Dissociation of early SEP components in unilateral traumatic section of the lower medulla

Spinal and scalp early SEPs were recorded, using a noncephalic reference electrode, in a patient with a traumatic cervicomedullary lesion causing unilateral loss of position sense. Cervical N11 and N13 and scalp-recorded far-field P14 SEPs were clearly dissociated following stimulation of the affected side. The findings suggest that the P14 component is generated above the foramen magnum, whereas the cervical N13 has a spinal generator.     

Anatomic origin and clinical application of the widespread N18 potential in median nerve somatosensory evoked potentials.

N18 is a broad negativity, with a duration of approximately 20 msec after positive far-field potentials and is recorded widely over the scalp using a noncephalic reference. Its origin has been controversial but its preservation after pontine or upper medullary lesion while loss after high cervical lesions suggested its medullary origin. Comparison with animal studies and direct recording studies in humans leads the authors to conclude that N18 is most likely generated at the cuneate nucleus by primary afferent depolarization. Namely, dorsal column afferents send collaterals to interneurons within the cuneate nucleus, which in turn synapse on presynaptic terminals of dorsal column fibers and depolarize them as a mechanism of presynaptic inhibition. In this way, an electrical sink is formed on presynaptic terminals, whereas their dorsocaudally situated axons serve as a source. The ventrorostral negative pole of the resultant dipolar potential must correspond to N18. The authors obtained a measure to evaluate medullary function objectively, and therefore N18 may be useful as a diagnostic tool for brain death. Usage of a C2S reference is essential for the accurate estimation of N18. Origins of other somatosensory evoked potential components related to the cuneate nucleus are also discussed.     

Clinical correlates of abnormal P14 in median SEPs

Recording median somatosensory evoked potentials (SEPs) from scalp and neck in separate channels with the use of an ear reference, 52 patients had abnormal scalp-recorded P14 associated with normal cervical-recorded N13. The patients had multiple sclerosis or other brainstem or high cervical cord lesions. Evidence of brainstem lesions was found in 35 patients on clinical examination or by brainstem auditory evoked potentials or blink reflex. Abnormalities of P14 were correlated highly with brainstem dysfunction, but high cervical cord lesions could not be excluded by this finding. The localizing value of SEP is improved by measuring the N13 and P14 peaks separately and assessing the cervical cord-brainstem conduction time.     

Anatomic origin of the cervical N13 potential evoked by upper extremity stimulation.

There is a large consensus, based on converging evidence, that N13 recorded at lower cervical levels has a segmental postsynaptic origin in the gray matter of the cervical cord and that because of the orientation of its dipole field, the Cv6-anterior cervical derivation should be used whenever the diagnostic problem requires that this potential be assessed selectively in terms of latency and amplitude. The diagnostic utility of the lower cervical N13 recording in dorsal horn deafferentation and in lesions at the Cv6-Cv8 metameric levels has been validated in all types of cervical cord lesions. Unfortunately, such clear-cut conclusions do not apply to the N13 potential recorded at upper cervical levels. Currently, this component is not considered to provide enough reliable information, in addition to P13-P14 scalp recordings, to be used routinely in the diagnosis of cervicomedullary lesions.     

Bipolar recording of short-latency somatosensory evoked potentials after median nerve stimulation

Generators of median short-latency somatosensory evoked potentials were studied with three orthodiagonal pairs of bipolar electrodes. N11 was attributed to the dorsal root and dorsal column volleys. N13 had at least two subcomponents, generator dipoles of which are directed horizontally (N13a) and axially (N13b). N13a was generated in the lower cervical cord. N13b (bipolar) and P14 far-field (noncephalic reference) appeared to originate in the cuneate nucleus or spinocerebellar tracts as well as in the medial lemniscus. Bipolar recordings were useful in localizing cervical cord lesions, which was impossible in conventional monopolar recordings.     

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.     

Stability of N20 onset or peak latency in median somatosensory evoked potentials

We analyzed onset and peak latencies of the N20 response of median nerve somatosensory evoked potentials (SEPs) in 21 healthy subjects by simultaneous recordings with noncephalic or ear reference from multiple scalp sites. The cortical onset was defined as the fork at which the contralateral parietal and frontal or ipsilateral parietal waves diverged. We found the N20 onset unchanged between noncephalic and ear reference recordings, or among the recordings around the contralateral centroparietal scalp. The N20 peak was prolonged when the recording position moved posteriorly. We suggest that N20 onset latency is more stable than N20 peak.     

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.     

Effect of cervical spinal cord lesions on early components of the median nerve somatosensory evoked potential

Clinical interpretation of median somatosensory evoked potentials (SEPs) is usually based on latency measurements of selected waveforms. The "cervicomedullary" potential (N14) is commonly recorded by measuring the voltage difference between cervical spine and frontal electrodes. This cervicomedullary potential is actually a composite waveform that is generated by several distinct neural structures. We present evidence that placement of additional recording electrodes to delineate the multiple cervical components of the median SEP enhances ability to detect and localize cervical cord lesions.     

The dissociation of early SEP components in lesions of the cervico-medullary junction: a cue for routine interpretation of abnormal cervical responses to median nerve stimulation

In non-cephalic reference records the lesions of upper cervical cord and medulla dissociate SEPs to median nerve stimulation, cervical N11 and N13 potentials being preserved whereas later components, generated above the foramen magnum, are absent or desynchronized and delayed. This was observed in 4 patients with space occupying lesions of the cervico-medullary junction. In three of them serial postoperative SEP records demonstrated a progressive normalization of the responses following decompression. During normalization delayed cortical components could reappear on the scalp before the far-field P14 positivity. Before surgery the widespread N18 potential was absent, at least on one side, in the 4 patients and was never found to be dissociated from the P14 component. The reversibility of early SEP dissociations after surgery allowed a documented study of the abnormal patterns of cervical to Fz responses that may be observed with various lesions of the cervical cord, including demyelination. When the P14 component is delayed because of conduction slowing it is injected as an abnormal 'N14' in the Cv6-Fz response; in this situation the use of a non-cephalic reference is necessary to make the distinction between the cervical N13 potential and brain-stem 'N14' negativity.     

Short-latency somatosensory evoked potentials in brain death

Summary Simultaneous recording of somatosensory evoked potentials to median nerve stimulation above the upper and lower neck in brain-dead patients revealed that all cervical responses were preserved in 10%, whereas a marked reduction in amplitude or even loss of N 13b at the level of the C2 spinous process was observed in 90%. Of the patients, 55% revealed an additional loss of N 13a, recorded at the level of the C7 spinous process; in 15% all cortical and spinal evoked potentials were missing, but Erb's point waves were still normal. These results suggest two different origins of the main negative waves (N 13a and N 13b), recorded above the upper and lower cervical spinal cord. N 13a (C7) is supposed to arise in the dorsal horn at the C6/7 level, N 13b (C2) in the cervicomedullary junction.     

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.     

The subcortical generated somatosensory evoked potentials in non-cephalic,cephalic, and anterior neck referenced recordings in a patient with a cervico-medullary lesion: a clue to the identification of the P14/N14 and N13 generators

Summary Median nerve somatosensory evoked potentials (SEPs) were studied in a patient before and after the development of a cervico-medullary lesion. The first examination demonstrated normal subcortical generated potentials N13 and N14. The second examination, following a subarachnoid haemorrhage at the cervico-medullary junction, displayed a delayed and reduced amplitude P14/N14 peak on both sides. P14/N14 showed the same latency in all montages, using noncephalic, cephalic and anterior neck references. The N13 component was not significantly changed in latency compared with the first examination. The latencies of the N13 peak were variable in the different montages. They increased from the lower (C7) to the upper (C2) neck, whereas the latency of the N13 onset was identical in all montages. This alteration might be caused by a delayed near-field activity at C2 overlapping the N13 component. These results fit the hypothesis of two major generators responsible for subcortical SEPs; a near-field N13 component at the level of the lower neck and a far-field P14 component arising from the level of the cervico-medullary junction. An additional minor near-field activity generated by the cuneate nucleus is suspected.     

Scalp recorded P13 and spinal recorded N13 in short latency somatosensory evoked potentials

Using non-cephalic reference and by median nerve stimulation, P 13 component and N 13 component are recorded on the scalp (scalp P 13) and the posterior neck (spinal N 13), respectively, in the short latency somatosensory evoked potentials (SSEP). The purpose of this study is to disclose the origin, characteristics and clinical significance of these two components. Ten healthy volunteers served for normal subjects. Ten patients with pontine lesion or brain death were studied. The effect of barbiturate was also studied in additional 5 patients during anesthesia for cranioplastic surgeries. Electrical stimuli of 0.2 msec square wave pulse were used in routine examination. To confirm the effects of stimulation frequency, 3, 6, 9, 12, 15, 18, 21, 24 and 27 Hz were also used in normal subjects. Recording electrodes were placed in the following sites. (1) Scalp electrode at the Shagass' point contralateral to the stimulated side (Par.). (2) Posterior neck electrode on the spinous process of the fifth cervical vertebrae (Cv5), (3) Anterior neck electrode on the thyroidal cartilage (Ant. C). (4) Erb's electrode just above the mid-clavicular point ipsilateral to the stimulation. Erb's electrode contra-lateral side of stimulation was used as a reference. Spinal N 13 on posterior neck reversed its polarity into P 13 (spinal P 13) on the anterior cervical electrode. A study with different stimulus rates revealed that the latency of scalp P 13 significantly prolonged at 24 Hz stimulation. On the other hand, the latency of spinal N 13-P 13 easily prolonged even at 18 Hz. This suggested that spinal N 13-P 13 were generated polysynaptically.(ABSTRACT TRUNCATED AT 250 WORDS)     

Scalp-recorded short and middle latency peroneal somatosensory evoked potentials in normals: comparison with peroneal and median nerve SEPs in patients with unilateral hemispheric lesions

Peroneal somatosensory evoked potentials (SEPs) were performed on 23 normal subjects and 9 selected patients with unilateral hemispheric lesions involving somatosensory pathways. Recording obtained from right and left peroneal nerve (PN) stimulations were compared in all subjects, using open and restricted frequency bandpass filters. Restricted filter (100-3000 Hz) and linked ear reference (A1-A2) enhanced the detection of short latency potentials (P1, P2, N1 with mean peak latency of 17.72, 21.07, 24.09) recorded from scalp electrodes over primary sensory cortex regions. Patients with lesions in the parietal cortex and adjacent subcortical areas demonstrated low amplitude and poorly formed short latency peroneal potentials, and absence of components beyond P3 peak with mean latency of 28.06 msec. In these patients, recordings to right and left median nerve (MN) stimulation showed absence or distorted components subsequent to N1 (N18) potential. These observations suggest that components subsequent to P3 potential in response to PN stimulation, and subsequent to N18 potential in response to MN stimulation, are generated in the parietal cortical regions.     

Anatomic origin of P13 and P14 scalp far-field potentials.

After median nerve stimulation, noncephalic or earlobe reference montages enable one to record over the scalp a well-defined, positive far-field response, which has been labeled the P14 or P13-P14 complex. It has been ascertained that this wave is generated in the caudal brainstem. Its use is reliable and sometimes mandatory in assessing a number of diseases that affect primarily the brainstem, such as multiple sclerosis or coma. Because of its complex shape as well as discrepant findings in the literature, it is still debated whether this potential is produced by a single or by multiple serial generators. The authors present these different views and summarize the different recording methods, while bearing in mind that some recording techniques are more suitable for routine purposes and others are preferred in selected cases, when more information regarding caudal brainstem function is required.     

Neural generators of tibial nerve P30 somatosensory evoked potential studied in patients with a focal lesion of the cervicomedullary junction

The tibial nerve P30 potential was studied in 6 patients with focal lesions located in the vicinity of the cervicomedullary junction. P30 potential was unaffected while cortical P39 was abnormal in the patients with a supramedullary lesion affecting the somatosensory pathway just above its decussation. Conversely, P30 was abnormal in the presence of a lesion situated caudally to the cervicomedullary junction affecting the lower limb sensory fibers just below their decussation. Median nerve P14 behaved similarly to the P30 potential in these cases. These clinical observations suggest that P30 potential, as P14 of median nerve somatosensory evoked potentials, is generated in the lower brain stern probably before the decussation of the sensory fibers; nucleus gracilis and medial lemniscus fibers in the lower brain stem are probably the anatomical structures generating P30 potential. This suggests that P30 potential may be used to study intraspinal and intracranial conduction times separately in the afferent somatosensory pathways. © 1996 John Wiley & Sons, Inc.     

Identification of a negative bitemporal component (N300) of the event-related potentials demonstrated by noncephalic recordings

We studied the scalp distribution of auditory event-related potentials (P300), using simultaneously a cephalic (linked ears) and a noncephalic (balanced sternovertebra) reference. The recordings with noncephalic reference showed that infrequent, attended auditory stimuli evoke a negative bitemporal component (N300) as well as a positive vertex component (P300).     

Bit-mapped colour imaging of the potential fields of propagated and segmental subcortical components of somatosensory evoked potentials in man

Early somatosensory evoked potentials (SEPs) to median or ulnar nerve stimulation were recorded with non-cephalic reference from neck, oesophagus and scalp in normal young adults. Transit times and durations were estimated for different components. SEP fields were mapped with up to 24 skin electrodes around the neck or along the midline neck and scalp, and projected onto a 2-dimensional plane for bit-mapped colour imaging. The posterior neck N11 is a near-field potential propagated caudorostrally in the dorsal column, associated with a positive P11 far field beyond termination of the cuneate bundle. A true phase reversal of the posterior neck N13 into an anterior neck P13 is substantiated, identifying a segmental generator with horizontal axis in dorsal horn. The N13-P13 represents postsynaptic excitatory potentials in interneurones of layers IV-V of the dorsal horn. It is not reflected in any scalp far field. The duration and onset latency of N13-P13 are in line with this interpretation. A new montage of posterior-to-anterior neck can enhance this component without introducing extraneous potentials. The P14 far field does not extend below the inion and presents distinct features. Neck-to-front scalp montages confound the SEP components generated in the spinal cord and above the foramen magnum respectively, but may serve to estimate N11 onset latency.