Early Cortical Potentials Research Articles

P122 Contribution of integrated somatosensory and auditory inputs to the cortical response evoked by transcranial magnetic stimulation: A sham TMS-EEG study

Transcranial Magnetic Stimulation (TMS) can effectively stimulate non-invasively the human cortex. The TMS-evoked cortical response can be recorded with electroencephalography (EEG). However, TMS also stimulates our senses by stimulating peripheral trigeminal nerve fibers and creating a loud click. This implies that the TMS-evoked EEG response not only reflects neural activity induced by transcranial excitations of neurons but also neural activity due to somatosensory and auditory stimulation. To characterize the contribution of multisensory peripheral stimulation to TMS-evoked cortical potentials (TEPs), we recorded the evoked EEG response caused by a somato-auditory sham condition which mimicked real TMS. In 20 healthy individuals, TMS was delivered with a figure-of-eight coil over two target sites (posterior parietal cortex and superior frontal gyrus) using two different coil orientations, perpendicular or parallel to sulcus orientation. The sham condition comprised of simultaneous somatosensory and auditory stimulation over the same hotspots as for real TMS. Somatosensory stimulation was achieved via cutaneous electrical stimulation of the scalp, while the TMS coil was used for auditory stimulation ensuring no electric field was induced in the brain by physically separating the coil from the scalp. EEG was acquired with a 61-channel TMS-compatible EEG system. While the early cortical potentials evoked by real or sham TMS differed, TEPs were closely matched in terms of shape and spatial distribution for late components of the evoked EEG responses 70–200 ms after the TMS pulse (see Fig. 1 Download : Download high-res image (666KB) Download : Download full-size image ). This was also the case for the N100 which has been commonly attributed to TMS-induced cortical inhibition. The resemblance of the EEG responses evoked by real and sham TMS challenges the notion that TEPs are mainly reflecting transcranial excitation of cortical neurons. This work has been funded by the Novo Nordisk Foundation Interdisciplinary Synergy Program 2014 [“Biophysically adjusted state-informed cortex stimulation (BASICS); Grant No. NNF14OC0011413].

ID 319 – Is the presence of late evoked potentials (N100 wave) a good predictor of survival in comatose patients?

Objective The persistence of both early cortical responses (N20, Pa) and late associative potentials (vertex potentials, N100) has been shown to improve the probability of return to consciousness of comatose patients. However, the prognostic value of late responses without early cortical potentials has not been documented. Methods We report results in 5 comatose patients in whom late N100 responses could be recorded in the absence of reproducible early cortical auditory and/or somatosensory potentials. The etiologies of coma were: anoxic–ischemic after cardiopulmonary arrest (3), brainstem hemorrhage (1) and ischeamic stroke (1). Results All patients showed reproducible N100 waves but absence of early cortical auditory and/or somatosensory responses. The EEG was non-reactive in 3 patients. All 5 patients had a poor clinical outcome, toward either death or vegetative state. Discussion The presence of N100 wave without previous recordable potentials may be explained either by alternative parallel pathways, or by re-synchronization of an altered ascending volley. Whatever the explanation, the presence of N100 wave may be associated with a good neurological outcome only if preceded by early cortical potentials (Pa and N20), but not if early responses are absent. Key message Caution should be exerted in interpreting the prognostic value of the N100 wave alone.

Not an Aspirin: No Evidence for Acute Anti-Nociception to Laser-Evoked Pain After Motor Cortex rTMS in Healthy Humans

High-frequency repetitive transcranial magnetic stimulation (HF-rTMS) has shown efficacy in relieving neuropathic pain. Whether its analgesic effect also applies to acute physiological nociception remains unclear due to previous contradictory findings. To provide an in-depth investigation of the effects of motor cortex HF-rTMS on acute laser-evoked pain and excitability of nociceptive networks in healthy subjects. Randomized, placebo-controlled, double-blind, cross-over study in 20 healthy participants. Laser heat stimuli at nociceptive threshold were delivered to the right hand, allowing assessment of: (a) subjective pain intensity and unpleasantness; (b) laser-evoked potentials (LEPs, 128 electrodes) and their source model; (c) sympathetic skin responses, and (d) spino-thalamic pathway excitability. Data were collected before and 20 minutes after a session of neuro-navigated 20 Hz rTMS to the contralateral motor cortex. Subjective pain reports to thermal laser pulses, amplitude of late cortical potentials and sympathetic skin responses were decreased after cortical stimulation, to a similar extent whether it was active or placebo. Early cortical potentials and nociceptive network excitability remained identical before and after rTMS, as did anatomical sources of LEPs. Our results do not provide evidence for a genuine anti-nociceptive effect of rTMS on acute physiological pain. We suggest that motor cortex rTMS may act upon high-order networks linked to the emotional and cognitive appraisal of chronic pain, and/or modulate pathologically sensitized networks, rather than change the physiological transmission within an intact nervous system. Such dichotomy is reminiscent of that observed with most drugs used for neuropathic pain.

The association between later cortical potentials and later phases of postural reactions evoked by perturbations to upright stance

Previous studies have suggested that early cortical potentials (e.g. N1) that are evoked by perturbations to upright stance are associated with sensory processing of the initial perturbation and that later potentials may represent cognitive processing of this perturbation. However, it has also been suggested that later cortical potentials could reflect sensory and motor processing of later phases of the postural reaction. The current study set out to provide additional insight into the association between perturbation-evoked cortical potentials and postural reactions evoked by whole-body perturbations. By altering the deceleration onset of the perturbation, which altered the timing of later postural responses, we determined whether changes in later postural responses were associated with changes in later potentials. Based on previous work, we hypothesized that later potentials would not be associated with changes in later postural responses. During stance, seven healthy young adults were instructed to maintain their balance following two types of perturbations: (1) acceleration phase immediately followed by a deceleration phase (TASK 1), and (2) acceleration phase followed by a delayed deceleration phase (TASK 2). In spite of profound task differences in later postural responses, results revealed no significant differences in later potentials. This work provides additional support for the idea that latter elements of perturbation-evoked cortical responses are likely independent of evoked motor reactions required to maintain stability.

Sensorimotor organization in patients who have undergone hemispherectomy: a study with (15)O-water PET and somatosensory evoked potentials.

To identify cortical structures that subserve residual motor and sensory function in patients with congenital hemiparesis due to a porencephalic cyst, we examined, using [(15)O]H2O, PET and somatosensory evoked potentials (SEPs) in three patients with left-sided hemiparesis who had undergone hemispherectomy. Motor stimulation of the affected hand produced ipsilateral activation in the premotor area in all patients, the SMA in two patients, and SII in two patients. Vibrotactile stimulation resulted in activation of the ipsilateral SII in all subjects. Median nerve stimulation of the affected hand produced ipsilateral long-latency SEPs in fronto-centro-parietal areas, whereas stimulation of the non-affected hand produced normal early cortical potentials in the contralateral hemisphere. Our results suggest that residual function in the paretic hand is warranted through non-primary motor and sensory areas, and higher order associative areas in the intact hemisphere.

Visual Activation in α‐Chloralose‐anaesthetized Cats Does Not Cause Lactate Accumulation in the Visual Cortex as Detected by [1HINMR Difference Spectroscopy

The hypothesis that neuronal activation results in lactate accumulation due to mismatch between glucose and oxygen consumption was tested in the cat model of visual activation by monitoring cerebral metabolism with localized 1H nuclear magnetic resonance spectroscopy (MRS). Adult cats were anaesthetized with alpha-chloralose, paralysed and mechanically ventilated. Visual evoked potentials measured over the occipital cortex showed maximal amplitude at 2 Hz stimulation, but the latencies of the early cortical potentials, N1 and P1, were independent of stimulation frequency. High signal-to-noise ratio, short echo time volume-selected [1H]MRS was used to monitor cerebral lactate with a temporal resolution of 70 s. Difference proton spectroscopy unambiguously showed no lactate peak in the visual cortex during visual activation at stimulation frequencies ranging from 1 to 16 Hz. Absence of change in lactate concentration during visual stimulation was confirmed by averaging all the spectra acquired during activation and subtracting them from reference spectra collected in darkness, a procedure that had a calculated lactate detection limit of 0.17 mM. We also reduced the O2 in the inspired air to 13%, which decreased pO2 from 94.5 +/- 8.9 to 47.0 +/- 6.8 mmHg, during visual stimulation at 2 or 4 Hz. At this low PO2 level, visual stimulation did not cause lactate accumulation in the visual cortex, however. The present data show that neuronal activation to this degree in the cat brain is not associated with aerobic lactate production to an extent that can be detected with 1H MRS.

Anesthesia with Increasing Doses of Sufentanil and Midlatency Auditory Evoked Potentials in Humans

Our interest focused on the question whether sufentanil differs from alfentanil, fentanyl, and morphine with regard on its effects on midlatency auditory evoked potentials (MLAEP). Therefore, we studied MLAEP during general anesthesia with increasing doses of sufentanil in 16 patients scheduled for elective major urologic surgery. Anesthesia was induced with sufentanil (1 microgram/kg every 7 min to a total dose of 3 micrograms/kg). In 8 of 16 patients, further incremental doses of sufentanil were given to a total dose of 5 micrograms/kg. Auditory evoked potentials were recorded before and 5 min after every sufentanil dose on vertex (positive) and mastoids on both sides (negative). Latencies of the peaks V, Na, Pa, Nb, and P1 (ms), and amplitudes Na/Pa, Pa/Nb, and Nb/P1 (microV) were measured. In the awake state, MLAEP had high peak-to-peak amplitudes and a periodic waveform. During general anesthesia the brainstem response V was stable to increasing doses of sufentanil. There was a marked statistically significant increase in latency and decrease in amplitude of Nb and P1 after 1-2 micrograms/kg sufentanil, which remained stable under further sufentanil application. In contrast, the early cortical potentials Na and Pa increased only slightly in latencies. This increase was statistically significant at 4 micrograms/kg for Na and at 3 and 4 micrograms/kg for Pa. For the amplitudes Na/Pa and Pa/Nb there was only a slight and statistically insignificant reduction. After the largest dose of sufentanil (3-5 micrograms/kg) Na and Pa showed a similar pattern as in awake patients. We conclude that sufentanil does not differ essentially from alfentanil, fentanyl, and morphine with regard on its effects on MLAEP.

Midlatency Auditory Evoked Potentials and Explicit and Implicit Memory in Patients Undergoing Cardiac Surgery

A high incidence of intraoperative awareness during cardiac surgery has been reported. Midlatency auditory evoked potentials (MLAEP) have been used recently as an indicator of awareness. In the current study, memory for information presented during anesthesia was investigated using MLAEP as one experimental indicator in 45 patients scheduled for elective cardiac surgery. In all patients general anesthesia was maintained using high-dosage fentanyl (1.2 mg.h-1). In addition, the patients of group 1 (n = 10) received flunitrazepam (1.2 mg.h-1), the patients of group 2 (n = 10) isoflurane (0.6-1.2 vol%), and the patients of group 3 (n = 10) propofol (4-8 mg.kg-1.h-1). Group 4 (n = 15) served as a control, and those patients were assigned randomly to one of the anesthetic regimes. After sternotomy and before cardiopulmonary bypass, an audiotape, which included an implicit memory task, was presented to the patients of groups 1-3. Auditory evoked potentials were recorded while the patients were awake and during general anesthesia immediately before and after the audiotape presentation. Latencies of the brain stem peak V and the early cortical potentials Na and Pa were measured. Three to 5 days postoperatively no patient had a clear explicit memory of intraoperative events. However, there were statistically significant differences in the incidence of implicit recall among the groups. Five patients in the flunitrazepam-fentanyl group, 1 patient in the isoflurane-fentanyl group, 1 patient in the propofol-fentanyl group, and no patient in the control group showed an implicit memory of the intraoperative tape message. In the awake state, MLAEP showed high peak-to-peak amplitudes and a periodic waveform. In the patients with implicit memory postoperatively, MLAEP continued to show this pattern during general anesthesia. The early cortical potentials Na and Pa did not increase in latency or decrease in amplitude before or after the audiotape presentation. In contrast, in the patients without implicit memory, MLAEP waveform was severely attenuated or abolished. Na and Pa showed marked increases in latencies and decreases in amplitudes or were completely suppressed. In 9 patients, including all patients (7 of 9) with implicit memory, Pa latency increased less than 12 ms, and 21 of 23 patients without implicit memory showed a Pa latency increase of greater than 12 ms during anesthesia and the audiotape presentation. Therefore, the Pa latency increase of greater or less than 12 ms may provide sensitivity of 100% and specificity of 77% in distinguishing patients with implicit memory from patients without implicit memory postoperatively. When the early cortical potentials of MLAEP are preserved during general anesthesia, auditory information may be processed and remembered postoperatively by an implicit memory task.

後脛骨神経刺激体性感覚誘発電位を用いた前大脳動脈血流一時遮断時の術中モニタリング

Posterior tibial nerve somatosensory evoked potentials (SEPs) were monitored intraoperatively in 22 patients with anterior communicating artery (Acom) aneurysms and 3 patients with distal anterior cerebral artery (ACA) aneurysms. Changes in peak latency and amplitude of the early cortical potentials of SEPs were evaluated. In 14 cases without temporary occlusion, the SEPs did not change during the surgical course. In 11 patients with temporary occlusion of A1 segment for Acom aneursms, lasting from 3 to 44 minutes, 10 demonstrated variable changes of P37-N46 interpeak amplitude. In 1 case, SEP signals remained stable. The P37 and N46 peak latency were not prolonged more than 2 msec in all cases. Significant SEP changes (a decrease in P37-N46 amplitude more than 50% to baseline value) were found in 4 cases. In these cases, the temporary occlusion was used intermittently, and the occlusion time did not go over 10 minutes per occlusion. In 3 cases, the wave form of SEP recoved to the baseline after the release of temporary occlusion. However, 1 case where the SEP did not fully recover suffered from transient motor paresis of a unilateral lower extremity. Despite the large variability of territories of ACA, intraoperative posterior tibial nerve SEP monitoring was helpful in the operative management such as temporary vessel occlusion.

EFFECTS OF INCREASING DOSES OF ALFENTANIL, FENTANYL AND MORPHINE ON MID-LATENCY AUDITORY EVOKED POTENTIALS

We have studied dose-dependent effects of alfentanil, fentanyl and morphine on mid-latency auditory evoked potentials (MLAEP). Anaesthesia was induced with alfentanil 100 micrograms kg-1 every 5 min to a total dose of 500 micrograms kg-1 (group I, n = 10), fentanyl 10 micrograms kg-1 every 7 min to a total dose of 50 micrograms kg-1 (group II, n = 10) or morphine 1 mg kg-1 for induction and 0.5 mg kg-1 every 15 min to a total dose of 3 mg kg-1 (group III, n = 10). MLAEP were recorded before and 3-15 min after every opioid dose on vertex (positive) and mastoids on both sides (negative). Latencies of the peaks V, Na, Pa, Nb, P1 (ms) and amplitudes Na/Pa, Pa/Nb and Nb/P1 (microV) were measured. Fast-Fourier transformation was used to calculate power spectra of the AEP. In the awake state, MLAEP had high peak-to-peak amplitudes and a periodic waveform. Power spectra indicated high energy in the 30-40 Hz frequency range. During general anaesthesia with increasing doses of alfentanil, fentanyl and morphine, the brainstem response V was stable. There was a marked increase only in latency and decrease in amplitude of P1. In contrast, for the early cortical potentials Na and Pa, only small increases in latencies and decreases in amplitudes were observed. After the largest doses of alfentanil (500 micrograms kg-1), fentanyl (50 micrograms kg-1) and morphine (3 mg kg-1), Na, Pa and Nb showed a similar pattern as in awake patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Facilitation of somatosensory evoked potentials by exploratory finger movements.

Modification of somatosensory processing depending on the behavioral setting was studied. Active alternating movements of the fingers, passive tactile stimuli to the hand, and active exploration of objects were performed during recording of somatosensory evoked potentials (SEPs). SEPs were elicited by compound electrical median nerve stimulation and electrical stimulation at detection threshold of cutaneous median nerve fascicles identified by microneurography. Electrical stimulation was not time-locked to the studied condition. In comparison with SEPs at rest there was attenuation of early cortical potentials up to 25 ms post-trigger in all nonresting conditions. In stimulation of the compound median nerve as well as of isolated cutaneous fascicles of a hand actively exploring an object there was an additional increased negativity, peaking at 28 ms. This facilitory effect was independent of attentional focusing and was absent during exploration using the ipsilateral, non-electrically stimulated hand. In patients with parietal lesions the facilitatory effect was diminished on the affected side. Spline interpolated brain maps at this latency based on 32-channel recordings in healthy volunteers showed a shift of local contralateral positive maximum from frontal to parietal during exploration, indicating enhancement of a tangential dipole. It is suggested that in conditions involving close sensorimotor interaction such as exploratory hand movements there is preactivation of a cortical area which is located in the central sulcus and receives cutaneous somatosensory inputs.

Pre- and postcentral somatosensory evoked potentials in Huntington's disease: Effects of stimulus repetition rate

We recorded frontal, central and parietal somatosensory evoked potentials (SEPs) to median nerve stimulation in 20 patients with Huntington's disease (HD) and in a group of normal controls. Two stimulus repetition rates, 1 Hz and 5 Hz, were employed. In HD patients the early cortical potentials (latency range 20–30 ms) at all 3 recording locations were replaced by a widespread, broadly configured N20-25 deflection, while later potentials at 40–80 ms did not significantly differ from those of normals. In contrast to the early P22, P27 and N30 potentials in normals, the N20-25 potential in the patients was not significantly modified by changing the stimulus repetition rate. At 40–80 ms the stimulus rate effects were similar in the patients and normals. The results show that early pre- and postcentral SEPs are both pathological in HD, while later frontal and parietal components can be totally preserved. The early N20-25 in HD is possibly a subcortical potential, seen due to unmasking in the absence of early cortical deflections.