The motor response potential after distal and proximal stimulation: studies in healthy volunteers and in polyneuropathies (author's transl)]

Muscle responses evoked distally and proximally were recorded in median and in peroneal nerves from controls and patients with polyneuropathies of different origin. The following parameters were studied in the individual muscle response: 1. the amplitude of the potential, measured peak to peak, 2. the amplitude of the negative phase, 3. the total duration of the potential, 4. the duration of the negative phase, 5. the area covered by the negative phase. Results of the proximal measurements were divided by those of the distal records. Distal motor latencies and nerve conduction velocities were also determined. In controls a loss of amplitude of 10-15% and an equal reduction of the area covered by the negative phase was noted in proximally evoked responses and the duration of the negative phase was increased by 2-7% when compared with distal measurements. In some polyneuropathies these parameters showed significantly pathological changes, although distal motor latency, amplitude and nerve conduction velocity were still within the normal range. Comparison of distally and proximally evoked muscle potentials may thus lead to further information about the mode of conduction in altered motor nerves.     

A micro-electrode study of peripheral neuropathy in man. Part 2. Responses to conditioning stimuli.

Surface, needle and micro-electrode recordings were obtained from sensory nerves of patients with various types of peripheral neuropathy. Changes in amplitude and conduction velocity of nerve action potentials were measured after a single conditioning stimulus and after tetanic stimulation for 2 min. In patients with hereditary forms of axonal degeneration (AD), recovery processes of nerve fibres of all conduction velocities were normal; in acquired forms of AD fibres with conduction velocity less than 30 m/sec had greater and more prolonged post-tetanic depression than control nerves of similar conduction velocity. Where neuropathy was associated with segmental demyelination (SD), fibres of all conduction velocities had prolonged recovery processes after both single and tetanic stimulation. The changes were especially marked at higher skin temperature, and were greater than the changes seen in nerves with acquired forms of AD. Finally, 2 sural nerves were studied during the process of Wallerian degeneration after a biopsy had been obtained proximally, and recovery processes did not change during the period of degeneration. Perceptual abnormalities were similar in AD and SD. It is suggested that changes in recovery processes of nerve fibres with segmental demyelination or regeneration after injury contribute to the perceptual abnormalities which occur in clinically encountered peripheral neuropathies.     

Effect of ischaemia on sensory potentials of normal subjects of different ages

In 73 normal subjects, from 10 to 82 years of age, maximum orthodromic sensory nerve conduction velocity was measured in the median nerve before and during a 30 minute period of vascular occlusion. During ischaemia progressive slowing in conduction velocity, decrease in amplitude, and increase in duration of the sensory action potential evoked at wrist and elbow by supramaximal stimulation of digit III were observed. However, a statistically significant difference (P<0·05 to P<0·01) between subjects was noted by grouping them by age: the older the subject, the longer the persistence of sensory response and the less marked the slowing in conduction velocity. The mechanism of the phenomenon has been discussed in relation to a similar longer resistance to ischaemia found in peripheral nerves of diabetic and uraemic patients.     

Conduction of nervous impulses in spinal roots and peripheral nerves of dystrophic mice

Conduction was studied in the sacral ventral roots and ventral tail nerves of dystrophic mice (dy/dy) and phenotypically normal littermates. In myelinated ventral root fibers of normal mice, conduction velocity was uniform with internodal conduction time45 ± 5 μsec (26 °C). In ventral root fibers of dystrophic mice, conduction velocity was decreased and strikingly non-uniform; both saltatory and continuous conduction were observed in different portions of the same nerve fiber. Continuous conduction with velocity <2 m/sec (26 °C) was characteristically observed in mid-root where the axons are bare; conduction was saltatory close to the exit from the spinal canal and near the spinal cord where the axons are myelinated.Maximum conduction velocity in ventral tail nerves was21 ± 3 m/sec for dystrophic mice and31 ± 4 m/sec for littermate controls (37 °C). Internodal lengths were somewhat decreased in the dystrophic peripheral nerves but there was no significant difference in maximum fiber diameters, myelin thickness or nodal morphology between dystrophic and normal nerves.     

Impairment of repetitive impulse conduction in experimentally demyelinated and pressure-injured nerves

Repetitive impulse conduction was studied in segmentally demyelinated peripheral nerves in guinea-pigs with experimental allergic neuritis (EAN) and in pressure-injured frog sciatic nerves. Normal guinea-pig sciatic-peroneal nerves maintained at 37°C conducted compound action potentials with only minor amplitude decreases at stimulus frequencies up to 200/sec. In contrast, nerves in EAN guinea-pigs maintained at 37°C demonstrated a rapidly progressive decrease in action potential amplitude when stimulated as slowly as 10-25/sec. The decrease is greater the higher the frequency of stimulation. At 100 stimuli/sec all EAN preparations showed more than a 50% reduction in action potential amplitude. These effects are reversible. In pressure-injured frog sciatic nerves similar effects occurred at stimulus frequencies as low as 50/sec. Normal frog nerves conducted up to 200 impulses/sec with little amplitude decrease. The probable mechanism and clinical significance of these results are discussed.     

Sensory group Ia proximal conduction velocity

The fastest median and ulnar velocities derived by recording motor and mixed nerve action potentials, F waves, H-reflexes, and somatosensory evoked potentials (SEPs) were compared. H-reflex recording was facilitated by employing selective group Ia excitation during voluntary muscular contraction. Mixed nerve, SEP, and H velocities, considered to predominantly reflect group Ia conduction, measured 63.2 +/- 3.2 m/sec, 63.4 +/- 4.5 m/sec, and 67.2 +/- 4.3 m/sec, respectively, between the wrist and elbow. Conventional motor conduction velocity was significantly slower (58.3 +/- 5.1 msec), but F velocity, which although nonuniform is also a measure of motor conduction, was 68.4 m/sec. Mean F latency was considered more reliable and representative than minimum F latency. F and H velocities accelerated proximally by 4.5 m/sec. They complement each other when evaluating motor and sensory group Ia conduction. The H-reflex and SEP use identical stimulus characteristics and when simultaneously recorded allow direct comparison of the fastest conducting peripheral and central sensory pathways.     

Method of studying conduction velocity in sensory fibers of the peripheral nerves and spinal cord. The averaging technic

The author describes a method of measuring conduction velocity in sensory fibres based on averaged evoked potentials. In the method potentials are recorded with surface electrodes over the nerves of the upper extremity at three sites: wrist, elbow and branchial plexus. The further route of the central neuron was represented by two responses from the cervical spinal cord at the C2 level, and first component N1 of the cortical response. The method makes possible distinguishing of damage to the peripheral part from that to the central part of the sensory system. Checking of the method in 15 healthy subjects made possible determination of conduction velocity which was stable for all measuring points in the peripheral nerve and spinal cord and was 75 m/sec, while at the distance from the spinal cord to the cortex it was only 58 m/sec. The author discusses in detail the technique of recording and reading of evoked potentials, whose amplitudes may be below 0.5 microV and latency is read with an accuracy of 0.1 msec.     

Peroneal nerve orthodromic sensory conduction technique: normative data

In some definite patients, a standard neurophysiological tool may not solve a complete differential diagnosis in common nerve peroneal neuropathy. In this study we have assessed a new simple procedure to study the orthodromic sensory conduction of both the superficial peroneal nerves (SPN) and deep peroneal nerves (DPN) in a heterogeneous group of 55 normal subjects. The mean sensory orthodromic conduction velocity of the SPN was 58.35 m/s. The mean sensory orthodromic conduction velocity of the mixed nerve action potential (MNAP) of the DPN was 55.27 m/s. The sensory conduction velocity, the amplitude of sensory-evoked potentials of SPN and DPN across the fibular head and the normative values are discussed. Our results confirm that these recording methods are easy to repeat and reliable in identifying peroneal neuropathy. An erratum to this article can be found at     

Effect of magnesium on nerve conduction velocity during regular dialysis treatment

Serial nerve conduction velocities in the peroneal and ulnar nerves have been measured in 10 patients on regular dialysis treatment over a three year period. Each patient alternated between phases on dialysis with magnesium-containing dialysate (1·5-1·7 m-equiv/l.) and phases on `magnesium-free' dialysate (0·2 m-equiv/l.). Plasma magnesium concentrations were high both pre- and post-dialysis during magnesium-containing dialysis, and normal to low on magnesium-free dialysis. All patients had defects in nerve conduction, mainly asymptomatic. Increases in nerve conduction velocity coincided with magnesium-free dialysis, and decreases occurred when the patients reverted to magnesium-containing dialysate. The significance of the correlation by the sign test was P<0·0005. It is concluded that extracellular magnesium levels can influence the rate of nerve conduction in vivo.     

Normal sensory conduction in the saphenous nerve in man.

Measurements of the sensory conduction velocity and the parameters of nerve action potentials in the saphenous nerve offer many advantages, compared with measurements in other nerves of the leg, regarding accuracy and the time required to complete the investigations. Therefore, the electroneurographical examination of the saphenous nerve is recommended in the early diagnosis of polyneuropathies and is indispensable in the exact diagnosis of proximal neuropathies and lesions of the femoral nerve. In the present study we indicate the proximal and distal segments of the saphenous nerve and illustrate the nerve action potentials from 70 normal subjects.     

Peripheral neuropathy in abetalipoproteinemia

We studied the peripheral neuropathy of three sisters with abetalipoproteinemia. Clinically, a sensory neuropathy progressively increased in severity. There was a diminution in the amplitude of sensory action potentials and a slight-to-moderate slowing in maximum sensory conduction velocity, initially most marked in distal portions of the nerves. Motor conduction was normal, although EMG indicated subclinical signs of partial chronic denervation. The sural nerves showed a decreased number of large fibers (greater than 7 micron); in the patient with the neuropathy of shortest duration, small fibers and clusters of regenerating fibers indicated regeneration. In the two patients with advanced neuropathy, one-half the segments of teased fibers showed paranodal demyelination. Also, unmyelinated fibers showed evidence of regeneration.     

Conduction velocity and temporal dispersion of the nerve volleys evoked by air-puff stimulation of the index finger and palm.

Air-puff stimuli were delivered to 5 successive sites (3 cm increments) over the index finger and palm to record propagating sensory nerve action potentials (SNAPs) from surface electrodes over the median nerve at the wrist. SNAPs consisted of a series of individual peaks (N1, P1, P2, N2 and P3) and the corresponding peaks in the records with stimulation at the various locations could be identified. The apparent conduction velocity of the first peak determined from the stimulation point at the finger tip to the wrist was 38 m/sec. With stimulation of the more proximal locations it became even slower. This paradoxical slowing is due to an increasing effect in the calculation of conduction velocity of the utilization time at the receptors for air-puff stimulation at progressively proximal sites. Segmental conduction velocity estimated between adjacent stimulus sites was 10-20 m/sec faster than the distal conduction velocity between the finger tip and the wrist. Within each segment, the conduction velocities of the individual peaks were not significantly different. These findings, together with invariant durations of the negative components (N1 and N2) in the propagating SNAPs along the ascending digital nerves, lead to the conclusion that the separate peaks are not the result of temporal dispersion due to differences in conduction velocity of skin afferents, but are primarily due to a more peripheral receptor mechanism involving variable delays in activation of different classes of mechanoreceptors.     

Ulnar nerve lesions associated with the carpal tunnel syndrome

Electrophysiological studies were performed on median and ulnar nerves in 234 cases of carpal tunnel syndrome. Abnormalities of the ulnar nerve sensory action potential were found in 39·3% of cases. The amplitude of the ulnar nerve sensory action potential was related to the amplitude of the median nerve sensory action potential, and to the median nerve motor conduction velocity in the forearm. The findings suggest that in a significant proportion of patients with carpal tunnel syndrome, a more generalized subclinical neuropathy may be present.     

Electrophysiologic evaluation of spinal cord motor conduction

Spinal cord motor conduction was determined by stimulating with a monopolar needle at the C5 cord level and recording evoked motor potentials from the ipsilateral tibialis anterior muscle. Minimal F wave and direct motor latencies from the peroneal nerve were used to calculate peripheral conduction time. Mean velocity index (defined as the distance from C5 to L4 divided by central conduction time) of 15 normal subjects was 64.9 m/sec (SD 7.5). In 5 patients with multiple sclerosis the mean velocity index was 40.6 m/sec (SD 6.5), whereas in 3 patients with cervical myelopathies, due to extradural compression, the mean velocity index was 32.8 m/sec. A repeat study in one of the latter patients, 4 days after removal of a C5 disc, documented a marked improvement in cord conduction. In a patient with a thoracic and cervical syrinx, cervical cord stimulation on the clinically affected side failed to evoke a motor potential, whereas the unaffected side was normal. This method provides a simple and effective way to evaluate spinal cord motor conduction using routine electrodiagnostic equipment.     

Carpal tunnel syndrome: correlations between pressure measurement and intraoperative electrophysiological nerve study

In 19 carpal tunnel syndrome (CTS) patients and 4 control subjects a catheter was introduced into the carpal tunnel and slowly retracted in 5 mm steps. Pressure was measured with the continuous infusion technique. In the same group of patients and controls, median nerve antidromic sensory action potential (aSAP) was detected intraoperatively stimulating proximally (S1), in the center (S2), and distally (S3) to the carpal tunnel and recording from the third finger (R). Sensory conduction velocity (SCV) and aSAP amplitude were considered in S1-S2, S2-S3 and S3-R segments. The intracarpal tunnel pressure was significantly higher in CTS patients than in controls, with the highest values located between 25 and 35 mm distal to the proximal border of the flexor retinaculum. SCV and aSAP amplitude were also decreased most often in the distal part (S2-S3) of the carpal tunnel.     

Mixed nerve action potentials in acquired demyelinating polyneuropathy

Uncertainty about motor and sensory contributions in abnormal nerves has limited the use of mixed nerve action potentials (MNAPs). We recorded MNAPs in 21 patients with an acquired demyelinating neuropathy, 18 age-matched control subjects, and 10 patients with an axonal polyneuropathy. Bipolar and unipolar recordings from median and ulnar nerves were made above the elbow after electrical stimulation of the nerves at the wrist. Antidromic digital sensory action potentials and motor conduction velocity were also recorded for both nerves. In 19 median and 12 ulnar nerves from demyelinating polyneuropathy patients, compared with control subjects, MNAP amplitudes were significantly reduced (mean, 6 μV vs. 31 μV), MNAP velocities were mildly reduced (mean, 50 m/s vs. 62 m/s), motor conduction velocities were significantly reduced (mean, 33 m/s vs. 57 m/s), and MNAPs were significantly dispersed, with markedly prolonged rise times (mean, 2.0 ms vs. 1.0 ms). Compared with the axonal polyneuropathy group, MNAP amplitudes from the median nerve were similarly reduced (mean, 8 μV vs. 9 μV), MNAP velocities were only slightly slower (mean, 52 m/s vs. 58 m/s), but the rise times were significantly prolonged (mean, 2.0 ms vs. 1.2 ms). We conclude that, in acquired demyelinating neuropathies, the onset and, in some cases, the whole MNAP is from afferent fibers, which can be abnormally dispersed, and that, over the same segment, MNAP velocity is less affected than motor conduction velocity. 1995.© 1995 John Wiley &Sons, Inc.     

Length-dependent weakness and electrophysiological signs of secondary axonal loss in chronic inflammatory demyelinating polyradiculoneuropathy

In chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) the pathophysiology underlying permanent muscle weakness and sensory loss was studied in 22 stabilized long-term CIDP patients clinically characterized using isokinetic dynamometry, quantitative sensory testing, and neuropathy scores. Conduction velocity (CV), distal latency (DLAT), minimal F-wave latency (FLAT), compound muscle action potential (CMAP), and amplitude decay between distal and proximal stimulation sites were determined in the median, ulnar, peroneal, and tibial motor nerves and sensory CV and nerve action potentials in the median and sural nerves. Amplitude of CMAP and the DLAT were related to quantitative muscle strength, whereas CV, FLAT, amplitude decay, and dispersion were not consistently related to strength. Furthermore, CMAP and muscle strength were significantly more reduced distally than proximally. In conclusion, the electrophysiological signs of axonal loss and the associated length-dependent muscle weakness suggest secondary axonal loss in addition to primary demyelination in CIDP.     

The carpal tunnel syndrome: localization of conduction abnormalities within the distal segment of the median nerve.

Palmar stimulation was used to assess median nerve conduction across the carpal tunnel in 61 control patients and 105 patients with the carpal tunnel syndrome. With serial stimulation from midpalm to distal forearm the sensory axons normally showed a predictable latency change of 0.16 to 0.21 ms/cm as the stimulus site was moved proximally in 1 cm increments. In 47 (52 per cent) of 91 affected nerves tested serially, there was a sharply localized latency increase across a 1 cm segment, most commonly 2 to 4 cm distally to the origin of the transverse carpal ligament. In these hands, the focal latency change across the affected 1 cm segment (mean +/- SD: 0.80 +/- 0.22 ms/cm) averaged more than four times that of the adjoining distal (0.19 +/- 0.09 ms/cm) or proximal 1 cm segments (0.19 +/- 0.08 ms/cm). In the remaining 44 (48 per cent) hands, the latency increase was distributed more evenly across the carpal tunnel. Unlike the sensory axons the motor axons were difficult to test serially because of the recurrent course of the thenar nerve, which may be contained in a separate tunnel. The wrist-to-palm latency was significantly greater in the patients with carpal tunnel syndromes than in the controls for sensory (2.18 +/- 0.48 ms v 1.41 +/- 0.18 ms) and motor axons (2.79 +/- 0.93 ms v 1.50 +/- 0.21 ms). Consequently, there was considerable difference between the carpal tunnel syndromes and controls in SNCV (38.5 +/- 7.5 m/s v 57.3 +/- 6.9 m/s), and MNCV (28.2 +/- 4.5 m/s v 49.0 +/- 5.7 m/s). In the remaining distal segment, however, there was only a small difference between the two groups in sensory (1.48 +/- 0.28 ms v 1.41 +/- 0.22 ms) and motor latency (2.15 +/- 0.34 ms v 2.10 +/- 0.31 ms). The exclusion of the relatively normal distal latency made it possible to demonstrate mild slowing across the carpal tunnel in 36 (21 per cent) sensory and 40 (23 per cent) motor axons of 172 affected nerves when the conventional terminal latencies were normal. Sensory or motor conduction abnormalities were found in all but 13 (8 per cent) hands. Without palmar stimulation, however, an additional 32 (19 per cent) hands would have been regarded as normal.     

Distal neuropathy in experimental diabetes mellitus

Although nerve conduction slowing is a well-accepted abnormality in rats with acute experimental diabetes, reports of neuropathological changes in diabetic rat nerves have been inconsistent. To examine this further, we studied electrophysiological and morphological features of posterior tibial nerves and their distal branches from four-week streptozotocin-induced diabetic rats and matched controls. Diabetic rat posterior tibial motor conduction was slowed (mean ± 1 SD, 34.8 ± 3.1 m/sec; controls, 41.2 ± 2.5 m/sec), and evoked muscle response amplitudes were only half of control values. Using quantitative techniques, we documented a diminution in number of the largest myelinated fibers in otherwise normal mid posterior tibial nerves, with an increase in the smaller sizes, indicating either a degree of axonal atrophy or impaired fiber growth during development. The principal pathological finding was active breakdown of myelinated fibers in the most distal motor twigs of hind foot muscles supplied by posterior tibial branches, with preservation of fibers in more proximal segments of these nerves. This anatomical lesion in diabetic nerves could account for both observed conduction slowing and lowered muscle response amplitudes. A consistent feature in both diabetic and control mid lateral plantar nerves was a zone of demyelination that apparently occurs at this natural site of nerve entrapment in rats. Taken together, the pathological abnormalities of peripheral nerve in acute experimental diabetes are best explained as resulting from a distal axonopathy.     

F response and somatosensory and brainstem auditory evoked potential studies in HMSN type I and II.

To evaluate conduction along the proximal and distal segments of motor and sensory long limb nerves, as well as along the very short acoustic nerve, F response and somatosensory and brainstem auditory evoked potential were studied in a series of patients with hereditary motor and sensory neuropathy (HMSN) types I and II. A diffuse and comparable slowing of conduction in proximal and distal nerve segments, as well as along the acoustic nerve, seems to favour a primary myelin defect in HMSN I. F response and motor conduction velocity showed a similar derangement in both proximal and distal motor segments. Latencies of somatosensory evoked potentials were symmetrically prolonged and correlated with motor nerve impairment. Central conduction times were normal. Studies of brainstem auditory evoked potentials showed a high incidence of acoustic nerve involvement, the most evident abnormality being a statistically significant increase in the latency of the I wave. Our data seem to support the presence of primary myelinopathic damage in HMSN I.