Daisuke Naka

The somatosensory evoked magnetic fields.

Averaged magnetoencephalography (MEG) following somatosensory stimulation, somatosensory evoked magnetic field(s) (SEF), in humans are reviewed. The equivalent current dipole(s) (ECD) of the primary and the following middle-latency components of SEF following electrical stimulation within 80-100 ms are estimated in area 3b of the primary somatosensory cortex (SI), the posterior bank of the central sulcus, in the hemisphere contralateral to the stimulated site. Their sites are generally compatible with the homunculus which was reported by Penfield using direct cortical stimulation during surgery. SEF to passive finger movement is generated in area 3a or 2 of SI, unlike with electrical stimulation. Long-latency components with peaks of approximately 80-120 ms are recorded in the bilateral hemispheres and their ECD are estimated in the secondary somatosensory cortex (SII) in the bilateral hemispheres. We also summarized (1) the gating effects on SEF by interference tactile stimulation or movement applied to the stimulus site, (2) clinical applications of SEF in the fields of neurosurgery and neurology and (3) cortical plasticity (reorganization) of the SI. SEF specific to painful stimulation is also recorded following painful stimulation by CO(2) laser beam. Pain-specific components are recorded over 150 ms after the stimulus and their ECD are estimated in the bilateral SII and the limbic system. We introduced a newly-developed multi (12)-channel gradiometer system with the smallest and highest quality superconducting quantum interference device (micro-SQUID) available to non-invasively detect the magnetic fields of a human peripheral nerve. Clear nerve action fields (NAFs) were consistently recorded from all subjects.

Effects of distraction on pain perception: magneto- and electro-encephalographic studies

After a painful CO2 laser stimulation to the skin, the magnetoencephalography (MEG) response (164 ms in average peak latency) was not affected by distraction, but the sequential electroencephalography (EEG) responses (240-340 ms), probably generated by a summation of activities in multiple areas, were markedly affected. We suspect that the MEG response, whose dipole is estimated in the bilateral second somatosensory cortex (SII) and insula, reflects the primary activities of pain in humans.

Somatosensory evoked magnetic fields following passive finger movement

The somatosensory evoked magnetic field (SEF) following passive finger movement and electrical stimulation of finger was studied in 10 normal subjects. Four main components were identified in SEFs recorded at the hemisphere contralateral to the moved finger: 1M(P), 2M(P), 3M(P) and 4M(P). The 1M(P) was clearly identified only in three subjects and was smaller than other components. The equivalent current dipoles (ECDs) of 1M(P) were located around the finger area of the primary sensorimotor cortex and oriented either posteriorly or anteriorly. We speculate that it was generated in areas 3a or 2 of the primary sensory cortex. The 2M(P) and 3M(P) were usually combined as one large deflection with two peaks. Because the ECDs of 2M(P) and 3M(P) were located around the finger area of the sensorimotor cortex and both oriented posteriorly, they were considered to be generated in area 4 and/or 3b, and their activities have temporal overlapping. The 4M(P) has large inter-individual difference in terms of amplitude and latency. The ECD of 4M(P) was also located around the finger area of the primary sensorimotor cortex, and oriented anteriorly. The 4M(PI), the main component recorded from the hemisphere ipsilateral to the moved finger, was located in the upper bank of the sylvian fissure, probably the second sensory cortex (SII). Five components, 1M(E), 2M(E), 3M(E), 4M(E) and 4M(EI), corresponding to 1M(P), 2M(P), 3M(P), 4M(P) and 4M(PI), were identified following electrical stimulation of the same finger. However, SEFs following passive movement were clearly different from SEFs following electrical stimulation, in terms of waveforms and source locations, probably due to differences of ascending fibers and receptive fields.

Sensory perception during sleep in humans: a magnetoencephalograhic study

We reported the changes of brain responses during sleep following auditory, visual, somatosensory and painful somatosensory stimulation by using magnetoencephalography (MEG). Surprisingly, very large changes were found under all conditions, although the changes in each were not the same. However, there are some common findings. Short-latency components, reflecting the primary cortical activities generated in the primary sensory cortex for each stimulus kind, show no significant change, or are slightly prolonged in latency and decreased in amplitude. These findings indicate that the neuronal activities in the primary sensory cortex are not affected or are only slightly inhibited during sleep. By contrast, middle- and long-latency components, probably reflecting secondary activities, are much affected during sleep. Since the dipole location is changed (auditory stimulation), unchanged (somatosensory stimulation) or vague (visual stimulation) between the state of being awake and asleep, different regions responsible for such changes of activity may be one explanation, although the activated regions are very close to each other. The enhancement of activities probably indicates two possibilities, an increase in the activity of excitatory systems during sleep, or a decrease in the activity of some inhibitory systems, which are active in the awake state. We have no evidence to support either, but we prefer the latter, since it is difficult to consider why neuronal activities would be increased during sleep.

Simple and novel method for measuring conduction velocity of A delta fibers in humans.

We report a simple new method for measuring the conduction velocity (CV) of A delta fibers in normal subjects. A large positive component of somatosensory evoked potential (SEP) whose peak latency was approximately 250 ms was clearly recorded only when strong electrical stimulation causing a definite painful feeling was applied to the skin. The CV of the peripheral nerve was calculated by measuring the latency difference of this component between the distal-stimulated SEP and proximal-stimulated SEP and the distance between two stimulus sites. The CV was approximately 11.4 m/s, (range 8.8-15.9 m/s), in the range of A delta fibers. The sleep effect on pain-related SEP was also observed in 3 subjects. The amplitude of pain-related SEP decreased with the progress of sleep stage. This simple and novel method is available in most clinics and should be very useful in investigating the physiologic functions of peripheral nerves in patients as well as normal subjects.

Magnetoencephalographic responses to painful impact stimulation

Magnetoencephalographic (MEG) field recordings are unique to detect current dipoles in SI and SII. Few devices are available for painful mechanical stimulation in magnetically shielded MEG rooms. The aim of the present MEG (dual 37-channel biomagnetometer) study was to investigate the location of the cortical generators evoked by painful impact stimuli of different intensities. An airgun was placed outside the shielded MEG room, and small plastic bullets were fired at the arm and trunk of the subjects in the room. The velocity of the bullet was measured and related to the evoked pain intensity. Stimuli were delivered for each of the following three conditions: strong pain intensity elicited from the upper arm and upper trunk; weak pain intensity elicited from the upper trunk. The evoked MEG responses had a major component with the characteristically polarity-reversal deflections indicating a dipole located beneath the coils. The response could be estimated by a single current dipole. When the estimated locations of the dipoles were superimposed on the individual magnetic resonance images (MRIs), consistent bilateral activation of areas corresponding to the secondary sensory cortices (SII) was found.

Effects of visual and auditory stimulation on somatosensory evoked magnetic fields.

DESIGN AND METHODS We investigated the effects of continuous visual (cartoon and random dot motion) and auditory (music) stimulation on somatosensory evoked magnetic fields (SEFs) following electrical stimulation of the median nerve on 12 normal subjects using paired t test and two way ANOVA for the statistics. RESULTS In the hemisphere contralateral to the stimulated nerve, the middle-latency components (35-60 ms in latency) were significantly enhanced by visual, but not by auditory stimulation. The dipoles of all components within 60-70 ms following stimulation were estimated to be very close each other, around the hand area of the primary sensory cortex (SI). In the ipsilateral hemisphere, the middle-latency components (70-100 ms in latency), the dipoles of which were estimated to be in the second sensory cortex (SII), were markedly decreased in amplitude by both the visual and auditory stimulation. CONCLUSIONS These changes in waveform by visual and auditory stimulation are thought to be due to the effects of the activation of polymodal neurons, which receive not only somatosensory but also visual and/or auditory inputs, in areas 5 and/or 7 as well as in the medial superior temporal region (MST) and superior temporal sulcus (STS), although a change of attention might also be a factor causing such findings.

Structure of the auditory evoked magnetic fields during sleep.

We studied the effects of sleep on auditory evoked magnetic fields following pure tone stimulation applied to the right ear of 10 healthy normal volunteers to investigate the changes in the processing of auditory perception in the primary auditory cortex. Dual 37-channel biomagnetometers were used to record auditory evoked magnetic fields over the bilateral temporal lobes in response to presented tones. Auditory evoked magnetic fields were compared for three stimulus frequencies (250, 1000 and 4000 Hz) and three sleep stages (awake state, sleep stages 1 and 2). Four main components, M50, M100, M150 and M200, were identified with latencies of approximately 50, 100, 150 and 200 ms, respectively. The latency of each component had a tendency to be prolonged with the depth of sleep stage in all frequencies. The amplitude ratios of the early-latency components (M50 and M100) showed a tendency of reduction compared with the same components in the awake state. By contrast, the amplitude ratios of the long-latency components (M150 and M200) were significantly enhanced with an increase in the sleep stage compared with the same components in the awake state. The equivalent current dipoles of all components in all conditions were detected at the superior temporal cortex (the primary auditory cortex). As for the changes in the equivalent current dipole location of each component, the equivalent current dipole was detected in the more posterior and medial region in responses to the high-frequency tone (1000 and 4000 Hz) compared with those to 250 Hz tone stimulation. Although the equivalent current dipoles of the early-latency components (M50 and M100) were in regions more anterior and superior compared to those in the awake state, there was no consistent tendency of changes in equivalent current dipole locations between each sleep stage in the late-latency components (M150 and M200). These findings are probably due to the difference in generating mechanisms between the early- and late-latency components.

Somatosensory evoked magnetic fields and potentials following passive toe movement in humans

The somatosensory evoked magnetic fields (SEFs) and evoked potentials (SEPs) following passive toe movement were studied in 10 normal subjects. Five main components were identified in SEFs recorded around the vertex around the foot area of the primary sensory cortex (SI). The first and second components, 1M and 2M, were identified at approximately 35 and 46 ms. Equivalent current dipoles (ECDs) of both 1M and 2M were estimated around SI in the hemisphere contralateral to the movement toe, and were probably generated in area 3a or area 2, which mainly receive inputs ascending through muscle and joint afferents. The large inter-individual difference of 1M and 2M in terms of ECD orientation was probably due to a large anatomical variance of the foot area of SI. The third and fourth components, 3M and 4M, were identified at approximately 62 ms and 87 ms, respectively. They appeared to be a single large long-duration component with two peaks. Since the 3M and 4M components were significantly larger than the 1M and 2M components in amplitude and their ECD location was significantly superior to that of 1M and 2M, we suspected that they were generated in different sites from those of 1M and 2M, probably area 3b or area 4. Four components, 1E, 2E, 3E and 4E, were identified in SEPs, which appeared to correspond to 1M, 2M, 3M and 4M, respectively. The variation observed in the scalp distribution of the primary component, 1E, could be accounted for by the variation of the orientation of ECD of the 1M component. There was a large difference in the waveform of the long-latency component (longer than 100 ms) between SEFs and SEPs. The 5E of SEPs was a large amplitude component, but the 5M of SEFs was small or absent. We speculate that this long-latency component was generated by multiple generators.

Effects of tactile interference stimulation on somatosensory evoked magnetic fields following tibial nerve stimulation.

Tactile stimulation of the hand interferes with somatosensory evoked brain responses following electrical median nerve stimulation. This effect was studied in eight normal subjects by magnetoencephalography (MEG). When stimulation was applied to the hand ipsilateral to the stimulated nerve, only the third response (3M) was enhanced in five subjects, but other responses were attenuated in all subjects. These interference effects were probably due to interactions in areas 3b and 1. After stimulation of the contralateral hand, only the second response (2M) was enhanced in six subjects. This effect was probably due to the intracerebral interactions mediated through the corpus callosum.