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Objective: To investigate whether recording from deep intracerebral (IC) electrodes can disclose laser evoked potential (LEP) components generated under the cerebral cortex., Methods: LEPs were recorded to hand and/or perioral region stimulation from 7 patients suffering from Parkinson's disease, who underwent implant of IC electrodes in the globus pallidum pars interna (GPi), in the subthalamic nucleus (STN) and in the pedunculopontine nucleus (PPN). LEPs were obtained from the IC electrode contacts and from the Cz vertex, referred to the nose., Results: The scalp traces showed a triphasic response (P1-N2-P2). The IC electrodes recorded two main components (ICP2 and ICN2), showing the same latencies as the scalp N2 and P2 potentials, respectively. The ICP2-ICN2 complex was sometimes preceded by a ICP1 wave at the same latency of the scalp P1 response., Conclusions: The LEP components recorded from the IC electrodes mirrored the ones picked up from the Cz lead, thus suggesting that they are probably generated by the opposite pole of the same cortical sources producing the scalp responses., Significance: In the IC traces, there was no evidence of earlier potentials possibly generated within the thalamus or of subcortical far-field responses. This means that the nociceptive signal amplification occurring within the cerebral cortex is necessary to produce identifiable LEP components.

Since a number of patients with Parkinson's Disease (PD) complain of painful sensations, we studied whether the central processing of nociceptive inputs is abnormal in PD. To test this hypothesis, we recorded scalp CO(2) laser evoked potentials (LEPs) to hand skin stimulation in 18 pain-free PD patients with unilateral bradykinetic-rigid syndrome (hemiparkinson) during the off state and in 18 healthy subjects. This technique allows us to explore non-invasively the functional status of some cerebral structures involved in nociceptive input processing. In both PD patients and control subjects, CO(2) laser stimulation gave rise to a main negative N2 potential followed by a positive P2 response at vertex peaking at a latency of about 200 and 300ms, respectively. These potentials are thought to originate from several brain structures devoted to nociceptive input processing, including the cingulate gyrus and insula. PD patients and normal subjects showed comparable N2 and P2 latencies, whereas the N2/P2 peak-to-peak amplitude was significantly lower in PD patients (regardless of the clinically affected body side) than in controls. LEPs were even recorded after acute L-dopa administration in 7 additional PD patients. L-dopa administration yielded no significant change in N2/P2 amplitude as compared to the off state. These results suggest an abnormal nociceptive input processing in pain-free PD patients which appears to be independent of clinical expression of parkinsonian motor signs and is not affected by dopaminergic stimulation.

It is well known that scalp potentials evoked by nonpainful visual and auditory stimuli are enhanced in amplitude when preceded by pre-stimulus low-amplitude alpha rhythms. This study tested the hypothesis that the same holds for the amplitude of vertex N2-P2 potentials evoked by brief noxious laser stimuli, an issue of interest for clinical perspective. EEG data were recorded in 10 subjects from 30 electrodes during laser noxious stimulation. The artifact-free vertex N2-P2 complex was spatially enhanced by surface Laplacian transformation. Pre-stimulus alpha power was computed at three alpha sub-bands according to subject's individual alpha frequency peak (i.e. about 6-8Hz for alpha 1, 8-10Hz for alpha 2 and 10-12Hz for alpha 3 sub-band). Individual EEG single trials were divided in two sub-groups. The strong-alpha sub-group (high band power) included halfway of all EEG single trials, namely those having the highest pre-stimulus alpha power. Weak-alpha sub-group (low band power) included the remaining trials. Averaging procedure provided laser evoked potentials for both trial sub-groups. No significant effect was found for alpha 1 and alpha 2 sub-bands. Conversely, compared to strong-alpha 3 sub-group, weak-alpha 3 sub-group showed vertex N2-P2 potentials having significantly higher amplitude (p<0.05). These results extend to the later phases of pain processing systems the notion that generation mechanisms of pre-stimulus alpha rhythms and (laser) evoked potentials are intrinsically related and subjected to fluctuating "noise". That "noise" could explain the trial-by-trial variability of laser evoked potentials and perception.

Our study aimed at investigating the nociceptive contribution to the somatosensory evoked potentials after electrical intramuscular stimulation (mSEPs) at painful intensity. Scalp mSEPs were recorded in 10 healthy subjects after electrical stimulation of the left brachioradialis muscle at three intensities: non-painful (I2), slightly painful (I4) and moderately painful (I6). For each intensity, mSEPs were recorded in a neutral condition (NC) in which subjects did not have any task, and in an attention condition (AC) in which subjects were asked to count the number of stimuli. In both NC and AC, the N120 and P220 amplitudes were significantly higher at I6 than at I2. While the N120 amplitude did not vary between NC and AC, the P220 amplitude was significantly higher in AC than in NC at all stimulus intensities. Our results suggest that nociceptive inputs contribute to the N120 amplitude increase at painful stimulus intensity, while the P220 amplitude is more sensitive to changes of subjects' attention level. Therefore, the N120 amplitude increase to moderately painful stimuli, as compared to non-painful stimuli, may represent a marker of the activation of the muscular thin myelinated afferents.

The oesophagus, stomach, duodenum and sigmoid colon were electrically stimulated in 12 healthy volunteers with a thin nasal endoscope. The painful cortical evoked potentials (EPs) were recorded from 64 surface electrodes. The early EPs with latencies < 200 ms were studied and the corresponding dipole sources were calculated. The electrical current intensities needed to evoke pain were highest in the stomach and duodenum, compared to the other segments (F = 7.8; P < 0.001; post hoc analysis P < 0.05). The EP latencies after stimulation of the stomach and sigmoid colon were shorter compared with those to stimulation of the oesophagus and duodenum (all P values < 0.001). The EP amplitudes were higher to oesophagus stimulation (all P values < 0.001 except for the early positivity). The potential fields obtained after stimulation of the most distal segments (duodenum and sigmoid colon) were in general distributed more posteriorly compared to those recorded in the more proximal regions. The EP topographies to stimulation of all gut tracts were explained by a bilateral source in the second somatosensory (SII) area, by a dipole in the anterior cingulate cortex (ACC), and by a bilateral generator in the insular cortex. However, the position of the sources significantly changed depending on the stimulated gut tract. Moreover, while the SII and ACC sources were initially activated to oesophagus and stomach stimulation, the ACC and insular activities were the earliest ones after stimulation of the lower gut segments. The findings reflect differences in pathways and brain processing of visceral nociceptive inputs coming from either upper or lower gut and may improve our understanding of the brain-gut axis in health and disease.

Objectives: Our study aimed at investigating the effect of repetitive recordings on somatosensory evoked potentials (SEPs) related to spatial attention in a population of healthy elderly subjects., Methods: Fifteen healthy elderly subjects were tested for six consecutive days using a somatosensory oddball paradigm, in which target stimuli were applied above the elbow and the non-target stimuli on the ipsilateral shoulder. Brain electrical activity was recorded from six scalp electrodes (Fz, Cz, F3, F4, T3 and T4)., Results: The N140 response to target stimuli showed a significantly decreased amplitude across the sessions with the lowest value during the fourth day of recording and with a partial recovery at the sixth day. On the contrary, the amplitude of the N140 response to non-target stimuli and that of the P300 potential to target stimuli were not significantly modified., Conclusions: The significant amplitude reduction of the N140 potential in target, but not in non-target recordings across sessions, suggests that the voluntarily oriented attention is reduced by stimulus repetition, while the automatic attention is not.

The aim of the study was to evaluate the effect of tonic pain evoked by topical application of capsaicin on the somatosensory sensation of warmth. The warmth pathways were studied in ten healthy subjects by recording the scalp potentials evoked by non-painful warm laser stimuli delivered on both the right and left perioral region (warmth C-fiber related laser-evoked potentials (C-LEPs)). Tonic pain was induced by topical capsaicin application above the lateral part of the right upper lip. The area of primary and secondary hyperalgesia were mapped. C-LEPs were obtained from 31 scalp electrodes before, during, and after capsaicin application. C-LEPs from the right perioral region were evoked by laser stimuli delivered to the area of secondary hyperalgesia during capsaicin application and on both the areas of primary and secondary hyperalgesia after capsaicin removal. While the lateralized N1/P1 component (around 185 ms of latency) was not affected by the capsaicin, the amplitudes of the later vertex C-LEPs (around 260 and 410 ms of latency for the N2a and P2 potentials, respectively) evoked from the secondary hyperalgesic area on the right side and from a symmetrical non-hyperalgesic area on the left perioral region were significantly decreased during capsaicin application and after capsaicin removal, as compared with the baseline recordings. At the same times, the rating of the laser-evoked warmth sensation was reduced significantly. This inhibitory effect can occur at brainstem level and is possibly due to: 1) trigemino-cortico-trigeminal circuits, similar to those mediating the classical diffuse noxious inhibitory control, or 2) an increased background activity of the capsaicin-insensitive A-fibers, which mediate the secondary hyperalgesia. Probably due to a peripheral inhibitory mechanism, neither reliable C-LEP components nor warmth sensation were evoked by laser pulses delivered to the primary hyperalgesic area. This is the first neurophysiological evidence in humans of an inhibitory effect of pain on warmth sensation.

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.

Objective: To investigate the possible contribution of the primary somatosensory area (SI) to pain sensation., Methods: Depth recordings of CO2 laser evoked potentials (LEPs) and somatosensory evoked potentials (SEPs) were performed in an epileptic patient with a stereotactically implanted electrode (Talairach coordinates y=-23, z=40) that passed about 10 mm below the hand representation in her left SI area, as assessed by the source of the N20 SEP component., Results: The intracerebral electrode was able to record the N20 SEP component after non-painful electrical stimulation of her right median nerve. The N20 potential showed a phase reversal in the bipolar montage (at about 31 mm from the midline), which confirms that the electrode was located near its generator in area 3b. In contrast, no reliable response was recorded from the SI electrode after painful CO2 laser stimulation of the right hand. An N2-P2 response was evoked at the vertex electrode (Cz), thus demonstrating the effectiveness of the delivered CO2 laser stimuli., Conclusions: Since the N20 SEP component originates from the anterior bank of the post-central gyrus (area 3b), our result suggests that this part of SI does not participate in LEP generation. In fact, the previously published LEP sources in the SI area estimated from scalp recordings are about 10-17 mm posterior of the electrode in our patient, suggesting that they are more likely located in area 1, 2 or posterior parietal cortex.

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.

The study aim was to evaluate the effect of different attentional tasks on the amplitudes and latencies of painful and non-painful contact heat evoked potentials (CHEPs). CHEPs were recorded in 12 healthy subjects during two experimental conditions, in which attention was oriented towards the intensity and the distress caused by the stimuli and were compared with CHEPs recorded during a neutral condition. The painful heat stimulation produced a negative potential at Cz vertex with a latency around 540 ms (Cz/N540), a positive peak at Cz electrode around 730 ms (Cz/P730) and, lastly, a positive peak around 1000 ms (Pz/P1000) in the Pz traces. The Cz/P730 wave was significantly higher in amplitude only during the painful stimulation and is probably related to coding the nociceptive activity. Varying the attentional target towards different properties of the stimulus did not cause any significant change in CHEP responses amplitude and latencies compared with the neutral condition. Our results suggest that CHEPs represent a reliable functional measure of the nociceptive pathways and that they are generated by the activation of different cerebral areas involved in pain processing. The high activation level of each of these area or their spatial neighbouring might explain the strong similarity of CHEP components recorded during different attentional manipulations.

Our study aimed at investigating the scalp topography of ultra-late CO(2) laser evoked potentials (LEPs), which are related to C fiber activation, and at exploring the effect of attention deviation on ultra-late LEPs. Brain responses to non-painful CO(2) laser stimuli were recorded in ten healthy subjects in three different conditions: (i) neutral condition in which subjects did not have any task; (ii) distraction condition in which subjects were asked to perform a mathematical task; and (iii) attention condition in which subjects had to count the number of stimuli. In all subjects, also A fiber-related late LEPs were recorded after painful CO(2) laser stimulation. The ultra-late LEPs in attention condition included an earlier negative potential (ultra-late N1) in the contralateral temporal region and a simultaneous frontal positive response (ultra-late P1). Later, a vertex biphasic component (ultra-late N2a and ultra-late P2) was identifiable. The vertex ultra-late LEP amplitude was significantly decreased in both neutral and distraction condition. Ultra-late LEPs showed a longer latency than late LEPs, but the scalp distributions of both ultra-late and late LEPs were very similar, thus suggesting that the same cerebral areas may be involved in their generation. Since attention deviations have a strong effect on ultra-late LEP amplitude, the subject's attention should be addressed to CO(2) laser stimuli when ultra-late LEPs are used for clinical purposes.

To elucidate whether the selective electrical stimulation of muscle as well as cutaneous afferents evokes modality-specific responses in somatosensory evoked potentials (SEPs) recorded on the scalp of humans, we compared scalp SEPs to electrical stimuli applied to the median nerve and to the abductor pollicis brevis (APB) motor point. In three subjects, we also recorded SEPs after stimulation of the distal phalanx of the thumb, which selectively involved cutaneous afferents. Motor point and median nerve SEPs showed the same scalp distribution; moreover, very similar dipole models, showing the same dipolar time courses, explained well the SEPs after both types of stimulation. Since the non-natural stimulation of muscle afferents evokes responses also in areas specifically devoted to cutaneous input processing, it is conceivable that, in physiological conditions, muscle afferents are differentially gated in somatosensory cortex. The frontocentral N30 response was absent after purely cutaneous stimulation; by contrast, it was relatively more represented in motor point rather than in mixed nerve SEPs. These data suggest that the N30 response is specifically evoked by proprioceptive inputs., (Copyright 2002 Wiley Periodicals, Inc.)

Contact heat evoked potentials (CHEPs) were collected in 12 healthy subjects by stimulating the forearm skin with a couple of thermodes at a painful intensity. The stimulated area was 628 mm(2) and the repetition rate was 0.1 Hz. The electroencephalogram was recorded by 31 electrodes placed on the scalp according to an extended 10-20 System. A dipolar model explaining the scalp CHEP distribution was built by using the brain electrical source analysis. The model includes two dipoles located bilaterally in the perisylvian region, one dipole in the deep midline region and two dipoles located bilaterally in the deep temporal lobe. This dipolar model is very similar to that previously described to explain the topography of evoked potentials to radiant heat stimulation by laser pulses. Since laser stimuli activate the nociceptive fibres, the strong similarity of the cerebral dipoles activated by contact heat stimuli and by laser pulses suggests that only nociceptive inputs are involved in the scalp painful CHEP building. Therefore, CHEP recording can be useful for clinical examination of the nociceptive system.