The role of somatosensory evoked potentials in spinal dysraphism – do they have a prognostic significance?

Somatosensory evoked potentials (SEP) are not routinely used in spinal dysraphism. In this study 38 patients (29 children and 9 adults) with spinal dysraphism were prospectively studied with the objective of evaluating whether SEPs were a prognostic tool that could be used to predict clinical improvement after repair of a spinal dysraphic lesion. For all patients, preoperative SEP and postoperative SEP (within 1 week of operation) were recorded. Fifteen of these patients also had follow-up postoperative SEP recordings taken within 3 months of operation. A clinical examination was performed at the time of each SEP. Thirty patients had tethered cord, 12 had diastematomyelia and 15 had intra- and/or extradural tumours, which included lipomas and dermoid and epidermoid tumours. Twenty-one children and all adults had abnormal preoperative SEPs. Sixteen children and 4 adults had improved SEPs postoperatively. All these children and 2 of the 4 adults also experienced clinical improvement. Improvement in SEPs preceded clinical improvement in 12/20 patients. We observe that SEPs have a good prognostic value. Received: 14 December 1997     

Distribution of brainstem somatosensory evoked potentials following upper and lower limb stimulation.

OBJECTIVE: Because somatosensory evoked potentials (SEP) to lower limb stimulation have not been recorded from the brainstem to the extent that upper limb SEPs have been studied, we compared brainstem recordings in response to both median nerve (MN) and posterior tibial nerve (PTN)stimulation. METHODS: SEPs were recorded directly from the dorsal surface of the brainstem in four patients with fourth ventricle tumors. RESULTS: Following MN stimulation, medullary SEPs were characterized by a major negativity (N1) preceded by a small positivity (P1) and followed by a large positivity (P2). In the pons, triphasic waves with predominant negativity were obtained. With PTN stimulation, similar medullary SEPs with a P1'-N1'-P2' configuration and pontine SEPs with a triphasic waveform were obtained. CONCLUSIONS: Since the distribution of PTN SEP was identical to that of MN SEP, PTN SEPs are thought to be generated by mechanisms similar to those for MN SEP. Thus, the P1' and N1' of medullary SEP would be generated by the dorsal column fibers that terminate in the nucleus, with P2' possibly arising postsynaptically in the nucleus. The triphasic PTN SEP from the pons reflects an axonal potential generated in the medial lemniscal pathway.     

Somatosensory evoked potentials and magnetic resonance imaging in syringomyelia.

Somatosensory evoked potentials (SEPs) to median and posterior tibial stimulation were obtained in 22 patients with syringomyelia. All patients had magnetic resonance imaging (MR) which defined the maximum transverse diameter of the syrinx as well as its longitudinal extension. SEP was abnormal in 16 (72%) patients. Median and posterior tibial SEPs were abnormal in 11 and 15 patients respectively. Both tests were abnormal in 10 patients. Ten patients showed absence of one or more central potentials (P/N13, N20, N22) and 7 patients demonstrated increased conduction times (N9-N20, P/N13-N20, N22-P40). The mean maximum transverse diameter of the syrinx was 7.5 mm in patients with normal SEPs and 16.2 mm in patients with abnormal SEPs. Abnormal SEP was observed in all 5 patients with loss of position sense, in 9 of 13 (69%) with loss of superficial pain and temperature, and 1 of 2 patients with motor deficit only. Central SEP abnormalities were observed in 3 of 5 patients with sensory deficits indistinguishable from a peripheral neuropathy and in 2 patients in the asymptomatic extremity. Three of 4 patients with syringomyelia and Chiari malformation had a normal SEP.     

Effect of electroconvulsive shock on the somatosensory evoked potential in the rat

The effect of electroconvulsive shock (ECS) on the cortical somatosensory evoked potential (SEP) was studied in 25 male rats. SEPs were recorded after stimulation of the contralateral forepaw. Animals were curarized and artificially ventilated but not anesthetized. The magnitude of the ECS was 80 mA for 600 ms which produced tonic-clonic convulsions lasting an average 54 s in noncurarized control animals. SEPs were recorded during the ictal period and then at intervals for 20 min. ECS initially caused the total abolition of all components of the SEP implying a significant but transient effect on activity propagated in specific and also possibly diffuse somatosensory pathways. The reappearance of the SEP coincided with the cessation of convulsive movements and the return of the corneal reflex. The return of the waveform to near baseline condition corresponded to the regaining of the righting reflex at approximately 3 min in the control animals. The most persisting change in the SEP waveform was in the shape of the late high-amplitude component (N2) which may reflect activity in the reticular formation. Following ECS, N2 reappeared with a peak latency notably decreased (approximately 1 ms) in comparison with the mean baseline recording. There was also an attenuation in the amplitude of N2 which remained significantly depressed (at less than 50% of mean baseline amplitude) throughout the post-ECS recording period. The results are compared with the relatively few studies of the acute effects of ECS on evoked potentials in psychiatric patients and also with a neuroendocrine theory which argues that the principal site and mode of action of ECS lies in the diencephalon.     

Somatosensory-evoked potentials indicate increased unpleasantness of noxious stimuli in response to increasing stimulus intensities in the rat

Recently, it has been shown in rats that specific characteristics of somatosensory-evoked potentials (SEPs) recorded from different sites on the scalp correlate differently to the amount of unpleasantness experienced by the animal following noxious stimulation. It was shown that the SEP recorded from vertex (Vx-SEP) did correlate with the unpleasantness, whereas the SEP recorded from the primary somatosensory cortex (SI-SEP) did not. In the present study, we further investigated the relationship between the Vx-SEP, SI-SEP and the unpleasantness of noxious stimuli. Therefore, different groups of rats were subjected to a SEP fear-conditioning paradigm in which the unconditioned stimulus (US), represented by noxious stimuli applied to evoke SEPs, was paired to a conditioned stimulus (CS) represented by a tone. Different stimulus intensities of the US were applied in the different groups. After CS-US presentation, CS-induced fear-conditioned behaviour was analysed in relation to the characteristics of the Vx- and SI-SEP during CS-US presentation. Results showed that increasing stimulus intensities led to increased SEP amplitudes, which were paralleled by an increased amount of CS-induced fear-conditioned behaviour. No differences between Vx-SEP and SI-SEP were found. The increase in the SEPs in parallel with the increased amount of fear-induced behaviour further supports the SEP to be a potentially valuable tool for studying acute pain and analgesia in animals.     

Central and peripheral SEP defects in neurologically symptomatic and asymptomatic subjects with low vitamin B12 levels

Somatosensory evoked potentials (SEPs) following median nerve stimulation were abnormal in 7 patients with sensory impairment due to vitamin B12 deficiency. Extensor plantar reflexes indicated a central sensory pathway lesion in 4 cases and absent tendon jerks suggested peripheral neuropathy in 4, but median nerve SEPs indicated a predominantly central lesion without marked peripheral nerve involvement in 6 and an axonal neuropathy without CNS involvement in 1. The latter had evidence of central slowing of conduction in SEPs following posterior tibial nerve stimulation. Consequently, it is suggested that the brunt of sensory pathway involvement usually falls on the CNS, although peripheral neuropathy may occur as the major abnormality in some cases. In 2 patients SEPs showed a marked improvement following treatment with vitamin B12 injections, one consistent with restored central conduction and the other with recovery from peripheral neuropathy. No peripheral or central SEP abnormalities were seen in 18 dairy-produce eating vegetarians with low vitamin B12 levels, although 6 reported mild sensory symptoms suggestive of peripheral neuropathy and 3 had corroborative clinical signs.     

Somatosensory evoked potentials in comatose patients: correlation with outcome and neuropathological findings

Summary Subcortical and early cortical somatosensory evoked potentials (SEPs) were recorded in 63 comatose patients and classified into five salient SEP grades, which were defined as follows: grade 1, normal SEP; grade 2, SEPs with a clearly recognizable scalp component N20, normal central conduction time but clearly distorted wave N20–P25; grade 3, SEPs with a still recognizable N20 but delayed central conduction time and severely altered wave N20–P25; grade 4, SEPs with absence of N20 but with a more or less recognizable P15; grade 5, SEPs with absence of both N20 and P15. When these five patterns were compared with outcome, it was found that bilaterally normal SEPs or only unilaterally distorted SEPs were generally followed by good outcomes. Bilaterally altered SEPs (grade 2 or 3) were indicative of reduced chances of full recovery. The great majority of patients showing either grade 4 or 5 SEPs died within a few days after the recording session. In 31 patients, it was found post mortem that grade-2 SEPs reflected cortical brain damage, whereas grade-3 SEPs correlated well with subcortical lesions. In post-traumatic patients, this SEP pattern coresponded to diffuse subcortical shearing lesions. Patients with grade 4 or 5 SEPs were found to have severe brain oedema giving rise to transtentorial herniation, which was combined with secondary midbrain haemorrhage and tonsillar herniation in all patients with bilateral grade-5 SEPs.     

Somatosensory evoked potentials (SEPs) recorded from deep brain stimulation (DBS) electrodes in the thalamus and subthalamic nucleus (STN).

OBJECTIVE: To examine the location of deep brain stimulation (DBS) electrode somatosensory evoked potentials (SEPs) and determine the generators of the median nerve SEPs recorded in thalamus and subthalamic nucleus (STN). METHODS: SEPs were recorded from contacts of DBS electrodes and microelectrodes in thalamus and STN to establish the latencies of N13, N18 and N20 in 24 patients (8 tremor, 4 chronic pain, 12 Parkinson disease) undergoing chronic DBS. RESULTS: A large SEP with a mean latency of 17.9+/-1.7 ms was recorded from thalamic contacts. Phase reversal occurred at the horizontal level of the anterior commissure-posterior commissure line. Smaller potentials with similar latency but no reversal could be recorded from STN electrodes. CONCLUSIONS: We propose that the thalamic SEP is generated by excitatory post-synaptic potentials in sensory relay neurons in nucleus ventrocaudalis. A small potential in STN at a similar latency, may be due to volume conduction from thalamus. Intraoperative and postoperative SEP recordings from DBS electrodes could be used to determine the optimal position of the contacts relative to the sensory pathways and the choice of contacts for chronic stimulation.     

Orientation of attention and sensory gating: an evoked potential and reaction time study in cat

Somesthetic-evoked potentials (SEPs) were recorded in eight cats trained to perform a reaction time task (RT). The preparatory period (PP) preceding the RT began with the cat placing its paw in a box and ended 1.5 s later with a paw-withdrawal signal, an imperative stimulus (IS). In experiment 1 (E1), the IS took the form of a vibration in the box, whereas in experiment 2 (E2) a tone was used. The SEPs were elicited by electrical stimulation delivered to the paw once per trial and at a different moment during the last second of each PP. The SEPs were recorded in the lemniscus medialis (LM), the centrum medianum (CM), and over the anterior suprasylvian gyrus (ASSG). During the PP of E1 (four cats), SEPs recorded in the CM and over the ASSG were found to be significantly depressed. No significant change was noted, however, in those recorded in the LM. No significant SEP depression was found in any of the structures in E2 (four cats). Comparison between the two experiments revealed notable differences at both the thalamic and cortical levels. Moreover, SEP depression diminished as the moment for the IS approached. While, in E1, this occurred in the CM and over the ASSG, in E2 it was found in the CM only. Lemniscal and thalamic SEP amplitude was found to be correlated with performance. These findings are discussed in terms of orientation of attention, discrimination, and sensory gating.     

Dissociation of thalamic high frequency oscillations and slow component of sensory evoked potentials following damage to ascending pathways.

OBJECTIVE: Somatosensory evoked potentials (SEPs) recorded from the thalamus have a slow component and high frequency (approximately 1000 Hz) oscillations (HFOs). In this study, we examined how lesions in the sensory afferent pathway affect these components. METHODS: Thalamic SEPs to contralateral median nerve stimulation were recorded from deep brain stimulation electrodes in two patients. Patient 1 had spinal cord injury at the C4/5 level. Patient 2 had multiple sclerosis with mid brain lesions. Seven patients with no brain or cervical spinal cord lesions served as controls. RESULTS: In both patients, the low frequency component of the SEP (LF SEP) was delayed and/or prolonged and greatly decreased in amplitude compared with controls. HFOs were recorded in both patients. The latencies of onset and peak of the HFOs were approximately the same as those of the LF SEPs and their amplitudes were similarly reduced. However, their frequency was similar to that of the control group. Cortical SEPs were absent in both patients. CONCLUSIONS: Normal frequencies of thalamic HFOs in association with increased peak latencies, and decreased amplitudes provide further evidence that the HFOs are likely due to intrinsic oscillations in the thalamus rather than high frequency synchronous inputs. SIGNIFICANCE: Thalamic HFOs are closely associated with the LF SEP but are generated by a different mechanism.     

Unusual scalp recorded somatosensory evoked potentials after removal of a large intraventricular meningioma

Very unusual scalp recorded SEPs were seen in a case after removal of a large intraventricular meningioma. One day before death (ten days after surgery) when the patient was moribund, SEPs from the clinically and radiologically affected hemisphere in which a hematoma and thalamic infarct were found, had a normal latency and were decreased in amplitude. SEPs from the clinically and radiologically nonaffected hemisphere, where only minimal findings were seen, had an abnormally short latency (16.9 msec) and the CCT was only 3.1 msec. We do not offer any logical explanation of these unusual SEP findings from both hemispheres shortly before death.     

Development of a rat model to assess the efficacy of the somatosensory-evoked potential as indicator of analgesia

Drug-induced changes in somatosensory-evoked potentials (SEPs) are considered to reflect an altered nociceptive state. Therefore, the SEP is proposed to be a parameter of analgesic efficacy. However, at present, SEPs have not been studied in relation to animal pain. The present study aims to develop a rat model in which this relationship can be studied based on Pavlovian fear conditioning. Therefore, rats, implanted with epidural electro-encephalogram recording electrodes, were randomly assigned to either a paired or random-control group and subjected to an aversive-to-appetitive transfer paradigm. During the aversive phase, the SEP-stimulation paradigm (5 mA square wave pulses, n = 72, of 2 ms duration each, with a stimulus frequency of 0.5 Hz; total duration 144 s) was used as the unconditioned stimulus (US), while a tone (40 s, 1500 Hz, 85 dB sound pressure level) was used as the conditioned stimulus (CS). During the appetitive phase, the CS was presented paired to the presentation of a sugar pellet. When compared to the random-control group, the paired group showed significantly more freezing behavior and significantly less reward-directed behavior in response to the CS in the appetitive phase. In addition, SEPs were not significantly affected by fear conditioning. Based on these results, we conclude that the SEP-stimulation paradigm can be successfully employed as a US in fear conditioning. In future studies, fear conditioning can be carried out under different levels of an analgesic regimen to allow the changes in SEP parameters to be compared to changes in fear-induced behavior making this model potentially useful to validate SEP parameters as indicators of analgesia.     

Middle-latency somatosensory evoked potentials after stimulation of the radial and median nerves: component structure and scalp topography.

Somatosensory evoked potentials (SEPs) after radial nerve stimulation are studied less frequently than those after median nerve stimulation. Therefore, little is known about their component structure and scalp topography. We investigated radial nerve SEPs after electrical stimulation at the left wrist. For comparison, the median nerve was also stimulated at the wrist. SEPs were recorded with 15 scalp electrodes (bandpass 0.5-200 Hz) in 27 healthy subjects. The waveform of the radial nerve SEP at a contralateral parietal lead was comparable to that of the median nerve SEP, consisting of P14, N20, P30, and N60. In spite of comparable stimulus intensities, SEP amplitudes were smaller after radial than after median nerve stimulation. Significant latency differences were found only for N20 (earlier for median nerve) and P30 (earlier for radial nerve). The duration of the primary complex N20-P30 thus was significantly shorter for the radial nerve. Whereas N20 and P30 were present with either earlobe or frontal reference, N60 had a prerolandic maximum and was best recorded with a bipolar transverse derivation. In addition, another middle-latency negativity (N110) was found near the secondary somatosensory cortex, which had previously been described only for radial nerve stimulation. In standard SEP derivations, the N110 is riding on the ascending limb of the vertex negativity. It could best be recorded in low temporal leads versus a midline reference. The scalp topographies of P30, N60, and N110 were similar for radial and median nerve stimulation.     

Prediction of 'awakening' and outcome in prolonged acute coma from severe traumatic brain injury: evidence for validity of short latency SEPs.

OBJECTIVE: To evaluate the prognostic value of somatosensory evoked potentials (SEPs) in severe traumatic brain injury (TBI) considering both 'awakening' and disability. METHODS: SEPs were recorded in 60 severe TBI with duration of acute coma>7 days. N20-P25 amplitudes, their side-to-side asymmetry and CCT were measured. SEPs on each hemisphere were classified as normal (N), pathological (P) or absent (A). 'Awakening' and disability were assessed after at least 12 months using Glasgow Outcome Scale (GOS). SEP predictive value was compared with GCS and EEG reactivity RESULTS: Seventy-five percent regained consciousness. 29/60 had a good outcome (GOS 4-5) and 31/60 had a bad outcome (GOS 1-3). According to the ROC curve, SEP findings were classified in 3 grades. Grade I (NN, NP) had PPV of 93.1% for 'awakening' and 86.2% for good outcome. Grade III (AA) had PPV of 100% for bad outcome and 72.7% for 'awakening'. Grade II (PP, NA, PA) was associated with the wider range of outcome. A multivariate analysis including SEP grading, GCS and EEG reactivity did not increase the percentage of cases prognosticated by SEP alone. CONCLUSIONS: We confirm the high predictive value of SEPs in TBI, which is greater than GCS and EEG reactivity. Indeed, SEP grades I and III were able to predict the correct prognosis in more than 80% of severe TBI. Therefore, SEPs should be used more widely in the prognosis of severe TBI. SIGNIFICANCE: Differently from post-anoxic, in post-traumatic coma the presence of normal SEPs has a favourable predictive value both for 'awakening' and disability. We think that in literature enough attention has still not been paid to this finding.     

Somatosensory evoked potentials in intraspinal tumors

SEPs have been recorded in 15 patients with spinal cord tumors (mostly ependymomas) and in 5 patients with cord compression due to meningiomas (3 cas), neuromas (1 case) or neurosarcoma (1 cas). All the patients have been operated on so that precise informations were available on the histology and the location of the tumor. SEPs were monitored during surgery in 8 patients. The main conclusions of this study are as follows: There was a good correlation between the somatosensory troubles for touch, vibration sense and joint position sense, and SEPs abnormalities, however, SEPs may be clearly abnormal in the absence of any somatosensory deficit when the dorsal columns are compressed and not infiltrated by the tumor. In the latter situation the reverse dissociation (i.e., normal SEPs with somatosensory troubles) may be observed. The possibility of a dissociation between normal N11 and N13 cervical components and absent P14 far field components (non-cephalic reference) has been confirmed in 6 patients with cervicomedullary tumors. In 3 of them, this dissociation was found to be reversible and early SEPs returned to normal after surgery. Peroperative monitoring of scalp SEPs recorded with a non-cephalic reference electrode allowed the detection of transient SEP abnormalities related with a traction on the dorsal columns of the cord. SEP monitoring is recommended for any surgical removal of tumor that needs a posterior myelotomy.     

Early somesthetic evoked potentials and sensory deficits in thalamic and juxta-thalamic lesions. Clinical, electrophysiological and x-ray computed tomographic study in 70 patients

Somatosensory Evoked Potentials (SEPs) have been recorded in 70 patients presenting a thalamic or capsular CT scan lesion. The loss of SEP parietal components confirmed the deafferentation of somatosensory cortex in infarctions of geniculothalamic or anterior choroidian arteries territory. SEPs were found to be normal in infarctions of other arterial territories, in agreement with the clinical evidence of normal somatosensory performances. In patients with haematomas, especially when located in the thalamus, there was no clear correlation between lesion sites and SEP data. Abnormal parietal responses were always associated to impaired tactile and joint sensations. The correlation was less significant for vibration sense. In four cases of selective loss of pain sensation SEPs were normal. In seven patients with abnormal parietal responses sterognosis was normal, a situation which is never encountered in cortical lesions. SEPs reliably documented the degree of somatosensory loss in patients with tactile extinction phenomenon. Contralateral parietal responses were reduced in four patients with tactile extinction but no attentional deficit for other sensory modalities. Thus normal SEPs are a prerequisite to consider thalamic neglect syndrome as a pure attentional disorder. Moreover SEPs demonstrated that there was no long-lasting deafferentation of somatosensory cortex in ataxic hemiparesis. It was found that selective loss of post-or prerolandic SEP components could occur in capsular lesions. This finding favors the hypothesis of parallel and independant thalamo-parietal and thalamo-frontal somatosensory projections that may be selectively damaged in lesions of thalamocortical radiations.     

Antidromic corticospinal tract potential of the brain.

OBJECTIVE: To describe a novel potential component (antidromic corticospinal tract potential, ACSP) of the brain after translaminar spinal stimulation of a relaxed patient during scoliosis surgery. To study the origin of this component and to compare its source to known sources of the somatosensory evoked potentials (SEPs). METHODS: We studied 17 consecutive patients during posterior scoliosis surgery. SEPs and ACSPs were elicited by translaminar spinal stimulation at the Th 2 and L 1 levels. ACSPs and SEPs were recorded on the scalp midline. Neurogenic motor evoked potentials (NMEPs) were recorded on the popliteal spaces. Preoperative tibial SEPs were also recorded. RESULTS: ACSP was distinctly separated from the corresponding spinally evoked cortical SEP that showed longer latency than the ACSP. ACSPs decreased and disappeared when stimulation was moved to the caudal direction in the conus region while SEP persisted. In addition, the hemispheric origin of ACSP was confirmed with multichannel midline recordings of the scalp and neck. Thus there was no confusion to the response of nucleus gracilis, corresponding the P 31 response of the tibial nerve SEP. CONCLUSIONS: The origin of ACSP seemed to be in the rostral part of the corticospinal tract. ACSP diminished in the conus region when stimulation was moved caudally and it disappeared when the stimulus was given to the root level. This proves that ACSP is not a response of the somatosensory tract, instead ACSP represents antidromic response of the pyramidal tract. ACSP can be used in monitoring of the motor tracts during scoliosis surgery together with NMEPs.     

Evaluation of reference sites for scalp potentials evoked by painful and non-painful sural nerve stimulation.

The objective of this study was to evaluate reference sites for recording the middle- and long-latency scalp potentials elicited by painful and non-painful sural nerve stimulation. Somatosensory evoked potentials (SEPs) were recorded from the scalp, the mastoid, the earlobe, the neck, and the wrist. Each site was referenced to the sterno-vertebral (SV) electrode, which is a balanced non-cephalic reference with essentially no ECG contamination. There was little or no activity recorded between the wrist and SV, and the SV was located within a region extending from the rostral neck to the wrist where the potentials were stable over space. Hence, the SV reference is indifferent for the middle- and long-latency potentials evoked by painful and non-painful sural nerve stimulation. There was, however, significant activity recorded from the earlobe and mastoid, sites which are frequently used as references for the SEP. It is important that investigators using these cephalic references to study the middle- and long-latency peaks of the SEP be aware of this activity as it will distort SEPs recorded from single sites and the SEP scalp topography, distortions which could unnecessarily complicate their interpretation.     

The Waveforms of the Group Mean SEP of Each Sex*

Abstract: With SEPs recorded from age-matched normal human subjects, 100 males and 100 females, 22.34 ± 1.69 years, it was confirmed that the Group Mean SEP of each sex each converges to a given waveform which significantly differed from each other. The waveform of the Group Mean SEP for females consisted of the 12 components, and was approximately tetraphasic within 500 msec in latency, while that for males consisted of the same components except for N₄ and P₄. There was a high convex arch with P₄ (82 msec) between P₂ and N₆ for females, but a low hollow slope without the peak for males. With Scaled SEPs, which were converted from SEPs by Amplitude Scaling, the results similar to those with SEPs were obtained.     

Abnormal gating of somatosensory inputs in essential tremor.

OBJECTIVE: To study whether sensorimotor cortical areas are involved in Essential Tremor (ET) generation.BACKGROUND: It has been suggested that sensorimotor cortical areas can play a role in ET generation. Therefore, we studied median nerve somatosensory evoked potentials (SEPs) in 10 patients with definite ET.METHODS: To distinguish SEP changes due to hand movements from those specifically related to central mechanisms of tremor, SEPs were recorded at rest, during postural tremor and during active and passive movement of the hand. Moreover, we recorded SEPs from 5 volunteers who mimicked hand tremor. The traces were further submitted to dipolar source analysis.RESULTS: Mimicked tremor in controls as well as active and passive hand movements in ET patients caused a marked attenuation of all scalp SEP components. These SEP changes can be explained by the interference between movement and somatosensory input ('gating' phenomenon). By contrast, SEPs during postural tremor in ET patients showed a reduction of N20, P22, N24 and P24 cortical SEP components, whereas the fronto-central N30 wave remained unaffected.CONCLUSIONS: Our findings suggest that in ET patients the physiological interference between movement and somatosensory input to the cortex is not effective on the N30 response. This finding thus indicates that a dysfunction of the cortical generator of the N30 response may play a role in the pathogenesis of ET.