Search PubMed⌕ Search

Biomedical subjects

R Kakigi

Publications and source records attributed to R Kakigi.

At least 109 records · Page 6Linked to original sources
PubMed1996

Intracerebral interactions caused by bilateral median nerve stimulation in man: a magnetoencephalographic study.

Somatosensory evoked magnetic fields (SEFs) following stimulation of the median nerves bilaterally ('bilateral' waveform) were examined in normal subjects to determine the interference effects of activation of sensory areas in bilateral hemispheres. SEFs following right median nerve stimulation and those following left median nerve stimulation were summated ('summated' waveform). A 'difference' waveform was induced by subtraction of the 'bilateral' waveform from 'summated' waveform. Short-latency deflections showed no consistent differences between the 'summated' and 'bilateral' waveforms, but the middle-latency deflection. N60m-P60m, in the 'bilateral' waveform was significantly (P < 0.01) smaller than that in the 'summated' waveform. The long-latency deflection, the N90m-P90m, in the 'bilateral' waveform was markedly (P < 0.001) reduced in amplitude as compared with the 'summated' waveform. The differences were clearly identified in the 'difference' waveform, in which the main deflections, U90m-D90m, were found in all subjects. Equivalent current dipoles (ECDs) of the short- and middle-latency deflections were located in the primary sensory cortex (SI) contralateral to the stimulated nerve, but ECDs of the N90m-P90m and U90m-D90m were located in bilateral second sensory cortices (SII) which are considered to receive ascending signals from bilateral sides of the body.

Adult↗
PubMed1996

Effects of judgement process on motor evoked potentials in Go/No-go hand movement task.

We examined the motor evoked potentials (MEP) of the forearm muscles following transcranial magnetic stimulation after the Go/No-go reaction-time hands movement in ten normal subjects. Facilitation of MEP of the agonistic muscles and suppression of MEP of the antagonistic muscles were recognized during the 'Go' session, while the MEPs of both muscles were markedly suppressed in the 'No-go' session. We considered that this MEP changes reflected the inhibition on the pyramidal tract during the 'No-go' session.

Adult↗
PubMed1996

Effects of sleep on somatosensory evoked responses in human: a magnetoencephalographic study.

We studied the effects of sleep on somatosensory evoked magnetic fields (SEFs) following median nerve stimulation in normal subjects, to investigate the changes of functional processing of sensory perception in the primary and second sensory cortices (SI and SII). The early components, 1M, 2M and 3M, which were generated in SI contralateral to the stimulated nerve, showed no significant change of latency or amplitude in stage 1 or 2 as compared with those in the awake state. The long-latency response, 4M whose latency was about 100 ms, was significantly enhanced in stage 2. The 4M was considered to be generated in SI and SII in the awake state, but the enhanced 4M in stage 2 was restricted in SI. The 4M(I) generated in SII of the hemisphere ipsilateral to the stimulated nerve, corresponding to 4M in the contralateral hemisphere, was absent during sleep. These findings were probably due to the difference of activities between SI and SII during sleep, that is, an increase of sensitivity to somatosensory stimulation in SI but a decrease or disappearance in SII.

Adult↗
PubMed1996

Differentiation of receptive fields in the sensory cortex following stimulation of various nerves of the lower limb in humans: a magnetoencephalographic study.

The authors investigated magnetoencephalography following stimulation of the posterior tibial (PT) and sural (SU) nerves at the ankle, the peroneal nerve (PE) at the knee, and the femoral nerve (FE) overlying the inguinal ligament in seven normal subjects (14 limbs) and confirmed its usefulness in clarifying the detailed differentiation of the receptive fields in the lower limb area of the primary sensory cortex in humans. The results were summarized as follows: 1) the equivalent current dipoles (ECDs) estimated by the magnetic fields following stimulation of the PT and SU were located very close to each other, along the interhemispheric fissure in all 14 limbs. They were directed horizontally to the hemisphere ipsilateral to the stimulated nerve. 2) The ECD following stimulation of the FE was clearly different from that seen in the other nerves, in terms of the location and/or direction, in all 14 limbs. The ECDs of 14 limbs were classified into two types according to the distance of ECD location between PT and FE; Type 1 (> 1 cm, nine limbs) and Type 2 (< 1 cm, five limbs). The ECD following FE stimulation was located on the crown of the postcentral gyrus or at the edge of the interhemispheric fissure in Type 1 and was close to the ECDs following PT and SU stimulation along the interhemispheric fissure in Type 2. 3) The ECD following PE stimulation was located along the interhemispheric fissure in all 14 limbs as for PT and SU. Its location was slightly but significantly higher than that of PT and SU in Type 1 and was close to ECDs following PT and SU stimulation in Type 2. The present findings indicated that approximately 65% (nine of 14) of the limbs showed the particular receptive fields compatible with the homunculus. Large inter- and the intraindividual (left-right) differences found in the present study indicated a significant anatomical variation in the area of the lower limb in the sensory cortex of humans.

Adult↗
PubMed1996

Pain relief by various kinds of interference stimulation applied to the peripheral skin in humans: pain-related brain potentials following CO2 laser stimulation.

Pain perception is changed by various kinds of interference stimulation applied to the peripheral skin in humans. We investigated pain-related somatosensory evoked brain potentials (pain SEPs) following CO2 laser stimulation applied to the hand or foot in normal subjects, to elucidate the underlying mechanisms. A pain visual analogue scale (VAS) was also scored to determine the degree of subjective feeling of painful sensation. The following stimulations were applied as the interference: (1) vibration, (2) active and passive movements of the hand or foot, (3) noxious warming by hot water (46 degrees C) and (4) noxious cooling by ice water (0 degrees C). These interference stimulations were applied not only to the same hand or foot as the laser stimuli but also to the contralateral hand or foot. Significant changes in the amplitude of pain SEPs and VAS score were observed to some degree for each type of interference, and we concluded that gate control theory and diffuse noxious inhibitory control were the most appropriate hypotheses to account for this particular phenomenon of pain relief. Some movement-related cortical activities were also considered to be an important factor. These findings could not be accounted for by simple changes in the subjects' attention. Pain relief was more prominent at the second pain ascending through C fibers than that of the first pain ascending through Adelta fibers. The responsible sites for this phenomenon are considered to be the dorsal horn of the spinal cord, the brainstem and some parts of the brain such as the second sensory cortex and the cingulate cortex.

Brain↗
PubMed1996

Recurrent demyelinating transverse myelitis in a high titer HBs-antigen carrier.

A 46-year-old man who was an extremely high titer hepatitis B surface (HBs)-antigen carrier had three attacks of acute demyelinating transverse myelitis associated with signs of meningeal irritation. Each episode showed good response to corticosteroid therapy. The cerebrospinal fluid was characterized by elevated levels of myelin basic protein (MBP) and predominating CD4+CD29+ helper-inducer T cells during the acute stages, and also by persistently positive HBs antigen. There were neither autoantibodies nor evidence of vasculitis. However, circulating immune complexes composed of HBs antigen disappeared after treatment, indicating that immunity to hepatitis B virus played a role in the demyelinative lesion formation in the central nervous system (CNS). In light of the animal studies demonstrating autoimmunity triggered by molecular mimicry between MBP and hepatitis B virus antigens, this patient may serve as a rare example of CNS demyelination in humans with the same autoimmune etiology.

Autoantigens↗
PubMed1995

Somatosensory evoked magnetic fields after mechanical stimulation of the scalp in humans.

Somatosensory evoked magnetic fields after mechanical stimulation by air-pressure-induced tapping which was applied to the forehead and occiput were examined in normal human subjects. The equivalent current dipole (ECD) of the initial magnetic field, 1M, was identified in the primary somatosensory cortex (SI) in the hemisphere contralateral to the stimulation. The ECD of the subsequent magnetic fields, 2M, was identified in bilateral second sensory cortices (SII). The ECD position of 1M in SI generated after the scalp stimulation was closely inferior to the hand area of the SI, which was consistent with the well-known somatotopic organization, 'homunculus'.

Adult↗
PubMed1995

Pain-related magnetic fields following painful CO2 laser stimulation in man.

The initial somatosensory evoked magnetic fields following painful heat stimulation by CO2 laser beam applied to the upper and lower limb were investigated in normal subjects. The main deflections, 'Pain MA' and 'Pain ML' following the arm and leg stimulation, respectively, were identified in the bilateral second sensory cortices (SII). The onset latencies of Pain MA and Pain ML were approximately 150 and 200 ms, respectively. No consistent equivalent current dipole was found in other areas including the primary sensory cortex in each hemisphere. Therefore, we consider that neurons in the bilateral SII are initially activated following painful heat stimulation.

Adult↗
PubMed1995

Topography of somatosensory evoked magnetic fields following posterior tibial nerve stimulation.

The topography of somatosensory evoked magnetic fields (SEFs) following stimulation of the right and left posterior tibial nerves was investigated in 5 normal subjects (10 nerves). The main deflections N37m-P45m-N60m-P75m and their counterparts P37m-N45m-P60m-N75m were identified in the hemisphere contralateral to the stimulated nerve. Their equivalent current dipoles (ECDs) were located in the foot area of the primary sensory cortex (SI), probably in area 3b. Restricted minor deflections, P40m-N40m and N50m-P50m, were considered to be generated in area 1 in SI. As the generator sources of P37m-N37m, P40m-N40m and N45m-P45m were temporarily changed and interfered with each other, the direction of ECDs appeared to be rotated with the passage of time. Small middle-latency deflections, N100m-P100m, were clearly identified in 2 subjects. ECDs of these deflections were found in the second sensory cortex (SII), in both hemispheres, although they were clearer in the hemisphere contralateral to the stimulated nerve. In conclusion, short- and middle-latency SEFs are mainly generated in area 3b in SI contralateral to the stimulated nerve, and responses generated in area 1 of SI and SII affect the SEFs to some degree, but interindividual differences are large compared with SEFs evoked by upper limb stimulation.

Adult↗
PubMed1995

Pain-related somatosensory evoked magnetic fields.

Somatosensory evoked magnetic fields (SEFs) following painful electrical stimulation of the finger were investigated in 5 normal subjects. Equivalent current dipoles (ECDs) of deflections shorter than 100 msec in latency were located in the primary sensory cortex (SI) in the hemisphere contralateral to the stimulated finger following either non-painful or painful stimulation. Two main deflections, N100m-P100m and N250m-P250m, were independently identified following painful stimulation, although they were not found in SEFs following non-painful weak stimulation. ECDs of the N100m-P100m were considered to be located in the bilateral second sensory cortices (SII). ECDs of the N250m-P250m were identified in the bilateral cingulate cortices and SII, but the intersubject difference was large. Therefore, we considered that contralateral SI and bilateral SII were initially activated by painful noxious stimulation, and then multiple areas including bilateral SII and cingulate cortices were activated. In EEG recordings (evoked potentials), no potential corresponding to N100m-P100m was found, probably because it was difficult to record activation in SII by EEG recordings. The P250 potential which corresponded to the N250m-P250m was clearly identified, probably because activation of multiple areas generated large long-duration EEG potentials which were maximal around the vertex, unlike MEG recordings.

Adult↗
PubMed1995

Gating of somatosensory evoked responses during active finger movements magnetoencephalographic studies.

The "gating" effects caused by active finger movements on somatosensory evoked magnetic fields (SEFs) following stimulation of the median nerve were examined in normal subjects. The effects of the interfering stimulus were best demonstrated by subtracting the "interference" wave forms from the "control" wave forms to derive the "difference" wave form. The short-latency cortical deflections, N20m-P20m, P30m-N30m and P25m-N35m were significantly attenuated with no latency changes. In contrast, the following middle-latency deflections, the N40m-P40m and the P60m-N60m were clearly changed in terms of latency and duration by the interference. The D30m-U30m and the U60m-D60m in the "difference" wave form were derived from these interference changes. It is considered that the gating effects on all deflections took place in the hemisphere contralateral to the stimulated median nerve, because all of the equivalent current dipoles (ECDs) of the short- and the middle-latency deflections in the "control", "interference" and "difference" wave forms were located there. The gating effects on the short-latency deflections were suggested to be due to the interactions between the neurons in areas 1 and 3b, which were activated by sensory inputs from cutaneous mechanoreceptors, and the neurons in area 3a which were activated by sensory inputs from the muscle spindles. The gating effects on the middle-latency deflections may mainly be due to the excitations of neurons in area 4 caused by either continuous movement-related activities or by sensory inputs spreading from the sensory cortex.

Adult↗
PubMed1994

Diffuse noxious inhibitory control. Reappraisal by pain-related somatosensory evoked potentials following CO2 laser stimulation.

The effects of DNIC (diffuse noxious inhibitory control) in humans were evaluated by means of pain SEPs (somatosensory evoked potentials) and pain visual analogue scale (VAS) following CO2 laser stimulation applied to the left knee while conditioning stimuli (non-noxious and noxious thermal stimuli) applied to the right hand. Pain SEPs were recorded from scalp electrodes following laser stimulation applied to the left knee during various conditions as follows: (1) control (without any interference), (2) non-noxious (dipping the right hand in water at 41 degrees C for 3 min), (3) noxious (dipping the right hand in water at 46 degrees C for 3 min), and (4) after-effect (3-6 min after taking the hand from the water at 46 degrees C). The present pain SEPs findings confirmed the presence of DNIC in humans, and indicates: (1) degree of pain relief was significantly correlated with changes in pain SEPs, particularly a marked decrease in amplitude, and a decrease in VAS; (2) DNIC was more effective on the second pain than the first pain; (3) the effect of DNIC gradually increased over time, but it rapidly disappeared after the conditioning stimuli ceased; and (4) DNIC was not due merely to changes of attention. I propose that the site responsible for DNIC is the brainstem or the spinal cord rather than the cerebral hemisphere.

Adult↗
PubMed1994

Do patients with Down's syndrome recognize Mickey Mouse?

In 47 patients with Down's syndrome who were too retarded to understand a conventional oddball paradigm, we studied event-related potentials (ERPs) by using task-irrelevant visual stimuli. As the patients had expressed interest in Disney cartoons and books, five pictures of Disney characters such as Mickey Mouse or Peter Pan were employed as the rare stimuli, and nine ordinary scenes such as mountains as the frequent stimuli. Five sets were constructed by intermingling each rare picture with nine frequent pictures, and each picture was presented on a TV screen. ERPs to the rare stimuli (N270-P380), which were different from the averaged waveforms to frequent stimuli and electrooculograms (EOGs), were clearly recorded in 35 out of 47 patients. Only 24 of these patients had ERPs using a conventional auditory oddball paradigm. The peak latencies in patients were significantly prolonged relative to age-matched normal controls, probably due to a slowed neural processing. The amplitude in patients was slightly larger than normal controls, probably due to the patients' greater interest or surprise when confronted with the Disney characters.

Adolescent↗
PubMed1994

Somatosensory evoked magnetic fields following median nerve stimulation.

Topography of somatosensory evoked magnetic fields (SEFs) following stimulation of the median nerve were investigated in normal subjects. N20m-P30m-N40m-P60m and their counterpart, P20m-N30m-P40m-N60m, were identified in the hemisphere contralateral to the stimulated median nerve. Their equivalent current dipoles (ECDs) were considered to be located in the hand area of area 3b in the primary sensory cortex (SI). Restricted deflections, P25m and N25m, were considered to be generated in area 1 in SI. Therefore, short-latency deflections less than 40 ms were considered to be hybrids of ECDs generated in areas 3b and 1. Middle-latency deflections, N90m-P90m, were considered to be generated in the second sensory cortex (SII), but they were greatly affected by the much stronger fields generated in SI. The N30m deflection, which was a magnetic reflection of the N30 potential of somatosensory evoked potentials (SEPs), were widely recorded in the frontal area. The generator site of N30 of SEPs is considered to be the supplementary motor area (SMA). However, ECDs of N30m were located in SI, and no significant ECD generated in the frontal area including SMA was detected. No significant deflections other than small N90m-P90m in SII were identified in the hemisphere ipsilateral to the stimulated nerve. No significant deflections whose ECDs were generated in the mid-parietal area were identified. In conclusion, short- and middle-latency SEFs are mainly generated in area 3b in SI contralateral to the stimulated median nerve, and responses generated in area 1 of SI and SII affect the SEFs to some degree.

Adult↗
PubMed1994

[Evoked potentials].

Recent advances of evoked potentials, mainly pain-related somatosensory evoked potentials following CO2 laser stimulation (pain SEPs), were summarized. A small negative and a large positive potential, the N240-P340 and the N300-P400 following the hand and the foot stimulation, were identified in normal subjects. Conduction velocity of the A delta fibers and the spinothalamic tract was approximately 10 m/sec. Pain SEPs were significantly decreased in amplitude and the marked pain relief was induced by vibration applied to the area where laser stimulation was applied. This finding was compatible with the gate control theory. Active and passive movements of the limbs remote from and adjacent to the stimulated area significantly decreased pain SEPs in amplitude. This indicated the particular interactions between pain perception and movement-related cortical activities taken place in some areas of the brain. The theory, diffuse noxious inhibitory controls (DNIC) proposed by Le Bars et al., was also confirmed by pain SEPs. Pain SEPs were useful in clinical testing. Pain SEP findings showed a significant correlation with the clinical impairment of pain sensation, and the subclinical lesions of the ascending pathways of the painful sensation were detected by pain SEPs.

Electroencephalography↗
PubMed1994

[Brain potentials following painful stimulation in humans].

When a CO2 laser beam is applied to the skin, subjects feel a "pin-prick" sensation. We have investigated somatosensory evoked potentials following CO2 laser stimulation (laser SEP) in normal subjects, and confirmed that signals following CO2 laser stimulation ascend through A-delta fibers and the spinothalamic tract. Its conduction velocity is approximately 10 m/s. Change in pain perception produced by the application of movement and various modalities of sensation to areas adjacent to, and remote from, the painful stimulus was investigated by means of laser SEPs. We investigated pain SEPs and conventional electrically stimulated SEPs in patients with various neurological diseases including peripheral neuropathies, syringomyelia, multiple sclerosis and HTLV-I-associated myelopathy (HAM), and found a good correlation between laser SEP findings and the degree of impairment of pain-temperature sensations. Laser SEPs could be used to find subclinical abnormalities in some patients.

Adult↗
PubMed1993

Scalp topography of somatosensory evoked potentials following median and posterior tibial nerve stimulation in Down's syndrome.

The scalp topography of somatosensory evoked potentials (SEPs) following stimulation of the median and posterior tibial nerve of 39 patients with Down's syndrome was compared with that of age-matched normal controls using significance probability mapping (SPM). The maximal area of each potential in Down's syndrome was similar to that in normal controls, but the scalp distribution was wider. The amplitudes of all components, except the N45 and P59 potentials of the posterior tibial nerve SEPs, were greater in Down's syndrome, and the t values calculated by SPM were significantly greater. However, the difference of SEP maps between Down's patients and aged controls (over 65 years) was much smaller than that between Down's patients and age-matched controls. Therefore, we conclude that the generator sources and generating mechanisms of SEPs in Down's syndrome are not different from those of normal control, however SEP potentials in Down's syndrome are remarkably enhanced, resulting in a wider distribution, probably due to accelerated aging in Down's patients.

Adolescent↗