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Biomedical subjects

I Mogyoros

Publications and source records attributed to I Mogyoros.

At least 37 records · Page 2Linked to original sources
PubMed1999

Conduction block in carpal tunnel syndrome.

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 degrees, 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.

Action Potentials↗
PubMed1998

Activity-dependent hyperpolarization of human motor axons produced by natural activity.

1. The changes in excitability of motor axons produced by natural activity were measured in six healthy subjects using voluntary contractions lasting 15 s, 30 s and 1 min, by recording the changes in stimulus current required to produce a compound muscle action potential of approximately 60 % of maximum. 2. On cessation of the contractions there was a prominent increase in the current required to produce the target potential, accompanied by an increase in rheobase, a decrease in strength-duration time constant, and an increase in axonal supernormality. These changes indicate that the hypoexcitability was due to axonal hyperpolarization. 3. The activity-dependent hypoexcitability increased in depth and duration the longer the contraction. Following a 1 min contraction, it produced a 24 % increase in threshold, waning over 15 min. The hypoexcitability was greater than in cutaneous afferents tetanized to produce an equivalent rate-dependent stress. 4. It is concluded that natural activity results in substantial hyperpolarization of active axons and that, for similar discharge rates, the degree of hyperpolarization is greater in motor axons than cutaneous afferents. The greater effect of activity on the excitability of motor axons could be due to less inward rectification and less persistent Na+ conductance than in sensory axons. It is suggested that motor axons may therefore be more susceptible than cutaneous afferents to conduction block at sites of impaired safety margin for impulse conduction.

Adult↗
PubMed1998

Ischemic resistance of cutaneous afferents and motor axons in patients with amyotrophic lateral sclerosis.

Compared with control subjects, patients with amyotrophic lateral sclerosis (ALS) have been reported to experience less or no paresthesias during and after release of ischemic compression of the upper arm for 10 min. This is reminiscent of the resistance to ischemia of diabetic patients, in whom sensory and motor axons undergo less ischemic depolarization and less postischemic hyperpolarization than in control subjects. The present study compared the changes in axonal excitability produced by ischemia for 10 min in 21 patients with ALS and 14 age-matched control subjects. Fewer patients reported intraischemic or postischemic paresthesias and the intensity of paresthesias was less, but this was significant only for postischemic paresthesias. There were quantitatively similar changes in refractoriness, supernormality, and strength-duration time constant during ischemic compression, but the increase in excitability of motor axons was less during the second half of ischemia in the patients. After release of ischemia the postischemic hyperpolarization was greater in the ALS patients, the opposite of what occurs in diabetes. These changes could reflect reduced intraneural K+ accumulation due to loss of motor axons or an alteration in nerve metabolism or membrane properties. Either way, the present study has failed to confirm previous reports of "ischemic resistance" in ALS, and indicates that the changes in axonal properties in ALS are not analogous to those in diabetes mellitus.

Adult↗
PubMed1998

Quantitative description of the voltage dependence of axonal excitability in human cutaneous afferents.

The voltage dependence of indices of axonal excitability were quantified for cutaneous afferents in eight normal subjects, using the threshold for a target compound sensory action potential as a measure of membrane potential. The membrane potential was altered using subthreshold depolarizing and hyperpolarizing currents of various sizes (-50% to +50% of threshold). Refractoriness and supernormality were determined as the threshold change required to produce the target potential when preceded by a supramaximal stimulus at appropriate conditioning-test intervals. The strength-duration time constant (tauSD) was calculated from the threshold currents using unconditioned test stimuli of 0.1 and 1 ms. There was a near-linear relationship between each of these indices and the reciprocal of threshold (a measure of 'excitability'). It is argued that the voltage dependencies of refractoriness and tauSD largely reflect the behaviour of transient and persistent Na+ channels, respectively, and that the present data therefore quantify aspects of Na+ channel behaviour in human nerves.

Axons↗
PubMed1998

Strength-duration properties of sensory and motor axons in amyotrophic lateral sclerosis.

In normal subjects, the strength-duration time constant is longer for cutaneous afferents than for motor axons, probably because the former express a greater non-inactivating (persistent) Na+ conductance that is active at threshold. Using a threshold-tracking system the strength-duration properties of cutaneous afferents and motor axons were recorded from 23 patients with amyotrophic lateral sclerosis, and compared with those of 32 healthy subjects. In control subjects and patients, the strength-duration time constant of sensory fibres declined with age, and there was no difference between the two groups when age was taken into account. The motor time constant did not change with age when expressed as a percentage of the time constant for sensory fibres in the same nerve, but was significantly longer for the patients than control subjects. In addition, motor rheobase was significantly lower for the patients, when expressed as a percentage of sensory rheobase. There was an inverse relationship between the time constant and rheobase for sensory and motor axons, and this was the same for the patients and the control subjects, suggesting that the variations in time constant within and between the groups were related to the expression of a common factor. Measurements of refractoriness and supernormality provided no evidence for a difference in resting membrane potential between the patients and control subjects. These findings are consistent with the interpretation that motor axons of the patients with amyotrophic lateral sclerosis have a greater persistent Na+ conductance than normal motor axons. This could contribute to the ectopic activity responsible for fasciculation.

Adult↗
PubMed1997

Paraesthesiae induced by prolonged high frequency stimulation of human cutaneous afferents.

1. The present study has explored the behaviour of human cutaneous afferents following conduction of prolonged trains of impulses at 200 Hz for 10-20 min, correlating the resultant changes in excitability with the perception of paraesthesiae. 2. Tetanization for 10 min resulted in activity-dependent changes in axonal excitability, with an initial period of hyperexcitability, followed by a long-lasting subexcitability. All subjects experienced paraesthesiae soon after cessation of the tetanic train, and these subsided gradually over 16 min. 3. Longer tetanic trains of 20 min duration resulted in greater changes in axonal excitability, but with paraesthesiae of a similar time course. The post-tetanic increase in excitability was abolished when short tetanic trains were delivered > 30 min before long trains, but all subjects still experienced paraesthesiae. 4. Threshold distributions following tetanic stimulation for both 10 and 20 min established that all axons contributing to the sensory volley underwent a uniform pattern of post-tetanic threshold changes. There was no evidence of a bimodal distribution with some axons hyperpolarized and others depolarized, as occurs with motor axons. However, the excitability changes were graded, with axons of lowest threshold undergoing a proportionately greater increase in excitability than axons of higher threshold. 5. The post-tetanic excitability changes were greater at the site of stimulation than elsewhere along the peripheral nerve. However, DC polarizing currents applied at this site failed to alter the sensation of paraesthesiae in the post-tetanic period. Furthermore, local anaesthetic block of the peripheral nerve proximal to the stimulation site failed to suppress the paraesthesiae. 6. The uniform pattern of post-tetanic threshold changes for cutaneous afferents differs from the bimodal distribution seen with post-ischaemic and post-tetanic motor axons. This difference in behaviour may reflect greater inward rectification and greater expression of a non-inactivating threshold conductance in cutaneous afferents. It is suggested that the ectopic activity responsible for paraesthesiae in the post-tetanic period arises from a more central site than the peripheral nerve.

Action Potentials↗
PubMed1997

Excitability changes in human cutaneous afferents induced by prolonged repetitive axonal activity.

1. The present study was undertaken to document the excitability changes produced by prolonged high-frequency trains of impulses in cutaneous afferents of six human subjects. 2. Trains of supramaximal stimuli at 200 Hz for 2 min or less produced a prolonged depression in excitability, consistent with activation of the electrogenic Na+-K+ pump. Trains of longer duration resulted in an initial period of hyperexcitability which, with 10 min trains, was associated with the sensation of paraesthesiae in all subjects. This transient hyperexcitability gradually gave way to a long-lasting period of hypoexcitability. 3. The excitability changes were reproducible, and were accompanied by corresponding changes in supernormality, refractoriness, strength-duration time constant and rheobase current, suggesting that the changes in axonal excitability reflected a change in membrane potential. 4. The transient increase in excitability that follows tetanic trains of 10 min had qualitatively similar effects on cutaneous axons as ischaemia or application of a depolarizing current. The post-tetanic changes in the supernormal period of sensory axons were those expected from the changes in excitability, without evidence of a gross distortion in its time course, as has been previously demonstrated in a hyperstimulated human motor axon. 5. It is concluded that the post-tetanic hyperexcitability of human sensory axons is probably driven by increased K+ accumulation in the restricted diffusion space under the myelin sheath, much as in motor axons, the differences in behaviour of sensory and motor axons being explicable by greater inward rectification in sensory axons.

Adult↗
PubMed1997

Excitability changes in human sensory and motor axons during hyperventilation and ischaemia.

This study was undertaken to compare the excitability changes of sensory and motor axons during hyperventilation and ischaemia, and to determine why ectopic impulse activity develops more readily during hyperventilation, and in sensory fibres. During hyperventilation for 20 min, all six subjects reported paraesthesiae in the hand and face, and four out of the six developed muscle twitching and cramps, associated with significant decreases of 20-30% in the threshold current required to produce sensory and motor potentials of constant size. During ischaemia four out of the six subjects reported paraesthesiae, but none reported muscle twitching. There were significant decreases of 15-20% in threshold for sensory and motor fibres. Ischaemia produced a marked decrease in supernormality, an increase in refractoriness and an increase in latency of the test compound sensory or motor potential, changes that were not seen with hyperventilation. The decrease in threshold during these manoeuvres was associated with a significant increase in strength--duration time constant (tau SD), indicating a relatively greater decrease in rheobase current. Using the technique of latent addition, we found that the changes in tau SD were consistent with a recently proposed model in which non-inactivating, voltage-dependent 'threshold channels' (presumably persistent Na+ channels) are active at resting potential. The failure of hyperventilation to alter conduction velocity, refractoriness or supernormality appreciably indicates that, unlike ischaemic depolarization, hyperventilation does not increase inactivation of conventional Na+ channels or activation of K+ channels, and this implies that the hyperventilation-induced increase in excitability is not the result of conventional depolarization, as seems to occur during ischaemia. These results suggest that hyperventilation has a rather selective action on the threshold channels, and they help to explain its greater effectiveness compared with ischaemia in provoking ectopic discharges. The greater expression of threshold channels in sensory than in motor fibres can explain why hyperventilation induces paraesthesiae before fasciculation and why only paraesthesiae occur during ischaemia.

Action Potentials↗
PubMed1996

Effects of femoral nerve stimulation on the electromyogram and reflex excitability of tibialis anterior and soleus.

The present study was undertaken to determine whether femoral nerve stimulation would produce heteronymous reflex responses in tibialis anterior (TA) and soleus, demonstrable by averaging the electromyogram (EMG) produced by a voluntary contraction, and whether the responsible changes in excitability were sufficient to affect the H reflexes of TA and soleus. In both muscles, femoral stimuli produced short-latency, presumably monosynaptic excitation, better defined in poststimulus averages of unrectified EMG, followed by long-lasting inhibition, better defined in averaged rectified traces. The H reflexes underwent changes at appropriate latencies. The thresholds for excitation and inhibition were, respectively, below and above threshold for the quadriceps M wave. The heteronymous responses were largely independent of stimulus rate and, within limits, scaled with the level of background contraction. The ability to define these heteronymous connections using relatively simple methodology extends their utility. Such tests may prove useful in probing pathophysiological mechanisms in individual patients.

Adult↗
PubMed1996

Activity-dependent changes in impulse conduction in a focal nerve lesion.

The present study was undertaken to determine whether, in patients with a focal nerve lesion, the axonal hyperpolarization produced by conduction of brief trains of impulses would result in conduction block in cutaneous afferents, thus indicating a site of impaired safety margin for impulse transmission. In 25 patients with focal conduction slowing across the carpal tunnel segment of the median nerve, a conditioning train of 10 supramaximal stimuli at 200 Hz resulted in a reduction in amplitude and an increase in latency of the test volley set up by a supramaximal stimulus. These changes exceeded those seen in control subjects, but followed a similar time course, with full recovery within 150 ms. There was a significant correlation between these changes and the severity of the compression neuropathy as indicated by the degree of focal conduction slowing in routine nerve conduction studies. Control data suggested that the measured changes in amplitude could be explained by temporal dispersion of the compound sensory volley. This view was supported by measurements of the changes in amplitude (and latency) in normal subjects during acute compression before conduction block had developed. In addition, there were similar linear relationships between the activity-dependent amplitude reduction and the corresponding change in latency for both the patients and the control subjects, indicating that there was no need to invoke factors additional to those operating in the control subjects to explain the greater amplitude depression in the patients. It is concluded that, although the depression in amplitude was greater in patients than in healthy subjects, the magnitude of this change can be explained by temporal dispersion of the abnormal compound sensory action potential associated with greater conduction slowing. Activity-dependent conduction block may play little role in the pathophysiology of carpal tunnel syndrome.

Action Potentials↗
PubMed1996

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.

Adult↗
PubMed1996

Differences in the recovery of excitability in sensory and motor axons of human median nerve.

Following conduction of an action potential there is a stereotyped sequence of changes in excitability as axons are initially refractory, then superexcitable and finally subexcitable. These activity-dependent oscillations in excitability subside over 100 ms and together constitute the recovery cycle. The present study was undertaken first to document the recovery cycle of sensory and motor axons of different threshold and, secondly, to compare the changes in sensory axons with those in motor axons. A computerized threshold-tracking system was used to measure recovery cycles in six healthy subjects; stimuli were applied to the median nerve at the wrist. Changes in the threshold required to produce an antidromic compound sensory action potential (CSAP) and an orthodromic compound muscle action potential (CMAP) of fixed amplitude (30%, 50% and 70% of maximal) were recorded following a single supramaximal conditioning stimulus. Normalized recovery cycles were identical for axons of different threshold, whether sensory or motor, and were reproducible on repeat testing. However, there were significant differences between the changes in sensory and motor axons, with greater supernormality and greater late subnormality in motor axons. The greater changes in motor axons could not be explained by differences in the strength-duration properties of sensory and motor axons. There are biophysical differences in the properties of sensory and motor axons and these differences may underlie the differential susceptibility of sensory and motor axons in peripheral nerve disorders.

Adult↗
PubMed1996

Changes in excitability and impulse transmission following prolonged repetitive activity in normal subjects and patients with a focal nerve lesion.

The present study was undertaken to document the excitability changes produced by prolonged high-frequency trains of impulses and to determine whether these changes in excitability would impair neural transmission in cutaneous afferents of patients with focal slowing of conduction across the carpal tunnel. A submaximal test stimulus was used to measure the changes in axonal excitability following trains of supramaximal stimuli delivered at 200 Hz for 30 s, 1 min or 2 min. These trains produced a prolonged depression in excitability in normal axons with gradual recovery to control levels over 20-30 min, presumably due to hyperpolarization associated with activation of the electrogenic Na+/K+ pump. The decrease in excitability was demonstrable at nerve segments remote from the site of tetanic stimulation. Based on these findings, the effects on neural transmission were then assessed in normal subjects and patients using a supramaximal test stimulus following a 1-min tetanic train. In normal subjects there was a small activity-dependent decrease in amplitude of the compound sensory action potential (CSAP) associated with a prolongation in its latency. In patients with focal slowing of conduction across the carpal tunnel there was a more marked post-tetanic prolongation in latency, but the reduction in amplitude of the maximal CSAP was no greater than in the control subjects. It is concluded that activity-dependent conduction block is not a major cause of symptoms in carpal tunnel syndrome. It is suggested that the conduction slowing seen in patients with mild-moderate carpal tunnel syndrome could result from mechanisms other than demyelination.

Action Potentials↗
PubMed1995

Homonymous and heteronymous monosynaptic reflexes in biceps brachii.

Using poststimulus time histograms, it has been reported that stimulation of the median nerve at the elbow produces a monosynaptic EPSP in voluntarily active single motoneurons of the human biceps brachii. The present study was undertaken to: (i) determine whether such stimulation could evoke a reproducible reflex response in biceps brachii; and (ii) establish the optimal conditions for eliciting the reflex under clinical conditions. Twelve normal subjects were studied. No reflex response was recordable when biceps brachii was relaxed. A reflex response with a mean latency of 14.0 ms (+/- 0.96 ms) could be recorded during a background voluntary contraction. The response was small (0.5-4.5% of the maximal M wave) but symmetrical, and could be obtained in all subjects. The responsible afferents appear to be rapidly conducting fibers from forearm flexor muscles and the latencies of the response were consistent with a monosynaptic reflex. Reflex amplitude increased with stimulus intensity and contraction strength. Stimulus rate did not affect amplitude significantly. It is concluded that a reproducible heteronymous monosynaptic reflex can be recorded from the contracting biceps brachii on stimulation of the median nerve at the elbow. Although smaller than the homonymous H reflex evoked by stimulation at Erb's point, it was technically easier to demonstrate that the EMG potential was of reflex origin (rather than part of an M wave). These reflexes should be of value in the assessment of the C-5/C-6 segments and the upper trunk of the brachial plexus.

Adult↗
PubMed1995

Reproducibility of a heteronymous monosynaptic reflex in biceps brachii.

The present study provides normal data for a new technique to assess conduction across the C5/C6 segments by recording a heteronymous monosynaptic reflex response from the contracting biceps brachii in response to stimulation of the median nerve in the cubital fossa. The reflex responses were reproducible and symmetrical, with a mean latency of 14.8 msec (S.D. 1.4 msec) and an absolute side-to-side differences of 0.5 msec (S.D. 0.29 msec). Latency was significantly correlated with both age and height, and multiple regression analysis provided the following equation: latency (msec) = 0.091 x height (in cm) + 0.036 x age (years) - 1.988. Amplitudes had wide scatter (22-365 microV on the right side) and positive skew. An amplitude less than 40% of that for the other side would be outside the 90th percentile. Five cases are described to illustrate the potential clinical utility of this test. However, whether this reflex is of diagnostic value can be answered only by a prospective study comparing it with other routine investigations.

Adult↗
PubMed1995

Activity-dependent changes in impulse conduction in normal human cutaneous axons.

The present study was undertaken to determine if the axonal hyperpolarization produced by a brief train of impulses would impair neural transmission in cutaneous afferents of normal human subjects (n = 25). To assess changes in axonal excitability, a submaximal test stimulus was conditioned by a train of 10 supramaximal stimuli at 200 Hz. This produced a depression in excitability lasting up to 100 ms, demonstrable at nodes of Ranvier remote from the site of stimulus application, and probably due to activation of a slow K+ conductance. The effects of this change in excitability on neural transmission were assessed using a supramaximal test pulse. This revealed small but significant activity-dependent decreases in amplitude at conditioning-test intervals up to 20 ms and increases in latency at intervals up to 70 ms. Both the amplitude decrease and the latency increase were greater the longer the conduction distance. The reduction in amplitude of the compound sensory potential could be explained by temporal dispersion due to the increase in latency. It is concluded that, at the nodes of normal cutaneous afferents, the safety margin for impulse generation is sufficiently high that the activity-dependent hyperpolarization does not produce conduction block. It is likely that the previously described reductions in the amplitude of the compound sensory action potential in response to brief trains of stimuli were due to dispersion of the volley, not conduction failure, and that conduction failure does not occur in normal cutaneous axons solely by activation of slow K+ conductances.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗