Somatosensory evoked potentials from the thalamic sensory relay nucleus (VPL) in humans: correlations with short latency somatosensory evoked potentials recorded at the scalp

Somatosensory evoked potentials (SEPs) were recorded in humans from an electrode array which was implanted so that at least two electrodes were placed within the nucleus ventralis posterolateralis (VPL) of the thalamus and/or the medial lemniscus (ML) of the midbrain for therapeutic purposes. Several brief positive deflections (e.g., P11, P13, P14, P15, P16) followed by a slow negative component were recorded from the VPL. The sources of these components were differentiated on the basis of their latency, spatial gradient, and correlation with the sensory experience induced by the stimulation of each recording site. The results indicated that SEPs recorded from the VPL included activity volume-conducted from below the ML (P11), activity in ML fibers running through and terminating within the VPL (P13 and P14), activity in thalamocortical radiations originating in and running througn the VPL (P15, P16 and following positive components) and postsynaptic local activity (the negative component). The sources of the scalp-recorded SEPs were also analyzed on the basis of the timing and spatial gradients of these components. The results suggested that the scalp P11 was a potential volume-conducted from below the ML, the scalp P13 and P14 were potentials reflecting the activity of ML fibers, the small notches on the ascending slope on N16 may potentially reflect the activity of thalamocortical radiations, and N16 may reflect the sum of local postsynaptic activity occurring in broad areas of the brain-stem and thalamus.     

Spine and scalp somatosensory evoked potentials in normal subjects and patients with spinal cord disease: Evaluation of afferent transmission

Spine and scalp somatosensory evoked potentials (SEPs) to peroneal nerve stimulation were recorded from 20 normal subjects using 1 restricted and 3 open frequency filter bandpasses. Spine to spine and spine to scalp propagation velocities were calculated. Of those recording parameters investigated, optimal recordings were obtained using an open bandpass (5–1500 or 30–1500 Hz) and recording from 3 surface spine bipolar channels and 1 scalp bipolar channel. This method was then investigated in 40 patients with disease of the spinal cord and peripheral nervous system. Focal spinal cord compressive lesions generally resulted in slowing of spine to spine and spine to scalp propagation velocities. Diffuse or multifocal lesions of the spinal cord generally resulted in the absence of scalp responses. Although there was no consistent correlation of the SEP findings with the sensory exam, there was a correlation of the SEP findings with the clinical prognosis.     

Comparison of scalp distribution of short latency somatosensory evoked potentials (SSEPs) to stimulation of different nerves in the lower extremity

SSEPs to stimulation of the CPN at the knee and PTN, PN and SN at the ankle were recorded from 15 cephalic sites and compared in 8 normal subjects. The configuration, amplitude, peak latency and distribution of P27, N35 (CPN) and P37, N45 (PTN, PN and SN) were analyzed. The configuration and distribution of SSEPs to stimulation of the 3 nerves at the ankle were similar across subjects. Both P37 and N45 were greatest in amplitude at the vertex and at recording sites ipsilateral to the side of stimulation. At contralateral sites either negative (N37) or negative, positive, negative potentials were recorded. The peak latency of N37 was the same or slightly less than that of P37. CPN-SSEPs were lower in amplitude and their configuration and scalp distribution showed much greater intersubject variability. This suggests that complex mechanisms which variably interact with one another are reflected in scalp SSEPs to CPN stimulation at the knee. The larger amplitude plus the minimal intersubject variability in morphology and topography of PTN-SSEPs indicate that this nerve is the most suitable for routine clinical use.     

Subject-based P1 latency inter-root comparison,a method to evaluate P1 latency in scalp recorded somatosensory evoked potentials obtained with sensory nerve stimulation in the lower extremities

The purpose of the present study was to establish a method that allows the general use of subject-based criteria to evaluate P1 latency in scalp recorded somatosensory evoked potentials obtained with stimulation of the sural (S1), superficial peroneal (L5) and saphenous (L4) nerves bilaterally. The nerves were stimulated at the same distance from the registration electrode.Two groups of normal nerve roots were studied: (1) nerve roots on both sides in 20 asymptomatic volunteers, and (2) neuroradiologically normal nerve roots on the asymptomatic side in 22 patients with unilateral sciatica.The results presented show that the P1 latencies after stimulation of the 6 different nerves in the same person can be regarded as equal. On this basis 2 criteria to evaluate P1 latency by within-subject P1 latency inter-root comparison were defined. They were the difference between P1 latency of 1 registration and (1) that of any one of the other 5 registrations and (2) the mean P1 latency of the other registrations.The variability of these subject-based criteria and the width of their reference limits were compared to those of the population-based criteria of height- and height-age-corrected P1 latency. This comparison showed that the use of within-subject P1 latency inter-root comparison should enhance the ability to demonstrate small bilateral P1 latency prolongations at the same segmental level.     

Comparison in man of short latency averaged evoked potentials recorded in thalamic and scalp hand zones of representation

Recordings were performed in the thalamus of 13 patients suffering from either abnormal movements or intractable pain, with the aim of delimiting the region to be destroyed or stimulated in order to diminish the syndrome. In 11 of these patients averaged evoked potentials were recorded simultaneously from the scalp and specific thalamus (VP) hand area levels following median nerve stimulation. These recordings were done during the operation or afterwards when an electrode was left in place for a program of stimulation.The latencies of onsets and peaks on the scalp ‘P15’ were compared with those of the VP wave; a clear correspondence was found. Moreover, when increased stimulation was used, both waves began to develop in parallel. Thus in the contralateral ‘P15’ a component exists due to the field produced by the thalamic response. To explain the presence of an ipsilateral scalp ‘P15’ wave, we propose that a second wave having the same latency and a slightly shorter peak exists on the scalp due to a field produced by a brain-stem response. This double origin of ‘P15’ is also shown by the different changes which the ipsilateral and contralateral waves present during changes in alertness.The scalp ‘N18–N20’ is also composed of at least 2 components. The first peak appears on the scalp with a latency shorter than that of the negativity which develops in the thalamus. The N wave, moreover, increases in latency with rapid stimulus repetition. We propose with others that ‘N18’ is a cortical event reflecting the arrival of the thalamo-cortical volley. The second component, ‘N20,’ has a peak latency closely correlated to that of the thalamic negativity. This component was present alone in ‘N’ when rapid stimulation (> 4/sec) was used, which did not change the thalamic response. It must be a field produced by the thalamic negativity.     

Effects of hypothermia on short latency somatosensory evoked potentials in humans

Short latency somatosensory evoked potentials (SSEPs) elicited by median nerve stimulation were monitored in 14 adult patients undergoing cardiac surgery under cardiopulmonary bypass and induced hypothermia. SSEPs were recorded at 1–2°C steps as the body temperature was lowered from 37°C to 20°C to determine temperature-dependent changes. Hypothermia produced increased latencies of the peaks of N₁₀, P₁₄ and N₁₉ components, the prolongation was more severe for the later components so that N₁₀−P₁₄ and P₁₄−N₁₉ interpeak latencies were also prolonged. The temperature-latency relationship had a linear correlation. The magnitude of latency prolongation (msec) with 1°C decline in temperature was 0.61, 1.15, 1.56 for N₁₀,P₄ and N₁₉ components, respectively, and 0.39 and 0.68 for interpeak latencies N₁₀−P₁₄ and P₁₄−N₁₉, respectively. The rise time and duration of the 3 SSEP components increased progressively with cooling. Cortically generated component, N₁₉ was consistently recordable at a temperature above 26°C, usually disappearing between 20°C and 25°C. On the other hand, more peripherally generated components, N₁₀ and P₁₄, were more resistant to the effect of hypothermia; P₁₄ was always elicitable at 21°C or above, whereas N₁₀ persisted even below 20°C. The amplitude of SSEP components had a poor correlation with temperature; there was a slight tendency for N₁₀ and P₁₄ to increase and for N₁₉ to decrease with declining temperature. Because incidental hypothermia is common in comatose and anesthetized patients, temperature-related changes must be taken into consideration during SSEP monitoring under these circumstances.     

Cortical potentials evoked by epidural stimulation of the cervical and thoracic spinal cord in man

Scalp somatosensory evoked potentials (SEPs) were recorded after electrical stimulation of the spinal cord in humans. Stimulating electrodes were placed at different vertebral levels of the epidural space over the midline of the posterior aspect of the spinal cord. The wave form of the response differed according to the level of the stimulating epidural electrodes. Cervical stimulation elicited an SEP very similar to that produced by stimulation of upper extremity nerves, e.g., bilateral median nerve SEP, but with a shorter latency. Epidural stimulation of the lower thoracic cord elicited an SEP similar to that produced by stimulation of lower extremity nerves. The results of upper thoracic stimulation appeared as a mixed upper and lower extremity type of SEP. The overall amplitudes of SEPs elicited by the epidural stimulation were higher than SEPs elicited by peripheral nerve stimulation. In 4 patients the CV along the spinal cord was calculated from the difference in latencies of the cortical responses to stimulation at two different vertebral levels. The CVs were in the range of 45–65 m/sec. The method was shown to be promising for future study of spinal cord dysfunctions.     

Amplitude and latency characteristics of spinal cord motor evoked potentials in the rat

The motor evoked potential (MEP) has become a valuable component of neurophysiological monitoring. A better understanding of the characteristics of the normal MEP is needed before one can fully appreciate the effects of injury on the MEP. We describe characteristic patterns of spinal cord MEPs, recorded epidurally, in response to transcranial (dura-to-palate) brain stimulation in a rat model. Series of signal averaged MEP responses at a duration of 100 μ sec were recorded at T_10/11, T_12/13, and L_1/2 in 8 normal rats. We used a much greater range of current intensities (0.5–65 mA) than has been studied previously. Also, we studied the gradual development of the MEP wave form using smaller increments of current strength than have been reported previously. We confirmed in rats our earlier report in cats that long latency peaks appear first at low intensities while short latency peaks appear with higher intensities (Konrad et al. 1988). We also report average peak latencies over the range of stimulus intensities used for each recording level in each rat. In some rats, conduction velocities of several MEP peaks were calculated, and they range from 35 to 42 m/sec. These velocities are consistent with values reported in the literature for extrapyramidal pathways. Our rat model provides a method of measuring spinal cord potentials at three levels with no trauma to the spinal cord. Therefore, it can be used to repeatedly test motor function in chronic studies of spinal cord injury.     

A method of calculating spinal cord transit time from potentials evoked by tibial nerve stimulation in normal subjects and in patients with spinal cord disease

Somatosensory potentials were evoked by stimulation of the tibial nerve at the ankle and recorded over the spine and scalp in 16 normal subjects and 26 patients with known or suspected spinal cord disease, with the aim of developing a method of measuring spinal sensory conduction velocity using a tolerable number of stimuli, applied unilaterally to alert subjects.In normal subjects N21 was consistently recorded overL1 vertebra and in most subjects a complex, N27/N29/P33, was recorded over the cervical spine referred to the vertex. Constant latencies at different spinal levels and, in one subject, comparison with the latency of the ascending volley indicate that the complex was not derived from the spinal cord but from more rostral structures, and therefore only transit time, rather than velocity, could be measured.In patients with clinically definite multiple sclerrosis, even with minimal clinical signs, the N27/N29/P33 complex was always abnormal. Abnormalities in this and other forms of spinal cord disease were commonly absence or distortion of the complex, prolonged transit time being rare. The clinical value of the method is limited by the very low amplitude of the responses.     

Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23).In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.Topographical studies of early cortical SEPs are useful for detecting each component in abnormal SEPs     

Intracranial recording of short latency somatosensory evoked potentials in man: Identification of origin of each component

In normal subjects the short latency SEPs generally consisted of 3 positive waves (P9, P11, P14) and a succeeding negative wave (N20). To determine the origins of these waves we have made intracranial records from 17 patients, which suggest the following results. P9 originates in stimulated median nerve peripheral to the dorsal roots such as brachial plexus, P11 in the dorsal column of the cervical cord, P14 in the cuneate nucleus and medial lemniscal pathway, and N20 in the cerebral cortex. On the basis of intracranial and intraspinal records, the onset of P11 indicates the arrival of the afferent volley at the cord entry and the peak latency of P11 its arrival time at the C1–2 level dorsal column. The onset latency of P14 indicates the onset of postsynaptic events in cuneate nucleus neurons and the peak latency of P14 arrival at the midbrain.From the ventral surface of the brain-stem 3 positive waves (P′9, P′11, P′14) like the initial positive components of the scalp short latency SEPs (P9, P11, P14) were recorded. The amplitude of P′14 was large compared to that of P14. The peak latencies of P′14 recorded at the medulla and the pons were shorter than that of P14 by 0.7–0.8 msec and 0.2–0.5 msec, respectively. The peak latency of P′14 at the midbrain was almost the same as that of P14. By measuring the distance between the recording electrodes in the brain-stem and the peak latency difference of P′14, the fastest lemniscal conduction velocity was estimated as 56 m/sec.     

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.     

The relationships among the severity of spinal cord injury,motor and somatosensory evoked potentials and spinal cord blood flow

To characterize the changes in axonal function in the motor and somatosensory tracts of the cord after spinal cord injury (SCI) and to correlate these changes with spinal cord blood flow (SCBF), the relationships among the severity of SCI, motor and somatosensory evoked potentials (MEPs and SSEPs) and SCBF were examined. Fifteen rats received a 1.5 g (n = 5), 20 g (n = 5) or 56 g (n = 5) clip compression injury of the cord at C8. SCBF at the injury site was measured by the hydrogen clearance technique 35 min before and 30 min after SCI. Concomitantly MEPs from the cord at T10 (MEP-C) and from the sciatic nerve (MEP-N) and SSEPs were recorded.A linear relationship (r = −0.89, P < 0.002) was found between the severity of SCI and the reduction in SCBF at the injury site. Linear discriminant analysis revealed that both the MEP (P < 0.0001) and SSEP (P < 0.003) were significantly related to the severity of SCI. Furthermore, the amplitude of the MEP (r = 0.65, P < 0.0001) and SSEP (r = 0.58, P < 0.0011) was significantly correlated with the posttraumatic SCBF. Multiple regression revealed that both the severity of cord injury and the degree of posttraumatic ischemia were significantly related to axonal dysfunction after SCI. While the MEP was more sensitive to injury than the SSEP, the SSEP more accurately distinguished between mild and moderate severities of cord injury.Axonal conduction in the motor and somatosensory tracts of the cord was significantly correlated with the reduction in posttraumatic SCBF and, therefore, these data provide quantitative evidence linking posttraumatic ischemia to axonal dysfunction following acute cord injury. Furthermore, this study validates the hypothesis that the combined recording of MEPs and SSEPs is an accurate technique to assess the physiological integrity of the cord after injury.     

Nerve,spinal cord and brain somatosensory evoked responses: a comparative study during electrical and magnetic peripheral nerve stimulation

Somatosensory evoked potentials (SEPs) and compound nerve action potentials (cNAPs) have been recorded in 15 subjects during electrical and magnetic nerve stimulation. Peripheral records were gathered at Erb's point and on nerve trunks at the elbow during median and ulnar nerve stimulation at the wrist. Erb responses to electrical stimulation were larger in amplitude and shorter in duration than the magnetic ones when ‘electrical’ and ‘magnetic’ compound muscle action potentials (cMAPs) of comparable amplitudes were elicited. SEPs were recorded respectively at Cv7 and on the somatosensory scalp areas contra- and ipsilateral to the stimulated side. SEPs showed a statistically significant difference in amplitude only for the brachial plexus response and for the ‘cortical’ N20-P25 complex; differences were not found between the magnetic and electrical central conduction times (CCTs) or for the peripheral nerve response latencies. Magnetic stimulation preferentially excited the motor and proprioceptive fibres when the nerve trunks were stimulated at motor threshold intensities.     

Electrophysiological characteristics of lumbosacral evoked potentials in patients with established spinal cord injury

Surface electrodes positioned over the S1 and T12 vertebrate and referenced to T6 were used to record spinal potentials evoked by unilateral stimulation of the posterior tibial nerve at the knee. Data were collected on 24 patients who received spinal cord injuries 2 months to 31 years previously. The recording sites were below the level of spinal injury. The lumbosacral evoked potentials (LSEPs) were compared with the results of measurements obtained from 19 neurologically healthy subject. Additional data were collected on each patient to characterize segmental reflex responses and preservation of sensory and motor functions associated with the L5 through S2 segments of the spinal cord. Assuming that the LSEP reflects demonstrate a degree of spinal cord dysfunctions caudal to the area of injury in s substantial number of the patients with spinal cord injury which we studied.     

Short latency somatosensory and spinal evoked potentials: Power spectra and comparison between high pass analog and digital filter

Medium nerve somatosensory evoked potentials (SSEPs) and intraoperative spinal evoked potentials were analyzed using different analog and zero phase shift digital high pass filter and by power spectrum. Additionally, high pass analog and digital filtering was performed on various sine, triangular and rectangular waves manufactured by a wave form generator. Recordings were also transformed to the 1st and 2nd time derivatives.The great abundance of spectral energy for scalp recorded median nerve SSEPs was below 125 c/sec but lower energy fast frequency components consistently extended to 500 c/sec. Power spectrum of the Erb's point compound nerve action potential revealed a wide band of spectral energy commencing at about 50–100 c/sec, peaking at about 250–270 c/sec and extending to nearly 1000 c/sec. This suggests that synchronous axonal activity generates predominantly faster frequencies above 100 c/sec.High pass analog filter confers phase non-linearity which results in various distortions including latency shift and a morphological change which may be visually similar to the 1st or 2nd time derivatives. High pass zero phase shift digital filter removes selected low frequencies without accompanying phase distortion. This accentuates fast peaks seen at open bandpass as well as transition points between baseline and component ascent or descent. Zero phase shift digital filter may also generate peaks that are not visualized at open pass but which reflect the sum of frequencies which were not removed by filtering. These peaks do not necessarily correspond to discrete singular neuroanatomical structures.Although peaks observed in high pass analog and digital filter appear similar and comparable, their underlying activity may be of different origin. This is because high pass analog filter projects a considerable amount of overlap from earlier onto later waves.For clinical correlation it is important that restricted bandpass analog or digitally filtered recordings be compared with open pass data. Only those peaks visualized in both open and restricted bandpass can be considered authentic. Examples of spinal and scalp SSEPs indicate that selective filtering may, under certain circumstances, distinguish axonal or lemniscal from synaptic generators.