seen with ischaemic compression (Mogyoros et al., 1997), though they developed more slowly with wrist extension, presumably because the site of maximal compression was more distal. While the excitability changes are those expected from an ischaemic compressive lesion, the extent to which they can be attributed to compression, ischaemia or traction on the nerve can be debated. There was no direct compression or ischaemia but compressive forces could have been exerted by traction on the nerve, particularly if the nerve was `tethered' in the carpal tunnel (McLellan and Swash, 1976). Accordingly, the excitability changes cannot be used as evidence that nerve stretch and stretch-sensitive channels were involved in the axonal depolarization, though they cannot be excluded.
Pathophysiology of carpal tunnel syndrome
The present results are consistent with the development of an ischaemic compressive block within the carpal tunnel during wrist extension. It is therefore pertinent to address the extent to which the abnormalities in patients with carpal tunnel syndrome can be explained on this basis.
The paraesthesiae experienced during the development of an ischaemic/compressive block are relatively mild, though a dull discomfort can be prominent when the block is severe. The most intense paraesthesiae are felt on release of the block, perhaps implying that in carpal tunnel syndrome the characteristic symptoms result more from release of compression than from ongoing compression. In addition, patients commonly complain of transient numbness on waking, and this is associated with intense paraesthesiae, much as might be expected during recovery from compression block.
In nerve conduction studies on patients with carpal tunnel syndrome, the characteristic findings are focal conduction slowing and CSAPs of reduced amplitude. Often these occur in patients with no objective sensory loss (as in the present study). As already mentioned, low-amplitude CSAPs could result from temporal dispersion of the compound volley rather than conduction block or axonal loss and, if this is so in carpal tunnel syndrome, preservation of sensation would not be surprising. The conduction slowing that occurs in depolarized axons is probably due to inactivation of Na+ channels (Hodgkin and Huxley, 1952), so that fewer are available for the generation of action potentials. This mechanism is also responsible for conduction slowing during the relatively refractory period and, accordingly, axonal refractoriness is greatly enhanced when axons are depolarized (Figs 3 and 4). The maximal slowing seen in the present study, presumably due to this mechanism, was ~0.5 ms. However, the slowing across the carpal tunnel averaged ~1 ms for the patients in this study, and it was demonstrable when the patients had no symptoms and, presumably, were not at that moment suffering from nerve compression. If ischaemic compression contributes to the conduction slowing in patients, as the present study argues, additional factors must also operate.
It is important to note that the present study required a CSAP of at least 5 µV, and was therefore restricted to patients with mild or moderate carpal tunnel syndrome. It is likely that, while ischaemic/compression may be important in carpal tunnel syndrome, morphological factors such as axonal loss, axonal attenuation, disordered myelination and intraneural fibrosis are also important, perhaps more so in patients with more prominent clinical deficits. A number of factors could contribute to the focal slowing of conduction, and it is likely that these vary in different patients and with lesions of different severity. It seems reasonable to question whether a myelin disturbance occurs in all patients and the extent to which it contributes to the conduction slowing. Even in those with a more severe disorder, attenuation of axons at the site of compression would result in conduction slowing over the attenuated segment, and it remains to be established whether and to what extent disturbed myelination contributes to the conduction disturbance (or to the ectopic activity responsible for paraesthesiae) in patients with this syndrome.
Hyperpolarization does not delay conduction block
In previous studies from this laboratory, attempts were made, without success, to precipitate conduction block in cutaneous afferents by causing them to conduct high-frequency trains of impulses (Kiernan et al., 1996b; Miller et al., 1996). The rationale was that, if the conduction slowing was due to demyelination and if low-amplitude CSAPs indicated some conduction block at rest, the hyperpolarization that results from activity might cause conduction block at the site of demyelination where the safety margin for impulse conduction would be low (Bostock and Grafe, 1985). However, the hyperpolarization due to activity would not be expected to impair conduction if axons were depolarized, as occurs in an ischaemic/compressive lesion.
The possibility that hyperpolarization might have a `protective' effect in patients with an ischaemic/compressive lesion prompted experiments to determine whether hyperpolarizing currents would alter the development of conduction block due to direct nerve compression. In this light, the failure of hyperpolarization to alter the development of conduction block in compressive lesions was disappointing. However it indicates only that the depolarizing change in membrane potential may not be the most important factor in the development of conduction block. The focal ischaemia that accompanies compression will paralyse the electrogenic Na+/K+ pump and other energy-dependent processes, and there will be abnormal ion accumulation on either side of the axonal membrane, factors that will not be reversed merely by changing membrane potential.
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Acknowledgments |
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The work was supported by Glaxo Wellcome Australia Ltd and the National Health and Medical Research Council of Australia.
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Received July 16, 1998. Revised November 14, 1998. Accepted January 18, 1999.
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