Pain-related somatosensory evoked potentials following CO2 laser stimulation of foot in man

Since our previous study of pain somatosensory evoked potentials (SEPs) following CO₂ laser stimulation of the hand dorsum could not clarify whether the early cortical component NI was generated from the primary somatosensory cortex (SI) or the secondary somatosensory cortex (SII) or both, the scalp topography of SEPs following CO₂ laser stimulation of the foot dorsum was studied in 10 normal subjects and was compared with that of the hand pain SEPs and the conventional SEPs following electrical stimulation of the posterior tibial nerve recorded in 8 and 6 of the 10 subjects, respectively. Three components (N1, N2 and P2) were recorded for both foot and hand pain SEPs. N1 of the foot pain SEPs was maximal at the midline electrodes (Cz or CPz) in all data where that potential was recognized, but the potential field distribution was variable among subjects and even between two sides within the same subject. N1 of the hand pain SEPs was maximal at the contralateral central or midtemporal electrode. The scalp distribution of N2 and P2, however, was not different between the foot and hand pain SEPs. The mean peak latency of N1 following stimulation of foot and hand was found to be 191 msec and 150 msec, respectively, but there was no significant difference in the interpeak latency of Nl-N2 between foot and hand stimulation. It is therefore concluded that NI of the foot pain SEPs is generated mainly from the foot area of SI. The variable scalp distribution of the N7 component of the foot pain SEPs is likely due to an anatomical variability among subjects and even between sides.     

Somatotopy of human hand somatosensory cortex revealed by dipole source analysis of early somatosensory evoked potentials and 3D-NMR tomography

Somatosensory evoked potentials (SEPs) to median nerve and finger stimulation were analyzed by means of spatio-temporal dipole modelling combined with 3D-NMR tomography in 8 normal subjects. The early SEPs were modelled by 3 equivalent dipoles located in the region of the brain-stem (B) and in the region of the contralateral somatosensory cortex (T and R). Dipole B explained peaks P14 and N18 at the scalp. Dipole T was tangentially oriented and explained the N20-P20, dipole R was radially oriented and modelled the P22. The tangential dipole sources T were located within a distance of 6 mm on the average and all were less than 9 mm from the posterior bank of the central sulcus. In 6 subjects the tangential sources related to finger stimulation arranged along the central sulcus according to the known somatotopy. The radial sources did not show a consistent somatotopic alignment across subjects. We conclude that the combination of dipole source analysis and 3D-NMR tomography is a useful tool for functional localization within the human hand somatosensory cortex.     

Glossopharyngeal evoked potentials in normal subjects following mechanical stimulation of the anterior faucial pillar

The anterior faucial pillar, which is innervated by the glossopharyngeal nerve, is thought to be important in eliciting the pharyngeal swallow in awake humans. Glossopharyngeal evoked potentials (GPEP), elicited by mechanically stimulating this structure, were recorded from 30 normal adults using standard averaging techniques and a recording montage of 16 scalp electrodes. Ten of the subjects experienced a desire to swallow in response to stimulation. Repeatable responses were recorded from all 30 subjects. The GPEPs recorded from the posterior scalp were W-shaped and consisted of P1, N1, P2, N2 and P3 peaks. Mean latencies of P1, N1 and P2 were 11, 16 and 22 msec, respectively, for both left and right pillar stimulation. In contrast, latencies of N2 and P3 varied significantly between left and right pillar stimulation. Mean latencies of N2 and P3 were 27 and 34 msec for left, and 29 and 35 msec for right pillar stimulation. Topographical maps acquired at peak latencies for P1, N1 and P2 revealed consistent asymmetrical voltage distributions between the two hemispheres; the largest responses were recorded from the hemisphere ipsilateral to the side of stimulation. The scalp topography of N2 and P3 varied between male and female subjects as well as between left and right pillar stimulation. These findings support the hypothesis that mechanical stimulation to the anterior faucial pillar alone can elicit repeatable responses from the central nervous system. The integration of this subcortical/cortical activity with that of the medullary swallowing center may play an important role in eliciting the pharyngeal swallow.     

Topography of middle-latency somatosensory evoked potentials following painful laser stimuli and non-painful electrical stimuli

The aim of this study was to compare cerebral evoked potentials following selective activation of Aβ and Aδ fibers. In 15 healthy subjects, Aβ fibers were activated by electrical stimulation of the left radial nerve at the wrist. Aδ fibers were activated by short painful radian heat pulses, applied to the dorsum of the left hand by a CO₂ laser. Evoked potentials were recorded with 15–27 scalp electrodes, evenly distributed over both hemispheres (bandpass 0.5–200 Hz). The laser-evoked potentials exhibited a component with a mean peak latency of 176 msec (N170). Its scalp topography showed a parieto-temporal maximum contralateral to the stimulus side. In contrast, the subsequent vertex negativity (N240), which appeared about 60 msec later, had a symmetrical scalp distribution. Electrically evoked potentials showed a component at 110 msec (N110), that had a topography similar to the laser-evoked N170. The topographies of the N170 and N110 suggest that they may both be generated in the secondary somatosensory cortex. There was no component in the electrically evoked potential that had a comparable interpeak latency to the following vertex potential: for N60 it was longer, for N110 it was shorter. On the other hand, in the laser-evoked potentials no component could be identified the topography of which corresponded to the primary cortical component N20 following electrical stimulation.     

Giant central N20-P22 with normal area 3b N20-P20: an argument in favour of an area 3a generator of early median nerve cortical SEPs?

Generators of early cortical somatosensory evoked potentials (SEPs) still remain to be precisely localised. This gap in knowledge has often resulted in unclear and contrasting SEPs localisation in patients with focal hemispheric lesions. We recorded SEPs to median nerve stimulation in a patient with right frontal astrocytoma, using a 19-channel recording technique. After stimulation of the left median nerve, N20 amplitude was normal when recorded by the parietal electrode contralateral to the stimulation, while it was abnormally enhanced in traces obtained by the contralateral central electrode. The amplitude of the frontal P20 response was within normal limits. This finding suggests that two dipolar sources, tangential and radial to the scalp surface, respectively, contribute concomitantly to N20 generation. The possible location of the N20 radial source in area 3a is discussed. The P22 potential was also recorded with increased amplitude by the central electrode contralateral to the stimulation, while N30 amplitude was normal in frontal and central traces. We propose that the radial dipolar source of P22 response is independent from both N20 and N30 generators and can be located either in 3a or in area 4. This report illustrates the usefulness of multichannel recordings in diagnosing dysfunction of the sensorimotor cortex in focal cortical lesions.     

Unmasking of cortical SEP components by changes in stimulus rate: a topographic study

We performed topographic mapping of somatosensory responses to median nerve stimulation delivered at 2, 5 and 10 Hz. Parietal N20 was significantly attenuated in 10 Hz somatosensory evoked potentials (SEPs), while central P22 diminished between 2 and 5 Hz, remaining stable thereafter. The single component most affected by increasing stimulus rate was N30, which abated by more than 50% in 10 Hz SEPs, as compared with basal responses. N30 attenuation disclosed the existence of an earlier negative component, N24, which appeared as a notch on the N30 ascending slope in 2 Hz SEPs, but became a well-defined peak at higher stimulus rates. The N24 negativity was not significantly modified by stimulus rate; it had a parietal counterpart (P24) with the same peak latency and identical behavior during the experimental procedure. Both P24 and N24 could be differentiated from central P22 on the basis of topographical distribution and response to stimulus frequency. P22 topography could be the result of a radially oriented generator, while P24/N24 appeared as the two poles of a neural source tangential to the scalp. P27 was seen in 40% of the subjects only; it is suggested that P27 is itself a composite potential to which the generator of N30 could contribute in part. We conclude that there is no single “optimal” stimulation rate for SEP recording. On the contrary, combination of different frequencies of stimulation should enhance the diagnostic utility of this technique by allowing a more selective assessment of overlapping activities.     

Frontal distribution of early cortical somatosensory evoked potentials to median nerve stimulation

The topography of early frontal SEPs (P20 and N26) to left median nerve stimulation was studied in 30 normal subjects and 3 patients with the left frontal bone defect. The amplitudes of P20 and N26 were maximum at the frontal electrode (F4) contralateral to the stimulation and markedly decreased at frontal electrodes ipsilateral to the site of stimulation. There was, however, no latency difference of P20 and N26 between ipsilateral and contralateral frontal electrodes. These results suggest that the origin of the ipsilateral and contralateral P20 and N26 is the same. The wide distribution of P20 and N26 over both frontal areas could be explained by assuming a smearing effect from generators actually located in the rolandic fissure and motor cortex.     

Short latency somatosensory evoked potentials recorded around the human upper brain-stem

We analyzed the intracranial spatiotermporal distributions of the N18 component of short median nerve somatosensosry evoked potentials (SSEPs) in 3 patients with epilepsy. In these patients, depth electrodes were implanted bilaterally into the frontal and temporal lobes, with targets including the amygdala and hippocampus; the latter two targets are close to the upper pons and midbrain.In this study N18 was divided into the initial negative peak (N18a) and the following prolonged negativity (N18b). Mapping around the upper pons and midbrain showed that: (1) the amplitude of the first negativity, which coincided with scalp N18a, was larger contralateral to the side of stimulation, but showed no polarity change around the upper brain-stem; and (2) the second negativity, which was similar to scalp N18b, did show an amplitude difference or a polarity change. This wave appeared to reflect a positive-negative dipole directed in a dorso-ventral as well as dorso-lateral direction from the midbrain, where positivity arises from the dorsum of the midbrain, contralateral to the side of the stimulation.Recordings from depth electrode derivations oriented in a caudo-rostral direction suggest that N18a and N18b may in part reflect neural activity originating from the upper pons to midbrain region which projects to the rostral subcortical white matter of the frontal lobe as stationary peaks.     

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

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

SEPs in two patients with localized lesions of the postcentral gyrus

Scalp distributions of median nerve SEPs were studied in normal controls and 2 patients with localized lesions of the postcentral gyrus. In controls, parieto-occipital electrodes registered N20-P27 while frontal electrodes registered P20-N27. Other small components, parieto-occipital P22 and frontal N22, were recognized in about half of the control records. The wave forms at a frontal and a parieto-occipital electrode, both distant from the central region, formed exact mirror images of each other concerning N20-(P22)-P27 and P20-(N22)-N27. Electrodes near the central region contralateral to the stimulation registered cP22-cN30 (central P22 and central N30). When the postcentral gyrus was damaged, N20/P20-P27/N27 and cP22-cN30 were eliminated and the only remaining components were a frontal negative wave (frN) and a contralateral parieto-occipital positive wave (poP). Digital nerve stimulation also evoked poP and frN in both cases. In case 2, poP coincided with P22 of the non-affected side. The following generators were proposed; N20/P20-P27/N27: area 3b, cP22-cN30: areas 1 and 2, poP/early frN (= P22/N22): area 4 at the anterior wall of the central sulcus (due to direct thalamic inputs to motor cortex), late frN: uncertain (SMA?, SII?).     

Early deflections of cerebral magnetic responses to median nerve stimulation

We have recorded early components of somatosensory evoked magnetic fields with a sensitive 7-channel first-order gradiometer using a wide recording passband (0.05–2000 Hz) and high sampling frequency (8000 Hz). The left median nerve was stimulated at the wrist and responses were recorded over the right hemisphere. The responses typically consisted of a N20m peaking at 18–20 msec, a small P22m peaking at 21–23 msec and a P27m peaking at 29–31 msec. The topography of N20m could be explained by a tangential current dipole in the posterior wall of the central sulcus (probably in area 3b). The equivalent dipoles of P27m were located on average 10 mm antero-medially to the sources of N20m. This suggests that P27m may get a contribution from the anterior wall of the central sulcus. An increase of stimulus repetition rate from 2 to 5 Hz decreased the amplitude of P27m more than that of N20m, which implies that these two deflactions are generated by different neural netwoks.     

Theta Burst Stimulation Applied over Primary Motor and Somatosensory Cortices Produces Analgesia Unrelated to the Changes in Nociceptive Event-Related Potentials

Continuous theta burst stimulation (cTBS) applied over the primary motor cortex (M1) can alleviate pain although the neural basis of this effect remains largely unknown. Besides, the primary somatosensory cortex (S1) is thought to play a pivotal role in the sensori-discriminative aspects of pain perception but the analgesic effect of cTBS applied over S1 remains controversial. To investigate cTBS-induced analgesia we characterized, in two separate experiments, the effect of cTBS applied either over M1 or S1 on the event-related brain potentials (ERPs) and perception elicited by nociceptive (CO₂ laser stimulation) and non-nociceptive (transcutaneous electrical stimulation) somatosensory stimuli. All stimuli were delivered to the ipsilateral and contralateral hand. We found that both cTBS applied over M1 and cTBS applied over S1 significantly reduced the percept elicited by nociceptive stimuli delivered to the contralateral hand as compared to similar stimulation of the ipsilateral hand. In contrast, cTBS did not modulate the perception of non-nociceptive stimuli. Surprisingly, this side-dependent analgesic effect of cTBS was not reflected in the amplitude modulation of nociceptive ERPs. Indeed, both nociceptive (N160, N240 and P360 waves) and late-latency non-nociceptive (N140 and P200 waves) ERPs elicited by stimulation of the contralateral and ipsilateral hands were similarly reduced after cTBS, suggesting an unspecific effect, possibly due to habituation or reduced alertness. In conclusion, cTBS applied over M1 and S1 reduces similarly the perception of nociceptive inputs originating from the contralateral hand, but this analgesic effect is not reflected in the magnitude of nociceptive ERPs.     

Pain-related somatosensory evoked potentials following CO2 laser stimulation in man

0ain-related somatosensory evoked potentials (SEPs) following CO₂ laser stimulation were analyzed in normal volunteers. Low power and long wavelength CO₂ laser stimuli to the hand induced a sharp pain which was associated with a large positive component, P320, recorded over the scalp. Amplitude decreased and latency increased with reduction in stimulus intensity and subjective pain feeling. P320 was maximal at the vertex but was distributed widely over the scalp. There were no topographic differences between left- and right-hand stimulation, or between hand and chest stimulation. Lidocaine injection to produce anesthetic nerve block resulted in loss of P320, but the potential was relatively preserved during ischemic nerve block. No potential corresponding to P320 could be recorded following electrical or mechanical tactile stimulation.We consider P320 to be generated by impulses arising from pain stimuli and ascending through Aδ fibers. We propose the thalamus as a generator source from considering its scalp topography, but pain-specific cognition or perception may also be involved in generating this potential.     

Effect of stimulus rate on the cortical posterior tibial nerve SEPs: a topographic study

We performed topographical mapping of somatosensory evoked potentials (SEPs) in response to posterior tibial nerve stimulation delivered at 2, 5 and 7.5 Hz in 15 healthy subjects. P37 was significantly attenuated at 5 and 7.5 Hz and the N50 component attenuated only at 5 Hz, its amplitude remaining stable for further increases in stimulus frequency. Frontal N37 and P50 potentials showed no significant decrease when the stimulus repetition frequency was changed from 2 to 7.5 Hz. P60 showed an attenuation of the amplitude only at 7.5 Hz. Latency and scalp topographies of all cortical components examined remained uncharged for the 3 stimulus rates tested The optimal stimulus rate for mapping of tibial nerve SEPs was lower than 5 Hz. The distinct recovery function of the contralateral N37-P50 and ipsilateral P37-N50 responses suggests that these potentials arise from separate generators     

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.     

Pain Modulation in Waking and Hypnosis in Women: Event-Related Potentials and Sources of Cortical Activity

Using a strict subject selection procedure, we tested in High and Low Hypnotizable subjects (HHs and LHs) whether treatments of hypoalgesia and hyperalgesia, as compared to a relaxation-control, differentially affected subjective pain ratings and somatosensory event-related potentials (SERPs) during painful electric stimulation. Treatments were administered in waking and hypnosis conditions. LHs showed little differentiation in pain and distress ratings between hypoalgesia and hyperalgesia treatments, whereas HHs showed a greater spread in the instructed direction. HHs had larger prefrontal N140 and P200 waves of the SERPs during hypnotic hyperalgesia as compared to relaxation-control treatment. Importantly, HHs showed significant smaller frontocentral N140 and frontotemporal P200 waves during hypnotic hypoalgesia. LHs did not show significant differences for these SERP waves among treatments in both waking and hypnosis conditions. Source localization (sLORETA) method revealed significant activations of the bilateral primary somatosensory (BA3), middle frontal gyrus (BA6) and anterior cingulate cortices (BA24). Activity of these contralateral regions significantly correlated with subjective numerical pain scores for control treatment in waking condition. Moreover, multivariate regression analyses distinguished the contralateral BA3 as the only region reflecting a stable pattern of pain coding changes across all treatments in waking and hypnosis conditions. More direct testing showed that hypnosis reduced the strength of the association of pain modulation and brain activity changes at BA3. sLORETA in HHs revealed, for the N140 wave, that during hypnotic hyperalgesia, there was an increased activity within medial, supramarginal and superior frontal gyri, and cingulated gyrus (BA32), while for the P200 wave, activity was increased in the superior (BA22), middle (BA37), inferior temporal (BA19) gyri and superior parietal lobule (BA7). Hypnotic hypoalgesia in HHs, for N140 wave, showed reduced activity within medial and superior frontal gyri (BA9,8), paraippocampal gyrus (BA34), and postcentral gyrus (BA1), while for the P200, activity was reduced within middle and superior frontal gyri (BA9 and BA10), anterior cingulate (BA33), cuneus (BA19) and sub-lobar insula (BA13). These findings demonstrate that hypnotic suggestions can exert a top-down modulatory effect on attention/preconscious brain processes involved in pain perception.     

Origin of frontal N15 component of somatosensory evoked potential in man

Origin of the frontal somatosensory evoked potential (SEP) by median nerve stimulation was investigated in normal volunteers and in patients with localized cerebrovascular diseases, and the following results were obtained.

• 1.(1) In normal subjects, SEPs recorded at F3 (or F4) contralateral to the stimulating median nerve were composed of P12, N15, P18.5 and N26. Similar components were recognized in SEP recorded at Fz.
• 2.(2) In patients in whom putaminal or thalamic hemorrhages had destroyed the posterior limbs of the internal capsules, frontal N15 and parietal N18 (N20) disappeared. These components were also absent in patients with cortical (parietal) infarctions. Among these patients, the thalamus was not affected in cases with putaminal hemorrhages and cortical infarctions.

These facts indicate that the generator of the frontal N15 does not exist in the thalamus but that it originates from the neural structure central to the internal capsule, which suggests a similarity to the generator of the parietal N18.Because N15 was recorded in the midline of the frontal region with shorter latency than parietal N18, the frontal N15 might represent a response to the sensory input of the frontal lobe via the non-specific sensory system.     

Bit-mapped somatosensory evoked potentials and muscular reflex responses in man: comparative analysis in different experimental protocols

Bit-colour maps of somatosensory evoked potentials (SEPs) and muscular responses from forearm and hand muscles were simultaneously recorded after median nerve stimulation. Subjects were asked either to relax totally (A), or to contract the examined muscle continuously and isometrically at 10–20% (B) and 80–100% (C) of the maximal strength. Isotonic contractions ipsilateral (D) and contralateral to the stimulus (E) were also examined. Both SEPs and EMG responses were elicited by individual near-motor threshold pulses delivered at 0.2/sec to the median nerve at the elbow. SEPs were maximal in amplitude during complete relaxation, whilst all the components following the parietal N20 were depressed by muscle contraction. Such decrements affected predominantly the parietal and frontal peaks of positive polarity during condition B, whilst the frontal negative component (wave N30) dropped remarkably in conditions C and D. Early EMG responses (V1 = spinal circuitry) were usually absent in condition A; they were present together with later components (= V2 possibly long-loop, transcortical circuitry) in C and D, whilst they were alone recordable in B and E. The amplitudes of the frontal wave N30 in SEPs and of V2 in LLRs were inversely correlated. This observation is consistent with the hypothesis that a change in the reactivity of the sensorimotor brain areas to afferent impulses is coupled to LLR elicitation in forearm and hand muscles.     

Median and tibial nerve somatosensory evoked potentials: middle-latency components from the vicinity of the secondary somatosensory cortex in humans

The topography of the middle-latency N110 after radial nerve stimulation suggested a generator in SII. To support this hypothesis, we have tried to identify a homologous component in the tibial nerve SEP (somatosensory evoked potential). Evoked potentials following tibial nerve stimulation (motor+sensory threshold) were recorded with 29 electrodes (bandpass 0.5–500 Hz, sampling rate 1000 Hz). For comparison, the median nerve was stimulated at the wrist. Components were identified as peaks in the global field power (GFP). Map series were generated around GFP peaks and amplitudes were measured from electrodes near map maxima. With median nerve stimulation, we recorded a negativity with a maximum in temporal electrode positions and 106±12 ms peak latency (mean±SD), comparable to the N110 following radial nerve stimulation. After tibial nerve stimulation the latency of a component with the same topography was 131±11 ms (N130). Both N110 and N130 were present ipsi- as well as contralaterally. Amplitudes were significantly higher on the contralateral than the ipsilateral scalp for both median (3.1±2.4 μV vs. 1.7±1.6 μV) and tibial nerve (1.9±1.2 μV vs. 0.6+1 μV). The topography of the N130 can be explained by a generator in the vicinity of SII. The latency difference between median and tibial nerve stimulation is related to the longer conduction distance (cf. N20 and P40). The smaller ipsilateral N130 is consistent with the bilateral body representation in SII.     

Short latency somatosensory evoked potentials following mechanical taps to the face. Scalp recordings with a non-cephalic reference

Trigeminal somatosensory evoked potentials were recorded over the scalp using non-cephalic reference sites following mechanical taps to the face. A negative wave form, Nf17, was recorded bilaterally with its highest amplitude over the frontal scalp contralateral to the side of stimulation. A localized negative form, Np25, was recorded over the centro-parietal scalp contralateral to the side of stimulation. Np25 had an onset latency of 16.46 msec. The location and restricted spatial distribution of Np25 suggest that it represents the initial activation of the face area of the primary sensory cortex. The widespread bilateral nature of Nf17 and its latency of onset preceding that of Np25 suggest that Nf17 may be a ‘far-field’ potential reflecting activity in subcortical sensory pathways subserving the face.