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.     

Trigeminal motor nerve conduction: Deep temporal and mylohyoid nerves

This article describes nerve conduction studies of the deep temporal nerve (DTN) and the mylohyoid nerve (MHN) motor branches of the trigeminal nerve. These nerves were stimulated intraorally with a pediatric surface stimulator. Compound muscle action potentials were recorded over the temporalis and mylohyoid muscles with surface electrodes. Forty-two subjects were studied. In all subjects the MHN response was elicited bilaterally, giving an upper latency limit of 2.3 ms. The mean MHN amplitude was 4.9 mV (SD = 1.8 mV, minimum = 1.3 mV). The maximal side-to-side latency difference was 0.4 ms, and the maximal side-to-side amplitude difference was 2.2 mV. The DTN response was only elicited bilaterally in 25 (60%) subjects. The average DTN latency was 2.1 ms (SD = 0.3, maximum = 2.7 ms). The average DTN amplitude was 4.3 mV (SD = 2.0, minimum = 0.3 mV). The MHN responses were the least technically demanding, and were more consistently elicited than the DTN responses. These nerve conduction techniques should prove useful in patients with trigeminal nerve disorders. © 1996 John Wiley & Sons, Inc.     

Intracranial stimulation of the trigeminal nerve in man. I. Direct motor responses.

Direct electrical stimulation of the intracranial portion of the trigeminal nerve was performed in 23 subjects undergoing retrogasserian thermocoagulation for the treatment of idiopathic trigeminal neuralgia. In 16 subjects, who were having the operation for the first time, neurological examination was normal, as was neurophysiological testing of trigeminal function. Seven subjects were being operated for the second time, owing to a recurrence of symptoms. In all the subjects being operated for the first time, direct motor responses were obtained from ipsilateral temporalis, masseter and anterior belly of the digastric. The motor conduction velocity was equal for the fibres directed to all three muscles. This was estimated to be 54m/s in the masseteric nerve and 55-68 m/s in the intracranial portion of the trigeminal nerve. Patients who had undergone previous thermocoagulation had a considerably slower conduction velocity. It is supposed that myelin sheaths had been damaged at the first operation.     

Slowly conducting myelinated fibers in peripheral neuropathy.

The main component of the compound sensory action potential reflects the activity of large myelinated sensory fibers with diameters of greater than 9 micron(s). By recording the averaged potential using a needle electrode placed close to the nerve, small late components can be measured. The latency of these late components can be used to calculate minimum conduction velocity (CV); in normal subjects, average minimum CV is 15 m/s, corresponding to conduction in fibers of about 4 micron(s) in diameter. Minimum CV was measured in median, ulnar, and sural nerves of 187 patients with mild to severe neuropathic symptoms. A reduction in minimum CV was a sensitive measure of peripheral nerve dysfunction, often showing abnormalities when measures derived from the main component were normal. Patients with isolated abnormalities in minimum CV tended to have neuropathic symptoms but no signs of neuropathy. In addition, reduced minimum conduction velocity has implications for the pathology of different types of neuropathy. Slowing conducting potentials may originate from regenerating fibers, which may be of particular relevance in patients with neuropathic pain.     

Sensory conduction study of the infrapatellar branch of the saphenous nerve

Although neuropathies of the infrapatellar nerve (infrapatellar branch of the saphenous nerve, IPBSN) have been reported clinically, no electrophysiological method has been defined to evaluate IPBSN conduction. We therefore studied a total of 60 saphenous nerves and 60 IPBSNs from 36 volunteers. The IPBSN was stimulated medially with a surface electrode 2 cm below the patella. The response was recorded with a needle electrode located close to the nerve 1 cm lateral to the femoral artery in the inguinal region. Sensory nerve action potentials were obtained from each subject; mean latency of the first positive peak was 8.1 +/- 0.9 ms, conduction velocity was 54 +/- 4.4 m/s, and response amplitude was 1.3 +/- 1.1 microV. The method that we describe may be an easy and useful electrophysiological test for neuropathies of the IPBSN.     

Sensory and motor nerve conduction velocities and the latency of the H reflex during growth of the rat

The H reflex evoked in the plantar muscles of the rat hind limb was studied. The latency of the reflex and the conduction velocity of the sensory and motor nerves in the reflex arc were determined in rats of different sizes. Sensory conduction velocities were 38.8 ± (sd)5.8 m/s in 100- to 150-g rats and 60 ± 5.9 m/s in 450- to 500-g rats compared with motor conduction velocities of 30.1 ± 2.8 m/s in 100- to 150-g and 55.0 ± 6.9 m/s in 450- to 500-g rats. Both motor and sensory velocities were directly related to rat size. However, the latency of the H reflex evoked at the ankle was relatively independent of rat size. It was 6.62 ± 0.36 m/s in 100- to 150-g rats and 6.05 ± 0.43 m/s in 450- to 500-g rats with a mean for 39 rats from 100 to 500 g of 6.44 ± 0.41 ms. This method of determining motor and sensory conduction velocities in the rat is simple, does not necessitate killing the animal, and should prove useful in the study of experimental neuropathies.     

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.     

Assessment of motor pathways to masticatory muscles: An examination technique using electrical and magnetic stimulation

To study motor pathways to masticatory muscles, a new recording technique using surface electrodes was developed. The recording electrode was mounted on a spatula and inserted enorally into the pterygomandibular plica over the belly of m. masseter. Using this technique, mean latencies/amplitudes of the compound action potentials (CMAPs) in 18 healthy subjects were 1.2 ms/4.9 mV after electrical stimulation of the trigeminal nerve below the zygomatic arch, and 5.5 ms/1.1 mV after magnetic stimulation of the cortex. In 15 patients with unilateral lesions of the facial nerve, masticatory CMAPs had virtually symmetrical configuration, latency, and amplitude, excluding a major contribution of volume conducted activity from other cranial muscles. The technique was evaluated in patients after surgical treatment for trigeminal neuralgia. Patients with with retrogasserian thermocoagulation and central demyelinating lesions were consistently identified. © 1994 John Wiley & Sons, Inc.     

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.     

Clinical utility of dorsal sural nerve conduction studies

A technique of testing sensory nerve conduction of the dorsal sural nerve in the foot was used in 38 normal subjects and 70 patients with peripheral neuropathies. The normal dorsal sural sensory nerve action potential (SNAP) had a mean amplitude of 8.9 microV (range 5-15 microV), mean latency to negative peak of 4.0 ms (range 3.2-4.7 ms), and mean conduction velocity of 34.8 m/s (range 30-44 m/s). Optimal placement of the recording electrodes to obtain a maximal nerve action potential was proximal to digits 4 and 5. Cooling to below 25 degrees C prolonged the latency but did not decrease the SNAP amplitude. Among the patients with peripheral neuropathy, dorsal sural SNAP was absent in 68 (97%), whereas only 54 (77%) showed abnormalities of sural sensory conduction. The diagnostic sensitivity of sensory nerve conduction studies in peripheral neuropathies may be significantly improved by the use of this technique for evaluating the action potential of the dorsal sural nerve.     

Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients

The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 +/- 0.5 mmol/l (mean +/- SEM) within 15 min and kept approximately 15 mmol/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist - elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 m/s to 50.4 m/s (P less than 0.05) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P less than 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P less than 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P less than 0.01) during clamping. Motor nerve conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P less than 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P less than 0.001). We conclude that acute induction of hyperglycemia in long-term diabetics seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency.(ABSTRACT TRUNCATED AT 250 WORDS)     

Conduction velocity of the human spinothalamic tract as assessed by laser evoked potentials

To study the conduction velocity of the spinothalamic tract (STT) we delivered CO2 laser pulses, evoking pinprick sensations, to the skin overlying the vertebral spinous processes at different spinal levels from C5 to T10 and recorded evoked potentials (LEPs) in 15 healthy human subjects. These stimuli yielded large-amplitude vertex potentials consisting of a negative wave at a peak latency of about 200 ms followed by a positive wave at a peak latency of about 300 ms. The mean conduction velocity of the STT was 21 m/s, i.e. higher than the reported velocity of the corresponding primary sensory neurons (type II AMH). Because dorsal stimulation readily yields reproducible brain LEPs, we expect this technique to be useful as a diagnostic tool for assessing the level of spinal cord lesions.     

The medial calcaneal nerve: Anatomy and nerve conduction technique

We report a new technique for studying conduction in the medial calcaneal nerve (MCN). Dissection of 14 cadaver feet revealed the optimal G₁ site to be one third of the way from the apex of the heel to a point midway between the navicular tuberosity and the prominence of the medical malleous. Seventy-two feet (36 healthy volunteers) were studied using surface stimulation of the tibial nerve 10 cm proximal to the G₁ surface electrode. Averaging technique was not required. Reference values (mean ± 2 SD) were determined for MCN onset latency (2.0 ± 0.3 ms), peak latency (2.5 ± 0.3 ms), onset conduction velocity (61 ± 11 m/s), peak conduction velocity (40 ± 5 m/s), baseline-to-peak amplitude (18 ± 6 μV), and maximum intrasubject side-to-side differences in these values (0.3 ms, 0.3 ms, 15 m/s, 5 m/s, and 17 μV, respectively). This study provides an easily performed, reproducible method for electrophysiologic evaluation of the MCN.© 1995 John Wiley & Sons, Inc.     

Supraorbital nerve conduction study in normal subjects

There is currently no examination technique that allows direct measurement of supraorbital nerve conduction velocity and amplitude. Therefore, in this study we describe a novel nerve conduction technique that allows measurement of the supraorbital sensory nerve action potential (SNAP) distal to the supraorbital foramen. Supraorbital SNAPs were recorded bilaterally from 17 healthy volunteers using an antidromic technique. The SNAPs were consistently recordable over the site 6 cm lateral to the midline point that was marked 10 cm above the nasion. Measured parameters included peak latency (mean 2.3 ms, SD 0.3), amplitude (mean 14.6 μV; SD 10.5), and velocity (mean 51.3 m/s, SD 6.8). The mean percentage of interside difference in amplitude was 25.6% (SD 17.3). Cut-off values (97th percentile) were 2.7 ms (peak latency), 3.3 μV (amplitude), 41.9 m/s (conduction velocity), and 54.9% (interside difference in amplitude). Supraorbital SNAPs can be recorded in all normal subjects and used as a quantitative measure of the functioning large fibers in the nerve.     

脑干三叉神经诱发电位对三叉神经根部分切断术的临床应用研究

目的 评价脑干三叉神经诱发电位对三叉神经痛病人三叉神经根切断术的临床应用价值.方法 作者研究了36例经术前MRTA及术中探查除外神经血管接触的三叉神经痛病人,在三叉神经感觉根大部切断术过程中,通过术前、中、后记录BTEP以监测三叉神经传导功能;测定BTEP潜伏期及波幅参量的变化指导手术的进程.结果 36例病人患侧BTEP潜伏期延长、波幅降低,提示三叉神经痛患者三叉神经传导功能损害,术中待BTEP呈一直线后,不再继续切断神经根,术后疼痛均缓解,未遗三叉运动功能障碍.结论 脑干三叉神经诱发电位可以指导选择性三叉神经根切断术并防止三叉神经眼支损害的发生.     

Technique for studying conduction in the lateral cutaneous nerve of calf

We describe a novel technique for assessing conduction in the lateral cutaneous nerve of the calf (LCNC), a branch of the common peroneal nerve, based on a study of 32 healthy subjects. Both antidromic and orthodromic techniques were used in each of the 64 limbs to obtain a sensory nerve action potential (SNAP) of the LCNC over a distance of 12 cm. In 60 limbs (93.7%) a SNAP was obtainable with either the antidromic or orthodromic technique. In 21 limbs (32. 8%), the SNAP was obtained both antidromically and orthodromically. In 33 limbs (51.6%), the SNAP was obtained only antidromically, and in 6 (9.4%), only orthodromically. In four limbs, the response was unobtainable. Mean antidromic onset latency was 2.1 ms +/- SD 0.3, peak latency was 2.6 ms +/- SD 0.4, amplitude (without averaging) was 4.3 microV +/- SD 2.5, and conduction velocity was 60 m/s +/- SD 10. Mean orthodromic onset latency was 2.3 ms +/- SD 0.3, peak latency was 2.7 ms +/- SD 0.3, amplitude was 5.0 microV +/- SD 2.2, and conduction velocity was 52 m/s +/- SD 5. Utilization of this technique allows for more detailed localization of common peroneal nerve injury based on whether it is proximal or distal to the origin of the LCNC.     

Long-latency reflexes in contracted hand and foot muscles and their relations to somatosensory evoked potentials and transcranial magnetic stimulation of the motor cortex.

OBJECTIVE: The cortical relay time (CRT) for V2 of long-latency reflexes (LLRs) in the contracted thenar and short toe flexor muscles was studied. METHODS: LLRs and somatosensory evoked potentials (SEPs) were studied by electrical stimulation of the median or posterior tibial nerve. The CRT for V2 was calculated by subtracting the onset latency of cortical potentials in SEPs and that of motor evoked potentials (MEPs) by transcranial magnetic stimulation (TMS) from the onset latency of V2 in eight healthy subjects. RESULTS: The CRT for the thenar muscles was 11.4+/-0.9 ms (mean +/- SD), as the onset latency was 48.8+/-1.4 ms for V2, 16.0+/-1.2 ms for N20 and 21.3+/-1.1 ms for MEP, respectively. The CRT for the short toe flexor muscles was 3.0+/-1.3 ms, as the onset latency was 80.5+/-4.5 ms for V2, 35.3+/-1.8 ms for P38 and 42.2+/-2.0 ms for MEP, respectively. CONCLUSION: Significantly longer CRT for V2 for the thenar muscles (P<0.001, paired Student's t test) may indicate more synaptic relays as compared to that for the short toe flexor muscles.     

Assessment of trigeminal small-fiber function: brain and reflex responses evoked by CO2-laser stimulation

Laser pulses selectively excite mechano-thermal nociceptors and evoke brain potentials that may reveal small-fiber dysfunction. We applied CO2-laser pulses to the perioral and supraorbital regions and recorded the scalp laser-evoked potentials (LEPs) and reflex responses in the orbicularis oculi, masticatory, and neck muscles in 30 controls and 10 patients with facial sensory disturbances. Low-intensity pulses readily evoked scalp potentials consisting of a negative component with a latency of 165 ms followed by a positive component at 250 ms. In vertex recordings, the amplitude of LEPs exceeded 30 microV. Although only high-intensity pulses evoked reflex responses, some subjects showed--even to low-intensity pulses--an orbicularis oculi (blink-like) response that markedly contaminated the scalp recording. Scalp LEPs were abnormal in patients with hypalgesia and normal trigeminal reflexes and normal in patients with normal pain sensitivity and abnormal trigeminal reflexes. Possibly because of the high receptor density in this area and the short conduction distance, laser stimulation of the trigeminal territory yields low-threshold and large LEPs, which are useful for detecting dysfunction in peripheral and central pain pathways.     

Clinical utility of dorsal sural nerve conduction studies in healthy and diabetic children.

OBJECTIVE: Monitoring of the dorsal sural sensory nerve action potential (SNAP) is a sensitive method for detection of peripheral neuropathies. We tried to determine the normal dorsal sural nerve conduction values of the childhood population and assessed the clinical utility of this method in diabetic children who have no clinical sign of peripheral neuropathy. METHODS: In the study, 36 healthy and 27 diabetic children were included. In all subjects peripheral motor and sensory nerve studies were performed on the upper and lower limbs including dorsal sural nerve conduction studies. RESULTS: The dorsal sural SNAP mean amplitude was 8.24+/-3.08 microV, mean latency was 2.47+/-0.48 ms, mean sensory conduction velocity was 41.63+/-5.43 m/s in healthy children. Dorsal sural SNAPs were absent bilaterally in one diabetic patient. In the other 26 diabetic patients, the mean dorsal sural nerve distal latency was longer (2.93+/-0.63 ms, P = 0.004), mean SCV was slower than in healthy subjects (36.68+/-7.66 m/s, P = 0.005). However, dorsal sural nerve amplitude was not different between the groups. A dorsal sural nerve latency of more than 2.9 ms had a sensitivity of 50% and a specificity of 75%. A dorsal sural nerve velocity of less than 36 m/s had a sensitivity of 54% and a specificity of 92%. CONCLUSIONS: We designated the reference values of the dorsal sural nerve in healthy children. In addition, our findings suggest that dorsal sural nerve conduction studies may have value to determine neuropathy in the early stages in children with diabetes. SIGNIFICANCE: The dorsal sural nerve conduction studies in diabetic children may have value to determine the neuropathy in its early stages.     

Reduced sensory and motor conduction velocity in 25-week-old diabetic [ ] mice

Motor and sensory conduction velocities were measured in sural and tibial nerves of 25-week-old genetically diabetic ( ) mice and their nondiabetic littermates. For motor conduction velocity determination, the sciatic nerve was stimulated at the hip and the tibial nerve subsequently stimulated at the ankle while recording interosseous muscle potentials from needle electrodes placed in the foot. Sensory conduction velocities were determined by recording compound action potentials directly from sural and tibial nerves at the ankle after sciatic nerve stimulation. Control and diabetic conduction velocities were compared by Student's t test. The motor conduction velocity was reduced by approximately 20% from the control, and the distal motor latency was increased in mice by 22% more than the control latency. Conduction velocity was also reduced in some sensory fibers, an observation not previously reported in the mouse. Sensory fibers most severely affected were the faster-conducting fibers of the sural nerve, whose conduction velocity was decreased by 18% from the control. Slower-conducting sensory fibers in sural and tibial nerves were only midly affected, whereas fast-conducting sensory fibers of the tibial nerve appeared to remain normal. These data suggest that not all nerve fibers react alike to the diabetic state in the genetically diabetic ( ) mouse.