Lumbar cord potentials evoked by stimulation of the nerves of the lower limb in man

Lumbar cord potentials evoked by electrical stimulation of the posterior tibial and sural nerves at the ankle were recorded with monopolar epidural electrodes, at T11-T12 level in 20 subjects and were compared with surface recorded potentials. Two quadriplegic patients with spinal section were included in this group. Curare was given in two cases. Xylocaine block of peripheral nerve was carried out in 4 cases. Double shock study was done in 5 cases. The lumbar cord evoked potentials show two successive components: a 'primary' negative-positive spike response with a latency of 19-35 msec, and the 'secondary' waves with latencies up to 200 msec. The 'primary' response is mainly produced by the afferent volley in the fibres of the dorsal roots and of their intramedullary prolongations. There is no evidence which suggests that it is correlated with presynaptic inhibition. The secondary components may be divided into the early and the late waves. The early waves (40-90 msec) are related to the polysynaptic activities from the afferent fibres of small diameters. The late waves are under the influence of supraspinal mechanism and may be related to long-loop reflexes. The clinical implications of these evoked potentials are discussed.     

Analysis of reflex activity in cardiac sympathetic nerve induced by myelinated phrenic nerve afferents

Electrical stimulation of the phrenic nerve afferents evoked excitatory responses in the right inferior cardiac sympathetic nerve in chloralose-anaesthetized cats. The reflex was recorded in intact and spinal cats. The latency and threshold of the volley recorded from the phrenic nerve as well as of the cord dorsum potentials evoked by electrical stimulation of the phrenic nerve indicated that group III afferents were responsible for this reflex. The phrenicocardiac sympathetic reflex recorded in intact cats was followed by a silent period. The maximum amplitude of the reflex discharges was 800 microV, the latency was 83 ms and the central transmission time 53 ms. Duration of the silent period lasted up to 0.83 s. In spinal cats the reflex was recorded 5.5-8 h after spinalization. The maximum amplitude of the spinal reflex discharges ranged from 22 to 91 microV and the latency from 36 to 66 ms.     

Short latency somatosensory evoked potentials in patients with neurological lesions

Short latency somatosensory potentials following median nerve stimulation were recorded in patients grouped according to anatomic location of neurological lesion. Patients with cerebral lesions causing severe sensory deficit lacked a major positive wave of cortical origin that in normal subjects peaked at a mean latency of 20.5 ms. Patients with severe cervical spinal cord disease lacked all of the normal somatosensory response except for the earliest component attributed to peripheral nerve activity. Patients with brain-stem lesions showed delayed latencies of later waves and prolonged interwave latencies. However, auditory evoked potentials measured in the group with brain-stem lesions were more helpful in localization. Analysis of short latency somatosensory potentials can discriminate between peripheral nerve, spinal cord, brain-stem, and cerebral lesions. Further experience and refinement of technique of measurement should increase the value of this procedure.     

Modulation of single motor unit discharges using magnetic stimulation of the motor cortex in incomplete spinal cord injury

OBJECTIVES: Motor evoked potentials (MEPs) and inhibition of voluntary contraction to transcranial magnetic stimulation (TMS) of the motor cortex have longer latencies than normal in patients with incomplete spinal cord injury (iSCI) when assessed using surface EMG. This study now examines the modulation of single motor unit discharges to TMS with the aim of improving resolution of the excitatory and inhibitory responses seen previously in surface EMG recordings. METHODS: A group of five patients with iSCI (motor level C4-C7) was compared with a group of five healthy control subjects. Single motor unit discharges were recorded with concentric needle electrodes from the first dorsal interosseus muscle during weak voluntary contraction (2%-5% maximum). TMS was applied with a 9 cm circular stimulating coil centred over the vertex. Modulation of single motor unit discharges was assessed using peristimulus time histograms (PSTHs). RESULTS: Mean (SEM) threshold (expressed as percentage of maximum stimulator output (%MSO)) for the excitatory peak (excitation) or inhibitory trough (inhibition) in the PSTHs was higher (p<0.05) in the patients (excitation = 47.1 (5.9) %MSO; inhibition = 44.3 (3.2) %MSO) than in controls (excitation=31.6 (1.2) %MSO; inhibition = 27.4 (1.0) %MSO). Mean latencies of excitation and inhibition were longer (p<0.05) in the patients (excitation=35 (1.8) ms; inhibition = 47.1 (1.8) ms) than in the controls (excitation = 21.1 (1.6) ms; inhibition = 27 (0.4) ms). Furthermore, the latency difference (inhibition-excitation) was longer (p<0.05) in the patients (10.4 (2.1) ms) than in the controls (6.2 (0.6) ms). CONCLUSION: Increased thresholds and latencies of excitation and inhibition may reflect degraded corticospinal transmission in the spinal cord. However, the relatively greater increase in the latency of inhibition compared with excitation in the patients with iSCI may reflect a weak or absent early component of cortical inhibition. Such a change in cortical inhibition may relate to the restoration of useful motor function after iSCI.     

Evoked potentials recorded from scalp and spinous processes during spinal column surgery

Peroneal nerve evoked potentials were simultaneously recorded from scalp and from wire electrodes inserted into lumbar and thoracic spinous processes at multiple levels during surgery for correction of spinal column curvature in 43 patients. Spinal potentials progressively increased in latency rostrally. Over cauda equina and rostral spinal cord initially positive triphasic potentials were recorded. Over caudal spinal cord the response consisted of initial positive-negative diphasic potentials that merged with broad large negative and positive potentials. At rapid rates of stimulation, the initial diphasic component was stable but the subsequent potentials significantly diminished in amplitude. This suggests that the diphasic component reflects presynaptic activity arising in the intramedullary continuations of dorsal root fibers and that the subsequent components reflect largely postsynaptic activity. Scalp recordings at restricted bandpass (30-3000 c/sec) revealed well defined positive and negative potentials with mean peak latencies of 25.9 and 29.9 msec (PV-N1). The amplitudes and latencies of PV-N1 remained relatively stable throughout general anesthesia with halogenated agents which suggests that this component may be a reliable monitor of conduction within spinal cord afferent pathways during spinal surgery. Data are presented which suggest that selective filtering may help to distinguish faster frequency, synchronous axonal events from slower frequency, asynchronous axonal or synaptic events.     

Aberrant conduction in human peripheral nerve: ephaptic transmission?

Later motor responses were recorded from the foot muscles of patients with neuropathy after stimulation of the posterior tibial nerve at the ankle. The latencies were too short to involve the spinal cord, but latencies were reduced by more proximal stimulation, indicating that the pathway begins with proximal conduction. The response differed from previously reported "axon reflexes," because it appeared on supramaximal stimulation. It was attributed to reflection of an impulse at a discontinuity of the myelin sheath. In 2 of 32 subjects, stimulation of the medial plantar nerve in the great toe resulted in reproducible motor responses with latencies of 37 and 38 msec in the flexor hallucis brevis. Ephaptic transmission was implied.     

Conduction properties of epidurally recorded spinal cord potentials following lower limb stimulation in man

Spinal somatosensory evoked potentials were recorded in 35 neurologically normal patients undergoing surgery for scoliosis. During posterior procedures the recording electrodes were placed in the dorsal epidural space and during anterior operations in the intervertebral discs. Stimulation was of the tibial nerve in the popliteal fossa and the posterior tibial and sural nerves at the ankle. At thoracic levels the response consisted of at least 3 components with different peripheral excitation thresholds and spinal conduction velocities (range 35-85 m/sec). All components were conducted mainly in tracts ipsilateral to the stimulus, component 1 being most laterally located. At low stimulus intensity only the fastest activity was recorded but this was markedly delayed over low thoracic segments and was recorded as a repetitive discharge rostrally. Higher intensities elicited additional components which were conducted at a slower but relatively uniform velocity; consequently they might overlap with or even overtake the fast activity at mid-to-low thoracic levels. Component 1 was much less prominent when the posterior tibial nerve was stimulated at the ankle and absent from the (cutaneous) sural nerve response; remaining potentials were conducted at velocities similar to those of components 2 and 3 following tibial nerve stimulation at the knee. Small 'stationary' potentials were recorded at all thoracic levels, probably due to the change in conductivity as the volley entered the spinal cord. Efferent activity was recorded at and below the thoraco-lumbar junction, possibly related to the H-reflex or F-wave. Similar, although smaller, afferent potentials were recorded from the anterior side of the vertebral column. Component 1 is likely to be due to the stimulation of group 1 muscle afferents which terminate in the dorsal horn and activate second order neurones, many of whose axons go to form the ipsilateral dorsal spinocerebellar tract. Components 2 and 3 are believed to be largely cutaneous in origin and to be conducted mainly in the dorsal columns.     

The origins of lumbosacral spinal evoked potentials in humans using a surface electrode recording technique.

Somatosensory evoked potentials were recorded over the lumbar spine and scalp in 12 normal subjects after stimulating the posterior tibial nerve at the knee and ankle and the sural nerve at the ankle. The H-reflex from the soleus muscle was recorded at the same time. The effects of stimulus intensity, frequency of stimulation and vibration were assessed. It was concluded that when the posterior tibial nerve was stimulated in the popliteal fossa, three negative peaks were recorded over the lumbosacral area. They arose from activity in the dorsal roots, the dorsal horn of the spinal cord (SD) and the ventral roots. In contrast when the posterior tibial nerve and the sural nerve were stimulated at the ankle only two negative peaks were recorded, a dorsal root potential and a spinal cord dorsum potential. In addition the data suggested that the peripheral nerve fibres that are involved with generating the surface recorded spinal potential with mixed nerve stimulation are primarily muscle afferents.     

The effects of focal epileptic activity on the somatosensory evoked potentials in the rat

Summary The cortical somatosensory evoked potential (SEP) of the rat, evoked by contralateral forepaw stimulation, consisted of early (P 1 and N 1) and late components (P 2 and N 2). Microelectrode recording yielded evoked unitary responses of short latencies in the range of the early components and responses of longer latencies in the range of P 2. During the development of focal epilepsy after topical application of penicillin, the late components of SEP were enhanced and the enhanced late negativity corresponded to a surface negative cortical spike. The prominent enlargement of later components was associated with prolonged, often recurrent discharges of longer latency unitary responses and with enlarged local field potentials. Early components of SEP remained relatively unaffected and so did unitary responses with short latencies.Epileptic spike-conditioned SEPs in the cuneate nucleus, thalamic sensory relay nucleus and sensory cortex were depressed from 100 ms (cuneate nucleus) to about 300 ms (thalamus and cortex) subsequent to spike discharge. Transmission in the cuneate nucleus was least affected. Thalamic and cortical early components of SEP had similar time courses of recovery, which differed markedly from that of cortical late components. Our findings suggest that two different neuronal activities generate different components of SEP and are differentially involved in the epileptic activities, which results in the different amplitude recovery following spontaneous epileptic spike discharges.This work was supported by the Deutsche Forschungsgemeinschaft (German Research Council)     

Responses of cardiac vagus and sympathetic nerves to excitation of somatic and visceral nerves

Somato-vagal and somato-sympathetic reflex responses were studied by recording simultaneously the activity of cardiac vagal and sympathetic efferents following excitation of various somatic (and 1 visceral) nerves in chloralose-anesthetized dogs.Stimulation of pure cutaneous (infraorbital, superficial radial, sural nerves), muscle (gastrocnemius, hamstring nerves) and mixed nerves (sciatic, brachial, intercostal, spinal) with short trains of pulses inhibited the activity of cardiac vagus nerve and excited that of cardiac sympathetic nerve after a latency of approximately 40–60 ms, depending on the nerve stimulated. These responses were followed by the opposite response, i.e. excitation of vagus and long-lasting inhibition (`silent period') of sympathetic nerve activity. These biphasic reflex responses recorded from both autonomic nerves had similar latencies so that a clear reciprocal relationship was observed. In addition to the above reflex responses which were observed in most instances, two peaks of excitation of short duration were recorded from the vagus nerve, in some instances, and an ‘early (spinal) reflex’ in sympathetic nerve was also observed. Both excitatory and inhibitory responses described above in either nerve were readily evoked by excitation of Group II (Aβ), but not Group I (Aα), afferent fibers and increased in magnitude when Group III (Aδ) afferents were also excited. Group IV (C) afferent contributed insignificantly to the somato-vagal reflex. The vagus nerve discharge evoked by sinus nerve stimulation was inhibited during reflex inhibition produced by somatic nerve stimulation. The latency of such inhibition was less than 20 ms and lasted for 100 ms after sural nerve stimulation. We conclude that, as in case of the baroreceptor reflex and autonomic component of the ‘defense reaction’, the somato-vagal and somato-sympathetic reflex responses are reciprocal in nature.     

Segmental inhibitory reactions in the spinal cord of the frog in response to orthodromic motor neuron activation

Ventral root reflexes evoked by a single dorsal root volley were recorded in the isolated frog spinal cord. They varied from asynchronous, low-amplitude response to highly synchronized monosynaptic discharge in different preparations. The response to a testing stimulus could be facilitated or inhibited, respectively. The inhibition was weaker at interstimulus intervals of about 40-50 ms and stronger either at longer (60-100 ms) or at shorter (15-30 ms) intervals, thus testifying to the existence of at least two types of inhibition: early and late. Strychnine effectively blocked the late inhibition and facilitated the early one; d-tubocurarine considerably weakened both types of inhibition. A conclusion is made that the late (presynaptic) inhibition is produced by activation of the inhibitory systems through recurrent motoneuron axon collaterals. Recurrent activation may also take part in the origin of the early (postsynaptic) inhibition.     

Comparison of the human evoked electrospinogram recorded from the intrathecal, epidural and cutaneous levels.

In 30 patients (17 of whom had a clinically normal spinal cord) spinal cord potentials evoked by peripheral nerve stimulation were studied with computer averaging techniques in order to compare the intrathecal, epidural and skin records. In epidural and skin records, segmental spinal cord potentials either recorded from lower cervical or lower thoracic intervertebral levels often had similar shapes and latencies, especially with regard to the first component of the intrathecally recorded responses. The second slow component became less significant and was even absent in some cases. The amplitude of the first component was on average 33% of that recorded intrathecally when recorded epidurally and only 10% when recorded from the skin. In three cases potentials of very prolonged onset latency were recorded epidurally or cutaneously while in the same cases intrathecal records resulted in potentials with normal latencies. Cervical tract responses at the C6--7 intervertebral level after stimulation of the posterior tibial nerve were studied by the 3 recording methods. Epidural and skin records failed to reveal such a response regularly, while intrathecal recording invariably provided the cervical tract response. The 3 recording methods were discussed with respect to clinical applications and research. It can be stated with some reservation that epidural and skin surface recording techniques could be exploited it one could know the time of arrival segmental afferent inputs at the spinal cord.     

Long-latency,nonreciprocal reflex responses of antagonistic hind limb muscles after cutaneous nerve stimulation in the cat

The time course of changes in monosynaptic reflex amplitude, after conditioning from both ipsi- and contralateral sural nerves at different stimulus strengths, was studied on two antagonistic motoneuronal pools acting on ankle muscles in spinal cats. Attention was focused on late effects, namely those appearing after a dely of more than 30 ms from the cutaneous stimulus. With low-threshold afferent activation, at conditioning-test intervals to 30 ms, the ipsilateral extensor monosynaptic reflex, recorded from the proximal stump of L7 to S1 ventral roots, showed marked inhibition; at longer intervals, a late facilitation period (LFP) lasting to 100 ms was observed. Increasing stimulus strength did not modify the time course of reflex excitability, but might enhance the amount of the facilitatory effecct. On the flexor monosynaptic reflex, sural conditioning induced, after the expected early facilitation, a second facilitatory period, starting at about 30 ms and recovering at about 130 ms. The excitability of antagonistic contralateral motoneuronal pools was also influenced, showing again a LFP with the same time course. The LFP was present after stimulation of the sural and saphenous nerves and was absent after stimulation of a muscle nerve. These late, long-lasting and nonreciprocal facilitatory effects on flexor and extensor ipsilateral motoneurons were quite distinct from the early reciprocal responses, and were evoked by large cutaneous fibers. An interpretation is put forward in light of the primary afferent hyperpolarization of Ia afferent terminals. A correlation is tentatively proposed with the mechanism subserving the stumbling corrective reaction.     

Subcortical somatosensory evoked potentials after posterior tibial nerve stimulation in children

We report our normative data of somatosensory evoked potentials (SEP) after posterior tibial nerve (PTN) stimulation from a group of 89 children and 18 adults, 0.4-29.2 years of age. We recorded near-field potentials from the peripheral nerve, the cauda equina, the lumbar spinal cord and the somatosensory cortex. Far-field potentials were recorded from the scalp electrodes with a reference at the ipsilateral ear. N8 (peripheral nerve) and P40 (cortex) were present in all children but one. N20 (cauda equina) and N22 (lumbar spinal cord) were recorded in 94 and 106 subjects, respectively. P30 and N33 (both waveforms probably generated in the brainstem) were recorded in 103 and 101 subjects, respectively. Latencies increased with age, while central conduction times including the cortical component, decreased with age (up to about age 10 years). The amplitudes of all components were very variable in each age group. We report our normative data of the interpeak latencies N8-N22 (peripheral conduction time), N22-P30 (spinal conduction time), N22-P40 (central conduction time) and P30-P40 (intracranial conduction time). These interpeak latencies should be useful to assess particular parts of the pathway. The subcortical PTN-SEPs might be of particular interest in young or retarded children and during intraoperative monitoring, when the cortical peaks are influenced by sedation and sleep, or by anesthesia.     

Intraoperative recordings of spinal somatosensory evoked potentials to tibial nerve and sural nerve stimulation

Somatosensory evoked potentials (SSEPs) to stimulation of the tibial nerve at the knee (TN-K) and ankle (TN-A), and the sural nerve at the ankle (SN-A), were recorded from 3 or 4 spinal levels during surgery for scoliosis in 11 neurologically normal subjects. With stimulation of all 3 nerves, the propagation velocity along the spine was nonlinear: it was faster over cauda equina and midthoracic cord than over caudal spinal cord. Over the mid-thoracic cord, TN-K SSEP propagation was faster than that of TN-A and SN-A SSEPs, whereas over the caudal spinal cord these values were similar on stimulation of all 3 nerves. These data suggest that fast conducting second order afferent fiber systems contribute to spinal cord SSEPs evoked by stimulating both mixed and cutaneous peripheral nerves.     

Somatosensory evoked potentials induced by stimulating a variable number of nerve fibers in rat

Somatosensory evoked potentials (SEPs) were recorded from rat spinal cord (sSEPs) and cerebral cortex (cSEPs). Stimulus sites included either one or both sural nerve branches having different fiber populations (group A), or distal to a lesion of controlled size of the sural nerve made 1 week earlier (group B). In the two groups of animals, amplitudes of SEPs correlated with the quantity of large myelinated nerve fibers. Peak latencies of sSEPs in group A related to the ratio of sizes of transmitting fibers. sSEPs and cSEPs in both groups A and B could be recorded in a reproducible fashion by stimulating sural nerve branches or lesioned nerve trunks containing only 100 or less nerve fibers greater than 4 m?m in size. Thus, presence of sSEPs or cSEPs after stimulation distal to a lesion site does not insure that many nerve fibers have continuity with the central nervous system (CNS). © 1993 John Wiley & Sons, Inc.     

Posterior tibial and sural nerve somatosensory evoked potentials in dystrophia myotonica

Somatosensory evoked potentials (SEPs) were recorded in a group of 18 patients with dystrophia myotonica and in 28 control subjects after stimulating the right and left posterior tibial (SEP-PT) and sural (SEP-S) nerves at the ankles. Recording electrodes were placed in the popliteal fossae, overlying the L3 spinal vertebrae, and at the appropriate scalp sites. In all control subjects and dystrophia myotonica subjects SEP-PT latencies were shorter than equivalent SEP-S latencies, probably reflecting conduction along group I muscle afferents and along slower conducting cutaneous afferents, respectively. Intergroup comparisons revealed prolonged absolute and interpeak latencies in the dystrophia myotonica group, showing both peripheral and central somatosensory pathway involvement. Individual abnormal latencies which exceeded the control group mean plus 3 standard deviations were found in 66% of the dystrophia myotonica group, mainly due to prolonged peripheral conduction times. Results pointed to the concomitant involvement of both the posterior tibial and sural nerve somatosensory pathways in dystrophia myotonica.     

Conduction characteristics of somatosensory evoked potentials to peroneal, tibial and sural nerve stimulation in man

Lumbar spine and scalp short latency somatosensory evoked potentials (SSEPs) to stimulation of the posterior tibial, peroneal and sural nerves at the ankle (PTN-A, PN-A, SN-A) and common peroneal nerve at the knee (CPN-K) were obtained in 8 normal subjects. Peripheral nerve conduction velocities and lumbar spine to cerebral cortex propagation velocities were determined and compared. These values were similar with stimulation of the 3 nerves at the ankle but were significantly greater with CPN-K stimulation. CPN-K and PTN-A SSEPs were recorded from the L3, T12, T6 and C7 spines and the scalp in 6 normal subjects. Conduction velocities were determined over peripheral nerve-cauda equina (stimulus-L3), caudal spinal cord (T12-T6) and rostral spinal cord (T6-C7). Propagation velocities were determined from each spinal level to the cerebral cortex. With both CPN-K and PTN-A stimulation the speed of conduction over peripheral nerve and spinal cord was non-linear. It was greater over peripheral nerve-cauda equina and rostral spinal cord than over caudal cord segments. The CPN-K response was conducted significantly faster than the PTN-A response over peripheral nerve-cauda equina and rostral spinal cord but these values were similar over caudal cord. Spine to cerebral cortex propagation velocities were significantly greater from all spine levels with CPN-K stimulation. These data show that the conduction characteristics of SSEPs over peripheral nerve, spinal cord and from spine to cerebral cortex are dependent on the peripheral nerve stimulated.     

Electrophysiological changes in the fasciculus gracilis of the cat following chronic clioquinol administration

Clioquinol was administered to cats for more than 200 days, in order to investigate the neural mechanisms underlying the sensory disturbances of subacute myelo-opticoneuropathy (SMON). Electrophysiological examination, carried out under urethane-chloralose anesthesia, revealed that there were 3 major abnormalities in the surface potentials of the nucleus gracilis evoked by sural nerve stimulation, i.e., a reduction in the peak-to-peak amplitude, prolongation of the N wave, and a reduction in P wave amplitude. The reduction in P-wave amplitude suggested suppression of presynaptic inhibition. This was confirmed by excitability tests of the presynaptic terminals of sural nerve fibers within the nucleus gracilis. Recordings of orthodromic volleys in the fasciculus gracilis, elicited by sural nerve stimulation, showed an increase in temporal dispersion. Increased temporal dispersion was also evident from recordings of antidromic volleys in the sural nerve. Peripheral axons of primary sensory neurons in the sural nerve and their terminals within the spinal cord showed no significant functional abnormalities in the chronic clioquinol cat. It is suggested that primary axons in the fasciculus gracilis near the nucleus gracilis are affected by chronic clioquinol administration.     

The spinal cord processing of input from the superior sagittal sinus: pathway and modulation by ergot alkaloids

The effects of ergot alkaloids on field potentials and unit responses produced in the upper cervical spinal cord by stimulation of the superior sagittal sinus (SSS) were examined in 57 anesthetized cats. Electrical stimulation of the SSS produced field potentials and single-unit responses at latencies of 5–20 ms. Field potentials were abolished by section of the first division of the trigeminal nerve but were unaffected or increased by section of the upper cervical nerves. Field potentials were reduced or abolished by intravenous injection of ergotamine or dihydroergotamine (DHE). The evoked response of 41 units (34.4%) were suppressed by either i.v. or iontophoretic administration of ergotamine, DHE or ergometrine. The results suggest that ergot alkaloids exert an effect at a spinal cord relay centre which receives trigeminally mediated input from cranial blood vessels.