Generators of human spinal somatosensory evoked potentials

Somatosensory evoked potentials recorded over the spine with a noncephalic reference following posterior tibial nerve stimulation have several components. (1) A stationary, synapse-dependent, negative potential (N22) occurs synchronously with a positive potential, P22, recorded ventral to the spinal cord and is localized to the lumbar region overlying the lumbar root entry zone. The N22/P22 complex is attributed to activation of interneurons in the dorsal gray of the lumbar cord. (2) A traveling negative potential with a gradually increasing latency may be recorded from the sacral to the cervical region. Its short refractory period indicates that it is not dependent on transmission across a synapse. This activity is attributed to transmission of the afferent volley through the lumbosacral plexus, roots, and the dorsal columns of the spinal cord. (3) N29, a stationary, synapse-dependent negative potential, localizes to the rostral cervical spine and is attributed to activation of the gracile nucleus relay cells. Following stimulation of the median nerve or fingers, the waveforms recorded over the cervical spine with a noncephalic reference include (1) the proximal plexus volley, a traveling negative potential reflecting transmission through the proximal brachial plexus and roots; (2) the dorsal column volley (DCV), the latency of which gradually increases from the caudal to rostral cervical region (the DCV is attributed to transmission of the afferent volley through the dorsal columns of the cervical cord); and (3) N13, a stationary negative waveform, with a long refractory period consistent with its dependence on transmission across a synapse. Experimental animal and human studies indicate that the N13 waveform is dependent on activity of at least two generator sites, namely the dorsal gray of the cervical cord and the cuneate nucleus.     

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.     

Cervical somatosensory evoked potentials in the healthy subject: analysis of the effect of the location of the reference electrode on aspects of the responses

Cervical SEPs were recorded in 111 normal subjects following stimulation of the median nerve at the wrist, using 3 different sites for the reference electrode (Fz, earlobe, shoulder). It was shown that cephalic reference electrodes (Fz or earlobe) modify the wave form of the cervical response, because they pick up far-field SEPs (P9, P11, P13, P14) originating from cervical roots, spinal cord and brainstem. These far-field SEP components are injected as negativities in the activity recorded by the cervical electrode. The responses recorded with cephalic reference differ from those recorded at the same cervical site, with a non-cephalic reference in 3 main points: (1) the amplitude of negative components N11 and N13 is increased; (2) the onset latency of N11 is significantly shorter; (3) an N14 negativity is added, the origin of which is probably in the brainstem; this component may occupy the peak of the cervical negativity; thus the central conduction time, calculated as the time interval between N14 and N20, does not take into account the time for spinal propagation of the somatosensory afferent inputs. A topographic study of cervical responses in 10 normal subjects showed an increase of the onset latency of N11 (mean 0.89) from the lower cervical region to the cervico-occipital junction, provided that a non-cephalic reference is used. This result suggests that N11 corresponds to the travelling of action potentials in the ascending spinal somatosensory pathways. The use of a medio-frontal (Fz) reference electrode results in: (1) a masking of the latency shift of N11 latency because of the subtraction of the far-field Fz-recorded P11 component, the onset of which was found to be synchronous with the entry of afferent volleys in the lower cervical spinal cord; (2) a modification of the spatial organization of the responses, due to the subtraction of far-field scalp-recorded positivities P9, P11, P13 and P14, that creates negative N9, N11, N13 and N14 potentials far below the level where cervical roots enter the spinal cord.     

Subpially recorded cervical spinal cord evoked potentials in syringomyelia.

Intraoperative spinal cord evoked potentials (SCEPs) to median nerve stimulation were detected subpially from the dorsal surface of the cervical spinal cord in 5 patients with cervical syringomyelia and were compared to normal SCEPs obtained from the unaffected side in 6 patients during intraoperative monitoring of dorsal root entry zone lesion. Normal SCEP began with a positive deflection P9 and a complex N11/N13 with several low amplitude short potentials superimposed on the N11/N13. The complex was followed by a second negative potential N2 and a late prolonged positivity, P. In the 4 patients in whom median nerve somatosensory evoked potentials (SEPs) were present preoperatively, SCEP consisted of the N11 potential and the following low amplitude short (LAS) potentials, while the N13 wave was missing. In the fifth patient, in whom the preoperative median nerve SEP was missing, SCEPs were of much lower amplitude and shorter duration than normal. The potentials N2 and P were not recorded in any of our 5 patients. Changes in N13 wave, N2 and P potentials noted in syringomyelia were presumed to be the result of destruction of the spinal cord dorsal horn neurons caused by spinal cord central cavitation.     

Short latency potentials recorded from the neck and scalp following median nerve stimulation in man.

Short latency evoked potentials were recorded from sites overlying the cervical and thoracic vertebrae, the clavicles, mastoid processes and cerebral cortex, following percutaneous stimulation of median nerve fibres at the elbow, wrist and fingers in 23 normal subjects. At least four major early components each with simultaneous positive and negative constituents, plus the first component (N20) of the cortical response, were all found to be mediated by sensory afferent fibres with conduction velocity 65--75 m/sec in the forearm of one subject. Study of the distribution of these potentials, using reference electrodes located at Fz or over the lower part of the spine, has led to the proposal of generator sites in the brachial plexus (N9), spinal roots or dorsal columns (N11), spinal grey matter or brain stem (N13), and brain stem or thalamus (N14). Comparison with intrathecal recordings in man lends support to the view that N11 and N13 are generated in or adjacent to the spinal cord. It is hoped the findings may extend the clinical applications of a non-invasive technique for investigating the afferent sensory pathways in man.     

The cervical somatosensory evoked potential in man: far-field, conducted and segmental components

Somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded from neck and scalp electrodes in 23 normal adults using cephalic and non-cephalic (knee) references simultaneously. With a cephalic reference, the neck SEP consisted of several 'negative' potentials that had the same latency at all recording locations. Simultaneous recordings from neck-scalp, neck-knee and scalp-knee derivations demonstrated that scalp far-field potentials significantly contributed to neck-to-scalp recordings and obscured the cervical SEPs. With a non-cephalic reference, the neck SEP consisted of a prominent positive wave (P9) followed by a large negative component (N13). A small positive potential, P10, seen in the lower neck, gradually increased in latency and amplitude from lower to upper neck and appeared as a P11 potential at upper cervical levels. In lower neck recordings, a negative wave, N11, was also present and in some subjects exhibited a latency shift from lower to upper neck. P9, P11 and N11 had a short refractory period suggesting a presynaptic origin whereas N13 had a longer refractory period indicating a postsynaptic generator. The consensus that P9 originates in the peripheral nervous system is consistent with its rapid recovery cycle. The bipolar characteristics of N11 and P11 as well as their latency shift and their short recovery cycle suggest that they reflect activity in the cervical dorsal columns. N13, that displayed no latency shift and had a longer recovery cycle, may originate in spinal cord dorsal horn interneurons.     

Spinal cord potentials in traumatic paraplegia and quadriplegia.

Cortical, cervical and lumbar somatosensory evoked potentials were recorded following median and tibial nerve stimulation in patients with traumatic paraplegia and quadriplegia. The isolated cord was able to produce normal potentials even during spinal shock if the vertical extent of the lesion did not involve the generator mechanisms. The cervical potentials showed subtle changes in paraplegia at Th5 levels and below. In high cervical lesions the early cervical potentials may still be present but the later potentials were absent or, in partial lesions, delayed.     

Slow positive dorsal cord potentials activated by heterosegmental stimuli.

Heterosegmental slow positive waves (HSPs) and segmental spinal cord potentials were recorded from the cord dorsum in ketamine-anesthetized rats. Forepaw stimulation produced HSPs in the lumbo-sacral enlargement (lumbar HSPs), whereas hind paw stimulation evoked HSPs in the cervical cord (cervical HSP). Both the HSP and the secondary component of the slow positive wave (P2s) in the segmental spinal cord potential were highly vulnerable to anesthetics and completely disappeared after spinal cord transection at the C1/2 level, indicating that both the HSP and P2s are produced by a long feedback loop via supraspinal structures. The lumbar HSP evoked by forepaw stimulation was maximal in amplitude at the L5 level and more dominant in the ipsilateral cord dorsum than in the contralateral one, but widely distributed in the lumbo-sacral cord. A variability of onset (7-18 msec for cervical and 5-17 msec for lumbar HSPs) and peak (22-35 msec for cervical and 12-50 msec for lumbar HSPs) suggests the existence of several nuclei to form the feedback loops for descending impulses to produce the HSPs. There were no peak latency differences between the HSPs and P2s. Since there were several similar characteristics between the P2s and HSP such as a high vulnerability to anesthetic, a complete disappearance after high spinal transection and similar response curves to graded intensities of stimulation, there may be a close relationship between their feedback nuclei and the pathways mediating them. All wide dynamic range (WDR) neurons (12/12) in lamina V of Rexed responded to heterosegmental stimulation with inhibition of firing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evoked potentials and contingent negative variation during treatment of multiple sclerosis with spinal cord stimulation.

Cervical somatosensory evoked potentials, brainstem evoked potentials, visual evoked potentials, and the cerebral contingent negative variation were recorded in patients with definite multiple sclerosis before, during, and after spinal cord stimulation. Improvements were seen in the cervical somatosensory and brainstem evoked potentials but neither the visual evoked potential nor the contingent negative variation changed in association with spinal cord stimulation. The results indicate that spinal cord stimulation acts at spinal and brainstem levels and that the clinical improvements seen in patients are caused by an action at these levels rather than by any cerebral arousal or motivational effect. The evoked potentials were not useful in predicting which patients were likely to respond to stimulation.     

Differential recording of upper and lower cervical N13 responses and their contribution to scalp recorded responses in median nerve somatosensory evoked potentials.

To distinguish the different origins of cervical N13 potentials in median nerve somatosensory evoked potentials (SSEPs), cervical N13 potentials were recorded by two different montages. The abnormal patterns of the SSEPs were compared to the abnormal evoked spinal cord responses (ESCPs) recorded from posterior epidural space in 13 patients with various cervical lesions. SSEPs from the posterior cervical surface were recorded from the mid-cervical level with anterior neck reference (Cv5-AN) and from the upper cervical level with inion reference (Cv2-IN). Scalp responses were recorded from the parietal region contralateral to the stimulating side with non-cephalic reference (shoulder contralateral to stimulating side). ESCPs were recorded from the posterior epidural space using catheter electrodes or needle electrodes inserted into the ligamentum flavum. Lower cervical N13 (LC-N13) recorded from the Cv5-AN montage showed similar latency to upper cervical N13 (UC-N13) recorded from the Cv2-IN montage. The latency of the early part of the P13-P14 complex in the scalp montage was similar to that of the UC-N13 and the negative peak latency of the ESCPs recorded at the C2-3 level. Attenuation of the LC-N13 and relatively preserved UC-N13 and P13-P14 were characteristic in patients with cervical syringomyelia and compression cervical myelopathy at the mid-cervical levels. Attenuation of the UC-N13 with normal LC-N13 was characteristic in patients with cervical spondylotic myelopathy who showed conduction blockade of the ESCPs at the C3-4 level. In a patient with schwannoma at the C1-2 level, conduction blockade of the ESCPs was observed at the C1-2 level. P13 was normal but P14 was prolonged. UC-N13 and P13 latencies were similar to the negative peak latency of the ESCPs at the C2-3 level. We demonstrated that two different cervical N13 potentials can be recorded by two different montages and they represent different behavior in various spinal cord lesions. In addition, at least the early part of the P13-P14 complex originates in the upper cervical region. To distinguish two different cervical N13, it is useful to detect not only the cervical pathology but also the symptomatic cervical cord compression level in patients with cervical myelopathy.     

Median nerve somatosensory evoked potentials recorded with cephalic and noncephalic references in central and peripheral nervous system lesions.

Somatosensory evoked potentials (SSEP) to electrical stimulation of the median nerve by using cephalic and noncephalic references were studied to detect the generator sources of short latency evoked potentials in 29 patients with cerebral, brainstem, spinal and peripheral nerve lesions. Patients were divided into six groups according to the localization of their lesions: group 1: cortical and subcortical lesions, group 2: basal ganglion lesions, group 3: pons and mesencephalon lesions, group 4: diffuse cerebral lesions, group 5: cervical cord lesions, group 6: brachial plexus lesions. Potentials were recorded using cephalic and noncephalic references after median nerve stimulation. Evidence obtained from patients suggested the following origins for these short latency SSEPs: P9 may arise in brachial plexus, P11 in dorsal basal ganglions or dorsal column, P13 and P14 in the nucleus cuneatus and lemniscal pathways, N16 in subthalamic structures and most likely mid and lower pons, N18 from the thalamus and thalamocortical tract, and N20 from primary somatosensory cortex.     

Assessment of intraspinal and intracranial conduction by P30 and P39 tibial nerve somatosensory evoked potentials in cervical cord, brainstem, and hemispheric lesions.

In routine recordings of tibial nerve somatosensory evoked potentials (SEPs), a global central conduction time is evaluated by measuring the interval between the segmental spinal N22 potential, recorded in the lumbar region, and the cortical P39 potential. In this study, we tested the reliability of the scalp far-field P30 potential, which originates in the vicinity of the cervico-medullary junction, in order to evaluate separately intraspinal and intracranial conduction in normal subjects and patients with cervical cord and intracranial lesions. P30 and cortical P39 potentials were studied in 23 healthy subjects and in 70 patients with cervical cord (n = 47), brainstem (n = 11) or hemispheric lesions (n = 12) selected on the basis of neuroimaging--computed tomography (CT) or magnetic resonance (MR)--findings. Median nerve SEPs were also recorded in all patients. Of the several montages tested to obtain the P30 potential, the Fpz-Cv6 derivation gave the highest signal-to-noise ratio; it permitted to obtain a P30 potential that peaked at 29.2 +/- 1.6 ms in all normal subjects. P30 abnormalities were observed only in patients with cervical or cervico-medullary lesions; these were associated with a normal P39 in only two of 33 abnormal recordings. Conversely, P30 was consistently normal in lesions situated above the cervico-medullary junction whether associated with normal, delayed, or reduced P39. P30 abnormalities were subclinical in 42% of abnormal recordings. All patients with normal tibial and median nerve SEPs on both sides had normal touch, joint, and vibration sensation in the four limbs. There was a strong correlation between tibial nerve P30 and median nerve P14 data in the whole series of patients; both potentials behaved similarly in all cases of intracranial supramedullary lesions. Combined abnormalities of P30 and P39 potentials thus indicate that conduction is impaired at the spinal level and proved to be particularly informative for detecting spinal cord dysfunction in patients with neuroimaging evidence of a narrowed cervical canal. Recording of abnormal N13, P14, or P30 potentials provided evidence of a cervical cord dysfunction in 66% of patients who had a suspected spondylotic myelopathy. Recording of tibial nerve P30 potential has proven to give reliable and useful information when a separate assessment of intraspinal and intracranial somatosensory conduction is needed; it merits inclusion, as does the upper limb N13 potential, in the evaluation of patients whose MR image indicates cervical canal narrowing.     

Chronically implanted electrodes for repeated stimulation and recording of spinal cord potentials

We have recorded and characterized the spinal cord evoked potentials (SCEPs) from the epidural space in the halothane-anesthetized rats. A group of 11 adult Wistar male rats was chronically implanted with two pairs of epidural electrodes. SCEPs were repeatedly elicited by applying electrical stimuli via bipolar U-shaped electrodes to the dorsal aspect of the spinal cord at C3-4 or Th11-12 levels, respectively. Responses were registered with the other pair of implanted electrodes, thus allowing us to monitor the descending (stimulation cervical/recording thoracic) and ascending SCEPs (stimulation thoracic/recording cervical). We studied the time-dependent changes of several SCEP parameters, among them the latency and amplitude of two major negative waves N1 and N2. During 4-weeks' survival, all major components of recordings remained stable and only minor changes in some parameters of the SCEPs were detected. We concluded that this technique enables repeated quantitative analysis of the conductivity of the spinal cord white matter in the rat. Our results indicate that SCEPs could be used in long-term experiments for monitoring progressive changes (degeneration/regeneration) in long projection tracts, primarily those occupying the dorsolateral quadrants of the spinal cord. These include projections that are of interest in spinal cord injury studies, i.e. ascending primary afferents, and important descending pathways including corticospinal, rubrospinal, reticulospinal, raphespinal and vestibulospinal tracts.     

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.     

Synaptic and non-synaptic components of the human cervical evoked response

The human cervical evoked response comprises a main negative wave and a following positivity. The peak of the negative wave, N13, is preceded by a small notch, N11, on the ascending negativity and is followed by another notch, N14, on the descending negative slope. The mechanisms of the components in the human cervical evoked response are still subject to discussion. In the present study conventional neurophysiological techniques were applied to see whether the components were of synaptic or non-synaptic origin. Resistance to high-frequency stimulation, refractoriness as tested by train or double shock conditioning stimuli and the effect of graded stimulation revealed that N11 and N14 fulfilled the criteria of a non-synaptic origin. N13 and the positive wave had properties pointing to a synaptic origin, the latter evidently reflecting an inhibitory mechanism. Each component in the human cervical evoked response both morphologically and functionally resembled the well known subcomponents in the spinal cord dorsum potential in experimental animals.     

Effect of transcutaneous electrical nerve stimulation (TENS) on central nervous system amplification of somatosensory input

The effect of transcutaneous electrical nerve stimulation (TENS) on the central nervous system amplification process was investigated focusing on the dorsal column-medial lemniscal pathway, because the dorsal column nucleus was recently shown to receive multiple sources of sensory information, including pain. Short latency somatosensory evoked potentials (SSEPs) were recorded in ten healthy normal volunteers. Amplitude changes in each SSEP component (the N9 brachial plexus potential, the P14 potential that originates from the cervicomedullary junction, spinal N13/P13 generated by the cervical dorsal horn and the cortical N20/P25 potential) were studied at stimulus strenghts ranging from the threshold (40% maximum stimulus) to 2.5 times the threshold (maximum). The findings suggest that sensory amplification begins at the P14 generator source near the cuneate nucleus. There was no statistically significant difference in sensory amplification between P14 and cortical N20/P25, indicating that the cuneate nucleus is the main site of the central amplifying process. When TENS was applied to the palm distal to the median nerve stimulation used for SSEP, cortical N20/P25 amplification disappeared, evidence that TENS suppresses the central amplification phenomenon, most probably at the level of the cuneate nucleus. Received: 29 October 1996 Received in revised form: 13 October 1997 Accepted: 6 November 1997     

Recovery functions of spinal cord and subcortical somatosensory evoked potentials to posterior tibial nerve stimulation: intrasurgical recordings

The recovery function of evoked potentials to posterior tibial nerve stimulation was studied. Intrasurgical recordings were made from interspinous ligaments at lumbar levels and from high thoracic-low cervical level. In addition, surface recordings were obtained from neck-scalp derivations. The recovery function of the potentials recorded from lumbar and from high thoracic-low cervical spinal cord were very similar, showing an early period of supernormality (5-20 ms) followed by a period of subnormality which reached its lowest point at 40-60 ms. Assuming that the potentials recorded at the lumbar level reflect activity in the cauda equina, we conclude that the results support the hypothesis that the potentials recorded from the thoraco-cervical level reflect activity in the dorsal columns. The recovery curve of the amplitude between the far field potentials P27 (which most probably reflects activity of the afferent volley at the level of foramen magnum) and N30 (which, by latency criteria, would reflect lemniscal or thalamic activity) showed a similar shape but with a shorter duration of the periods of super- and subnormality. It is likely that this modification was due to the synapse at the gracilis nucleus. The first cortical component (P32) recorded in the neck-scalp derivation was totally abolished within the recovery period studied (50 ms interval).     

Properties of femoral venous afferent inputs and lumbosacral distribution of spinal evoked activity

The present studies were done to determine details of the anatomical and physiological characteristics of femoral-saphenous venous afferent input to the lumbar spinal cord. Gross anatomical examination revealed that afferent bundles could be seen coursing from the saphenous nerve to the femoral-saphenous vein. Compound action potentials elicited by femoral-saphenous venous afferent stimulation were recorded from the femoral nerve and in dorsal rootlets of the 6th lumbar cord segment. The compound action potentials included activity correlated with that of fibers conducting impulses at the rate of 31 to 61 m/s. Lumbar cord dorsum potentials elicited by femoral-saphenous venous afferent stimulation were abolished by rhizotomy of the most caudal rootlets of the 6th lumbar cord segment. L6 was also the cord segment from which the largest amplitude cord dorsum negative potentials were recorded, while action potentials with large late positive waves were recorded from more caudal cord segments. These observations suggested that the L6 segment contained the largest number of spinal neurons responding to primary femoral-saphenous venous afferent input, and that input reached the more caudal segments via intersegmental connections. A proposed physiological role of these afferents is briefly described.     

Developmental assessment of spinal cord and cortical evoked potentials after tibial nerve stimulation: effects of age and stature on normative data during childhood

Somesthetic information from lower extremities is processed by cerebral cortex after traversing the sensory pathways of peripheral nerve, spinal cord, brain-stem and thalamus. Clinical utility of somatosensory evoked potentials (SSEPs) during human development requires systematic analysis of normative data acquired during various stages of body growth and nervous system maturation. Accordingly, SSEPs after tibial nerve stimulation were studied in 32 normal awake children (1-8 years old) and compared with values obtained in young adults (18-40 years old). Potentials were recorded from the tibial nerve (N5), first lumbar spinous process (N14), seventh cervical spinous process (N20) and from the scalp, 2 cm behind the vertex (P28). In all children studied, the N5, N14 and N20 latencies were positively correlated with age and height yielding a predictive nomogram. An extremely variable electropositive cortical SSEP was recorded from Cz' which did not show a highly predictable linear relationship in association with a relatively poor correlation coefficient for height and age. It may be concluded that between 1 and 8 years of normal postnatal development, latencies reflecting peripheral nerve and lumbar spinal cord vary directly with height and age and can be represented by a simple cable model of a lengthening myelinated pathway. In contrast, the latency of the cortical SSEP reflects asynchronous maturation of elongating polysynaptic pathways and apparently requires a more complex model for prediction in order to enhance its clinical utility.     

Skin and epidural recording of spinal somatosensory evoked potentials following median nerve stimulation: correlation between the absence of spinal N13 and impaired pain sense

Summary A clinical lesion study and intraoperative epidural recordings were made to test the origin and clinical significance of the spinal N13 and P13 of somatosensory evoked potentials (SEP) that follow median nerve stimulation. Intraoperatively, the respective peak latencies of spinal P13 and N13 coincided with those of the N1 component of the dorsal cord potential and its phase reversed positivity. On both the ventral and dorsal sides of the cervical epidural space, maximal amplitude was at the C5 vertebral level to which nerve input from the C6 dermatome is the main contributor. The modality of sensory impairment in the hand dermatome was examined in selected patients with cervical lesions, who showed such normal conventional SEP components as Erb N9, far-field P9, P11, P14, N18 and cortical N20, with or without loss of spinal N13. Statistically, the loss of spinal N13 was associated with decrease of pain sensation in the C6 dermatome. This was interpreted as being due to damage to the central grey matter of the cord, including the dorsal horn. Our results suggest the spinal N13 and P13 originate from the same source in the C6 spinal cord segment and that they are good indicators for the detection of centromedullary cervical cord damage.