Sensory (1a) and F-wave conduction velocity in the proximal segment of the tibial nerve

The F-wave was used to estimate the fastest motor nerve conduction velocity (MNCV) along the proximal segment (spinal cord to knee) of the axons of the tibial nerve in 65 control subjects, 8 patients with diabetic polyneuropathy, and 4 patients with Charcot-Marie-Tooth disease. Terminal latencies and MNCV along the distal segment (knee to ankle) of the nerve were also estimated with the conventional M-response technique. This article describes another method for estimating sensory nerve conduction velocity (SNCV) along 1a fibers of the tibial nerve for the spinal cord-to-knee segment. Proximal and distal MNCV showed moderate slowing in patients with diabetic polyneuropathy and severe slowing in those with Charcot-Marie-Tooth disease. In 17 control subjects, proximal MNCV for the axons supplying the abductor hallucis muscle was compared to that estimated for the axons to the gastrocnemius muscle. MNCV for the proximal is faster than that for the distal small muscle. In 2 patients, M- and F-responses were not obtained from the abductor hallucis; in these patients, effective estimation of the proximal MNCV was made from the gastrocnemius muscle and showed marked reduction.     

The pathogenesis of pneumatic tourniquet paralysis in man.

The relative importance of ischaemic and direct mechanical injury to nerves compressed by a tourniquet, in the pathogenesis of tourniquet paralysis in man has not been established. To investigate this question, conduction in ulnar or median nerve fibres has been measured in healthy subjects both at the level of the pneumatic tourniquet and distal to the tourniquet. Measurement was prior to, for the period of tourniquet inflation, and following release of the tourniquet. The earliest conduction delays and block were observed at the level of the tourniquet, particularly across the proximal tourniquet border zone. However, a proximal to distal progression in conduction abnormalities distal to the tourniquet suggested that the earlier conduction abnormalities at the level of the tourniquet were primarily ischaemic in origin. Mechanical compression, however, probably contributed to disproportionate conduction delays and blocks across the border zones of the tourniquet.     

Conduction of the sciatic nerve in its proximal and distal segment in patients with ALS (amyotrophic lateral sclerosis)

Conduction in the proximal segment of the sciatic nerve was assessed by recording the latencies of M and H responses from soleus muscle, in the distal segment by comparing the latencies of M waves from the abductor hallucis muscle, obtained by stimulating the tibial nerve in the popliteal fossa and at the ankle. Data from 30 patients with amyotrophic lateral sclerosis (ALS) were compared with an age-matched group of healthy subjects. We observed an increase in the difference between the latencies of M and H responses from soleus, and a lengthening of the distal latency of the M wave from abductor hallucis. The motor conduction velocity of the tibial nerve was preserved. The functional significance of the data are discussed. It is suggested that they indicate a slowing of conduction in the proximal segment of the sciatic nerve and that they can be correlated with pathological findings in proximal nerves in ALS and in the experimental anterior horn cell disorder.     

Conduction velocity along human nociceptive reflex afferent nerve fibres.

The conduction velocity along the nociceptive flexor reflex afferent nerve fibres was investigated in human subjects. The posterior tibal nerve was stimulated at two sites by single painful electrical shocks of 1.0 ms duration and with adequate intensity and the reflex EMG discharges were recorded from the short head of the biceps femoris muscle. The fastest reflex conduction velocity along the posterior tibial nerve between the ankle and the popliteal fossa was about 10-25 m/s. Thus the fastest flexor reflex afferent fibres associated with a painful sensation were thought to be included in the A-delta group of cutaneous afferent nerve fibres.     

Changes in nerve function and nerve fibre structure induced by acute, graded compression.

Rabbit tibial nerves were subjected to direct, acute graded compression by means of an inflatable compression chamber. The acute and long term effects of 50, 200 and 400 mmHg applied for two hours on nerve function and nerve fibre structure were investigated. A pressure of 50 mmHg applied for two hours induced only minimal or no acute deterioration of maximal conduction velocity and nerve fibre structure. Conduction velocity was gradually reduced during compression at 200-400 mmHg pressure for two hours and in those cases the recovery of nerve conduction after pressure release was incomplete. Ultrastructural analysis revealed pronounced, early nerve fibre damage in these nerves. Three weeks after compression, nerves compressed at 50 mmHg for two hours had normal afferent and motor conduction velocity, although there were morphological signs of slight nerve fibre damage. Nerves compressed at 200 mmHg for two hours exhibited reduction of conduction velocity only at the level of compression, in contrast to the nerves compressed at 400 mmHg for two hours in which conduction velocity was reduced both at the level of compression and distal to the compressed segment. Morphologically, the nerves compressed at 200-400 mmHg for two hours showed varying degrees of demyelination and axonal degeneration three weeks after compression.     

Conduction velocity in the proximal segments of a motor nerve in the Guillain-Barré syndrome.

Conduction velocity from spinal cord to axilla (estimated using the F wave) has been compared with conduction velocity from axilla to wrist (measured in the conventional manner) in the motor fibres of the ulnar nerve in 17 controls subjects and in 11 patients with the Guillain-Barré syndrome (GBS). In the patients with GBS the conduction velocity was, in general reduced to a similar extent in both the proximal and the distal portions of the motor fibres, suggesting that the disease process is usually diffuse. In two patients, however, the conduction velocity in the proximal segment was disproportionally reduced and in one of these the conduction velocity in the distal segment was normal. It is concluded that the estimation of conduction velocity in the proximal segments of motor nerves may be of value in the assessment of patients with GBS.     

The non-linear relationship between nerve conduction velocity and skin temperature.

Median motor and sensory nerves were examined in 20 healthy subjects. Superficial stimulating and recording electrodes were used, and the nerves were examined at natural skin temperature, after cooling and after heating of the arm. The conduction velocity for the fastest and slow conducting sensory fibres (temperature range 17-37 degrees C), and for the fastest conducting motor fibres (temperature range 19-38 degrees C) increased non-linearly with increase in skin temperature. Similarly, distal motor latencies increased non-linearly with decrease in skin temperature. The effect of temperature was most pronounced in the low temperature range, and change in conduction velocity per degree centigrade was reduced toward higher skin temperature. Sensory nerve response duration increased linearly with decline in skin temperature. Sensory and motor amplitude did not show any significant relation to skin temperature.     

TULLIDORA (KARWINSKIA HUMBOLDTIANA) TOXIN MAINLY AFFECTS FAST CONDUCTING AXONS

Cats were given a single oral dose of ether extracts from tullidora ( Karwinskia hunboldtiana ) fruit which contains an identified neurotoxin. Acute experiments were performed 4–7 weeks after toxin administration when flaccid limb paralysis was evident. Normal cats were used as controls. The medial gastrocnemius, the soleus and the sural nerves were electrically stimulated and the unitary potentials evoked by the stimuli were extracellularly recorded from spinal root filaments to measure the conduction velocity of single fibres. In control cats, the average conduction velocity (CV) was greater in medial gastrocnemius motor fibres than in the afferent ones of the same nerve and the soleus motor axons, whereas in the sural nerve CV was less than in the aforementioned cases. The CV values and the proportion of fast conducting fibres (> 80 m/s) in each nerve were directly related ( r = 0.99). In treated cats, CV diminished in all the nerves studied, but the conduction velocity was further reduced in the faster fibres. Consequently, the motor division of the medial gastrocnemius nerve, normally composed of a high proportion (57%) of fast fibres, was more affected by tullidora and the sural nerve, which has the lowest proportion (0.7%) of these type of fibres, was the less affected. Our findings suggest that the preferential involvement of motor nerves in the experimental tullidora (buckthorn) neuropathy, as well as the preservation of somatic sensation in quadriplegic children accidentally poisoned with tullidora, are related to the distribution of axonal diameters in peripheral nerves.     

Prolonged conduction block with axonal degeneration. An electrophysiological study.

Serial electrophysiological studies were performed in a case of 'tourniquet paralysis' of the upper limb after the application of an Esmarch bandage above the elbow. Three months after onset of paralysis, nerve conduction was reduced to a quarter of normal between elbow and and axilla along the few fibres still conducting through the lesion, but was normal distal to the block. Seven months after nerve damage, EMG showed evidence of reinnervation after Wallerian degeneration, and half the nerve fibres had recovered from the conduction block. Thirteen months after nerve injury clinical examination and nerve conduction were normal, but EMG still showed evidence of partial denervation.     

Conduction in the motor neurons of the peripheral nerves in hemiplegia of cerebral origin

A study of motor nerve conduction velocities in median, ulnar, peroneal and tibial nerves bilaterally in 50 hemiplegic patients revealed a statistically significant slowing in the affected limbs compared with the unaffected side. The decrease of nerve conduction velocity was not related to any of the following factors: duration of stroke, degree of paralysis, degree of spasticity, side of paralysis, age of patients, and sex ef patients. The results can indicate that lower motor neurons are indeed affected by upper motor neuron lesions. The slowing of the nerve conduction velocity of motor peripheral nerves is probably due to the loss of trophic influence from higher centres or its decline. The author suggests that this phenomenon leads to a selective deterioration of thick nerve fibres while only thinner ones continue conducting impulses.     

Regeneration distal to a prolonged conduction block.

In 6 baboons a tourniquet round the knee was used to produce a prolonged local conduction block. This was followed, within a few days, by a surgical crush of the tibial or deep peroneal nerve at the ankle, in order to produce Wallerian degeneration distally. Electrophysiological recordings from small foot muscles were then used to study the time-course of regeneration in motor fibres. When the results were compared with those from crushed but unblocked nerves of the opposite leg, there was no evidence that either reinnervation of muscles or the subsequent maturation of the regenerating motor nerve fibres was delayed by the prolonged proximal conduction block.     

Nerve conduction during Wallerian degeneration in the baboon

Conduction in the lateral popliteal nerve of the baboon was studied during the course of Wallerian degeneration. Six nerves were examined. In each case the muscle response to nerve stimulation and the ascending nerve action potential were recorded daily until the nerve became inexcitable. The muscle response to nerve stimulation disappeared after four to five days, but ascending nerve action potentials could be recorded for a further two to three days. There was no change in maximal motor conduction velocity or in distal latency until the muscle response to nerve stimulation was severely reduced in amplitude. At this stage there was a consistent increase in distal latency, sometimes associated with a mild reduction in maximal motor velocity in the leg. There was no change in the velocity of ascending nerve action potentials. Histological studies confirmed the presence of degeneration in the terminal parts of the intramuscular nerve fibres at a time when the proximal parts of the same fibres were relatively normal.     

Transcranial magnetic stimulation studies in the Miller Fisher syndrome: evidence of corticospinal tract abnormality.

OBJECTIVES: To evaluate serial central motor conduction time in the Miller Fisher syndrome. METHOD: Three patients with classic Miller Fisher syndrome were evaluated clinically. They had serial central motor conduction times measured with transcranial magnetic stimulation and nerve conduction studies. Motor evoked potentials were recorded from the first dorsal interossei and abductor hallucis muscles. RESULTS: All three patients showed reduction in central motor conduction times in tandem with gradual clinical improvement at each review. CONCLUSIONS: There is electrophysiological evidence of a central reversible corticospinal tract conduction abnormality in the Miller Fisher syndrome.     

Early phase of vincristine neuropathy in man. Electrophysiological evidence for a dying-back phenomenon, with transitory enhancement of spinal transmission of the monosynaptic reflex

Ten patients with Hodgkin's disease were examined before and after each administration of vincristine sulfate (2 intravenous injections of 1.4 mg/m2 of body surface during the first week of each month for 3 months). The motor conduction velocity of the peroneal nerve, the conduction velocity in palmar sensory fibres of the median nerve, and the conduction velocity in the H reflex pathway remained unchanged. The amplitude of distal muscle (extensor digitorum brevis) and sensory nerve (median) potentials decreased, while the maximal response of more proximal muscles (soleus) was not significantly modified. The soleus T response quickly decreased, although at the same time the H response was increased in the days following administration of vincristine. Thus the T/H ratio seems to be the only convenient electrophysiological method of evaluating the functional impairment of primary afferent distal segments. These results show that vincristine induces a transitory excitability enhancement of the monosynaptic reflex. It is suggested that the drug may cause an increase in the firing rate in proximal segments of injured Ia fibres. Apart from this phenomenon the electrophysiological results lead to the conclusion that vincristine induces distal axonal degeneration, similar to that in other toxic neuropathies (e.g. acrylamide or n-hexane) where a dying-back process has been clearly demonstrated.     

Motor nerve conduction velocity distributions in man: results of a new computer-based collision technique

A new computer-based collision technique for direct measurement of the human motor nerve conduction velocity distribution is described. In contrast to previous collision techniques, the test muscle response is progressively cancelled to a null using an arrangement of proximal and distal stimuli which eliminates distortion of the test response caused by transient changes in nerve and muscle fibre conduction. The increased sensitivity of this new technique permits accurate measurement of the slowest 1% of alpha motor nerve fibres. We have used our modified collision technique to determine motor nerve conduction velocity distributions for the median nerve in 20 normal subjects aged between 19 and 59 (mean 35) years. 150% maximal stimulus intensities were used, with a controlled limb temperature of 35 degrees C. Group mean velocities (+/- S.D.) for the fastest (95%), mean (50%) and slowest (5% and 1%) motor fibres were 59.1 +/- 3.0, 56.9 +/- 2.9, 52.7 +/- 3.1 and 51.2 +/- 3.7 m/sec respectively. Data are also presented for the ulnar and peroneal nerves.     

Evaluation of distal and proximal axonal degeneration in patients with carpal tunnel syndrome.

In patients with carpal tunnel syndrome, varying degrees of demyelination and axonal degeneration occur in the median nerve. Only a few studies have examined axonal degeneration produced at proximal to the lesion. In this study proximal axonal degeneration was evaluated and compared with other parameters. In 40 consecutive CTS patient hands, distal latency (DL), compound muscle action potential amplitude (CMAP) and motor conduction velocity (MCV) were analyzed by conventional motor nerve conduction studies. Intrafascicular compound nerve action potential amplitude (N-CNAP) at the elbow after wrist simulation and its nerve conduction velocity (NCV) between wrist and elbow were also analyzed. The negative correlation of DL with CMAP was statistically significant (r = 0.577, p < 0.001). CMAP was correlated with either MCV (r = 0.537, p < 0.001) or N-CMAP (r = 0.710, p < 0.001). A significant correlation of MCV with NCV (r = 0.517, p < 0.001) was also indicated. There were no any other significant correlation among the parameters. In CTS the degree of demyelination and axonal degeneration influence the prognosis for nerve recovery after decompressive surgery. DL is mainly influenced by demyelination that results in conduction block and slowing at the carpal tunnel. CMAP and N-CNAP indicate the degree of axonal degeneration at distal and proximal to the compression site. As in electrophysiologic evaluation of mononeuropathies, proximal axonal degeneration is best assessed by both stimulation and recording electrode locationing proximal to the lesion. Recording of intrafascicular nerve action potential was a little invasive method, but it provided important informations. The negative correlation between DL and CMAP implies that distal axonal degeneration can occur in proportion to the conduction disturbance. Moreover, N-CNAP had a higher correlation with CMAP. The greater the distal axonal degeneration, the more the proximal axonal degeneration. Conduction velocity represents the velocity of the fastest conduction fiber, not the degree of axonal degeneration.     

Acute peripheral nerve compression in the baboon

As a model of acute pressure neuropathy (“Saturday night palsy”) in man, a weighted nylon cord lying across the limb has been used to produce local compression of the ulnar and anterior tibial nerves in anaesthetised baboons. Motor nerve conduction studies were carried out 18–24 hr after compression; in some animals they were repeated at intervals for periods of up to 16 weeks.In the ulnar nerve the results were variable, but in the anterior tibial nerve, compression by a 1.5 kg weight for 90 min regularly produced a severe or complete conduction block. In such cases the pressure on the skin over the nerve ranged from 1.6–2.1 kg/cm². A pressure of approximately 1.0 kg/cm² caused a partial conduction block with a conduction delay in the unblocked fibres. A pressure of 0.75 kg/cm² or less caused no conduction defect.When the periods of compression were extended from 90 min to 120, 150 or 180 min, the conduction blocks were accompanied by increasing amounts of Wallerian degeneration. The local blocks produced by the longer periods of compression were also slower to recover.The histological features of the lesions were basically similar to those described previously after nerve compression by a pneumatic tourniquet. In the large myelinated fibres there was displacement of the nodes of Ranvier along the fibres away from the site of pressure. This movement occurred in 2 zones near the edges of the lesion, the nodes at the centre of the lesion being spared. Accompanying the nodal displacement there was stretching of the paranodal myelin on one side of the node and invagination on the other. At the extreme edges of the lesion there was sometimes distension of the paranodal regions with thinning of the myelin.These changes were followed by demyelination and finally by remyelination. In the recovery phase irregular myelin swellings were seen which were similar in appearance to those seen previously in recovering nerves after a pneumatic tourniquet.These results, together with those described previously, indicate that in “Saturday night palsy” and similar pressure lesions of peripheral nerves, the conduction block is due to a direct mechanical effect of the applied pressure on myelinated fibres, and that ischaemia, due to compression of the intra-neural blood vessels, plays little if any part.     

Alteration of proximal conduction velocity at distal nerve injury in carpal tunnel syndrome: demyelinating versus axonal change.

The objective of this study was to determine the cause of median forearm motor conduction velocity (FMCV) slowing in patients with carpal tunnel syndrome, due to either focal conduction abnormality over wrist or retrograde conduction slowing, and to decide whether the slowing is related to severity of compression or not. Fifty carpal tunnel syndrome patients confirmed by conventional nerve conduction study with abnormal electromyography of the abductor pollicis brevis muscle were group 1, and 100 with normal electromyography, group 2. One hundred volunteers served as controls. In addition to conventional nerve conduction study of median and ulnar nerves, palmar stimulations for median mixed and motor nerves were also performed to calculate wrist-palm mixed nerve conduction time and motor conduction velocity (W-P MCV). For group 1, group 2, and control subjects, respectively, W-P MCV were 19.73+/-7.65 (mean+/-SD), 32.7+/-6.83, and 52.75+/-6.4 m/s, whereas median FMCV were 48.63+/-8.32, 54.42+/-2.11, and 57.86+/-4.24 m/s. There was a significant reduction in the W-P MCV (62.6%, P<0.00001) and a decrease in the median FMCV (15.95%, P<0.00001) in group 1, and 38% reduction in W-P MCV (P<0.00001) and 5.9% decrease in median FMCV (P<0.00001) in group 2 when compared with controls, but ulnar FMCV and sensory nerve conduction study results did not, suggesting the reduction of median W-P MCV is not parallel with that of median FMCV in both patients groups. Furthermore, there is a poor correlation of median FMCV and W-P MCV in patient groups, implying conduction blockage of the large myelinating fibers at the wrist, leaving only slower axons to be measured, is not the likely cause of reduction of FMCV. In addition, the reduction of compound muscle action potential amplitude of abductor pollicis brevis muscle, conduction block at wrist and weak correlation of median FMCV and compound muscle action potential amplitude of abductor pollicis brevis exclusively occurred in group 1. Therefore, the retrograde conduction slowing really occurs among patients with carpal tunnel syndrome-markedly in those with abnormal electromyography and mildly in those with only demyelination. This finding counters conventional wisdom that nerve function changes only in segments distal to injured sites.     

Abnormalities in the vagus nerve in canine acrylamide neuropathy

Dogs exposed to acrylamide develop a sensorimotor peripheral neuropathy and megaoesophagus. The presence of neuropathy was confirmed electrophysiologically and histologically. Hindlimb motor conduction velocity was reduced and there was a loss of large diameter myelinated fibres in the dorsal common digital nerve and the tibial nerve. The conduction velocity of vagal motor fibres innervating the thoracic oesophagus was not decreased; there was a reduction in the conduction velocity of the mixed nerve action potential of the vagus. Degenerating nerve fibres were observed in the vagus in the midthoracic region. The damage to vagal nerve fibres may be an important factor in the causation of megaoesophagus.     

Nerve conduction studies in experimental non-freezing cold injury: II. Generalized nerve cooling by limb immersion.

After immersion of the hind limb of the rabbit, up to the lower thigh, in a waterbath, at 1 degree C for 10 to 14 hours under light anesthesia, there was evidence of persistent nerve damage to the tibial nerve, which varied in severity in different animals. Nerve conduction studies, carried out within 24 hours of removal from the bath, showed that in a proportion of the motor and/or afferent fibers, there was conduction failure between the knee and ankle. This was followed, over the next 48 hours, by distal degeneration of the affected fibers. No persistent conduction block was seen. After distal degeneration had occurred, maximal conduction velocity was mildly reduced, suggesting that the fastest-conducting motor and afferent fibers had been particularly affected. Morphological studies confirmed preferential large myelinated fiber degeneration, the earliest lesions being seen in the leg at the level of the upper calf. Limb edema was not seen after cooling, and there was no histological evidence of muscle necrosis or damage to blood vessels. No abnormalities were seen in 4 control animals after hind limb immersion for 12 hours at temperatures of 30 to 35 degrees C. Possible reasons for the proximal site of myelinated nerve fiber damage during hindlimb cooling are discussed.