Normal proximal and delayed distal conduction in the pudendal nerves of patients with idiopathic (neurogenic) faecal incontinence.

The latency of the response in the external anal sphincter muscle following transcutaneous stimulation of the cauda equina at the L1 vertebral level was measured in nine women with neurogenic faecal incontinence (mean 7.3 SD 0.7 ms) and 11 normal subjects (mean 5.6 SD 0.6 ms) (p = 0.01). There was no difference in conduction velocity between the L1 and L4 vertebral levels thus supporting the suggestion that conduction delay in faecal incontinence occurs distally.     

Motor conduction velocity in the human spinal cord: slowed conduction in multiple sclerosis and radiation myelopathy.

Transcutaneous electrical stimulation of the central nervous system was used to measure motor conduction velocity in the human spinal cord in 21 subjects aged 22 to 75 years (mean 55 years), none of whom had neurological disease. The motor conduction velocity between the sixth cervical (C6) and first lumbar (L1) vertebral levels was 67.4 +/- 9.1 m/s. This probably represents conduction velocity in the corticospinal tracts. In these subjects the motor conduction velocity in the cauda equina, between the first lumbar (L1) and fourth lumbar (L4) vertebral levels, was 57.9 +/- 10.3 m/s. In four of five patients with multiple sclerosis, all with corticospinal signs in the legs, motor conduction velocity between C6 and L1 was slowed (41.8 +/- 16.8 m/s), but cauda equina conduction was normal (55.8 +/- 7.8 m/s). Similar slowing of spinal cord motor conduction was found in a patient with radiation myelopathy. This method should provide a relevant, simple clinical test in patients with spinal cord disease.     

Electrophysiological observations on the human pudendo-anal reflex.

A reproducible electrophysiological technique is described to determine the latency of reflex contraction of the external anal sphincter in response to stimulation of the dorsal genital nerve: the pudendo-anal reflex. This was studied in 38 asymptomatic control subjects and 20 women with neurogenic faecal incontinence, supplemented by determination of the mean motor unit potential duration (MUPD) of the external anal sphincter and anorectal manometry. The reflex latency in the control group was 38.5 +/- 5.8 (SD) ms and appeared to be independent of age or sex. Three patients with faecal incontinence had absent reflexes; the remainder showed significant prolongation of latency (56 +/- 12.2 SD ms) and diminution of amplitude. MUPD was prolonged in incontinence and showed significant correlation with the corresponding reflex latency determination (tau = 0.56, p less than 0.001). The latency of this polysynaptic spinal reflex hence provides a reliable index of neuropathy of the external anal sphincter.     

Perineal motor potentials to magnetic stimulation, pudendal evoked potentials and perineal reflex in women.

Motor potentials to transcranial and lumbar magnetic stimulation were recorded from the perineum in 14 healthy women. The response to transcranial stimulation presented an onset at 20.2 +/- 1.3 ms and a negative peak at 25.1 +/- 1.9 ms. Lumbar responses presented an onset at 5.1 +/- 0.8 ms, and the motor central conduction time measured 14.4 +/- 1.5 ms. Perineal reflex, cortical and lumbar pudendal evoked potentials were recorded after electrical stimulation of the labia minora. These tests are of possible clinical use in the evaluation of sphincter disturbances as they investigate the afferent and efferent pathways concerning pudendal nerve function.     

Visualization of the electrical activity of the cauda equina using a magnetospinography system in healthy subjects

ObjectiveTo establish a method to measure cauda equina action fields (CEAFs) and visualize the electrical activities of the cauda equina in a broadly aged group of healthy adults.MethodsUsing a 124-channel magnetospinography (MSG) system with superconducting interference devices, the CEAFs of 43 healthy volunteers (22–64 years of age) were measured after stimulation of the peroneal nerve at the knee. Reconstructed currents were obtained from the CEAFs and superimposed on the X-ray image. Conduction velocities were also calculated from the waveform of the reconstructed currents.ResultsThe reconstructed currents were successfully visualized. They flowed into the L5/S1 foramen about 8.25–8.95 ms after the stimulation and propagated cranially along the spinal canal. In 32 subjects (74%), the conduction velocities of the reconstructed currents in the cauda equina could be calculated from the peak latency at the L2–L5 level.ConclusionsMSG visualized the electrical activity of the cauda equina after peroneal nerve stimulation in healthy adults. In addition, the conduction velocities of the reconstructed currents in the cauda equina could be calculated, despite previously being difficult to measure.SignificanceMSG has the potential to be a novel and noninvasive functional examination for lumbar spinal disease.     

Soleus H-reflex to S1 nerve root stimulation

H-reflexes in normals were elicited by percutaneous electrical and magnetic stimulation of proximal nerve roots at the cauda equina. H-M interval to S1 nerve root stimulation at the level of the S1 foramen was 6.8 +/- 0.33 ms, with side to side difference of 0.16 +/- 0.13 ms. Compression/ischemia of the sciatic nerve in the mid-thigh abolished the H-reflex to stimulation of the tibial nerve at the popliteal fossa when the H-reflex to S1 nerve root stimulation was preserved. The length of the S1 nerve root in human cadavers was measured to be 17.5 +/- 03 cm, providing an estimated dorsal root conduction velocity of 67.3 m/s and a ventral root conduction velocity of 54 m/s. We conclude that the H-M interval to S1 root stimulation can provide reliable measures of conduction within the spinal canal including proximal afferents, anterior horn cells and ventral roots.     

Damage to the innervation of the voluntary anal and periurethral sphincter musculature in incontinence: an electrophysiological study.

In 40 women with idiopathic (neurogenic) faecal incontinence, 20 of whom also had stress urinary incontinence, single fibre EMG studies showed an increased fibre density in the external anal sphincter muscle. All these patients showed excessive descent of the pelvic floor on straining. The mean terminal motor latencies in the pudendal and perineal nerves, measured by a digitally-directed intrarectal stimulating technique, were increased when compared with 20 control subjects (p less than 0.01). The perineal nerve terminal motor latency was more markedly increased in the 20 patients with double incontinence than in those with faecal incontinence alone (p less than 0.01). These results provide direct electrophysiological evidence of damage to the innervation of the pelvic floor musculature in idiopathic faecal and double incontinence, and imply that idiopathic stress urinary incontinence may have a similar cause.     

Diagnostic value of cauda equina motor conduction time in lumbar spinal stenosis

ObjectiveLumbar spinal stenosis (LSS) is a chronic degenerative disease with pain in the back, buttocks and legs aggrevated by walking and relieved after rest without associated vascular disease of lower extremities observed in patients between 50 and 60 years. Several studies, using different methods indicated an association between slowing or blocking of root-nerve conduction and LSS. None of the previous research had applied the more conceivable methods such as recording the cauda equina potentials from the lumbar level or stimulating the spinal roots within the canal using either leg nerves or muscles. In this study, electrical lumbar laminar stimulation was used to demonstrate prolongation of cauda equina motor conduction time in lumbar spinal stenosis.MethodsTwenty-one LSS patients and age matched 15 normal control subjects were included in the study. Lumbar laminar electrical stimulation from L1 and L5 vertebra levels were applied by needle electrodes. Compound muscle action potential (CMAP) from gastrocnemius muscles were recorded bilaterally. Latency difference of CMAPs obtained from L1 and L5 spine levels were accepted as the cauda equina motor conduction time (CEMCT).ResultsCEMCT was significantly longer in patient group when compared to normal controls. Mean latency difference was 3.59 ± 1.07 msec on the right side, 3.49 ± 1.07 msec on the left side in LSS group, it was 1.45 ± 0.65 msec on the right side, 1.35 ± 0.68 msec on the left side on normal control group (p < 0.0001).ConclusionsThe prolongation of CEMCT was statistically and individually significant in patient group. This may indicate that lower lumbosacral motor roots were locally and chronically compressed due to lumbar spinal stenosis. Lumbar spinal stenosis may have induced local demyelination at the cauda equina level.SignificanceSince the prolongation of CEMCT was found only in patients with LSS, the method of laminar stimulation can be chosen for patients with uncertain diagnosis of LSS.     

Anal sphincter responses after perianal electrical stimulation.

By perianal electrical stimulation and EMG recording from the external anal sphincter three responses were found with latencies of 2-8, 13-18 and 30-60 ms, respectively. The two first responses were recorded in most cases. They were characterised by constant latency and uniform pattern, were not fatigued by repeated stimulation, were most dependent on placement of stimulating and recording electrodes, and always had a higher threshold than the third response. The third response was constantly present in normal subjects. It had the longest EMG response and the latency decreased with increasing stimulation to a minimum of 30-60 ms. This response represented the clinical observable spinal reflex, "the classical anal reflex". The latencies of the two first responses were so short that they probably do not represent spinal reflexes. This was further supported by the effect of epidural anaesthesia which left the first responses unaffected but abolished the classical anal reflex. The origin of the two first responses is discussed and models involving antidromal impulse propagation in the efferent fibre as the afferent limbs of the responses are proposed.     

Sensory potentials evoked by magnetic stimulation of the cervical spine

Magnetic stimulation of cervical spinal roots was shown to elicit sensory potentials (MESP) which could easily be recorded at the fingers with ring electrodes. The latency of the MESP recorded at digit I was significantly shorter and the amplitude higher than of digits III and V. The latencies were largely independent of stimulus strength. In an attempt to localize the place of depolarization, the latencies of these potentials were compared with the N11 of the SEP (reflecting the arrival in the spinal cord) and with F-wave latencies and motor evoked potentials (MEP) to abductor pollicis brevis. The MESP latencies showed a very constant difference with the N11, being 0.6 ms faster. The mean difference between F latency and MEP was 1.2 ms. It is concluded that the origin of these MESPs is very near the spinal foramina, possibly in the sensory ganglia. © 1993 John Wiley & Sons, Inc.     

Spinal evoked potential in the monkey

Computer-averaged evoked potential responses (EPs) to stimulation of the sciatic nerve and cervical spinal cord were recorded from the dura and skin over the cauda equina and spinal cord in seven monkeys, three with chronic spinal cord lesions. Sciatic EPs consisted of predominantly negative triphasic propagated potentials recorded at all spinal levels and greatest in amplitude over the cauda equina and caudal spinal cord. The conduction velocity of this EP was faster over the cauda equina and rostral spinal cord than over caudal cord segments. Triphasic potentials were succeeded by small negative potentials over the cauda equina and larger negative potentials over the lumbar enlargement. Sciatic EPs over the upper lumbar and thoracic cord were more sensitive to asphyxia than the initial triphasic potentials recorded over cauda equina and caudal cord but resisted changes from increasing the rate of stimulation up to 100 per second. Propagated thoracic EPs were preceded by nonpropagated potentials. The longer latency negative potentials occurring locally over the cauda equina and lower lumbar enlargement were abolished at levels of asphyxia and were attenuated at rates of stimulation that did not affect the preceding triphasic potentials. Following complete spinal cord transection, nonpropagated sciatic EPs were recorded in leads rostral to the section. In preparations with chronic partial cord hemisection involving dorsal and lateral quadrants, ipsilateral sciatic EPs had increased latency, reduced amplitude, and poor definition in the vicinity of and rostral to the lesion. Direct cervical cord stimulation elicited caudally propagated potentials which were followed by large, broad potentials over the lumbar enlargement.     

Lumbosacral evoked potentials (LSEPs) and cortical somatosensory evoked potentials (SEPs) in patients with lesions of the conus medullaris and cauda equina

Evoked potentials from unilateral stimulation of the posterior tibial nerve at the knee were recorded over the spinous processes S1, L4, L2, T12 and from the 'lower extremity' portion of the sensory cortex (Cz) in 29 patients who exhibited clinical and electromyographic signs of conus medullaris or cauda equina lesions. Simultaneous recording of the lumbosacral evoked potentials (LSEPs) and cortical somatosensory evoked potentials (SEPs) permitted evaluation of the relative effectiveness of the peripheral stimulus in eliciting responses in the lumbosacral segments of the spinal cord and in the cortex of the brain. In patients with cauda equina lesion, each major component of LSEP can be absent or the peak can have a reduced amplitude and a prolonged latency. The degree of impairment of the LSEP runs in parallel to the degree of severeness of the cauda equina lesion. The recording of LSEP responses with surface electrodes represents a reliable test for the detection of mild cauda equina abnormalities, but the surface recording technique is not sensitive enough to differentiate between severe incomplete and severe complete cauda equina lesions. On the other hand, concurrent recording of responses evoked at lumbosacral and cortical levels by the same stimuli did detect instances in which the first-order afferents were capable of delivering an adequate volley of impulses to evoke a sizeable cortical response without evidence of an associated postsynaptic response in the spinal cord. Such findings are good evidence of a problem localized in the gray matter of the spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

AAEM minimonograph #35: Clinical experience with transcranial magnetic stimulation

We elicited motor evoked potentials (MEPs) using transcortical magnetic stimulation in 150 control subjects aged 14 to 85 years and 275 patients with a variety of diseases. There were no significant side effects. Cortex-to-target muscle latencies measured 20.2 +/- 1.6 ms (thenar), 14.2 +/- 1.7 ms (extensor digitorum communis), 9.4 +/- 1.7 ms (biceps), and 27.2 +/- 2.9 ms (tibialis anterior). Central motor delay between the cortex and the C-7 and L-5 measured 6.7 +/- 1.2 ms and 13.1 +/- 3.8 ms, respectively. Mean spinal cord motor conduction velocity measured 65.4 m/s. MEP amplitude expressed as a percentage of the maximum M wave was never less than 20% of the M wave. A value of less than 10% is considered abnormal. MEP latency increases linearly with age and central motor delay is longer in older subjects. Compound muscle action potentials and absolute MEP amplitudes decreased linearly with age. In multiple sclerosis (MS), MEP latency and central delay were often very prolonged. The MEP was more sensitive than the SEP in MS. In amyotrophic lateral sclerosis, MEP latencies were only modestly prolonged; the characteristic abnormality was reduced amplitude. When pseudobulbar features predominated MEPs were often absent. The MEP was of normal latency in Parkinson's disease, but age-related amplitude was often increased. MEP latency and amplitude were normal in Huntington's disease. Abnormal MEPs persisted several months after stroke despite good functional recovery. The MEP could be used to advantage to demonstrate proximal conduction slowing and block in demyelinating neuropathies. In plexopathy, ability to elicit an MEP several days after onset of paresis was good evidence of neuronal continuity in motor fibers.     

Sacral sparing with cauda equina compression from central lumbar intervertebral disc prolapse.

Sparing of sensation in sacral dermatomes and of sphincter control was found in eight out of fourteen cases of severe cauda equina compression from massive central lumbar disc prolapse. Although the triangular shape of the lumbar spinal canal may be one factor for this it was found from a necropsy model that the increase in linear strain on the stretched roots of the cauda equina is least in the more centrally placed lower sacral roots. It is argued that the lower tension in these roots is determined by Young's Modulus.     

Magnetic-motor-root stimulation: Review

Magnetic stimulation can activate the human central and peripheral nervous systems non-invasively and virtually painlessly. Magnetic stimulation over the spinal enlargements can activate spinal nerves at the neuroforamina (magnetic-neuroforamina stimulation). This stimulation method provides us with information related to the latency of compound-muscle action potential (CMAP), which is usually interpreted as peripheral motor-conduction time (PMCT). However, this stimulation method has faced several problems in clinical applications. One is that supramaximal CMAPs were unobtainable. Another is that magnetic stimulation did not usually activate the spinal nerves in the spinal canal, i.e., the cauda equina, which prevented an evaluation of its conduction. For these reasons, magnetic-neuroforamina stimulation was rarely used to evaluate the conduction of peripheral nerves. It was mainly used to evaluate the conduction of the corticospinal tract using the parameter of central motor-conduction time (CMCT), which was calculated by subtracting PMCT from the latency of motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) over the primary motor cortex. Recently, supramaximal stimulation has been achieved in magnetic-neuroforamina stimulation, and this has contributed to the measurement of both CMAP size and latency. The achievement of supramaximal stimulation is ascribed to the increase in magnetic-stimulator output and a novel coil, the magnetic augmented translumbosacral stimulation (MATS) coil. The most proximal part of the cauda equina can be reliably activated using the MATS coil (magnetic-conus stimulation), thus contributing to the measurement of cauda equina conduction time (CECT) and cortico-conus motor-conduction time (CCCT). These recent developments in magnetic-motor-root stimulation enable us to more precisely evaluate the conduction of the proximal part of peripheral nerves and that of the corticospinal tract for lower-limb muscles. In this review article, we summarise the basic mechanisms, recent topics, clinical applications, comparison to electrical stimulation, pitfalls, safety and additional issues in magnetic-motor-root stimulation.     

Central and peripheral motor conduction to cremasteric muscle

The few electrophysiologic studies of the cremasteric muscle (CM) have mainly been restricted to the cremaster reflex with no reference to central and peripheral nerve conduction to the muscle, probably for technical reasons.Twenty-six normal adult male volunteers were studied by transcranial magnetic cortical stimulation (TMS) and stimulation of thoracolumbar roots. The genitofemoral nerve (GFN) was stimulated electrically at the anterior superior iliac spine and a needle electrode was inserted into the CM for conduction studies. The motor latency to the CM from the cortical TMS ranged from 20 to 33 ms among the subjects (25.8 +/- 2.9 ms, mean +/- SD). Magnetic stimulation of the lumbar roots produced a motor response of the CM within 9.6 +/- 1.9 ms (range, 6-15). The central motor conduction time to the CM was 16.5 +/- 2.8 ms (range, 10-21). Stimulation of the GFN produced a compound muscle action potential with a mean value of 6.4 +/- 1.8 (range, 4-10) ms in 23 of the 26 cases. Thus, central motor nerve fibers to the CM motor neurons exist, and there may be a representation area for the CM in the cerebral cortex. The GFN motor conduction time to the CM may have clinical utility, such as in the evaluation of the groin pain due to surgical procedures in the lower abdomen.     

Motor potentials of bulbocavernosus muscle after transcranial and lumbar magnetic stimulation: comparative study with bulbocavernosus reflex and pudendal evoked potentials.

Motor potentials of the bulbocavernosus muscle were recorded in 17 healthy subjects after transcranial and lumbar magnetic stimulation. The latencies (SD) were respectively: 22.9 (1.8) and 5.9 (0.4) ms. The central conduction time was 17.0 (2.5) ms. The bulbocavernosus reflex presented an onset at 34.5 (3.3) ms and a negative peak at 43.1 (3.9) ms. The cortical pudendal evoked potential was W shaped: the first peak had a latency of 35.4 (2.8) ms. The concurrent recording of motor potentials, bulbocavernosus reflex, pudendal evoked potentials gives a measure of peripheral and central, afferent and efferent neurological pathways related to pudendal nerve function.     

Somatosensory cerebral potentials evoked by stimulation of the lumbo-sacral spinal cord in normal subjects and in patients with conus medullaris and cauda equina lesions

Somatosensory cerebral evoked potentials were recorded by intrathecal stimulation of the lumbo-sacral cord and roots in 16 normal subjects and patients having cauda/conus injury (group A, 15 cases), compressive lesions of cauda equina (group B, 13 cases) and lesions of both types covering the lumbar cord (group C, 24 cases). The shape of the intrathecally evoked cerebral potential (IECP) was basically the same as that obtained by posterior tibial nerve stimulation from 12 normal subjects except that the early components were 10-15 msec shorter in latency in the former potential, with an average of 12 msec. IECPs were easily recorded in groups A and B, but a significant delay was found in both groups, especially group A. It was difficult to obtain the IECP in group C, When it could be recorded the latency increase was apparent. These findings were explained on the basis of degeneration of the ascending spinal nerve fibers proximal to the lesion site.     

Motor nerve conduction study in cauda equina with high-voltage electrical stimulation in multifocal motor neuropathy and amyotrophic lateral sclerosis

In this study we aim to establish a motor nerve conduction study (NCS) for the cauda equina and examine its usefulness in multifocal motor neuropathy (MMN) and amyotrophic lateral sclerosis (ALS). NCS of the tibial nerve proximal to the knee was performed with an optimized high-voltage electrical stimulation (HV-ES) method in 21 normal subjects, 5 with MMN, and 11 with ALS. HV-ES, but not magnetic stimulation, could supramaximally stimulate the cauda equina. Cauda equina motor conduction time determined by HV-ES, but not that with F-waves, correlated well with cauda equina length on magnetic resonance imaging. HV-ES revealed proximal lesions in 4 MMN patients but in none of the ALS patients. Importantly, 1 patient with "MMN without conduction block (CB)" had a CB in the cauda equina. Cauda equina motor conduction is better evaluated by HV-ES than with F-wave study or magnetic stimulation. HV-ES can help to distinguish MMN and "MMN without CB" from ALS.