Electroencephalography and Clinical Neurophysiology/Evoked Potentials Section最新文献

In this study of electrically-evoked auditory brain-stem responses (EABRs) elicited by cochlear nucleus stimulation, 3 waves were identified after the initial wave that is directly initiated by the electric stimulus. Varying the rate of periodic stimulation or the interval between pairs of stimuli revealed that the shorter the latency of a wave, the faster it recovered from activation (i.e. shorter refractory period). The slow recovery of the third wave and an accompanying contribution to the second wave could be accounted for by postsynaptic generation in the two medial superior olivary nuclei (MSO); the faster recovery of another contribution to the second wave by generation in an axonal tract bending around the contralateral MSO; and the fastest recovery of the first wave by another axonal pathway having larger axons. Comparison with the relative latencies and spatial distribution of an acoustically-evoked auditory brain-stem response (AABR) indicated that the third wave corresponds to wave V, the second to wave IV (called IVb), and the first to a wave that precedes wave IV (called IVa). The anatomical interpretations for the two later waves of the EABR are consistent with most of the extant data on the neural generators of AABR waves IV and V. Thus, the present data and analysis strengthen the identification of the electrically evoked responses as EABRs and provide a firmer foundation for intra-operative EABR monitoring to assist auditory brain-stem implant placement.

In the present study, the component structure of auditory event-related potentials (ERP) was studied in children of 7–9 years old by presenting stimuli with different interstimulus intervals (ISI). A short-term auditory sensory memory, as reflected by ISI effects on ERPs, was also studied. Auditory ERPs were recorded to brief unattended 1000 Hz frequent, `standard' and 1100 Hz rare, `deviant' (probability 0.1) tone stimuli with ISIs of 350, 700 and 1400 ms (in separate blocks). With the 350 ms-ISI, the ERP waveform to the standard stimulus consisted of P100-N250 peaks. With the two longer ISIs, in addition, the frontocentral N160 and N460 peaks were observed. Results suggested that N160, found with the longer ISIs, is a correlate of the adult auditory N1. In difference waves, obtained by subtracting ERP to standard stimuli from ERP to deviant stimuli, two negativities were revealed. The first was the mismatch negativity (MMN), which is elicited by any discriminable change in repetitive auditory input. The MMN data suggested that neural traces of auditory sensory memory lasted for at least 1400 ms, probably considerably longer, as no MMN attenuation was found across the ISIs used. The second, later negativity was similar to MMN in all aspects, except for the scalp distribution, which was posterior to that of the MMN.

Auditory electric and magnetic P50(m), N1(m) and MMN(m) responses to standard, deviant and novel sounds were studied by recording brain electrical activity with 25 EEG electrodes simultaneously with the corresponding magnetic signals measured with 122 MEG gradiometer coils. The sources of these responses were located on the basis of the MEG responses; all were found to be in the supratemporal plane. The goal of the present paper was to investigate to what degree the source locations and orientations determined from the magnetic data account for the measured EEG signals. It was found that the electric P50, N1 and MMN responses can to a considerable degree be explained by the sources of the corresponding magnetic responses. In addition, source-current components not detectable by MEG were shown to contribute to the measured EEG signals.

Objectives: We studied waveform changes associated with a focal conduction block in compression myelopathies.

Design and Methods: A total of 26 patients underwent serial intervertebral recording of spinal somatosensory evoked potentials (SSEPs) after epidural stimulation. The site of compression identified by abrupt reduction in size of the negative peak was designated as 0 level with the other levels numbered in order of distance assigning a minus sign caudally.

Results: Considering the response recorded at −4 as baseline (100%), SSEPs showed a progressive increase rostrally, reaching an average of 154% in amplitude and 216% in area at −1 followed by an abrupt decline to 32% and 31% at 0. The incremental change of the negative peak was accompanied by a small reduction in area of the initial positive component to 90% at −1 considering the value at −4 as baseline (100%).

Conclusions: The theory of solid angle approximation and the concept of phase cancellation best explain the apparently paradoxical enhancement of the negative peak which characterize typical waveform changes at the site of conduction block.

Auditory evoked potentials were recorded to onset and offset of synthesised instrumental tones in 40 normal subjects, 20 right-handed for writing and 20 left-handed. The majority of both groups showed a T-complex which was larger at the right temporal electrode (T4) than the left (T3). In the T4-T3 difference waveforms, the mean potential between latencies of 130 and 165 ms was negative in all right-handed subjects except two for whom the waveforms were marginally positive-going. Amongst the left-handers, however, this converse asymmetry was seen in 7 subjects, 5 of them more than 2 standard deviations from the mean of the right-handed group. The degree of asymmetry was not significantly correlated with the degree of left-handedness according to the Edinburgh Handedness Inventory. Asymmetry of the T-complex to instrumental tones appears to reflect the lateralisation of auditory `musical' processing in the temporal cortex, confirming evidence from other sources including PET that this is predominantly right-sided in the majority of individuals. The proportion of left-handers showing the converse laterality is roughly in accordance with those likely to be right-hemisphere-dominant for language. If linguistic and `musical' processes are consistently located in opposite hemispheres, AEPs to complex tones may prove a useful tool in establishing functional lateralisation.

We compared scalp somatosensory evoked potential (SEP) recordings by non-cephalic and earlobe reference in 14 healthy subjects and in 5 patients with lesions of the upper cervical cord. In healthy subjects, the scalp to earlobe montage tended to cancel all far-field potentials preceding the scalp P14. On the contrary, the P14 far-field was more difficult to identify in scalp to non-cephalic recordings, because in 12/14 cases it followed another far-field (P13), which was very close in latency to the P14. In 4 patients, the scalp to non-cephalic traces showed a single positive wave (P13/P14 complex) in the P14 latency range. If this complex had been labelled as P14, the somatosensory dysfunction would have been localised above the foramen magnum. On the other hand, the scalp to earlobe recording allowed correct localisation of the lesion since it showed the `real' and delayed P14 in two patients and no far-field response in the remaining two. Therefore, we propose the use of the scalp to earlobe montage as standard in routine examinations.

Objectives: Spatial analysis of the evoked brain electrical fields during a cued revealed an extremely robust anteriorization of the positivity of a P300 microstate in the NoGo compared to the Go condition (NoGo-anteriorization in a prevailing study). To allow a neuroanatomical interpretation the NoGo-anteriorization was investigated with a new three-dimensional source tomography method (LORETA) was applied.

Methods: The test contains subsets of stimuli requiring the execution (Go) or the inhibition (NoGo) of a cued motor response which can be considered as mutual control conditions for the study of inhibitory brain functions. 21-channel ERPs were obtained from 10 healthy subjects during a cued CPT, And analyzed with LORETA.

Results: Topographic analyses revealed significantly different scalp distributions between the Go and the NoGo conditions in both P100 and P300 microstates, indicating that already at an early stage different neural assemblies are activated. LORETA disclosed a significant hyperactivity located in the right frontal lobe during the NoGo condition in the P300 microstate.

Conclusions: The results indicate that right frontal sources are responsible for the NoGo-anteriorization of the scalp P300 which is consistent with animal and human lesion studies of inhibitory brain functions. Furthermore, it demonstrates that frontal activation is confined to a brief microstate and time-locked to phasic inhibitory motor control. This adds important functional and chronometric specificity to findings of frontal activation obtained with PET and Near-Infrared-Spectroscopy studies during the cued CPT, and suggests that these metabolic results are not due to general task demands.

Mismatch negativity (MMN) and N2b were elicited during a selective dichotic-listening task in 16 young (Y), 16 middle-aged (M) and 19 elderly (E) subjects to evaluate automatic and effortful memory comparison of auditory stimuli. Sequences of standard (80%) and deviant (20%) tones were dichotically presented to subjects in two runs. In each run, subjects were instructed to give a button-press response to the deviant (target) tones in the ear designated as attended and to ignore the input to the other ear.

Peak latencies, peak amplitudes and mean amplitudes were calculated for MMN and N2b components in each subject. MMN latency and amplitude were quite stable regardless of age, while N2b latency was significantly longer in M and E subjects than in Y subjects. These results are interpreted as reflecting that automatic processes of comparison in auditory memory of stimuli presented at short interstimulus intervals remain quite stable from 23 to 77 years of age; however, those requiring attentional effort decline with age.

Readiness potentials (RPs) preceding a trigger pulling movement were recorded in 9 right-handed male subjects. We investigated two tasks, non-purposive and purposive movement tasks. In this study we defined simple trigger pull as non-purposive, and target force production by pulling the trigger as purposive. In the non-purposive task, the subjects were instructed to pull the trigger at their own pace and at an easily-exerted force level. After two sessions in the non-purposive movement task, the subjects were submitted to the purposive movement task, and were requested to pull the trigger in an attempt to produce target force, the range of which was decided individually on the basis of mean force level in the second session of the non-purposive movement task. The RP preceding the purposive movement was larger than that preceding the non-purposive movement. In addition, enhancement of the RP was specific to the negative slope (NS′). Since neither peak force nor time to peak force of the movement differed in the two tasks, it was concluded that the increased NS′ was due to a psychological change associated with execution of the purposive movement.

Objective: To identify low-frequency activity in the pain-evoked potential at very late latencies, consistent with C-fiber transmission velocities.

Methods: Brief (1 ms) painful (intracutaneous) and two levels of non-painful (mild and strong) electrical pulses were applied to the index and middle fingers of the left hand. Evoked potentials (EPs) were recorded from 30 electrodes covering the entire scalp. Data from the 3 stimulus conditions (approximately 60 trials per condition per subject) were compared using the frequency domain technique of complex demodulation applied to single trial data. Subjects were 14 normal right-handed male human volunteers, aged 19–36 years.

Results: Using descriptive probability mapping, pain versus strong non-pain differences were found in grand average data as well as in 8 of 14 subjects, consisting of greater low-frequency power at latencies from 700 to 1100 ms at electrodes near the contralateral central sulcus and at the vertex.

Conclusions: There are topographically focal, pain versus non-pain differences in the 700–1100 ms latency range that can be seen using frequency-domain analytic techniques. These differences were not seen with traditional time domain analyses. They may be due to a C-fiber-related mechanism or to very late activity triggered by faster fibers.