Comparison of somatosensory evoked high-frequency oscillations after posterior tibial and median nerve stimulation.

OBJECTIVE: We compared the high-frequency oscillations (HFOs) evoked by posterior tibial nerve (PTN) and median nerve (MN) stimulation. METHODS: Somatosensory evoked potentials (SEPs) were recorded with a filter set at 10-2000 Hz to right PTN and to right MN stimulation in 10 healthy subjects. The HFOs were obtained by digitally filtering the wide-band SEPs with a band-pass of 300-900 Hz. RESULTS: HFOs were recorded in 8 of the 10 subjects for PTN, and in all subjects for MN stimulation. The HFOs after both PTN and MN stimulation started approximately at or after the onset of the primary cortical response (P37 and N20) and ended around the middle of the second slope. HFO amplitudes and area after PTN stimulation were significantly smaller than those after MN stimulation. HFO duration after PTN stimulation was markedly longer than that after MN stimulation. However, HFO interpeak latencies did not differ between the two nerves. CONCLUSIONS: The present findings suggest that the HFOs after PTN and MN stimulation reflect a neural mechanism common to the hand and foot somatosensory cortex.     

Interference of tactile and pain stimuli on thalamocortical signal processing in humans revealed by median nerve SEPs.

OBJECTIVE: We investigated the interference of tactile and painful stimuli on human early somatosensory evoked potentials (SEPs) including high frequency oscillations (HFOs) to further study thalamocortical processing of somatosensory information. METHODS: Multi-channel median nerve SEPs were recorded during (1) no interference, (2) sensory interference by tactile stimulation to digits 2 and 3, and (3) application of pain to the same digits. Spatio-temporal source analysis separated brain stem (S1), thalamic (S2) and two cortical sources (S3, S4), which were evaluated for the low (20-450 Hz) and high (450-750 Hz) frequency portion of the signal. RESULTS: Low frequency SEPs showed a decrease of activity at cortical source S3 during both conditions, while thalamic source S2 was significantly increased during pain interference. HFOs showed an increase of cortical source S3 and in trend of thalamic source S2 and cortical source S4 during both kinds of interference. CONCLUSIONS: Although the painful stimulus might not be specific for the nociceptive afferents, the present data affirm that at this early stage of sensory information processing within the primary sensory cortex (area 3b, area 1) pain is handled similar to sensory interference. SIGNIFICANCE: HFOs might represent an intrinsic "somatosensory alerting" system which reacts to both interference stimuli in a similar way, therefore indicating an interference without a qualitative evaluation.     

Effects of general anesthesia on high-frequency oscillations in somatosensory evoked potentials.

To determine the characteristics of high-frequency oscillations (HFOs) of cortical somatosensory evoked potentials (SEPs), the effect of general anesthesia on HFOs and low-frequency primary cortical responses was studied. The authors recorded SEPs elicited by median nerve stimulation directly from human brains of seven patients who underwent implantation of subdural electrodes before surgical treatment of intractable epilepsy. Recordings were made before and during general anesthesia. Changes in the number of HFOs and amplitude ratios of HFOs/primary cortical responses were analyzed. Under general anesthesia, the number of HFO peaks and the amplitude ratios were significantly decreased. General anesthesia induced remarkably decreased HFO activities when compared to low-frequency SEPs, suggesting that each of those originated from different generators. Possible relations between gamma-amino-butyric acid (GABA)ergic inhibitory interneurons and HFOs are discussed.     

Parietal generators of low- and high-frequency MN (median nerve) SEPs: data from intracortical human recordings.

OBJECTIVE: To identify low and high-frequency median nerve (MN) somatosensory evoked potential (SEP) generators by means of chronically implanted electrodes in the parietal lobe (SI and neighbouring areas) of two epileptic patients. METHODS: Wide-pass short-latency and long-latency SEPs to electrical MN stimulation were recorded in two epileptic patients by stereotactically chronically implanted electrodes in the parietal lobe (SI and neighbouring areas). To study high-frequency responses (HFOs) an off-line digital filtering of depth short-latency SEPs was performed (500-800 Hz, 24 dB roll-off). Spectral analysis was performed by fast Fourier transform. RESULTS: In both patients we recorded a N20/P30 potential followed by a biphasic N50/P70 response. A little negative response in the 100 ms latency range was the last detectable wide-pass SEP in both patients. Two HFOs components (called iP1 and iP2) were detected by mere visual analysis and spectral analysis, and were supposed to be originated within the parietal cortex. CONCLUSIONS: This was the very first study that recorded wide bandpass and high frequency SEPs by electrodes, exploring both the lateral and the mesial part of the parietal lobe and particularly that of the post-central gyrus.     

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.     

High-frequency oscillations change in parallel with short-interval intracortical inhibition after theta burst magnetic stimulation.

OBJECTIVE: Theta burst transcranial magnetic stimulation (TBS) causes changes in motor cortical excitability. In the present study, somatosensory-evoked potentials (SEPs) and high-frequency oscillations (HFOs) were recorded before and after TBS over the motor cortex to examine how TBS influenced the somatosensory cortex. METHODS: SEPs following electric median nerve stimulation were recorded, and amplitudes for the P14, N20, P25, and N33 components were measured and analyzed. HFOs were separated by 400-800 Hz band-pass filtering, and root-mean-square amplitudes were calculated from onset to offset. SEPs and HFOs were measured before and after application of either intermittent or continuous TBS (iTBS/cTBS; 600 total pulses at 80% active motor threshold) over the motor cortex. Motor-evoked potentials (MEPs) and short-interval intracortical inhibition (SICI) of the first dorsal interosseous muscle were examined before and after TBS. RESULTS: MEPs, SICI, and HFO amplitudes were increased and decreased significantly after iTBS and cTBS, respectively. Wide-band SEPs did not change significantly after TBS. CONCLUSIONS: TBS changed the cortical excitability of the sensorimotor cortices. Changes in HFOs after TBS were parallel to those in SICI. SIGNIFICANCE: The mechanisms of changes in HFOs after TBS may be the same as those in SICI.     

Somatosensory evoked high frequency oscillations recorded from subdural electrodes

OBJECTIVES: To examine high frequency oscillations (HFOs) of somatosensory evoked potentials (SEPs) recorded directly from subdural electrodes to investigate the relationship between the primary somatosensory cortex and HFOs. METHODS: SEPs were recorded directly from subdural electrodes previously implanted in 3 patients for clinical evaluation prior to surgical treatment of intractable epilepsy. RESULTS: The primary sensory cortex (area 3b) was proposed as the source of somatosensory HFOs, because the distribution of HFOs recorded from the subdural electrodes agreed with the distribution of the N20-P20 components of the somatosensory evoked potential. The somatosensory HFOs showed a strictly somatotopic source arrangement. There was a polarity inversion of the prophase component and also the N20-P20 component of HFOs across the central sulcus. However, the phase was synchronized in the latter part of the HFOs. CONCLUSIONS: We propose that the origins of the early and latter parts of HFOs are different, and that there was a clear somatotopy.     

Somatosensory evoked potentials and high-frequency oscillations in athletes

ObjectiveAthletes perform skilled movements during games and daily training. We hypothesized that the cortical representation in athletes differs from that in non-athletes.MethodsSomatosensory evoked potentials (SEPs) and high-frequency oscillations (HFOs) were recorded from seven healthy football players, seven healthy racquet players and seven healthy non-athletes. Electrical stimuli were delivered to the posterior tibial nerves and the median nerves, bilaterally. Cortical and spinal SEPs and sensory nerve action potentials (SNAPs) were recorded. SEPs were recorded by 0.3–3000 Hz filter. HFOs were separated by 400–800 Hz band-pass filtering. SNAPs were recorded by 20–2000 Hz filter.ResultsThe P37–N45 amplitude in football players and the N20–P25 amplitude in racquet players were significantly larger than those in non-athletes. The number of negative peaks of HFOs from the posterior tibial nerve in football players and the HFO amplitudes from the median nerve in racquet players were significantly larger than those in non-athletes. The earlier an individual started playing football, the larger the P37–N45 amplitude. Neither spinal SEPs nor SNAPs differed significantly among the three groups.ConclusionsDaily long-term training brings about plastic excitation in the somatosensory cortex representation of the trained limbs in athletes.SignificancePlastic changes in the somatosensory cortex are induced specifically by physical training.     

Unmasking of presynaptic and postsynaptic high-frequency oscillations in epidural cervical somatosensory evoked potentials during voluntary movement.

OBJECTIVE: To investigate the effect of the voluntary movement on the amplitude of the somatosensory evoked potentials (SEPs) recorded by an epidural electrode at level of the cervical spinal cord (CSC). METHODS: Fourteen patients underwent an epidural electrode implant at CSC level for pain relief. After the median nerve stimulation, SEPs were recorded from the epidural electrode and from 4 surface electrodes (in frontal and parietal regions contralateral to the stimulated side, over the 6th cervical vertebra, and on the Erb's point). SEPs were recorded at rest and during a voluntary flexo-extension movement of the stimulated wrist. Beyond the low-frequency SEPs, also the high-frequency oscillations (HFOs) were analysed. RESULTS: The epidural electrode contacts recorded a triphasic potential (P1-N1-P2), whose negative peak showed the same latency as the cervical N13 response. The epidural potential amplitude was significantly decreased during the voluntary movement, as compared to the rest. Two main HFOs were identifiable: (1) the 1200 Hz HFO which was significantly lower in amplitude during movement than at rest, and (2) the 500 Hz HFO which was not modified by the voluntary movement. CONCLUSIONS: The low-frequency cervical SEP component is subtended by HFOs probably generated by: (1) postsynaptic potentials in the dorsal horn neurones (1200 Hz), and (2) presynaptic ascending somatosensory inputs (500 Hz). SIGNIFICANCE: Our findings show that the voluntary movement may affect the somatosensory input processing also at CSC level.     

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.     

Evoked potentials in a man with a complete large myelinated fibre sensory neuropathy below the neck.

Cortical somatosensory evoked potentials (SEPs) were recorded from a man with a severe neuropathy without touch and proprioception below the neck. Peripheral neurophysiological tests showed a complete large myelinated fibre sensory neuropathy. Sensory threshold to electrical stimulation of the median nerve was 15 mA (normal 2-4 mA). With a stimulus of 39 mA, duration 400 microsecons, applied at the wrist a cortical SEP was recorded with a latency of 84 msec, giving a propagation velocity of 11.9 m/sec. At stimulation rates of above 3.3 Hz the SEP was absent. It is concluded that the SEPs recorded were conducted along A delta peripheral fibres.     

Contribution of different somatosensory afferent input to subcortical somatosensory evoked potentials in humans

ObjectivesTo investigate the subcortical somatosensory evoked potentials (SEPs) to electrical stimulation of either muscle or cutaneous afferents.MethodsSEPs were recorded in 6 patients suffering from Parkinson’s disease (PD) who underwent electrode implantation in the pedunculopontine (PPTg) nucleus area. We compared SEPs recorded from the scalp and from the intracranial electrode contacts to electrical stimuli applied to: 1) median nerve at the wrist, 2) abductor pollicis brevis motor point, and 3) distal phalanx of the thumb. Also the high-frequency oscillations (HFOs) were analysed.ResultsAfter median nerve and pure cutaneous (distant phalanx of the thumb) stimulation, a P1-N1 complex was recorded by the intracranial lead, while the scalp electrodes recorded the short-latency far-field responses (P14 and N18). On the contrary, motor point stimulation did not evoke any low-frequency component in the PPTg traces, nor the N18 potential on the scalp. HFOs were recorded to stimulation of all modalities by the PPTg electrode contacts.ConclusionsStimulus processing within the cuneate nucleus depends on modality, since only the cutaneous input activates the complex intranuclear network possibly generating the scalp N18 potential.SignificanceOur results shed light on the subcortical processing of the somatosensory input of different modalities.     

Influence of cholinergic circuitries in generation of high-frequency somatosensory evoked potentials.

OBJECTIVE: High-frequency oscillations (HFOs) evoked by upper limb stimulation reflect highly synchronised spikes generated in the somatosensory human system. Since acetylcholine produces differential modulation in subgroups of neurons, we would determine whether cholinergic drive influences HFOs. METHODS: We recorded somatosensory evoked potentials (SEPs) from 31 scalp electrodes in 7 healthy volunteers, before and after single administration of rivastigmine, an inhibitor of central acetylcholinesterase. Right median nerve SEPs have been analysed after digital narrow bandpass filtering (500-700 Hz). Raw data were further submitted to Brain Electrical Source analysis (BESA) to evaluate the respective contribution of lemniscal, thalamic and cortical sources. Lastly, we analysed by Fast Fourier transform spectral changes after drug administration in the 10-30 ms latency range. RESULTS: Rivastigmine administration caused a significant increase of HFOs in the 18-28 ms latency range. Wavelets occurring before the onset latency of the conventional N20 SEP did not show any significant change. A similar increase concerned the strength of cortical dipolar sources in our BESA model. Lastly, we found a significant power increase of the frequency peak at about 600 Hz in P3-F3 traces after drug intake. CONCLUSIONS: Our findings demonstrate that the cortical component of HFOs is significantly enhanced by cholinergic activation. Pyramidal chattering cells, which are capable to discharge high-frequency bursts, are mainly modulated by cholinergic inputs; by contrast, acetylcholine does not modify the firing rate of fast-spiking GABAergic interneurons. We thus discuss the hypothesis that cortical HFOs are mainly generated by specialised pyramidal cells.     

Somatosensory evoked high-frequency oscillations recorded directly from the human cerebral cortex.

OBJECTIVE: To elucidate the generator sources of high-frequency oscillations of somatosensory evoked potentials (SEPs), we recorded somatosensory evoked high-frequency oscillations directly from the human cerebral cortex. SUBJECTS AND METHODS: Seven patients, 6 with intractable partial epilepsy and one with a brain tumor, were studied. With chronically implanted subdural electrodes, we recorded SEPs to median nerve stimulation in all patients, and also recorded SEPs to lip and posterior tibial nerve stimulation in one. High-frequency oscillations were recorded using a restricted bandpass filter (500-2000 Hz). RESULTS: For the median nerve oscillations, all oscillation potentials were maximum at the electrodes closest to the primary hand sensorimotor area. Most oscillations were distributed similar to or more diffusely than P20/N20. Some later oscillations after the peak of P20 or N20 were present in a very restricted cortical area similar to P25. We investigated the phase change of each oscillation potential around the central sulcus. One-third of the oscillations showed phase reversal around the central sulcus, while later oscillations elicited in a restricted cortical area did not. High-frequency oscillations to posterior tibial nerve and lip stimulation were also maximum in the sensorimotor areas. Most of the lip oscillations showed phase reversal around the central sulcus, but most of the posterior tibial nerve oscillations did not. CONCLUSION: High-frequency oscillations are generated near the primary sensorimotor area. There are at least two different generator mechanisms for the median nerve high-frequency oscillations. We suspect that most oscillations are derived from the terminal segments of thalamocortical radiations or from the primary sensorimotor cortex close to the generator of P20/N20, and some later oscillations from the superficial cortex close to the generator of P25.     

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.     

Movement interference attenuates somatosensory high-frequency oscillations: contribution of local axon collaterals of 3b pyramidal neurons.

OBJECTIVES: We examined the effects of movement interference on high-frequency oscillations (HFOs) and N20m in 10 healthy subjects.METHODS: For the movement interference condition, somatosensory evoked magnetic fields (SEFs) following electric median nerve stimulation were recorded during voluntary movement of the digits. For the control condition, the SEFs were recorded without interference. The N20m and HFOs were separated by 3-300Hz and 300-900Hz bandpass filtering. Then, the peak-to-peak amplitudes were measured.RESULTS: Both interference/control amplitude ratios for the N20m and HFOs were smaller than 100%. In contrast, the HFO/N20m amplitude index, which was calculated by dividing the interference/control amplitude ratio for the HFOs with that for the N20m, was significantly greater in the movement interference condition than in the control condition.CONCLUSIONS: Although the overall amplitude of the HFOs was decreased by movement, enhancement of the HFOs by the movement was revealed by the HFO/N20m amplitude index. Thus, we suggest that the HFOs represent activity of the inhibitory interneurons excited by both thalamocortical afferent impulses and excitatory synaptic inputs from pyramidal neurons in area 3b through their local axon collaterals, thereby reflecting both feed-forward and feedback inhibitory effects onto the post-synaptic pyramidal neurons.     

Origins of the somatic N20 and high-frequency oscillations evoked by trigeminal stimulation in the piglets.

OBJECTIVE: In humans, the somatic evoked potentials (SEPs) and magnetic fields (SEFs) elicited by peripheral nerve stimulation contain high-frequency oscillations (HFOs) around 600 Hz superimposed on the initial cortical response N20. Responses elicited by snout stimulation in the swine also contain similar HFOs during the rising phase of the porcine N20. This study examined the generators of the N20 and HFOs in the swine. METHODS: We recorded intracortical SEPs and multi-unit activities in the sulcal area of the primary somatosensory cortex (SI) simultaneously with SEFs. The laminar profiles of the potential and current-source-density (CSD) were analyzed. RESULTS: The CSD analysis revealed that the N20 was produced by two dipolar generators, both directed toward the cortical surface. After the arrival of the initial thalamocortical volley in layer IV, the sink of the first generator shifted toward shallower layers II-III with a velocity of 0.109+/-0.038 m/s (mean+/-SD). The sink of the second generator moved to layer V. The initial thalamocortical axonal component of the HFO was produced by repolarizing current with the sink in layer IV. The CSD laminar profile of the postsynaptic component was very similar to the profile of intracortical N20. The current sink within each cycle of HFO propagated upward with a velocity of 0.633+/-0.189 m/s, indicating backpropagation. CONCLUSIONS: We propose that the N20 is generated by two sets of excitatory neurons which also produce the HFOs. Although the loci of synaptic inputs are unknown, these neurons appear to fire initially in the soma and produce backpropagating spikes toward distal apical dendrites. SIGNIFICANCE: These conclusions relate the N20 to the HFO and provide a new explanation of how the current underlying the N20 is invariantly directed toward superficial layers across species.     

High-frequency magnetic oscillations evoked by posterior tibial nerve stimulation

Magnetocephalographic recordings of the primary somatosensory response (P37m) and high-frequency oscillations (HFOs) evoked by posterior tibial nerve stimulation were obtained in normal subjects. Electrical stimuli were delivered to the posterior tibial nerve and magnetic recordings were taken over the superior aspect of the left hemisphere with a 37-channel biomagnetometer. In order to separate the high-frequency oscillations from the underlying P37m, the wide-band (0.1-1200 Hz) recorded responses were digitally filtered with a 500-800 Hz band-pass filter. The localization of the HFOs were estimated to be in somatosensory area 3b, very close to the P37m source. Our data suggest that the HFOs are somatotopically arranged in the primary somatosensory cortex, and are a ubiquitous phenomenon of the primary somatosensory cortex.     

Different origins of low- and high-frequency components (600 Hz) of human somatosensory evoked potentials.

OBJECTIVE: Human median nerve somatosensory evoked potentials (SEPs) contain a low-amplitude (<500 nV) high-frequency (approximately 600 Hz) burst of repetitive wavelets (HFOs) which are superimposed onto the primary cortical response 'N20.' This study aimed to further clarify the cortical and subcortical structures involved in the generation of the HFOs. METHODS: 128-Channel recordings were obtained to right median nerve stimulation of 10 right-handed healthy human subjects and in 7 of them additional to right ulnar nerve. Data were evaluated by applying principal component analysis and dipole source analysis. RESULTS: Different source evaluation strategies provided converging evidence for a cortical HFO origin, with two different almost orthogonally oriented generators being active in parallel, but with a phase shift of a quarter of their oscillatory period, while the low-frequency 'N20' is adequately modeled by one tangential dipole source. Median and ulnar derived low-frequency and HFO cortical sources show a somatotopic order. Additionally, generation of the HFOs was localized in subcortical, near-thalamic and subthalamic source sites. The near-thalamic dipole was located at significantly different sites in HFO and low-frequency data. CONCLUSIONS: The cortical HFO source constellation points to a 'precortical' source in terminals of thalamocortical fibers and a second intracortical HFO origin. Furthermore, HFOs are also generated at subcortical and even subthalamic sites. Near-thalamic, the HFO and low-frequency signals are generated or modulated by different neuron populations involved in the thalamocortical outflow.     

Transcranial direct current stimulation applied over the somatosensory cortex - differential effect on low and high frequency SEPs.

OBJECTIVE: Transcranial direct current stimulation (tDCS) has an influence on the excitability of the human motor cortex measured by motor evoked potentials (MEPs) after transcranial magnetic stimulation. Low and high frequency (HFOs) components of somatosensory evoked potentials (SEPs) were studied questioning whether a comparable effect can be observed after applying tDCS to the human somatosensory cortex. METHODS: Multichannel median nerve SEPs were recorded before and after applying tDCS of 1mA over a period of 9min with the cathode placed over the somatosensory cortex and the anode over the contralateral forehead and vice versa in a second session. The source activity of the N20, N30 and HFOs was evaluated before and after application of tDCS. RESULTS: After cathodal tDCS to the somatosensory cortex we found a significant reduction of the N20 source amplitude while there was no effect after anodal stimulation. For the N30 component and HFOs no change in source activity was observed. CONCLUSIONS: Corresponding to the results for the motor cortex a sustained reduction of the excitability of the somatosensory cortex after cathodal tDCS was shown. SIGNIFICANCE: We demonstrated differential effects of tDCS on the high and low frequency components of SEPs confirming the hypothesis of locally and functionally distinct generators of these two components.