Intracortical recordings of early pain-related CO2-laser evoked potentials in the human second somatosensory (SII) area.

We studied responses of the parieto-frontal opercular cortex to CO2-laser stimulation of A delta fiber endings, as recorded by intra-cortical electrodes during stereotactic-EEG (SEEG) presurgical assessment of patients with drug-resistant temporal lobe epilepsy. After CO2-laser stimulation of the skin at the dorsum of the hand, we consistently recorded in the upper bank of the sylvian fissure contralateral to stimulation, a negative response at a latency of 135 +/- 18 ms (N140), followed by a positivity peaking around 171 +/- 22 ms (P170). The stereotactic coordinates in the Talairach's atlas of the electrode contacts recording these early responses covered the pre- and post-rolandic part of the upper bank of the sylvian fissure (-27 < y < +12 mm; 31 < x < 57 mm; 4 < z < 23 mm), corresponding to the accepted localization of the SII area in man, possibly including the upper part of the insular cortex. The spatial distribution of these early contralateral responses in the SII-insular cortex fits wit that of the modeled sources of scalp CO2-laser evoked potentials (LEPs) and with PET data from pain activation studies. Moreover, this study showed the likely existence of dipolar sources radial to the scalp surface in SII, which are overlooked in magnetic recordings. Early responses also occurred in the SII area ipsilateral to stimulation peaking 15 ms later than in contralateral SII, suggesting a callosal transmission of nociceptive inputs between the two SII areas. Other pain responsive areas such as the anterior cingulate gyrus, the amygdala and the orbitofrontal cortex did not show early LEPs in the 200 ms post-stimulus. These findings suggest that activation of SII area contralateral to stimulation, possibly through direct thalamocortical projections, represents the first step in the cortical processing of peripheral A delta fiber pain inputs.     

The effects of auditory attention measured from human electrocorticograms.

OBJECTIVE: A central question in auditory electrophysiology has been whether selective attention can modulate exogenous components of the scalp-recorded N1 (the 'N1 effect'). Intracranial electrocorticograms were used in the current work to investigate this issue in greater anatomical detail. METHODS: Data were recorded from subdural electrodes placed across temporal cortex in 6 patient-volunteers undergoing diagnostic procedures for medically intractable epilepsy. Patients performed a dichotic listening task in which they alternately attended to a series of tones presented to both ears (mean ISI 800 ms) by responding to rare frequency deviants. RESULTS: Effects of attention were measured on the largest negative and positive waveform deflections observed between 70 and 220 ms post-stimulus for stimuli presented contralateral to grid location. Peak deflections were most often recorded from the upper bank of the posterior superior temporal gyrus at approximately 89 and 173 ms on average (labeled N90stg and P170stg, respectively). Selective attention had little effect on peak latencies but significantly increased the N90stg for 3 subjects, increased the P170stg for two subjects, and decreased the P170stg for two other subjects. CONCLUSIONS: Selective auditory attention can modulate neural response in auditory cortex. SIGNIFICANCE: The effects of attention on the scalp-recorded N1 component may arise in part from the enhancement of exogenous responses in temporal cortex.     

The effects of lesions of superior temporal gyrus and inferior parietal lobe on temporal and vertex components of the human AEP

We recorded auditory evoked potentials (AEPs) to 1 kHz tone bursts in controls and patients with unilateral lesions centered in posterior superior temporal gyrus and adjacent caudal inferior parietal lobule (STG) or in rostral inferior parietal lobule (IPL). Controls generated a vertex maximal N94 (N1b) and P200 (P2) and additional P45, N78 and N127 temporal AEP components (P45, N1a, N1c). Similar to prior reports, in controls the N1a was most prominent over the left temporal lobe and the P45 was largest over the right temporal lobe consistent with behavioral and anatomical data indicating differential organization of left and right human temporal lobe. The N1c was recorded equally from both T3 and T4 electrodes and was enhanced in the temporal site contralateral to the ear of stimulation. The patient groups had differential effects on AEPs. Unilateral STG lesions resulted in bilateral reductions of the N1b and P45 and marked unilateral reductions of the N1a and N1c over lesioned hemisphere. IPL lesions resulted in bilateral but non-significant reductions of the N1b and N1c. The scalp topography results in normal subjects combined with the effects of unilateral STG lesions provide supportive evidence that the temporal maximal components of the human AEP (P45, N1a, N1c) are generated by radially oriented neuronal dipole sources located in STG. The bilateral reduction of the N1b vertex response by unilateral STG lesions is compatible with a unilateral disruption of a vertically oriented dipole situated in the posterior superior temporal plane. The results emphasize the critical role of the superior temporal plane and lateral superior temporal gyrus in generation of human long latency AEPs.     

Intracranial auditory detection and discrimination potentials as substrates of echoic memory in children

In children, intracranial responses to auditory detection and discrimination processes have not been reported. We, therefore, recorded intracranial event-related potentials (ERPs) to both standard and deviant tones and/or syllables in 4 children undergoing pre-surgical evaluation for epilepsy. ERPs to detection (mean latency = 63 ms) and discrimination (mean latency = 334 ms) were highly localized to areas surrounding the Sylvian fissure (SF). These potentials reflect activation of different neuronal populations and are suggested to contribute to the scalp recorded auditory N1 and mismatch negativity (MMN).     

Scalp topography and dipolar source modelling of potentials evoked by CO2 laser stimulation of the hand

CO2 laser evoked potentials to hand stimulation recorded using a scalp 19-channel montage in 11 normal subjects consistently showed early N1/P1 dipolar field distribution peaking at a mean latency of 159 ms. The N1 negativity was distributed in the temporoparietal region contralateral to stimulation and the P1 positivity in the frontal region. The N1/P1 response was followed by 3 distinct components: (1) N2a reaching its maximal amplitude at the vertex and ipsilaterally to the stimulated hand, (2) N2b mostly distributed in the frontal region, and (3) P2 with a mid-central topography. Brain electrical source analysis showed that this sequence was explained, with a residual variance below 5%, by a model including two dipoles in the upper bank of the Sylvian fissure of each hemisphere, a frontal dipole close to the midline, and two anterior medial temporal dipoles, thus suggesting a sequential activation of the two second somatosensory areas, anterior cingulate gyrus and the amygdalar nuclei or the hippocampal formations, respectively. This model fitted well with the scalp field topography of grand average responses to stimulation of left and right hand obtained across all subjects as well as when applied to individual data. Our findings suggest that the second somatosensory area contralateral to the stimulation is the first involved in the building of pain-related responses, followed by ipsilateral second somatosensory area and limbic areas receiving noxious inputs from the periphery.     

Hemispheric asymmetry of late auditory evoked response induced by pitch changes in infants: influence of sleep stages

Late auditory evoked potentials (LAEPs) have been recorded in response to a 1000 Hz standard (occurrence 80%) or a 2000 Hz deviant (occurrence 20%) tone on the left (T3) and right (T4) temporal scalp in 6-week-old full-term newborns during pure quiet or active sleep states. Sleep states were permanently controlled by polygraphic recording including EEG, EOG, EMG, EKG and respiratory movements. During quiet sleep LAEPs consisted of a clear polygraphic response: N1-P2-N2. Mean latencies ranges in T3 and T4 were: N1 = 28–70 ms; P2 = 343–407 ms;N2 = 966–1178 ms; and P3 = 1461–1492 ms. During active sleep LAEPs consisted of a N1-P2-N2 response. Mean latency ranges on T3 and T4 were: N1 = 36–79 ms; P2 =278–304 ms; N2 = 555–620 ms. N2 latency was significantly shorter in AS than in QS. Amplitude of the N1-P2-N2 complex was significantly lower during active sleep. In response to standard stimuli, mean amplitudes and latencies of the LAEP were similar on T3 and T4 during active or quiet sleep states. In response to deviant stimuli mean amplitude of the N1-P2-N2 complex was significantly higher and mean latencies of N1 and N2 were significantly shorter on T3 during quiet sleep. No significant difference was observed during active sleep. These results confirm that sleep stages have a considerable influence on cortical auditory pathways. The auditory message is amplified during quiet sleep and inhibited during active sleep. Therefore sleep states need to be controlled to analyze LAEPs in young children. Furthermore our results show that unexpected auditory stimuli are differentiated in the temporal area of the left hemisphere of 6-week-old infants. This represents a functional correlate of the known hemispherical asymmetry in the speech region of the temporal cortex.     

Sequential temporo‐fronto‐temporal activation during monitoring of the auditory environment for temporal patterns

Subjects detected rarely occurring shifts between two simple tone‐patterns, in a paradigm that dissociated the effects of rarity from those of pitch, habituation, and attention. Whole‐head magnetoencephalography suggested that rare attended pattern‐shifts evoked activity first in the superior temporal plane (sTp, peak ～100 ms), then superior temporal sulcus (sTs, peak ～130 ms), then posteroventral prefrontal (pvpF, peak ～230 ms), and anterior temporal cortices (aT, peak ～370 ms). Activity was more prominent in the right hemisphere. After subtracting the effects of nonshift tones (balanced for pitch and habituation status), weak but consistent differential effects of pattern‐shifts began in aT at 90–130 ms, spread to sTs and sTp at ～130 ms, then pvpF, and finally returned to aT. Cingulate activity resembled prefrontal. Responses to pattern shifts were greatly attenuated when the same stimuli were ignored, suggesting that the initial superior temporal activity reflected an attention‐related mismatch negativity. The prefrontal activity at ～230 ms corresponded in latency and task correlates with simultaneously recorded event‐related potential components N2b and P3a; the subsequent temporal activity corresponded to the P3b. These results were confirmed in sensors specific for frontal or temporal cortex, and thus are independent of the inverse method used. Overall, these results suggest that auditory working memory for temporal patterns begins with detection of the pattern change by an interaction of anterior and superior temporal structures, followed by identification of the event and its consequences led by posteroventral prefrontal and cingulate cortices, and finally, definitive encoding of the event in anterior temporal areas. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.     

Age-related effects on superior temporal gyrus activity during an auditory oddball task

We used magnetoencephalography in combination with magnetic resonance imaging to investigate the effects of aging on the temporal dynamics of activity localized to several brain regions during an auditory oddball task. The most interesting effects were noted in the superior temporal gyrus as follows: (1) responses were generally stronger to rare than to frequent tones throughout the entire 600-ms time interval, and (2) increases in the amplitude of the 40-ms peak and the latency of the maximum late response were evident in the elderly. Although superior temporal gyrus activity has traditionally been associated with early sensory processing, these results suggest that superior temporal gyrus activity is also important for later decision-related processing.     

Auditory associative cortex dysfunction in children with autism: evidence from late auditory evoked potentials (N1 wave-T complex).

OBJECTIVES: Auditory processing at the cortical level was investigated with late auditory evoked potentials (N1 wave-T complex) in 4-8-year-old autistic children with mental retardation and compared to both age-matched normal and mentally retarded children (16 children in each group). METHODS: Two negative peaks which occurred in the 80-200 ms latency range were analyzed according to stimulus intensity level (50 to 80 dB SPL): the first culminated at fronto-central sites (N1b) and the second at bitemporal sites (N1c, equivalent to Tb of the T complex). The latter wave was the most prominent and reliable response in normal children at this age. RESULTS: Our results in autistic children indicated abnormalities of this wave with markedly smaller amplitude at bitemporal sites and pronounced peak latency delay (around 20 ms). Moreover, in both reference groups the intensity effect was found on both sides whereas in autistic children it was absent on the left side but present on the right. CONCLUSION: These findings in autistic children showing very disturbed verbal communication argue for dysfunction in brain areas involved in N1c generation i.e., the auditory associative cortex in the lateral part of the superior temporal gyrus, with more specific left side defects when auditory stimulus have to be processed.     

Automatic auditory off-response in humans: an MEG study

We recorded cortical activities in response to the onset and offset of a pure tone of long duration (LONG) and a train of brief pulses of a pure tone with an interstimulus interval of 50 ms (ISI–50 ms) or 100 ms (ISI–100 ms) by use of magnetoencephalograms in 11 healthy volunteers to clarify temporal and spatial profiles of the auditory on- and off-cortical response. Results showed that a region around the superior temporal gyrus (STG) of both hemispheres responded to both the onset and offset of the stimulus. The location of the source responsible for the main activity (N1m) was not significantly different between the on- and off-responses for any of the three tones. The peak latency of on-N1m was similar under the three conditions, while the peak latency of off-N1m was precisely determined by the ISI, which suggested that off-N1m is based on short-term memory of the stimulus frequency. In addition, there was a positive correlation of the N1m amplitude of N1m between the on- and off-responses among the subjects. The present results suggested that auditory on-N1m and off-N1m have similar physiological significance involved in responding to abrupt changes.     

Pain processing within the primary somatosensory cortex in humans

To investigate the processing of noxious stimuli within the primary somatosensory cortex (SI), we recorded magnetoencephalography following noxious epidermal electrical stimulation (ES) and innocuous transcutaneous electrical stimulation (TS) applied to the dorsum of the left hand. TS activated two sources sequentially within SI: one in the posterior bank of the central sulcus and another in the crown of the postcentral gyrus, corresponding to Brodmann's areas 3b and 1, respectively. Activities from area 3b consisted of 20- and 30-ms responses. Activities from area 1 consisted of three components peaking at 26, 36 and 49 ms. ES activated one source within SI whose location and orientation were similar to those of the TS-activated area 1 source. Activities from this source consisted of three components peaking at 88, 98 and 109 ms, later by 60 ms than the corresponding TS responses. ES and TS subsequently activated a similar region in the upper bank of the sylvian fissure, corresponding to the secondary somatosensory cortex (SII). The onset latency of the SII activity following ES (109 ms) was later by 29 ms than that of the first SI response (80 ms). Likewise, the onset latency of SII activity following TS (52 ms) was later by 35 ms than that of area 1 of SI (17 ms). Therefore, our results showed that the processing of noxious and innocuous stimuli is similar with respect to the source locations and activation timings within SI and SII except that there were no detectable activations within area 3b following noxious stimulation.     

Event-related potential P300 in cerebral infarction

N1, P2 and P300 potentials were studied in 20 cases of cerebral infarction and 47 healthy controls with standard technique of auditory event-related potentials. Healthy controls of both sexes, different ages, education levels and cognitive capacity did not show apparent differences in the latency of p300 (P greater than 0.05, respectively). The patient group, however, revealed significant (P less than 0.001) prolongation of latency of P300 (mean = 409.6 +/- 50 ms) as compared with 28 well matched healthy subjects (mean = 337.7 +/- 24 ms). Although there was some decline of amplitude of P300 in the patient group, the difference between the control and patient groups was not significant (P greater than 0.05). There was significant difference in the Cognitive Capacity Screening Examination findings between the control and patient groups (P less than 0.01), but it seemed that the evaluation of latency of cognition-related p300 might be more objective and sensitive (P less than 0.001).     

Normative data for lateral femoral cutaneous nerve SEPs.

AIMS OF THE STUDY: To determine normative values for somatosensory evoked potentials (SEPs) of the lateral femoral cutaneous nerve (LFCN). METHODS: The LFCN was stimulated at two points, one located 1 cm lateral to the midpoint of a line joining the anterior superior iliac spine (ASIS) and the patella (31 subjects), and the other one located 12 cm distal to the ASIS (24 subjects). Recordings were performed at Cz' (2 cm behind Cz)-Fz. RESULTS: Reproducible SEPs were obtained in all but one of the 31 subjects to ASIS-patella midpoint (mean P1 latency: 33.2+/-3.5 ms, mean side-to-side difference: 2.0+/-1.6 ms) and in all but three of the 24 subjects to stimulation 12 cm distal to the ASIS (mean P1 latency: 30.9+/-3.3 ms, mean side-to-side difference: 2.2+/-1.7 ms). CONCLUSIONS: Reliable SEPs can be obtained to LFCN stimulation. It is easier and, therefore, more convenient to stimulate the ASIS-patella midpoint.     

Memory-dependent auditory evoked potentials to change in the binaural interaction of noise signals.

When non-identical binaural noise signals suddenly become coherent in the two ears, or coherent noise suddenly becomes incoherent, long latency binaurally evoked potentials (BINEP) are elicited which consist of P70, N130 and P220 components. Responses of similar morphology and latency were recorded to a change in the frequency of monaural click trains. The responses to onset or offset of the click trains were 20-50 msec shorter in latency. BINEP are also evoked when the sound image suddenly shifts due to the introduction of a short inter-aural delay in coherent noise signals. Responses to "isolated" shifts occurring once every 7 sec were 2-3 times (N130) or 3-5 times (P220) larger than responses to "frequent" shifts (6/7 sec) of the same magnitude in the same direction. Responses to "infrequent" shifts (1/7 sec) interspersed with frequent shifts in the opposite direction were of intermediate size, significantly larger than frequent responses. The BINEP could reflect the activity of location-specific neurones in the auditory cortex, but it seems more likely that they are due to a common neuronal pool responsive to any shift in the location of the sound image. Similar neuronal pools may be concerned with the detection of change in other auditory dimensions such as pitch. The difference between isolated, infrequent and frequent responses suggests that the BINEP amplitude is dependent on a memory of the shifts which have occurred in the preceding few seconds. The underlying process may be similar or identical to that which governs generation of the "mismatch negativity."     

Ear movement induced by electrical cortical stimulation

Cortical areas that control ear movement have not been reported in humans. We describe a rare case in which ear auricle movement was induced by extraoperative electrical cortical stimulation. A 21-year-old man with intractable localization-related epilepsy was admitted for presurgical evaluation. Subdural electrodes were implanted over the right temporal and frontal regions. Tonic upward contraction of the left ear auricle was elicited by stimulating the subdural electrode on the posterior portion of the right superior temporal gyrus close to the end of the Sylvian fissure. No other body movements or auditory symptoms were elicited. A possible mechanism underlying this rare phenomenon is discussed.     

Deconvolution of 40 Hz steady-state fields reveals two overlapping source activities of the human auditory cortex.

Steady-state auditory evoked fields were recorded from 15 subjects using a whole head MEG system. Stimuli were 800 ms trains of binaural clicks with constant stimulus onset asynchrony (SOA). Seven different SOA settings (19, 21, 23, 25, 27, 29 and 31 ms) were used to give click rates near 40 Hz. Transient responses to each click were reconstructed using a new algorithm that deconvoluted the averaged responses to the different trains. Spatio-temporal multiple dipole modelling in relation to 3D MRI scans revealed two overlapping source components in both the left and right auditory cortex. The primary sources in the medial part of Heschl's gyrus exhibited a N19-P30-N40 m pattern. The secondary, weaker sources at more lateral sites on Heschl's gyrus showed a N24-P36-N46 m pattern. When applied to transient middle latency auditory evoked fields (MAEFs) recorded at SOAs of 95-135 ms, the primary sources imaged activities similar to the deconvoluted steady-state responses, but the secondary source activities were inconsistent. Linear summation of the deconvoluted source waveforms accounted for more than 96% of the steady-state variance. This indicates that the primary activity of the auditory cortex remains constant up to high stimulation rates and is not specifically enhanced around 40 Hz.     

Generators of middle- and long-latency auditory evoked potentials: implications from studies of patients with bitemporal lesions

We recorded middle- and long-latency auditory evoked potentials (AEPs) in 5 patients (ages 39-72 years) with bilateral lesions of the superior temporal plane. Reconstructions of CT sections revealed that primary auditory cortex had been damaged bilaterally in four of the patients, while in the fifth an extensive left hemisphere lesion included primary auditory cortex while a right hemisphere lesion had damaged anterior auditory association areas but spared primary auditory cortex. Normal middle-latency AEPs (MAEPs) were recorded at the vertex electrode in all of the patients. In 3 of the 5 patients, MAEPs also showed normal coronal scalp distributions and were comparable in amplitude following stimulation of either ear. Two patients showed abnormalities. In one case, Na (latency 17 msec)-Pa (latency 30 msec) amplitudes were reduced over both hemispheres following stimulation of the ear contralateral to the more extensive lesion. In another, with both subcortical and cortical involvement, the Pa was abolished over the hemisphere with the more extensive lesion. Long-latency AEPs were normal in 2 patients whose lesions were largely confined to the superior temporal plane. In 2 patients with lesions extending into the inferior parietal lobe, N1s were abolished bilaterally. In the fifth patient, the N1 showed a slight reduction over the hemisphere with the more extensive lesion. Middle- and long-latency AEPs were differentially affected by some lesions. For example, patients with absent N1s could produce normal Pas. A review of these results and those of previous studies of bitemporal patients suggests that abnormalities in middle- and long-latency AEPs do not necessarily reflect damage to primary auditory cortex per se, but rather the degree of damage to adjacent areas. Abnormalities in MAEPs are associated with subcortical lesions, or cortical lesions extensive enough to denervate thalamic projection nuclei. Abnormalities in the long-latency N1 reflect lesion extension into the multi-modal areas of the inferior parietal lobule. This area appears to exert a critical modulatory influence over N1 generators outside of the superior temporal plane.     

Cortical auditory system maturational abnormalities in children with autism disorder: an MEG investigation

Latency of electric (e.g., P1 and N1) and magnetic (e.g., M100) auditory evoked components depends on age in typically developing children, with longer latencies for younger (4-6 years) and shorter, adult-like latencies for older (14-16 years) children. Age-related changes in evoked components provide indirect measures of auditory system maturation and reflect changes that occur during development. We use magnetoencephalography (MEG) to investigate maturational changes in cortical auditory systems in left (LH) and right (RH) hemispheres in children with autism disorder (AD) and Controls. We recorded auditory evoked responses over left and right temporal lobes in 17 Control and 15 AD children in the age range 8-16 years and measured M100 latency as a function of age, subject group and hemisphere. Linear regression analyses of age and M100 latency provided an estimate of the rate of latency change (ms/year) by hemisphere and subject group. Controls: M100 latency for the group ranged from 100.8 to 166.1 ms and varied linearly in both hemispheres, decreasing at a rate of -4 ms/year (LH) and -4.5 ms/year (RH). AD: M100 latency ranged from 116.2 to 186.2 ms. Slopes of regression lines did not differ from zero in either LH or RH. M100 latency showed a tendency to vary with age in LH, decreasing at a rate of -4.6 ms/year. M100 latency in RH increased slightly (at a rate of 0.8 ms/year) with age. Results provide evidence for a differential auditory system development in AD children which may reflect abnormalities in cortical maturational processes in AD.     

Auditory evoked responses (AER) and augmenting-reducing phenomenon in patients with progressive supranuclear palsy (PSP)

Variations in amplitude and latency of P1, N1 and P2 waves of AER induced by increasing the stimulus intensity (augmenting-reducing) were measured in PSP patients and compared to those observed in normal subjects. The studied population included 17 patients (10 male, 7 female, mean age 66 +/- 8 yr) with a typical PSP symptomatology and 17 normal subjects (10 male, 7 female, mean age 66 +/- 9 yr). All subjects from both the groups showed a normal auditory threshold (less than 30 db SPL or a moderately increased threshold never exceeding 10 db SPL). Nine patients had normal BAER; 4 patients showed an abnormal III wave; 3 patients showed an abnormal V wave. One patient had a poorly individualized BAER. Latencies and amplitudes of P1, N1 and P2 waves derived from Cz and Fz (linked ear reference) were studied with 50, 60, 70 and 80 db intensities and for each patient slopes of amplitude-stimulus intensity and latency-stimulus intensity curves were studied. Although patients showed decreased AER amplitudes, the augmenting-reducing phenomenon was not different from controls regarding either latency or amplitude changes with increasing stimulus intensity. Previous studies had established a negative correlation between the augmenting-reducing responses and HVA levels in the cerebrospinal fluid (CSF). Similarity of augmenting-reducing mechanisms in PSP and normal subjects favors the hypothesis of unimpaired mesocortical and mesolimbic dopaminergic pathways in PSP. This hypothesis is also supported by postmortem studies using biochemical markers.