The functional organization of anti-predator behaviour in the pied flycatcher: a study of avian visual perception.
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In a patient with unilateral hearing impairment due to a predominantly ipsilateral pontine pathology, BAEP peak II in a vertex to ipsilateral mastoid derivation (BAEP-II) was preserved on stimulation of the affected ear. All later activity was lost. Intracranial recording from electrodes intraoperatively placed over both cochlear nuclei on the floor of the IVth ventricle showed potentials with size and wave form comparable to the scalp records. Thus only peripheral sources, distant from the ventricular electrode, seem to contribute to scalp BAEP-II. Upon stimulation of the unaffected ear considerably larger intracranial activity was seen with peak 2-4 wave shapes obviously different from the scalp BAEP II-IV. It is concluded that intracranial electrodes sense a complex field distribution predominantly originating in structures to which they are in close electrical connection. This activity, however, need not necessarily project to the scalp.
Brain-stem auditory evoked potentials (BAEPs) were recorded simultaneously from scalp electrodes and intraparenchymatous sites along a ponto-mesencephalic stereotactic penetration path in a patient with the unique condition of a brain-stem tumour which therapeutically necessitated radionuclide implantation but did not grossly affect scalp BAEPs. The data suggest major contributions to scalp peak III from the pons ipsilateral to the stimulated ear, to peak IV from both ipsi- and contralateral sources, and to peak V mainly from contralateral, more rostral sites. Some local activities evidently did not project to the scalp.
Upon conventional median nerve stimulation at the wrist early magnetic fields were recorded using a SQUID magnetometer. At the upper arm, mono- and biphasic compound nerve action fields were detected, depending on the subject's distribution of single fiber conduction velocities. At the upper thorax, brachial plexus fields reversed polarity at the level of Erb's point; their distribution was asymmetric, probably due to volume currents. At the upper lateral neck, fields from proximal plexus, spinal cord (P13m) and the primary somatosensory cortex contralateral to the sensor position were detected. The observed P13m field distribution agrees with the electrophysiological concept of a sagittal segmental dorsal horn generator.
Upon electrical median nerve stimulation wide-band scalp SEP recordings show a burst of high-frequency low-amplitude wavelets of uncertain origin. Digital high-pass filtering (above 400 Hz) of the primary cortical response ("N20") can separate the burst from the underlying "N20 proper" which itself is known to be generated by excitatory postsynaptic potentials (EPSPs) in area 3b. Here, neuromagnetic multichannel recordings show a close correlation between the spatial field distributions of the magnetic burst and of the magnetic "N20m" proper. It is concluded that somatosensory evoked magnetic high-frequency (600 Hz) wavelets have generators at or near the primary somatosensory cortex. Possible modes of generation comprise repetitive discharges conducted in the terminal segments of thalamocortical axons and postsynaptic contributions from neocortical neurons.
The authors report the case of a young female patient submitted to chemonucleolysis at L4-5 with collagenase, in whom severe tissue lesions affecting the cartilaginous end-plate, the vertebral bone, the posterior intervertebral ligament, the epidural fat, and the dura mater were verified at laminectomy, which had become necessary due to functional motor deterioration.
Brain-stem auditory evoked potentials (BAEPs) were recorded at intraparenchymatous sites along a ponto-mesencephalic stereotactic penetration path in a patient with the rare condition of a ponto-medullary lesion which required biopsy but did not grossly alter scalp BAEPs. Click stimuli were applied either monaurally (with contralateral masking noise against acoustic cross-talk; conditions 'R,' 'L') or binaurally (condition 'RL'). A binaural interaction trace ('BI') was derived by subtracting the sum of the monaural from the binaural responses: BI = (RL)-(R + L). Despite failure to obtain significant BI components above noise level for scalp BAEPs, at the lower pons clearly discernible, multiphasic BI activity could be recorded beginning at the peak latency of scalp wave III and extending over approximately the next 4 msec. Its amplitude rapidly fell off with distance toward more rostral, mesencephalic recording sites. In relation to this positive finding, the equivocality among some of the previous studies on the detection of BI components in human scalp BAEPs is tentatively rephrased in terms mainly of a low signal-to-noise ratio and of functional peculiarities introduced by the respective stimulation protocols.
Structural damage inflicted on membranes of excitable cells may evoke quasi-DC injury currents driven by the transmembrane resting potential gradient. In contrast to the usually invasive electrophysiological approaches, superconducting quantum interference devices (SQUIDs) measure the concomitant weak biomagnetic fields non-invasively as is shown here for acutely excised rat nerves or muscles. Analysis of the field distributions showed slowly decaying equivalent current dipole moments in the nanoampmeter range as generated by microamp nerve injury currents extending intra-axonally over millimeter distances. The geometric and kinetic parameters of this experimental design may allow in vivo recordings in human patients.
OBJECTIVE: Human median nerve somatosensory evoked potentials (SEPs) contain a low-amplitude (<500 nV) high-frequency (approximately 600 Hz) burst of repetitive wavelets (HFOs) which are superimposed onto the primary cortical response 'N20.' This study aimed to further clarify the cortical and subcortical structures involved in the generation of the HFOs. METHODS: 128-Channel recordings were obtained to right median nerve stimulation of 10 right-handed healthy human subjects and in 7 of them additional to right ulnar nerve. Data were evaluated by applying principal component analysis and dipole source analysis. RESULTS: Different source evaluation strategies provided converging evidence for a cortical HFO origin, with two different almost orthogonally oriented generators being active in parallel, but with a phase shift of a quarter of their oscillatory period, while the low-frequency 'N20' is adequately modeled by one tangential dipole source. Median and ulnar derived low-frequency and HFO cortical sources show a somatotopic order. Additionally, generation of the HFOs was localized in subcortical, near-thalamic and subthalamic source sites. The near-thalamic dipole was located at significantly different sites in HFO and low-frequency data. CONCLUSIONS: The cortical HFO source constellation points to a 'precortical' source in terminals of thalamocortical fibers and a second intracortical HFO origin. Furthermore, HFOs are also generated at subcortical and even subthalamic sites. Near-thalamic, the HFO and low-frequency signals are generated or modulated by different neuron populations involved in the thalamocortical outflow.
OBJECTIVE: Injury currents are a hallmark of acute lesions in polarized cells. Our objective was to develop a non-invasive technique for monitoring human near-DC injury currents in vivo. METHODS: Using diagnostic muscle biopsy as controlled paradigm, injury-related magnetic DC-fields were mapped for 60 min postsurgery over leg muscle lesions of 9 subjects. A 49-channel magnetometer was used in combination with a mechanical horizontal modulation of the subject beneath the sensor array. RESULTS: Magnetic DC-field maps showed salient differences between biopsy and contralateral legs in 8/9 patients with a characteristic slowly decaying field in all biopsy legs. A variety of anomalous DC-field patterns was recorded over the biopsy sites, corresponding to theoretically predicted geometric variations of equivalent DC-current dipoles, i.e. wound surfaces, pointing into opposing muscle fibre ends. By contrast, all control measurements showed an elongated dipolar DC-field pattern. Additionally, mean global DC-field strengths were significantly higher over biopsy legs compared to the contralateral site. CONCLUSIONS: Our pilot data illustrate that human injury currents can be detected using non-invasive magnetometry. Thus, DC-magnetometry may provide an essential new tool for clinical monitoring of injury currents, possibly also in brain tissue, e.g. in case of anoxic or peri-infarct depolarizations.
Functional neuroimaging techniques map neuronal activation indirectly via local concomitant cortical vascular/metabolic changes. In a complementary approach, DC-magnetoencephalography measures neuronal activation dynamics directly, notably in a time range of the slow vascular/metabolic response. Here, using this technique neuronal activation dynamics and patterns for simple and complex finger movements are characterized intraindividually: in 6/6 right-handed subjects contralateral prolonged (30 s each) complex self-paced sequential finger movements revealed stronger field amplitudes over the pericentral sensorimotor cortex than simple movements. A consistent lateralization for contralateral versus ipsilateral finger movements was not found (4/6). A subsequent sensory paradigm focused on somatosensory afferences during the motor tasks and the reliability of the measuring technique. In all six subjects stable sustained neuronal activation during electrical median nerve stimulation was recorded. These neuronal quasi-tonic activation characteristics provide a new non-invasive neurophysiological measure to interpret signals mapped by functional neuroimaging techniques.
The pericentral primary sensorimotor cortices generate the "mu rhythm" with a distinct spectral signature exhibiting two peaks, generated predominantly anterior (20 Hz) or posterior (10 Hz) to the central sulcus; it defines a "background" network state upon which somatosensory inputs will impinge. We used the high spatiotemporal resolution of magnetoencephalography to analyze the perturbation dynamics of these cortical rhythms in response to a series of paired electric median nerve stimuli: single trials were sorted off-line according to increasing power of the 10- or 20-Hz rebounds which occurred 300-600 ms after the first stimulus; using subaverages formed from the upper and lower 20% of this distribution, we analyzed somatosensory evoked fields (SEF) and power modifications caused by the second stimulus in the pair. We report three key findings: (1) the power level of rhythm rebounds triggered by the first stimulus predicted the rebound strength after the second stimulus applied 600 ms later; yet, it was uncorrelated across the 2.4-s interval separating subsequent stimulus pairs. (2) Conventional averaging camouflages substantial trial-to-trial variations of rhythm dynamics including, for example, even non-occurrences of rhythm rebounds. (3) For six of the seven subjects, the background rhythm power did not affect any SEF component; for the subject with the strongest rhythms only intracortically generated deflections (peaking after the thalamocortical input component N20m) varied as function of pre-stimulus 10- or 20-Hz power. Thus, the perturbation dynamics of the pericentral mu rhythm exhibits a significant intertrial variance, which becomes effective mainly at a time scale larger than 600 ms.
The first detection of the magnetic field of a stimulated peripheral nerve in man is presented. The measurement was performed noninvasively and in vivo on a healthy subject. The spatio-temporal field distribution is utilized to calculate the location of bioelectric activity on the basis of the equivalent current dipole model. The localization of the active nerve tissue is confirmed by a computer tomography image of the upper arm cross-section. Furthermore, a calculation of the total current distribution in the nerve explains the observed morphology of the signal.
Spatially restricted biological current distributions, like the primary neuronal response in the human somatosensory cortex evoked by electric nerve stimulation, can be described adequately by a current multipole expansion. Here analytic formulas are derived for computing magnetic fields induced by current multipoles in terms of an nth-order derivative of the dipole field. The required differential operators are given in closed form for arbitrary order. The concept is realized in different forms for an expansion of the scalar as well as the dyadic Green's function, the latter allowing for separation of those multipolar source components that are electrically silent but magnetically detectable. The resulting formulas are generally applicable for current sources embedded in arbitrarily shaped volume conductors. By using neurophysiologically relevant source parameters, examples are provided for a spherical volume conductor with an analytically given dipole field. An analysis of the signal-to-noise ratio for multipole coefficients up to the octapolar term indicates that the lateral extent of cortical current sources can be detected by magnetoencephalographic recordings.
The generators of high frequency bursts (600-Hz activity) detected at the parietal scalp over the primary somatosensory cortex after electrical stimulation of peripheral nerves are not yet known. We investigated the influence of benzodiazepine on the somatosensory-evoked 600-Hz activity by means of neuromagnetic measurements and source analysis. After oral administration of lorazepam, the latency of the 600-Hz burst activity was increased; specifically later peaks were delayed more than earlier peaks. In contrast, the latency of the concurrent primary cortical low frequency response (N20m) was not significantly changed. The source strengths of both N20m and 600-Hz bursts were significantly increased. Our results provide evidence for two components of the 600-Hz activity with a different generator structure.
Functional magnetic resonance imaging (fMRI) was used to examine the influence of non-painful electrical stimulus intensity on the BOLD response in human primary somatosensory cortex (SI). In ten healthy subjects, index and middle finger of the right hand were stimulated separately at two different stimulus intensities. The activated volume of single finger representations as well as the volume of representational overlap of the two activations increased following an increase in stimulus intensity. This effect was seen in two different subdivisions of SI, one in the depth of the central sulcus, presumably corresponding to Brodmann area (BA) 3b, and one on the crown of the postcentral gyrus, presumably corresponding to BA 1/2. Relative overlap (ratio of overlap volume to volume of individual finger representation) was larger in BA 1/2 than in BA 3b. Additionally, in both areas relative overlap increased significantly from low to high stimulus intensity. Relative overlap did not change when different correlation thresholds were employed arguing against an unspecific 'spillover effect'. Analysis of signal intensity time courses indicated that the response difference to high versus low stimulus strength was not present during the initial seconds of stimulation, during which both led to a similar signal intensity increase. Only during the following maintenance level of the response did the response to high stimulus intensity reach a significantly higher plateau level than the one due to low intensity stimulation, an effect which was present in both areas, BA 3b and BA 1/2, respectively.
Human cortical somatosensory evoked potentials (SEP) can be modified by concomitant motor tasks ('gating'), through peripheral occlusion and/or central mechanisms. The present study aimed (1) at refining earlier results concerning motor-gating of the primary cortical EPSP-related N20 response after electric median nerve stimulation, and (2) at providing first data on motor-gating of the 600 Hz SEP wavelet burst which occurs superimposed onto N20 and primarily reflects repetitive cerebral population spikes. In 12 healthy subjects median nerve SEP were elicited, using electrical stimuli with intensities below, at and above motor threshold, under either rest or an isometric fist clenching task. Amplitude and latency modifications were analysed for the peripheral compound action potential (CAP), low-frequency SEP components (N20, P25, N35 and P70) and the high-frequency burst. While the peripheral CAP remained unchanged, isometric motor innervation significantly attenuated N20, P25 and P70 amplitudes and shortened peak latencies progressively for all components after N20. In contrast, the high-frequency 600 Hz burst was modulated neither in amplitude nor in latency. Regular amplitude recruitment occurred for all components independent from the motor task, excluding channel saturation as an explanation for gating. We suggest that SEP gating under isometric motor innervation is a central process which selectively operates on specific SEP components and could partly reflect an "efference copy" mechanism.
'Gating' refers to a reduction of cortical somatosensory evoked potentials (SEP) under multiple simultaneous afferent inputs. This study used the opportunity for intrathalamic recordings in patients with movement disorders to clarify to what extent cortical SEP gating is preceded by thalamic gating. Recordings were performed in 10 patients, narcotised by intravenous propofol when receiving implantation of a therapeutic deep brain stimulator system. SEP were elicited by an 8.1-Hz median nerve stimulation at twice motor threshold and were recorded simultaneously from both intrathalamic and scalp electrodes before and after the application of the depolarising muscle blocker succinylcholine which eliminated both the background muscular tone and the repetitive muscle twitches caused by the median nerve stimulation. Peripheral compound action potentials recorded at the upper arm remained unchanged after complete muscle relaxation, proving a continuously effective nerve stimulation. In contrast, the primary cortical SEP component (N20) was significantly increased under succinylcholine (+17%). This cortical release from gating was not paralleled, however, by an increased thalamic response; rather, the primary thalamic response (P16) showed a slight (-9%) but highly significant amplitude reduction. As the recordings were performed in narcotised patients, any potentially variable attentional bias on part of the subjects can be excluded as confounding factor when comparing the two experimental conditions with vs. without reafferent somatosensory inflow. Thus, given the high signal-to-noise ratio of intrathalamically recorded SEP, the present study shows a distinct thalamo-cortical dissociation with the primary somatosensory cortex representing the predominant level exhibiting SEP gating.