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Biomedical subjects

M Shimojo

Publications and source records attributed to M Shimojo.

At least 55 records · Page 3Linked to original sources
PubMed1997

Effects of movement and movement imagery on somatosensory evoked magnetic fields following posterior tibial nerve stimulation.

We examined the "gating" effects caused by active and passive movements of toes and by "movement imagery" (mental moving of the toe without actual movements) on somatosensory evoked magnetic fields (SEFs) following stimulation of the posterior tibial nerve in normal subjects. Active and passive movements significantly attenuated the short- and middle-latency cortical components (P < 0.001) with no latency change, and the effects of the active movements were larger than those of the passive movements. In contrast, the subsequent long-latency component with a latency of about 100 ms was enhanced only by the active movements. Therefore, both centrifugal and centripetal mechanisms should be considered. The gating effects by movements on all components may occur in the primary sensory cortex (SI) in the hemisphere contralateral to the stimulated nerve, because all of the equivalent current dipoles (ECDs) of the components in the "control" and each "interference" waveform were located there. Active movements of the toes contralateral to the stimulated nerve caused no significant gating effect. The short-latency components were not consistently changed by "movement imagery", but the middle- and long-latency components were enhanced. Their ECDs were located in the SI contralateral to the stimulated nerve and in the SII in bilateral hemispheres. Therefore, we speculated that brain responses to somatosensory stimulation, particularly components generated in SII, were affected by volitional changes.

Adult↗
PubMed1997

Visual evoked cortical magnetic fields to pattern reversal stimulation.

We studied visual evoked magnetic fields to pattern reversal stimulation in six healthy subjects. Similar to the N75-P100-N145 components in visual evoked potentials, triphasic deflections, N75m-P100m-N145m, were clearly observed around the midoccipital position. A very small component, P50m, was occasionally observed preceding the N75m. Equivalent current dipoles (ECDs) of the main deflection, P100m, to quadrant-field stimulation were estimated near or around the calcarine fissure contralateral to the stimulation. The vertical ECD location of the P100m to the upper quadrant-field stimulation was estimated significantly lower (0.81 +/- 0.45 cm) than those to lower stimulation. These results were compatible with the retinotopic organization of the visual cortex (cruciform model) and suggested that the P100m originated in the striate cortex. The small P50m, although only a small number of ECDs could be estimated reliably, was located in the contralateral visual cortex. ECDs of the N75m were estimated mainly near or around the contralateral calcarine fissure. ECDs of the N145m were estimated also retinotopically, but with a greater vertical distance (2.90 +/- 1.09 cm) between upper and lower quadrant-field stimulation. MR-overlaid ECDs of the N145m suggested that these originated in the extrastriate cortex. No ECD was estimated when a probe was placed at the midfrontal position.

Adult↗
PubMed1997

Activity in posterior parietal cortex following somatosensory stimulation in man: magnetoencephalographic study using spatio-temporal source analysis.

We investigated the activation of posterior parietal cortex (PPC) to somatosensory stimulation in humans to determine its fundamental role as a somatosensory associated area using magnetoencephalography (MEG). We studied somatosensory evoked magnetic fields (SEF) after stimulation of median nerve, posterior tibial nerve and lip, and analyzed them by the single dipole model and also by the multidipole model using brain electric source analysis (BESA) system. In single source model analysis, the dipole at the peak latency of short-latency components following each site stimulation were located in the corresponding receptive fields in the primary somatosensory cortex (SI) contralateral to the stimulation. The dipole at the peak latency of the middle latency components were located in bilateral upper bank of Sylvian fissure (SII), By contrast, in the five-dipole model of BESA, the equivalent current dipoles (ECDs) of the middle-latency SEF after stimulation of median nerve and posterior tibial nerve were identified in the contralateral SI and in the bilateral SII and PPC, while all activities of middle-latency SEF after lip stimulation appeared to be restricted in the contralateral SI and bilateral SII. Around 80 msec in latency, the ECD location in PPC after median nerve stimulation was, on the average, 2.4 cm posterior, 2.9 cm medial and 2.6 cm superior to the hand area in SI. The ECD in PPC after posterior tibial nerve stimulation was also located posterior to the foot area in SI, but it was close to the SI area of foot, their distance being approximately 1.3 cm. ECD in PPC was almost equally demonstrated in each hemisphere. These findings suggested that the somatosensory associated cortex in PPC represented somatotopic organization in parallel with 'homunculus' in SI, but the hand area was much wider than the foot area. It was not clear whether the lip area in PPC was absent or was too close to be separated from the SI.

Adult↗
PubMed1997

Characterization of a human placental fructose-6-phosphate, 2-kinase/fructose-2,6-bisphosphatase.

A full-length cDNA, which encodes a human placental fructose-6-phosphate,2-kinase/ fructose-2,6-bisphosphatase, was constructed and expressed in Escherichia coli. The expressed protein, purified to homogeneity, showed a molecular weight of 58,000 by gel electrophoresis under denaturing conditions, compared to the deduced molecular weight of 59,410. The N-terminal sequence of 15 amino acids coincided with that of the deduced sequence. The active enzyme was a dimer as judged by molecular sieve filtration. The expressed enzyme was bifunctional with Vmax values of 142 and 0.2 milliunits/mg for the kinase and phosphatase activities, respectively. The phosphatase activity was extremely low, because one phosphatase active site residue was mutated, and consequently the kinase/phosphatase ratio was the highest among the known isozymes. Furthermore, the enzyme was phosphorylated by cAMP-dependent protein kinase, protein kinase C and also by [2-32P]fructose-2,6-bisphosphate. Phosphorylation by cAMP-dependent protein kinase and protein kinase C increased the maximal Fru-6-P,2-kinase activities by 1.8- and 1.1-fold, respectively. These results suggested that placental fructose-6-phosphate,2-kinase/ fructose-2,6-bisphosphatase is important in maintaining and regulating a relatively high rate of glycolysis in placenta.

Cyclic AMP-Dependent Protein Kinases↗
PubMed1997

Immunodetection of 11 beta-hydroxysteroid dehydrogenase type 2 in human mineralocorticoid target tissues: evidence for nuclear localization.

11 beta-Hydroxysteroid dehydrogenase (11 beta HSI) is an enzyme complex responsible for the conversion of hormonally active cortisol to inactive cortisone; two isoforms of the enzyme have been cloned and characterized. Clinical observations from patients with the hypertensive syndrome apparent mineralocorticoid excess, recently explained on the basis of mutations in the human 11 beta HSD2 gene, suggest that it is the 11 beta HSD2 isoform that serves a vital role in dictating specificity upon the mineralocorticoid receptor (MR). We have raised a novel antibody in sheep against human 11 beta HSD2 using synthetic multiantigenic peptides and have examined the localization and subcellular distribution of 11 beta HSD2 in mineralocorticoid target tissues. The immunopurified antibody recognized a single band of approximately 44 kDa in placenta, trophoblast, and distal colon. In kidney tissue, two bands of approximately 44 and 48 kDa were consistently observed. No signal was seen in decidua, adrenal, or liver. Immunoperoxidase studies on the mineralocorticoid target tissues, kidney, colon, and parotid gland indicated positive staining in epithelial cells known to express the MR: respectively, renal collecting ducts, surface and crypt colonic epithelial cells, and parotid duct epithelial cells. No staining was seen in these tissues in other sites. The intracellular localization of 11 beta HSD2 in kidney and colon epithelial cells was addressed using confocal laser microscopy. Parallel measurements of 11 beta HSD2 and nuclear propidium iodide fluorescence on sections scanned through an optical section of approximately 0.1 micron indicated significant 11 beta HSD2 immunofluorescence in the nucleus. In human kidney, colon, and salivary gland, 11 beta HSD2 protects the MR from glucocorticoid excess in an autocrine fashion. Furthermore, within these tissues, 11 beta HSD2, which had been considered to be a microsomal enzyme, is also found in the nucleus, suggesting that the interaction between the MR and aldosterone or cortisol is in part a nuclear event.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1997

18-Hydroxycortisol and 18-oxocortisol in Cushing's syndrome.

In patients with primary aldosteronism due to an aldosterone-producing adenoma and glucocorticoid-suppressible aldosteronism, 18-hydroxycortisol and 18-oxocortisol excretions are elevated. Both steroids are synthesized in the transitional zone between the zona glomerulosa and zona fasciculata. There are no reports concerning production of these steroids in Cushing's syndrome due to adrenal adenoma or hyperplasia, as far as we know. We determined the urinary excretion and serum concentration of 18-hydroxycortisol and 18-oxocortisol in eight patients with Cushing's syndrome (four due to adrenal adenoma, and four due to adrenal hyperplasia). Two of the four patients with adrenal adenoma had high levels of urinary and serum 18-hydroxycortisol and 18-oxocortisol; on the other hand all the patients with adrenal hyperplasia had normal urinary and serum levels of both steroids. Patients with high concentrations of 18-hydroxycortisol and 18-oxocortisol, however, showed no differences in clinical features, routine laboratory findings and hormonal data compared to patients with normal concentrations of 18-hydroxycortisol and 18-oxocortisol. Our data suggest that some adrenal adenomas causing Cushing's syndrome originate from transitional cells.

Adenoma↗
PubMed1996

Effects of tactile interference stimulation on somatosensory evoked magnetic fields.

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 magnetonecephalography (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.

Adult↗
PubMed1996

Reciprocal change of motor evoked potentials preceding voluntary movement in humans.

Reciprocal change of motor evoked potentials (MEPs) recorded from the agonist and antagonist muscles of the forearm was studied in 10 normal subjects in whom transcranial magnetic stimulation (TMS) was applied to the hand motor area before voluntary wrist movements. MEP recorded from the agonist muscles, that is, radial extensor muscles for wrist extension and ulnar flexor muscle for wrist flexion, were gradually facilitated with shortening of the interval between the magnetic stimulation and the voluntary muscle contraction. In contrast, MEP recorded from the antagonist muscles, that is, ulnar flexor muscle for wrist extension and radial extensor muscles for wrist flexion, were gradually suppressed as the interval shortened. The reciprocal change of MEP was recognized when TMS was applied within 60 ms prior to the voluntary movements. The present data confirmed that reciprocal change of MEP was recognized before voluntary movements; they further suggest that cortically originated reciprocal control of the corticospinal pathway may exist and that it may be generated just before the voluntary movement.

Adult↗
PubMed1996

Somatosensory evoked magnetic fields following stimulation of the lip in humans.

The topography of somatosensory evoked magnetic fields (SEFs) following stimulation of the upper and lower lips was investigated in 6 normal subjects. When the lateral side of the upper lip was stimulated, P20m and its counterpart, N20m, were identified in the hemisphere contralateral to the stimulated side. The equivalent current dipoles (ECDs) of N20m-P20m were considered to be located in lip area of the primary sensory cortex (SI). Middle latency deflections (N40m-P40m, N60m-P60m, and N80m-P80m) were identified in bilateral hemispheres. Their ECDs were located in the SI in both hemispheres. Long latency deflections (P110m-N110m) were recognized in both hemispheres, and their ECDs were located inferior to the SI, in an area considered to be the secondary sensory cortex (SII). When the midline of the lip was stimulated, similar short and middle latency deflections was also identified, but SII deflections (P110m-N110m) were decreased in amplitude. When the lower lip was stimulated, the ECDs of short and middle latency deflections were located at a site in the SI inferior to or near those elicited by upper lip stimulation. The ECDs of P110m-N110m were located in an area of the SII similar to that upon stimulation of the upper lip, but their orientations were different.

Adult↗
PubMed1996

Effects of noxious cooling of the skin on pain perception in man.

By means of somatosensory evoked brain potentials following painful CO2 laser stimulation (pain SEPs) and a pain visual analogue scale (VAS), we investigated changes in pain perception caused by noxious cooling of the skin in normal subjects. Pain SEPs were recorded from scalp electrodes following laser stimulation applied to the leg under various conditions as follows: (1) control (without any interference); (2) 46 degrees C foot (dipping the foot ipsilateral to the stimulated leg in hot water at 46 degrees C); (3) 0 degrees C foot (dipping the foot ipsilateral to the stimulated leg in ice water at 0 degrees C); and (4) 0 degrees C hand (dipping the hand contralateral to the stimulated leg in ice water at 0 degrees C). Marked decreases in amplitude of pain SEPs and VAS were observed under all conditions as compared with the control (P < 0.001); the degree of pain relief was significantly correlated with changes in pain SEPs. These changes were greatest in the '0 degrees C hand' condition, followed in decreasing order by '0 degrees C foot' and '46 degrees C foot', and there was a significant difference between '0 degrees C hand' and the '46 degrees C foot' condition. We considered that the decrease in pain is due to the diffuse noxious inhibitory control (DNIC). The reason why the degree of pain relief in '0 degrees C foot' condition was less than that in '0 degrees C hand' condition is unclear, but some particular spatial summation of two kinds of nociceptive impulses mediated by the same pathway might take place.

Adult↗
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

Adrenal 11 beta-hydroxysteroid dehydrogenase.

11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyzes the interconversion of cortisol (F) to inactive cortisone (E) in man (corticosterone (B) to 11-dehydrocorticosterone (A) in rodents) and plays a crucial role in regulating corticosteroid hormone action. Two isoforms of this enzyme have been characterized; a low affinity NADP(H)-dependent enzyme (11 beta-HSD1) and a high affinity NAD-dependent dehydrogenase (11 beta-HSD2). We have analysed the expression of 11 beta-HSD in the rodent and human adrenal gland and have investigated its role with respect to glucocorticoid-mediated catecholamine biosynthesis. Our studies indicated higher expression of 11 beta-HSD2 mRNA in male versus female intact mouse adrenal. Both 11 beta-HSD isoforms were detected in intact male rat adrenal homogenates. For the 11 beta-HSD1 isoform, NADPH-dependent oxo-reductase activity exceeded that of NADP-dependent dehydrogenase activity (188 versus 98 pmol/mg.protein.hr). In situ hybridisation studies indicated specific localisation of 11 beta-HSD1 mRNA to cells at the corticomedullary junction. 11 beta-HSD2 mRNA was uniformly distributed across the cortex and was low/absent in the medulla. Administration of glycyrrhizic acid in vivo (> 100 mg/kg for 4 days) resulted in inhibition of 11 beta-HSD1 mRNA and activity and a decrease in mRNA levels for the glucocorticoid-dependent enzyme, phenylethanolamine N-methyltransferase, whilst levels of the glucocorticoid-independent enzyme, tyrosine hydroxylase were unchanged. No 11 beta-HSD expression was observed in the rat phaeochromocytoma cell line, PC12 cells, nor in human normal adrenal gland or phaeochromocytoma specimens. There are marked species and sex differences in the expression of 11 beta-HSD isoforms within the adrenal. The role of 11 beta-HSD within the adrenal gland remains obscure, but at least in the rat, the expression of the reductase enzyme, 11 beta-HSD1, to the corticomedullary junction may serve to maintain high medullary glucocorticoid concentrations required for catecholamine biosynthesis.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1996

11 beta-Hydroxysteroid dehydrogenase in the rat adrenal.

11 beta-Hydroxysteroid dehydrogenase (11 beta-HSD) catalyses the interconversion of biologically active cortisol to inactive cortisone in man, and corticosterone to 11-dehydrocorticosterone in rodents. As such, this enzyme has been shown to confer aldosterone-selectivity on the mineralocorticoid receptor and to modulate cortisol/corticosterone access to the glucocorticoid receptor (GR). Two kinetically distinct isoforms of this enzyme have been characterized in both rodents and man; a low-affinity NADP(H)-dependent enzyme (11 beta-HSD1) which predominantly acts as an oxoreductase and, more recently, a high-affinity NAD-dependent uni-directional dehydrogenase (11 beta-HSD2). In this study we have analysed the expression of both 11 beta-HSD1 and 11 beta-HSD2 isoforms in rat adrenal cortex and medulla and have investigated their possible roles with respect to glucocorticoid-regulated enzymes mediating catecholamine biosynthesis in adrenal medullary chromaffin cells. Using a rat 11 beta-HSD1 probe and a recently cloned in-house mouse 11 beta-HSD2 cDNA probe, Northern blot analyses revealed expression of mRNA species encoding both 11 beta-HSD1 (1.4 kb) and 11 beta-HSD2 (1.9 kb) in the whole adrenal. Consistent with this, 11 beta-dehydrogenase activity (pmol 11-dehydrocorticosterone formed/mg protein per h, mean +/- S.E.M.) in adrenal homogenates, when incubated with 50 nM corticosterone in the presence of 200 microM NAD, was 97.0 +/- 9.0 and with 500 nM corticosterone in the presence of 200 microM NADP, was 98.0 +/- 1.4. 11-Oxoreductase activity (pmol corticosterone formed/mg protein per h) with 500 nM 11-dehydrocorticosterone in the presence of 200 microM NADPH, was 187.7 +/- 31.2. In situ hybridization studies of rat adrenal cortex and medulla using 35 S-labelled antisense 11 beta-HSD1 cRNA probe revealed specific localization of 11 beta-HSD1 mRNA expression predominantly to cells at the corticomedullary junction, most likely within the inner cortex. In contrast, 11 beta-HSD2 mRNA was more abundant in cortex versus medulla, and was more uniformly distributed over the adrenal gland. Negligible staining was detected using control sense probes. Ingestion of the 11 beta-HSD inhibitor, glycyrrhizic acid (> 100 mg/kg body weight per day for 4 days) resulted in significant inhibition of adrenal NADP-dependent (98.0 +/- 1.4 vs 42.5 +/- 0.4) and NAD-dependent (97.0 +/- 9.0 vs 73.2 +/- 6.7) 11 beta-dehydrogenase activity and 11-oxoreductase activity (187.7 +/- 31.2 vs 67.7 +/- 15.3). However, while levels of 11 beta-HSD1 mRNA were similarly reduced (0.85 +/- 0.07 vs 0.50 +/- 0.05 arbitrary units), those for 11 beta-HSD2 remained unchanged (0.44 +/- 0.03 vs 0.38 +/- 0.01). Levels of mRNA encoding the glucocorticoid-dependent enzyme phenylethanolamine N-methyltransferase which catalyses the conversion of noradrenaline to adrenaline, were also significantly reduced in those rats given glycyrrhizic acid (1.12 +/- 0.04 vs 0.78 +/- 0.04), while those for the glucocorticoid-independent enzyme tyrosine hydroxylase (1.9 kb), which catalyses the conversion of tyrosine to DOPA, were unchanged (0.64 +/- 0.04 vs 0.61 +/- 0.04). In conclusion, the rat adrenal gland expresses both 11 beta-HSD1 and 11 beta-HSD2 isoforms. 11 beta-HSD1 gene expression is localized to the adrenal cortico-medullary junction, where it is ideally placed to regulate the supply of cortex-derived corticosterone to the medullary chromaffin cells. This, together with our in vivo studies, suggests that 11 beta-HSD1 may play an important role with respect to adrenocorticosteroid regulation of adrenaline biosynthesis. The role of 11 beta-HSD2 in the adrenal remains to be elucidated.

11-beta-Hydroxysteroid Dehydrogenases↗
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↗
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↗