Comparison of electrophysiological findings between CIDP and HMSN-1]

Chronic inflammatory demyelinating polyneuropathy (CIDP) and hereditary motor sensory neuropathy type 1 (HMSN-1) are representative myelinopathies. In order to differentiate changes in acquired and congenital demyelinating neuropathies, we studied electrophysiologically 9 patients with active phase of CIDP (36.0 +/- 17.6 years old; mean +/- SD) and 7 patients with genetically-proven HMSN-1 A (56.0 +/- 13.6 years old). Motor conduction studies demonstrated longitudinal uniformity in HMSN-1, contrariwise focal conduction block or conduction delay in CIDP. The mean median nerve conduction velocity in the forearm segment and the mean CMAP amplitude stimulated at the wrist were not different between CIDP and HMSN-1 group; 31.8 +/- 7.2 m/sec and 5.6 +/- 2.8 mV in CIDP, and 26.7 +/- 9.8 m/sec and 3.2 +/- 2.6 mV in HMSN-1, respectively. Upper extremity polyneuropathy index (PNI), a mean percentage of normal for 6 indices concerning to the velocity and latency over two nerves obtained by motor conduction studies, was equal and around 50% on the average in each group. Conduction blocks were presented in 7 patients with CIDP and only one patient with HMSN-1. No sensory nerve action potential was recorded in 6 out of 9 patients with CIDP, and in 6 out of 7 patients with HMSN-1. Intrafascicular neurography of the median nerve, stimulated at the wrist and recorded from intrafascicularly inserted microelectrode at the elbow, revealed irregular multiphasic waves which signify severe temporal dispersion. Maximum conduction velocity was similarly reduced to 48 m/sec in CIDP and 44 m/sec in HMSN-1 on the average, but in one patient with HMSN-1 it was maintained to 63 m/sec with conspicuous temporal dispersion of the waveform. Amplitude of the compound nerve action potential (CNAP) decreased more (p < 0.01) in HMSN-1 (26 +/- 11 micro V) than in CIDP (72 +/- 25 micro V). Temporal dispersion of CNAP was prominent in HMSN-1 than in CIDP. In conclusion, electrophysiological changes were more homogeneous in the longitudinal distribution but more heterogeneous in the cross-sectional distribution in HMSN-1 than in CIDP.     

Muscle fiber conduction velocity related to stimulation rate

Muscle fiber conduction velocity in human biceps brachii muscle, produced by voluntary contraction and by contraction owing to microstimulation of a single motor unit, was measured with surface array electrodes. The conduction velocity of the fibers in the motor unit was calculated from the conduction time of the motor unit action potential along the electrode array and the electrode separation. With voluntary contraction, a conduction velocity of 4.25 +/- 0.43 m/sec (mean +/- S.D., n = 68) was obtained. In recording the surface EMG, the mean firing rate of the motor unit was 15.8 imp/sec (range 6-24 imp/sec). Significantly slower conduction velocity of 3.69 +/- 0.33 m/sec (mean +/- S.D., n = 56) was found after microstimulation (P less than 0.001). The higher the stimulation rate the higher was the conduction velocity. With increasing stimulus rates of 5, 10, 20 and 40 c/sec, the mean and S.D. of the conduction velocity were 3.74 +/- 0.33 m/sec (2.1% increase in the mean value to 1 c/sec stimulus rate), 4.16 +/- 0.37 m/sec (13.6%), 4.35 +/- 0.54 m/sec (18.8%) and 4.80 +/- 0.49 m/sec (31.1%), respectively. The firing rate for voluntary contraction was in the same range of the one obtained with 10-20 c/sec electrical stimulation, conduction velocity was the same in the two conditions. We conclude that measurement of muscle fiber conduction velocity should also be standardized with muscle fiber firing rate.     

Changes in nerve conduction velocity across the elbow due to experimental error

One diagnostic criterion for ulnar nerve mononeuropathy at the elbow (UNE) is a decrease in across-elbow nerve conduction velocity (NCV) > 10 m/s compared to the forearm segment. Distance and latency measurement errors are an inherent part of NCV calculations. Twenty electromyographers measured the latencies of stored ulnar compound muscle action potentials and measured the forearm and across-elbow distances along the ulnar nerve. Based on previously published equations, experimental error in NCV was calculated for various NCVs. The mean distances and standard deviations for the forearm and elbow segments were 212.5 +/- 2.1 mm and 86.7 +/- 4.2 mm, respectively. For an NCV of 55 m/s, a difference of 14 m/s between the two segments can occur from measurement error alone. Distance measurements about the elbow are fraught with interobserver errors rendering the resultant NCV of that segment of limited value as a sole criterion for the diagnosis of UNE.     

Sensory nerve action potentials in the evaluation of diabetic polyneuropathy]

In order to clarify the suitability of sensory nerve action potential(SNAP) in the evaluation of diabetic polyneuropathy, we studied measurements of SNAPs in the median, ulnar and sural nerves. Subjects were 253 patients with non-insulin dependent diabetes mellitus; 167 men and 86 women, aged 58.2 +/- 12.8(mean +/- SD) years old. Their diabetic history was 10.2 +/- 8.6 years. SNAPs were recorded antidromically from index finger, little finger and lateral to the Achilles tendon, respectively. Twenty-eight patients, in whom any one of the SNAPs couldn't be obtained, were already excluded from this study. The polyneuropathy index (PNI) was calculated from 12 indices concerning to the velocity or long distance latency in motor nerve conduction studies of 4 nerves. The PNI is known to be an excellent index to express the degree of diabetic polyneuropathy. Amplitude and conduction velocity in each nerve was 28.6 +/- 15.6 microV and 46.2 +/- 7.4 m/sec in the median nerve, 26.7 +/- 15.8 microV and 47.0 +/- 6.5 m/sec in the ulnar nerve, 13.1 +/- 6.5 microV and 43.1 +/- 6.0 m/sec in the sural nerve, respectively. The coefficient of correlation of the measurements between median and ulnar nerves was larger than other assortment of nerves. The coefficient of correlation of each measurement with PNI was around 0.40 in the amplitude and around 0.55 in the conduction velocity. Nevertheless, the mean value of the 3 nerves had a higher coefficient of correlation with PNI; 0.48 in the amplitude and 0.60 in the conduction velocity. SNAP measurements of a single nerve are often largely affected by the inter-individual differences, inter-nerve differences or measuring errors. But the mean value of the 3 nerves will be better in exploring the degree of diabetic polyneuropathy. Evaluation of diabetic polyneuropathy by SNAPs will be best achieved by using the mean value of these 3 nerves.     

Spinal sympathetic conduction velocity in humans

Simultaneous micro-electrode recordings of muscle sympathetic activity were made in the radial nerve at the mid-humerus level and the peroneal nerve at the fibular head in 8 healthy subjects. Sympathetic impulses occurred spontaneously in multi-unit bursts time-locked to the cardiac rhythm. There was a high degree of similarity between radial and peroneal neurograms with the radial bursts preceding corresponding peroneal ones by approximately 0.35 s. Utilizing this latency difference and previously determined values for peripheral sympathetic postganglionic conduction velocities, we calculated that the spinal conduction velocity for muscle sympathetic activity is 2.8 +/- 0.7 m/s (mean +/- SD). The result agrees with similar data from experimental animals.     

Sympathetic skin response: normal results in different experimental conditions.

(1) The sympathetic skin response (SSR) is a slow wave, generated in deep layers of the skin, resulting from reflex activation of the sudomotor sympathetic efferent fibres. The aim of this study was to define experimental conditions, best stimulation and recording procedures, and the criteria for validation of the responses. (2) Thirty normal subjects (aged 25-56) were tested. The stimulation was an electrical pulse train applied to the median nerve at the wrist, a binaural tone burst, or both simultaneously. Records were made with surface electrodes on hand and foot contralateral to the stimulated median nerve. (3) Response shape was most often biphasic in feet, biphasic or triphasic in hands. SSR amplitude was 3.1 +/- 1.8 mV in hands, 1.4 +/- 0.8 mV in feet. Normal mean onset latency was 1.5 +/- 0.08 sec for hand response, 2.05 +/- 0.10 sec for foot response. The mean conduction velocity along peripheral sympathetic nerve fibres was 1.40 +/- 0.14 m/sec in lower limbs. (4) Bimodal stimulation (burst + median) provided responses of larger amplitude. The influence of stimulation intensity was also investigated. A decrease in amplitude and lengthening of latencies were observed after 15-20 min of testing. (5) The criteria for validation of responses are discussed. The importance of central processing time in the response delay is pointed out. In good methodological conditions, SSR would appear to be a simple, effective means of assessing sympathetic sudomotor outflow in central and peripheral nervous system disorders.     

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.     

Posterior antebrachial cutaneous nerve conduction studies in normal subjects.

OBJECTIVE: The posterior antebrachial cutaneous (PABC) nerve is a sensory nerve that branches out from the radial nerve at the level of the spiral groove. Thus it can be affected in a radial nerve lesion at or proximal to its origin in the spiral groove. However, there has been limited knowledge about the normal values of PABC nerve conduction studies. This study was done to determine these normal values. METHODS: Sixty-three healthy adults (23 males) with a mean age of 41.5+/-10.6 (range, 20-90) years were recruited with informed consent. A total of 126 nerves were studied. The nerve conduction studies were performed using a Dantec Counterpoint EMG machine (Dantec, Skovlunde, Denmark). RESULTS: The mean+/-standard deviation values for the onset as well as peak latency, conduction velocity, amplitude and side-to-side amplitude ratio were 2.07+/-0.16 (range, 1.80-2.60) ms, 2.35+/-0.15 (range, 2.05-2.90) ms, 58.21+/-4.29 (range, 46.15-66.67) m/s, 6.10+/-2.11 (range, 2.90-13.00) microV and 0.83+/-0.12 (range, 0.60-0.99), respectively. There was a significant correlation between the subject age and the PABC onset and peak latencies as well as the amplitudes. CONCLUSIONS: The PABC nerve is assessable for nerve conduction studies and these normal values may be useful in evaluation of patients with suspected radial nerve lesions.     

Motor and sensory conduction along the posterior interosseous nerve

The posterior interosseous nerve (PIN) is the main distal branch of the radial nerve. It innervates most of the extensor muscles of the forearm and contains deep sensory fibres directed to the ligaments and joints of the wrist. The presence of deep sensory fibres allow measurement of sensory conduction (SCV) other than motor nerve conduction velocity (MCV) along this nerve. Normal values of motor and sensory conduction along the terminal branches of the radial nerve distal to the elbow are reported. The results accord well with data previously reported.     

Maturation of peripheral nerves in preterm infants. Motor and proprioceptive nerve conduction.

The peripheral nerve maturation (proprioceptive and motor nerve conduction velocities (PNCV and MNCV] was studied in 3 groups of newborn babies. Two groups of premature babies (PT), studied when they reached the expected date of birth (group I, gestational age (GA) at birth 27-31 weeks, n = 13, group II, GA at birth 32-35 weeks, n = 9), were compared to 10 normal full-term newborns (FT). The MNCV of PT babies was similar to that of FT babies: group I 22.8 +/- 3.3 m/sec (X +/- S.D.), group II 24.9 +/- 4.3 m/sec, FT 25.7 +/- 3.9 m/sec. PNCV was significantly lower in group I (18.1 +/- 5.9 m/sec) than in group II (28.3 +/- 6.4 m/sec) and in FT babies (32.0 +/- 7.4 m/sec) (P less than 0.001). Such a delay in maturation could be partly responsible for the neurological impairment often observed in PT babies.     

Study on the latency difference between compound muscle and sensory nerve action potentials]

In motor nerve conduction studies compound muscle action potentials (CMAPs) appear later than sensory nerve action potentials (SNAPs). This time lag originates from the conduction delay at the distal motor axon, neuromuscular transmission time and muscle action potential induction time. To investigate the latency difference between CMAPs and SNAPs we studied 46 healthy individuals, 46 patients with diabetes mellitus and 33 patients with carpal tunnel syndrome, using the lumbrical and interossei recording method. In this method the recording active electrode was placed on the 2nd lumbrical muscle and the reference electrode on the proximal palmar aspect of the index finger. Supramaximal stimulation was given to the median or ulnar nerve trunk at 9-cm proximal to the recording active electrode. The CMAP from the 2nd lumbrical muscle (L) and the SNAP from the digital nerve (N) were recorded after median nerve stimulation, and the CMAP from the 2nd interossei muscles (I) was recorded after ulnar nerve stimulation. The residual latency, which is arbitrary defined as the latency difference (L-N) in this study, was 1.38 +/- 0.15 (mean +/- SD) msec in healthy individuals. About 1 msec of the residual latency is regarded as the time for neuromuscular transmission and the time to evoke muscle activities. Thus, the conduction delay at the distal motor axon was calculated as about 0.4 msec in healthy individuals. The residual latency was relatively constant in 29 diabetic patients without conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) < or = 0.4 msec. Their sensory nerve conduction velocities (calculated from N latency) were always above 40 m/sec. On the other hand in diabetic patients with conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) > 0.4 msec, the residual latency gradually increased as the sensory nerve conduction velocity decreased. Their sensory nerve conduction velocities were mostly less than 40 m/sec. The similar relationship was observed in patients with carpal tunnel syndrome without diabetes mellitus. We consider that the diabetic neuropathy alone doesn't cause the increase of the residual latency. Instead, severe conduction delay across the carpal tunnel decreases the N velocity and increases the residual latency. We can also regard the relationship between the latency difference (L-N) and N velocity as being in inverse proportion. Perhaps the increase of the residual latency was simply caused by the proportional decrease in the conduction velocity at the distal motor axon, not by the special mechanism concerning to the carpal tunnel syndrome. This paper presented the electrophysiological changes seen in the distal segment secondary to the proximal entrapment.     

Remyelination by Schwann cell transplantation for CNS demyelinated axons: functional comparison with developmental myelination]

Transplantation of Schwann cells(SCs) induced remyelination of demyelinated rat dorsal column(DC) axons and improved conduction. To investigate the difference between developmental oligodendrocytic myelination and SC myelination in conductive functions of axons, we compared normally developmental DCs(10 days old, 22-23 days old, and adult rat), demyelinated DCs, and remyelinated DCs by SC transplantation. DCs of adult rats were demyelinated at T 11 by X-ray irradiation and ethidium bromide, and transplanted with SCs(3 x 10(4)) of adult rats. Three weeks later, the spinal cord was removed and pinned in a recording chamber and compound action potentials (CAPs) were recorded, to investigate conduction properties(conduction velocity, amplitude of CAP and response after high frequency stimulation). Normal DCs were recorded in same manner. Following transplantation of SCs, histological examination revealed SC-like patterns of remyelination of demyelinated axons. The conduction velocities of 10 days old DCs(1.7 +/- 3.4 m/s, n = 4) increased early to 8.1 +/- 3.3 m/s(22-23 days old, n = 7) and 12.2 +/- 1.5 m/s (adult, n = 5). After SC transplantation the velocity significantly improved 7.7 +/- 1.5 m/s(n = 5) compared to demyelinated axons(1.2 +/- 0.4 m/s, n = 7), but less than adult. A 600 Hz 0.5 sec stimulus train led to an amplitude decrement of 7.1 +/- 7.5%(n = 7) in demyelinated axons. Following transplantation, amplitude decreased in 66.2 +/- 11.9%(SC, n = 5), same as 22-23 days(71.7 +/- 11.7%, n = 7) old or adult(76.6 +/- 15.6%, n = 6). The recovery properties after high frequency stimulation developed earlier than conduction velocity. Following SC transplantation, the recovery properties improved to that of normal adult, but not conduction velocity. Lower conduction velocity may be due to shorter internode distance of remyelination after transplantation, same as 22-23 days old pups, than normal adult rats. Though anatomical difference and/or time after transplantation influenced the conduction, these result suggested SC remyelination might result in insufficient for conduction velocity.     

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.     

The conduction velocity of the descending spinal pathway to the renal sympathetic nerve in the cat

The conduction velocity of the descending spinal excitatory pathway to the renal sympathetic nerve was measured in five chloralose-anaesthetised, spinal cats (C1 transection). Electrical stimuli were delivered to the dorsolateral funiculus at three levels between segments C3 and T6, and responses recorded from the ipsilateral renal nerve. Spinal conduction velocity was calculated as 4.4 +/- 0.4 m/s (mean +/- SEM), from the latency difference of renal nerve volleys to stimulation at different cord levels. A contralateral pathway to the renal nerve was identified: this also ran in the dorsolateral funiculus, and crossed below segment T5. It conducted at 4.1 and 7.9 m/s (two cats). Renal preganglionic conduction velocity (greater splanchnic nerve) was 4.1 and 5.0 m/s (two cats). As the renal sympathetic nerve is functionally homogeneous, these conduction velocity measurements are of a functionally-defined sympathoexcitatory pathway.     

Wide spectrum of motor conduction velocity in Charcot-Marie-Tooth disease. An anatomico-physiological interpretation

Motor conduction velocity along the forearm segments of the ulnar and median nerves was studied in 25 patients with Charcot-Marie-Tooth disease. It was found that there was a spectrum of values between 68 and 10 m/sec for the ulnar and between 60 and 15 m/sec for the median nerve. Although a neuronal disorder is expected in patients with normal or slightly diminished conduction velocity values and a Schwann cell disorder is expected in those with marked slowing of conduction, alternative hypotheses are offered to reconcile those differences with the notion that these patients belong to an homogenous group.     

Hereditary motor-sensory neuropathy. II. Electrophysiological studies

Electrophysiological parameters (conduction velocity, distal latency, amplitude of evoked response) were analysed in two types of sensorimotor hereditary neuropathy isolated on the ground of the values of motor conduction velocity in the median nerve which was 38 m/sec. Using this criterion the studied material of 53 cases could be divided into two groups. Group I of 34 cases in which the mean conduction velocity in the median nerve was 16.2 m/sec, and group II of 19 cases had a mean conduction velocity in the median nerve of 50.7 m/sec. The evaluation of the degree of slowing down of conduction in both types showed similar values in individual cases and in families.     

AANEM Application

Introduction: This anatomical study evaluates the role and correlation of ultrasound (US) with anatomy in depicting the superficial branch of the radial nerve (SBRN) and to evaluate the feasibility of US guided perineural infiltration as a potential therapeutic option in Wartenberg syndrome. Methods: Twenty‐one arms from 11 non‐embalmed cadavers were examined with US. Under US guidance perineural injection with ink was performed proximal to the site where the SBRN perforates the forearm fascia. The distribution of ink around the nerve was evaluated with dissection. Results: US allowed the distinction of the SBRN segments and their relation to the fascia. In all cases, the subfascial segment was stained. In only 57% the subfascially applied ink also reached the subcutaneous compartment. Conclusions: With US it is possible to examine and differentiate all segments of the SBRN. US guidance can be used for perineural injection of all relevant segments. Muscle Nerve 50: 939–942, 2014     

Peripheral nerve function during hyperglycemic clamping in healthy subjects

The influence of hyperglycemia with physiological hyperinsulinemia on peripheral nerve function was studied in 10 non-diabetic subjects. Blood glucose concentration was raised from 3.8 +/- 0.2 mmol/l (mean +/- SEM) to 17.1 +/- 1.4 mmol/l (mean +/- SEM) within 15 min and kept at this level for 120 min by intravenous glucose infusion. Sensory and motor nerve conduction velocity, and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min of hyperglycemia. Mean sensory nerve conduction velocity increased from 57.7 m/s to 59.5 m/s (P less than 0.005) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia mean sensory nerve conduction velocity was 59.6 m/s (P less than 0.05). An insignificant increase was seen in motor nerve conduction velocity during hyperglycemia. Mean distal motor latency decreased from 3.1 ms to 3.0 ms (P less than 0.025) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia distal motor latency was 2.9 ms (P less than 0.05). We conclude that short term hyperglycemia with physiological hyperinsulinemia seems to increase sensory nerve conduction velocity and decrease motor latency.     

Conduction velocity in spinal descending pathways of baro- and chemoreceptor reflex

Activity in the white rami T3 and L2 or 3 has been recorded and averaged with respect to excitation of the carotid sinus baroreceptor afferents produced by the pulsatile blood pressure (baroreceptor reflex) and with respect to brief trains of electrical stimuli exciting low threshold chemoreceptor afferents in the left carotid sinus nerve (chemoreceptor reflex). Experiments were performed on chloralose anaesthetized cats with both vago-depressor nerves cut. From the latency difference between the onset of the responses at the thoracic and their arrival at the lumbar level the spinal conduction velocity for the pathway of each reflex has been calculated. The baroreceptor reflex pathway has slower spinal conduction velocity 3.3 +/- 0.7 m/sec than the chemoreceptor pathway 5.5 +/- 0.9 m/sec. These results indicate that there are separate descending spinal pathways for the two types of reflexes.     

Dorsal ulnar cutaneous nerve conduction: reference values

We investigated the reference values of the dorsal ulnar cutaneous nerve (DUC) sensory nerve conduction (SNC) in 66 healthy individuals. Measurements were processed using stimulating electrodes positioned between the ulnar bone and the flexor carpi ulnaris muscle, 11-13 cm proximal to the active electrode recording. Superficial recording electrodes were placed on the fourth intermetacarpal space. The mean sensory conduction velocity (SCV) in males was 63.7 - 0.16 x age +/- 3.36 m/s and in females was 57.7 +/- 3.37 m/s. The mean sensory nerve action potential (SNAP) amplitude in males was 19.5 +/- 10.7 microV and in females was 24.6 +/- 5.8 microV. The mean SNAP duration was 0.96 +/- 0.13 ms. No significant differences regarding the DUC-SCV, distal latency, and SNAP duration or amplitude were found between both sides of the same subject. The amplitude of the SNAP was higher in females than males. The effects of age on DUC-SCV were distinct for each gender.