Scalp topography of the short latency somatosensory evoked potentials following posterior tibial nerve stimulation in man

The scalp topography of the short latency somatosensory evoked potentials (SEPs) to unilateral posterior tibial nerve stimulation at the ankle was studied by using a non-cephalic reference in 22 normal young adults. At least 3 components (P28, N31 and N32) were identified preceding the major positive peak (P36). The first 2 components had similar peak latency at all scalp electrodes, and were considered to be generated in deep structures. However, N32 was localized to the hemisphere contralateral to the side of stimulation. P36 was maximal at the midline foot sensory area, or at the contralateral parasagittal area, and its amplitude decreased more steeply anteriorly than posteriorly. The peak latency of P36 progressively increased from ipsilateral to the side of stimulation in the coronal plane. P36 occurred earlier in the somatosensory area, and increased in peak latency anteriorly. Generator source of scalp-recorded far-field potentials (P28 and N31) remains to be elucidated. N32 might reflect activities of the thalamo-cortical pathway or an initial cortical response. P36 appeared to be generated in the somatosensory foot area.     

Topography and intracranial sources of somatosensory evoked potentials in the monkey. II. Cortical components

Averaged somatosensory evoked potentials (SEPs) and associated multiple unit activity (MUA) were recorded from a series of epidural and intracortical locations following stimulation of the contralateral median nerve in the monkey. Cortical components were differentiated from the earlier subcortical activity and the intracerebral distribution and sources of each cortical potential were determined. Under barbiturate anesthesia the SEP wave form is simplified and can be wholly attributed to two sources. The earliest cortical activity consists of a biphasic P10-N20 wave which is generated in the posterior bank of the central sulcus. A second wave form, P12-N25, originates in the crown of the postcentral gyrus. No other cortical areas are active. In the alert state the morphology of the surface SEP is complex and reflects the interaction of volume conducted activity from several adjacent cortical sources. The wave form overlying the hand area of the postcentral gyrus consists of P12, P20, P40, N45 and P110. Precentral recordings exhibit P10, P13, N13, N20, P24, N45 and P110. Six anatomical sources have been identified. P10 and N20 originate in the posterior bank of the central sulcus including areas 3a and 3b and are volume conducted in an anteroposterior direction. P12 originates in area 1 as well as the anterior portion of area 2. P20 is generated in the medial portion of the postcentral gyrus including area 5. The source of P40 lies within the lateral portion of the parietal lobe including area 7b. Two components were generated in precentral cortex: P13/N13 originates principally in area 4 within the anterior bank of the central sulcus and P24 reflects activity in the anteromedial portion of the precentral gyrus including area 6. The long latency SEP components, N45 and P110, are generated widely within the somesthetic areas of postcentral cortex. The early cortical SEP components recorded in the monkey closely resemble in configuration and topography those recorded from man although the latter are longer in latency, reflecting interspecies differences in the length of conduction pathways as well as in cortical processing time.     

Cortical and subcortical somatosensory evoked potentials to median nerve stimulation in man

In order to define the precise locations of precentral and postcentral gyri during neurosurgical operations, somatosensory evoked potentials to contralateral median nerve stimulation were recorded from the cerebral cortex in 19 cases with organic cerebral lesions which located near the central sulcus. In addition to that, distribution patterns of early components of SEPs were displayed by Nihonkoden Atac 450 in 3 cases who had bone defects after wide decompressive craniectomy but were without any sensory disturbances In 4 cases, in whom deep electrodes were inserted for the stereotaxic operations or other reasons, frontal subcortical SEPs were recorded in order to know the origins of frontal components of SEPs. From the parietal cortex, N19, P22 and P23 were observed. And from the frontal cortex, P20 and N25 were obtained. Their average peak latencies were as follows; (table; see text) Because all subjects had organic lesion in the brain, the peak latencies were a little bit longer, and their standard deviations were larger than those in normal cases. Usually, clear-cut phase reversal could be observed between N19 and P20 across the central sulcus. So, the precentral and postcentral gyri were easily identified during the operations. N19 and P23 appeared over the wide areas of the parietal cortex. Also, P20 and N25 were recorded almost whole areas of the frontal cortex. On the other hand, P22 appeared from relatively restricted part of the postcentral gyrus where sensory hand area might have been located. Depth recording from the frontal subcortical area revealed that P20 could be recorded from the bilateral frontal subcortical areas and there observed no phase reversal between the cortical and subcortical SEPs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nasopharyngeal recordings of somatosensory evoked potentials document the medullary origin of the N18 far-field.

Because the nasopharyngeal electrode provides non-invasive access to the ventral brain-stem at the medullo-pontine level we used it for recording somatosensory evoked potentials (SEPs) to median nerve stimulation (non-cephalic reference). After the P9 and P11 far-fields, the nasopharyngeal SEPs disclosed a negative-going component which was interpreted as the near-field equivalent of the P14 scalp far-field generated in the caudal part of the medial lemniscus. Nasopharyngeal SEPs also revealed a large N18 with voltage and features strikingly similar to those of the scalp-recorded N18 far-field. These results suggest that N18 is generated in the medulla and not more rostrally in the brain-stem. The use of a nasopharyngeal electrode as reference for topographic brain mapping is discussed. The paper documents the feasibility and relevance of nasopharyngeal recordings for non-invasive analysis of short-latency SEPs.     

Distinct fronto-central N60 and supra-sylvian N70 middle-latency components of the median nerve SEPs as assessed by scalp topographic analysis, dipolar source modelling and depth recordings.

OBJECTIVES: To investigate the possible contribution of the second somatosensory (SII) area in the generation of the N60 somatosensory evoked potential (SEP).METHODS: In 7 epileptic patients and in 6 healthy subjects scalp SEPs were recorded by 19 electrodes placed according to the 10-20 system. All epileptic patients but one were also investigated using depth electrodes chronically implanted in the parieto-rolandic opercular cortex. Scalp SEPs underwent brain electrical source analysis.RESULTS: In both epileptic patients and healthy subjects, scalp recordings showed two middle-latency components clearly distinguishable on the basis of latency and scalp distribution: a fronto-central N60 potential contralateral to stimulation and a later bilateral temporal N70 response. SEP dipolar source modelling showed that a contralateral perisylvian dipole was activated in the scalp N70 latency range whereas separate perirolandic and frontal sources were activated at the scalp N60 latency. Depth electrodes recorded a biphasic N60/P90 response in the parieto-rolandic opercular regions contra- and ipsilateral to stimulation.CONCLUSIONS: Two different middle-latency SEP components N60 and N70 can be distinguished by topographic analysis and source modelling of scalp recordings, the sources of which are located in the fronto-central cortex contralateral to stimulation and in the supra-sylvian cortex on both sides, respectively. The source location of the scalp N70 in the SII area is strongly supported by its spatio-temporal similarities with SEPs directly recorded in the supra-sylvian opercular cortex.     

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.     

Somatosensory evoked potentials recorded directly from human thalamus and Sm I cortical area.

Somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded from the nucleus ventralis caudalis. They consisted of monophasic or diphasic potentials with mean onset latency of 13.8 ms. More complex SEPs to median nerve stimulation were obtained from the cortex. The SEPs consisted of two major positive waves, P1 and P2, and were recorded over both the precentral and postcentral gyri, suggesting that somatosensory information converges to the motor cortex, probably to be used for the integration of critical motor activity. In two patients, it was noted that the motor representation of facial movements was larger than the correspondent sensory representation on the postcentral gyrus. This larger motor representation of the face and more specifically of the lips and tongue may be related to human acquisition of mimicry and articulation of language.     

Cortical potentials related to voluntary and passive finger movements recorded from subdural electrodes in humans

Movement-related potentials were recorded from subdural electrodes placed on the precentral and postcentral cortex in 3 patients undergoing operation for intractable epilepsy. With self-initiated index finger movement, a negative potential of 25 to 50 microvolts in amplitude, preceding onset of the electromyographic activity by 60 to 95 ms (or onset of movement by 150 to 230 ms), was recorded from the hand somatosensory postrolandic area in all 3 patients. A similar potential preceding the movement was recorded from the precentral hand motor area in one subject who was the only patient in whom the precentral electrodes were placed on the hand motor area. Following active and passive movements, a clearly defined positivity (18 to 32 ms after a photometer trigger) that reversed phase across the central fissure was recorded. The premovement potentials are most probably generated by pyramidal tract neurons and motor-function-related neurons located in the post- and prerolandic areas. The postmovement positivity is most probably due to short-latency kinesthetic reafferent activation of the posterior bank of the central fissure (equivalent to P2 of the somatosensory evoked potentials).     

Contribution of GABAergic cortical circuitry in shaping somatosensory evoked scalp responses: specific changes after single-dose administration of tiagabine.

OBJECTIVES: To determine whether conventional as well as high-frequency somatosensory evoked potentials (SEPs) to upper limb stimulation are influenced by GABAergic intracortical circuitry. METHODS: We recorded SEPs from 6 healthy volunteers before and after a single-oral administration of tiagabine. Conventional low-frequency SEPs have been obtained after stimulation of the median nerve, as well as after stimulation of the first phalanx of the thumb, which selectively involves cutaneous finger inputs. Median nerve SEPs have been further analyzed after digital narrow-bandpass filtering, to selectively examine high-frequency responses. Lastly, in order to explain scalp SEP distribution before and after tiagabine administration, we performed the brain electrical source analysis (BESA) of raw data. RESULTS: After tiagabine administration, conventional scalp SEPs showed a significant amplitude increase of parietal P24, frontal N24 and central P22 components. Similarly, BESA showed a significant strength increase of the second peak of activation of the first two perirolandic dipoles, which are likely to correspond to the N24/P24 and P22 generators. By contrast, no significant changes of high-frequency SEPs were induced by drug intake. CONCLUSIONS: Our findings support the view that both N24/P24 and P22 SEP components are probably generated by deep spiny cell hyperpolarization, which is strongly increased by inhibitory inputs from GABAergic interneurons. By considering the clear influence of inhibitory circuitry in shaping these SEP components, conventional scalp SEP recording could be useful in the functional assessment of the somatosensory cortex in different physiological and pathological conditions. By contrast, intrinsic firing properties of the cell population generating high-frequency SEP responses are unaffected by the increase of recurrent GABAergic inhibition.     

Brain-stem components of high-frequency somatosensory evoked potentials are modulated by arousal changes: nasopharyngeal recordings in healthy humans.

OBJECTIVE: Until now, the demonstration that early components of high-frequency oscillations (HFOs) evoked by electrical upper limb stimulation are generated in the brain-stem has been based on the results of scalp recordings. To better define the contribution of brain-stem components to HFOs building, we recorded high-frequency somatosensory evoked potentials (SEPs) in 6 healthy volunteers by means of a nasopharyngeal (NP) electrode. Moreover, since HFOs are highly susceptible to arousal fluctuations, we investigated whether eyes opening can influence HFOs at this level. METHODS: We recorded right median nerve SEPs from the ventral surface of the medulla by means of a NP electrode as well as from the scalp, in 6 healthy volunteers under two different arousal states (eyes opened versus eyes closed). SEPs have been further analyzed after digital narrow bandpass filtering (400-800 Hz). RESULTS: NP recordings demonstrated in all subjects a well-defined burst, occurring in the same latency window of the low-frequency P13-P14 complex. Eyes opening induced a significant amplitude increase of the NP-recorded HFOs, whereas scalp-recorded HFOs as well as low-frequency SEPs remained unchanged. CONCLUSIONS: Our findings demonstrate that slight arousal variations induce significant changes in brain-stem components of HFOs. According to the hypothesis that HFOs reflect the activation of central mechanisms, which modulate sensory inputs depending on variations of arousal state, our data suggest that this modulation is already effective at brain-stem level.     

Topographical features of the sensory-evoked responses in malformed brains

To reveal the functional organization of the somatosensory area in the dysgenetic cortex, somatosensory-evoked potentials were examined in seven patients with congenital brain anomalies diagnosed by magnetic resonance imaging, including six patients in whom multichannel recordings over the scalp were used. In four patients with polymicrogyria/pachygyria and two with lissencephaly, the early cortical responses, frontal P20 and parietal N20, were absent in the cortex contralateral to the stimulated side. The first cortical response was a positive wave that appeared predominantly over the centroparietal area in five patients, and in the frontal area in the other patient with polymicrogyria/pachygyria. These findings suggest that the differentiated somatosensory function is distributed normally in the centroparietal cortex in most cases of widespread cortical dysplasia. However, the absence of P20/N20 may indicate a hypoplastic central sulcus or functionally undifferentiated subdivision of the somatosensory cortex in these patients. The absence of cortical responses in the patient with holoprosencephaly may correspond with growth failure of the thalamocortical afferent projections in this disorder.     

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.     

Reduction in amplitude of the subcortical low- and high-frequency somatosensory evoked potentials during voluntary movement: an intracerebral recording study.

OBJECTIVE: To investigate whether the reduction of amplitude of the scalp somatosensory evoked potentials (SEPs) during movement (gating) is due to an attenuation of the afferent volley at subcortical level. METHODS: Median nerve SEPs were recorded from 9 patients suffering from Parkinson's disease, who underwent implant of intracerebral (IC) electrodes in the subthalamic nucleus or in the globus pallidum. SEPs were recorded from Erb's point ipsilateral to stimulation, from the scalp surface and from the IC leads, at rest and during a voluntary flexo-extension movement of the stimulated wrist. The recorded IC traces were submitted to an off-line filtering by a 300-1500 bandpass to obtain the high-frequency SEP bursts. RESULTS: IC leads recorded a triphasic component (P1-N1-P2) from 14 to 22 ms of latency. The amplitudes of the scalp N20, P20 and N30 potentials and of the IC triphasic component were significantly decreased during movement, while the peripheral N9 amplitude remained unchanged. Also the IC bursts, whose frequency was around 1000 Hz, were reduced in amplitude by the voluntary movement. CONCLUSIONS: Since the IC triphasic component is probably generated by neurons of the thalamic ventro-postero-lateral nucleus, which receive the somatosensory afferent volley, the P1-N1 amplitude reduction during movement suggests that the gating phenomenon involves also the subcortical structures.     

Spinal and early scalp-recorded components of the somatosensory evoked potential following stimulation of the posterior tibial nerve

Somatosensory evoked potentials (SEPs) were elicited by stimulation of the posterior tibial nerve (PTN) in 12 normal adults. Recording using both cephalic and non-cephalic references were obtained from multiple electrodes placed over the spine and scalp. Following PTN stimulation, the fastest recorded potentials of the afferent sensory volley proceeds up the spinal cord at constant velocity. After arrival of the volley at cervical cord levels, 3 widely distributed waves, P28, P31 and N34, are recorded from scalp electrodes. These 'far-field' potentials are followed by a localized positivity (P38) which has a peak voltage either at the vertex or just laterally toward the side of stimulation. A contralateral negativity (N38) was present in most individuals. We propose that P28 arises from medial lemniscus; that P31 is generated by ventrobasal thalamus; and that N34 is probably the result of further activity in thalamus and/or thalamocortical radiations. The P38/N38 complex represents the primary cortical response to PTN stimulation. Its most consistent characteristic is a positivity at the vertex or immediately adjacent scalp areas ipsilateral to the stimulated leg. The topography of the P38/N38 potential varies slightly from individual to individual in a manner consistent with a functional dipole situated in the leg and foot area on the mesial aspect of the postcentral gyrus, whose exact location and orientation changes in accordance with known variations in the location of the leg area.     

Median and tibial somatosensory evoked potentials. Changes in short- and long-latency components in patients with lesions of the thalamus and thalamo-cortical radiations

Alterations in short- and long-latency components of median and tibial somatosensory evoked potentials (SEPs) were studied in patients with lesions in the thalamus and thalamo-cortical radiations. When the lesions were located primarily in the ventro-posterior thalamus, the SEP changes consisted of the following combination: absence of response; decrease in response amplitude; delay in peak latency; and attenuation of median N20-P25 and tibial P40. The laterally situated ventro-posterior lesions tended to preferentially affect tibial SEPs whereas the medially situated lesions tended to preferentially affect median SEPs. The lateral thalamic lesions affected primarily the long-latency SEP components, whereas the medial thalamic lesions affected primarily the mid-latency or the mid- and long-latency SEP components. Corona radiata infarcts produced SEP changes similar to those with the ventro-posterior thalamic lesions except that absence of evoked responses was not observed. Subcortical infarcts tended to affect the mid- and long-latency SEP components with relative preservation of the short-latency components. The present data indicate that only the lesions involving the primary thalamic relay area affected all SEP components, particularly the short-latency components, and that the lesions in other thalamic areas can also influence the SEPs, particularly the mid- and long-latency components. The present study further demonstrates that a combined use of median and tibial SEPs is useful in delineating the topographic organization of the somatosensory system in the thalamus.     

Epilepsy in Schizencephaly: Abnormal Cortical Organization Studied by Somatosensory Evoked Potentials

Median nerve short-latency somatosensory evoked potentials (MN-SSEP) are recorded from the scalp to assess parietal lobe function and from the cortex to identify primary sensory and motor areas before epilepsy surgery. Nevertheless, the origins of many of the MN-SSEP waveforms and the reliability of this technique for localizing the central sulcus are not definitively known. We studied a child with a unilateral, closed, right parietal schizencephalic cleft and frequent simple partial seizures before the child underwent cortical resection. The sensory examination, neuroimaging, and electrical brain stimulation findings indicated a normal thalamus and an abnormal parietal lobe. Scalp-recorded MN-SSEPs showed intact widespread N18 potentials bilaterally, but absent right, although normal left parietal N20 and P27 waveforms. Cortically recorded MN-SSEPs could not localize the central sulcus owing to an absence of the expected negative potential over the right postcentral gyrus and the presence of waves with abnormal latencies over the precentral cortex. These findings suggest that: (a) the N18 potential probably originates at or below the level of the thalamus, (b) the N20 and P27 peaks are most likely generated by parietal cortex or white matter, and (c) cortically recorded MN-SSEPs can fail to localize the central sulcus before epilepsy surgery when congenital anomalies exist in the parietal lobe.     

Lateralization of the P22/N30 precentral cortical component of the median nerve somatosensory evoked potentials is different in patients with a tonic or tremulous form of cervical dystonia.

Somatosensory evoked potentials (SEPs) of the median nerve were recorded in 40 patients with the tonic and tremulous form of torticollis and in 40 healthy volunteers. Polymyographic recordings of the activity of cervical muscles were performed in all patients with cervical dystonia to determine the dystonic and antagonistic muscles. Patient SEPs were recorded during abnormal head movement. SEPs in 20 healthy volunteers were recorded with the head in the middle position. SEPs in another 20 healthy volunteers were recorded with the head rotated 60 degrees to the right. The mean peak-to-peak amplitude values of the precentral P22/N30 and the postcentral N20/P25 complexes and their mean side-to-side ratios were calculated in the F3 (F4), C3' (C4'), and C3+ (C4+) electrode positions in all four groups. In patients with the tonic form of torticollis (group I), an apparent mean P22/N30 amplitude increase was found above the hemisphere contralateral to the direction of head deviation in both precentral electrode positions, F3(4) and C3(4)'. A statistically significant difference was observed between group I and other patient and control groups. In patients with the tremulous form of torticollis (group II), an increase in the mean P22/N30 amplitude was found above both hemispheres in both precentral electrode positions F3(4) and C3(4)'; a significant difference was found between group II and both control groups. Lateralization of the P22/N30 component was found only in patients with the tonic form of torticollis. The mean side-to-side ratio of the precentral P22/N30 component amplitude was significantly different when group I was compared with either group II or control groups. No significant difference between group II and either control group was found. No significant abnormalities in the postcentral N20/P25 component were found in either the dystonic patients or in healthy control subjects. These results might indicate a different pattern of cortex excitability in patients with tonic versus tremulous forms of torticollis and therefore may implicate different underlying pathophysiological mechanisms in these two forms of disorder.     

Localisation of the sensorimotor cortex during surgery for brain tumours: feasibility and waveform patterns of somatosensory evoked potentials

OBJECTIVE: Intraoperative localisation of the sensorimotor cortex using the phase reversal of somatosensory evoked potentials (SEPs) is an essential tool for surgery in and around the perirolandic gyri, but unsuccessful and perplexing results have been reported. This study examines the effect of tumour masses on the waveform characteristics and feasibility of SEP compared with functional neuronavigation and electrical motor cortex mapping. METHODS: In 230 patients with tumours of the sensorimotor region the SEP phase reversal of N20-P20 was recorded from the exposed cortex using a subdural grid or strip electrode. In one subgroup of 80 patients functional neuronavigation was performed with motor and sensory magnetic source imaging and in one subgroup of 40 patients the motor cortex hand area was localised by electrical stimulation mapping. RESULTS: The intraoperative SEP method was successful in 92% of all patients, it could be shown that the success rate rather depended on the location of the lesion than on preoperative neurological deficits. In 13% of the patients with postcentral tumours no N20-P20 phase reversal was recorded but characteristic polyphasic and high amplitude waves at 25 ms and later made the identification of the postcentral gyrus possible nevertheless. Electrical mapping of the motor cortex took up to 30 minutes until a clear result was obtained. It was successful in 37 patients, but failed in three patients with precentral and central lesions. Functional neuronavigation indicating the tumour margins and the motor and sensory evoked fields was possible in all patients. CONCLUSION: The SEP phase reversal of N20-P20 is a simple and reliable technique, but the success rate is much lower in large central and postcentral tumours. With the use of polyphasic late waveforms the sensorimotor cortex may be localised. By contrast with motor electrical mapping it is less time consuming. Functional neuronavigation is a desirable tool for both preoperative surgical planning and intraoperative use during surgery on perirolandic tumours, but compensation for brain shift, accuracy, and cost effectiveness are still a matter for discussion.     

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.