Biomedical subjects

S Miyamoto

Publications and source records attributed to S Miyamoto.

At least 19 recordsLinked to original sources

PubMed2000

Nonconvulsive focal inhibitory seizure: subdural recording from motor cortex.

The authors obtained an ictal electrocorticogram with chronically implanted subdural electrodes from a 30-year-old man with a low grade glioma in the right postcentral gyrus who had a focal inhibitory seizure of the left arm. During the ictal paresis, the authors observed epileptic discharges in the positive arm motor area of the right precentral gyrus and in its rostral area, but not in the negative motor area. The epileptic activity probably inhibited the spinal motoneuron pool without eliciting excitatory activity in the corticospinal pathway.

Adult↗

PubMed2000

Autosomal dominant temporal lobe epilepsy in a Japanese family.

We described autosomal dominant familial temporal lobe epilepsy in a Japanese family in which three individuals (one man and his two children) were affected. Their seizures commonly consisted of auditory symptoms and infrequent nocturnal generalized seizures. Repeated EEGs did not provide confirmative epileptiform discharges, but cranial MRI in one patient showed mild left hippocampal atrophy, and decreased glucose metabolism in the left temporal area was demonstrated by 18F-deoxyglucose positron emission tomography (FDG-PET). A confirmative diagnosis in one of the patients by FDG-PET was helpful for diagnosis in other patients in the same family. Seizure onset was adolescent commonly among the three patients, but better seizure control was achieved in the father as compared with the two children.

Adult↗

PubMed2000

Negative inotropic effect of endothelin-1 in the mouse right ventricle.

Effects of endothelin-1 on the contraction and cytosolic Ca(2+) concentrations (¿Ca(2+)(i)) of the mouse right ventricle were investigated. Endothelin-1 (1-300 nM) elicited a negative inotropic effect in a concentration-dependent manner. The endothelin-1-induced negative inotropy was antagonized by a selective endothelin ET(A) receptor antagonist, BQ-123 (cyclo ¿Asp-Pro-Val-Leu-Trp-; 3, 10 microM). Endothelin-1 reduced the peak amplitudes of both the ¿Ca(2+)(i) transient and contraction without changing inward Ca(2+) current. The relationship between peak amplitude of ¿Ca(2+)(i) and peak force generated by changing the extracellular Ca(2+) concentration (¿Ca(2+)(o)) was not affected by endothelin-1. In addition, the trajectory of the ¿Ca(2+)(i)-contraction phase plane diagram obtained at 2 mM ¿Ca(2+)(o) in the absence of endothelin-1 was superimposable on that obtained at 4 mM ¿Ca(2+)(o) in the presence of endothelin-1 (300 nM). Endothelin-1 (300 nM) translocated protein kinase C from cytosol to membrane, suggesting activation of protein kinase C. Further, a selective protein kinase C inhibitor, bisindolylmaleimide I (10 microM), inhibited the endothelin-1-induced negative inotropy. These results suggest that endothelin-1 elicits negative inotropy by reducing the amplitude of the ¿Ca(2+)(i) transient without changing inward Ca(2+) current through the activation of the endothelin ET(A) receptor followed by protein kinase C activation in the mouse right ventricle.

Animals↗

PubMed2000

A switch in distinct I kappa B alpha degradation mechanisms mediates constitutive NF-kappa B activation in mature B cells.

Inducible activation of cytoplasmic NF-kappa B/Rel transcription factors occurs via proteasome-dependent degradation of an associated inhibitor, termed I kappa B alpha. Mature B lymphocytes constitutively express nuclear NF-kappa B, which is important for their long-term survival. The intrinsic mechanisms by which B cells constitutively activate NF-kappa B are unknown. In this paper we demonstrate that maintenance of NF-kappa B activity in primary B cells is mediated by a novel calcium-dependent, but proteasome-independent, mechanism. Moreover, we show that differentiation of conditionally transformed pre-B cells is accompanied by a switch from proteasome-dependent to proteasome-independent degradation of I kappa B alpha. Our findings indicate that I kappa B alpha degradation mechanisms are dynamic during B cell development, and ultimately establish constitutive NF-kappa B activity in mature B lymphocytes.

Animals↗

PubMed2000

NF-kappaB activation by camptothecin. A linkage between nuclear DNA damage and cytoplasmic signaling events.

Activation of the transcription factor NF-kappaB by extracellular signals involves its release from the inhibitor protein IkappaBalpha in the cytoplasm and subsequent nuclear translocation. NF-kappaB can also be activated by the anticancer agent camptothecin (CPT), which inhibits DNA topoisomerase (Topo) I activity and causes DNA double-strand breaks during DNA replication to induce S phase-dependent cytotoxicity. Here we show that CPT activates NF-kappaB by a mechanism that is dependent on initial nuclear DNA damage followed by cytoplasmic signaling events. NF-kappaB activation by CPT is dramatically diminished in cytoplasts and in CEM/C2 cells expressing a mutant Topo I protein that fails to bind CPT. This response is intensified in S phase cell populations and is prevented by the DNA polymerase inhibitor aphidicolin. In addition, CPT activation of NF-kappaB involves degradation of cytoplasmic IkappaBalpha by the ubiquitin-proteasome pathway in a manner that depends on the IkappaB kinase complex. Finally, inhibition of NF-kappaB activation augments CPT-induced apoptosis. These findings elucidate the progression of signaling events that initiates in the nucleus with CPT-Topo I interaction and continues in the cytoplasm resulting in degradation of IkappaBalpha and nuclear translocation of NF-kappaB to attenuate the apoptotic response.

Apoptosis↗

PubMed2000

Biosynthesis and post-translational processing of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1). N-linked glycosylation affects cell-surface expression and ligand binding.

LOX-1 (lectin-like oxidized low density lipoprotein receptor-1) is a type II membrane protein belonging to the C-type lectin family that can act as a cell-surface receptor for atherogenic oxidized low density lipoprotein (Ox-LDL) and may play crucial roles in atherogenesis. In this study, we show, by pulse-chase labeling and glycosidase digestion, that LOX-1 is synthesized as a 40-kDa precursor protein with N-linked high mannose carbohydrate chains (pre-LOX-1), which is subsequently further glycosylated and processed into the 48-kDa mature form within 40 min. Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1. Cell enzyme-linked immunosorbent assay, flow cytometry, and immunofluorescence confocal microscopy demonstrated that the deglycosylated form of LOX-1 is not efficiently transported to the cell surface, but is retained in the endoplasmic reticulum or Golgi apparatus in tumor necrosis factor-alpha-activated bovine aortic endothelial cells, but not in BLOX-1-CHO cells. Radiolabeled Ox-LDL binding studies revealed that the deglycosylated form of LOX-1 expressed on the cell surface of BLOX-1-CHO cells has a reduced affinity for Ox-LDL binding. Taken together, N-linked glycosylation appears to play key roles in the cell-surface expression and ligand binding of LOX-1.

Amidohydrolases↗

PubMed2000

Formation of platelet aggregates after attacks of coronary spastic angina pectoris.

Using a novel laser-light scattering method, we examined platelet aggregability, especially small-sized platelet aggregates, at baseline and after spontaneous coronary spastic attacks in 14 patients with coronary spastic angina, and before and after anginal attacks during an exercise test in 11 patients with stable exertional angina. The number of small-sized platelet aggregates after coronary spastic anginal attacks increased significantly, but not in patients with stable exertional angina. These results imply that an increase in the number of small-sized platelet aggregates from coronary spasm may be a trigger for coronary thrombosis via medium- and large-sized platelet aggregates.

Acetylcholine↗

PubMed2000

Bone regeneration by transforming growth factor beta1 released from a biodegradable hydrogel.

This paper describes the sustained release of transforming growth factor beta1 (TGF-beta1) from a biodegradable hydrogel based on polyion complexation for the enhancement of bone regeneration activity. Basic TGF-beta1 was adsorbed onto the biodegradable hydrogel of acidic gelatin with an isoelectric point of 5.0 by an electrostatic interaction. The TGF-beta1 could not be adsorbed onto basic gelatin. When acidic gelatin hydrogels incorporating 125I-labeled TGF-beta1 were implanted into the back subcutis of mice, the radioactivity decreased with time and the in vivo retention of TGF-beta1 was prolonged with a decrease in the water content of hydrogels. The higher the water content of hydrogels, the faster their biodegradation. The in vivo retention of TGF-beta1 correlated well with that of gelatin hydrogels, indicating that TGF-beta1 was released from the gelatin hydrogel as a result of hydrogel biodegradation. The ability of TGF-beta1-incorporated into acidic gelatin hydrogels to induce bone regeneration was evaluated in a rabbit calvarial defect model. Eight weeks after treatment, the gelatin hydrogels with water contents of 90 and 95 wt% induced significantly high bone regeneration compared with those with lower and higher water contents and free TGF-beta1. This indicates that the sustained release of TGF-beta1 from the hydrogel with suitable in vivo degradability is necessary to effectively enhance its osteoinductive function. Rapid hydrogel degradation will result in a retention time of TGF-beta1 which is too short to induce bone regeneration. It is possible that the slow degradation of the hydrogel physically blocked TGF-beta1-induced bone regeneration at the skull defect. It can be concluded that the gelatin hydrogel is a promising matrix of TGF-beta1 release to induce skull bone regeneration.

Absorbable Implants↗

PubMed2000

A nuclear export signal in the N-terminal regulatory domain of IkappaBalpha controls cytoplasmic localization of inactive NF-kappaB/IkappaBalpha complexes.

Appropriate subcellular localization is crucial for regulation of NF-kappaB function. Herein, we show that latent NF-kappaB complexes can enter and exit the nucleus in preinduction states. The nuclear export inhibitor leptomycin B (LMB) sequestered NF-kappaB/IkappaBalpha complexes in the nucleus. Using deletion and site-directed mutagenesis, we identified a previously uncharacterized nuclear export sequence in residues 45-54 of IkappaBalpha that was required for cytoplasmic localization of inactive complexes. This nuclear export sequence also caused nuclear exclusion of heterologous proteins in a LMB-sensitive manner. Importantly, a LMB-insensitive CRM1 mutant (Crm1-K1) abolished LMB-induced nuclear accumulation of the inactive complexes. Moreover, a cell-permeable p50 NF-kappaB nuclear localization signal peptide also blocked these LMB effects. These results suggest that NF-kappaB/IkappaBalpha complexes shuttle between the cytoplasm and nucleus by a nuclear localization signal-dependent nuclear import and a CRM1-dependent nuclear export. The LMB-induced nuclear complexes could not bind DNA and were inaccessible to signaling events, because LMB inhibited NF-kappaB activation without affecting the subcellular localization of upstream kinases IKKbeta and NIK. Our findings indicate that the dominant nuclear export over nuclear import contributes to the largely cytoplasmic localization of the inactive complexes to achieve efficient NF-kappaB activation by extracellular signals.

Amino Acid Motifs↗

PubMed2000

Effects of NK-104, a new hydroxymethylglutaryl-coenzyme reductase inhibitor, on low-density lipoprotein cholesterol in heterozygous familial hypercholesterolemia. Hokuriku NK-104 Study Group.

The clinical efficacy of NK-104, a novel and totally synthetic hydroxymethylglutaryl-coenzyme A reductase inhibitor, was assessed in 30 patients (men/women = 15/15, mean age 51 years) with heterozygous familial hypercholesterolemia. After a placebo phase of >4 weeks, NK-104 was given at an initial dose of 2 mg/day for 8 weeks, which was increased to 4 mg/day for a further 8 weeks. As a result of 2 mg/day of NK-104 treatment, mean +/- SD of total and low-density lipoprotein cholesterol levels decreased significantly (p<0.0001) from baseline, namely from 8.80+/-1.38 to 6.11+/-1.09 mmol/L (-31%) and from 6.81+/-1.52 to 4.09+/-1.03 mmol/L (-40%), respectively. They decreased further (p<0.0001) as a result of 4-mg/day administration, to 5.52+/-0.81 mmol/L (-37%) and 3.55+/-0.85 mmol/L (-48%), respectively. Changes in high-density lipoprotein cholesterol levels failed to reach statistical significance. Serum triglyceride levels decreased significantly (p<0.0001) from baseline as a result of 4 mg/day of NK-104, from 1.99+/-1.72 to 1.35+/-0.90 mmol/L (-23%). Serum apolipoprotein B, CII, CIII, and E levels significantly decreased: mean changes from baseline at the end of the study were -41% (p<0.0001), -27% (p<0.0001), -19% (p = 0.002), and -37% (p<0.0001), respectively. On the other hand, apolipoprotein AI and All levels significantly increased as a result of the treatment: + 10% (p = 0.002) and +6% (p = 0.008), respectively. There were no adverse events observed in either clinical or laboratory findings that could be attributed to the treatment. These results suggest that the potency of NK-104 appears to be dose-dependent, and that NK-104 is safe and well tolerated in the treatment of patients with heterozygous familial hypercholesterolemia, and thus also provides a new therapeutic choice for subjects requiring lipid-modifying therapy.

Female↗

PubMed2000

Levels of rheumatoid factor isotypes, metalloproteinase-3 and tissue inhibitor of metalloproteinase-1 in synovial fluid from various arthritides.

When synovial effusion is the only symptom, it is often difficult to make an exact diagnosis of the arthritic disease. To distinguish various types of arthritis with synovial effusion, we measured the levels of matrix metalloproteinase-3 (MMP-3, Stromelysin), tissue inhibitor of metalloproteinase-1 (TIMP-1) and rheumatoid factor (RF) isotypes in synovial fluid (SF) from patients with rheumatoid arthritis (RA), osteoarthritis (OA), pyogenic arthritis (PA), pseudogouty arthritis (PG), gouty arthritis (GA) and traumatic arthritis (TA). SF was aspirated from the knee joint or the ankle joint. Levels of IgG-, IgM- and IgA-RF isotypes were measured by ELISA. Levels of MMP-3 and TIMP-1 in SF were simultaneously determined by a one-step EIA system. Levels of IgG-RF, IgM-RF and MMP-3 in SF from RA patients were significantly higher than those in OA, PA, PG, GA and TA. However, IgA-RF in SF from RA patients, when compared with PA and GA, did not show a significantly increased level. In addition, TIMP-1 in SF from RA, when compared with PA and TA, also has not shown a significantly increased level. Therefore, in addition to analysing clinical data, measurements of IgG-RF, IgM-RF and MMP-3 in SF may contribute in distinguishing RA from other arthritic diseases.

Adolescent↗

PubMed2000

Effect of 1,25(OH)2D3 on expression of estrogen receptor-alpha mRNA on rat osteosarcoma cell line (ROS 17/2.8).

In order to investigate the regulatory mechanisms of estrogen receptors (ER) in bone cells, changes in ER-alpha mRNA levels of rat osteosarcoma cell line (ROS 17/2.8) before and after exposure to 1,25(OH)2D3 and 17-beta estradiol respectively were measured by quantitative polymerase chain reaction using an internal standard. ER mRNA levels in the ROS 17/2.8 cultured with the medium alone had 5.029 +/- 1.623 mol/g total RNA x 10(-13) and were not statistically different from those cultured in the presence of 1,25(OH)2D3 at concentrations of 10(-12) M and less. ER mRNA levels in the ROS 17/2.8 cell line showed a small but a significant increase as a result of stimulation by 1,25(OH)2D3 at concentrations of 10(-10) and 10(-11) M. However, ER mRNA levels in ROS 17/2.8 cultured in the presence of 1,25(OH)2D3 at concentrations of 10(-9) M were not statistically different from those of the control. On the other hand, the expression of ER in ROS 17/2.8 cells cultured for 3 hours with various doses of 1,25(OH)2D3 showed, by immunoblotting methods, a significant increase at the dose of 10(-10) M in the expression of ER. Although a physiological significance is obscure, these observations suggest that 1,25(OH)2D3 plays a part in the expression of ER in ROS 17/2.8. No significant changes were seen in the expression of ER mRNA and the synthesis of ER as a result of stimulation by the estradiol.

Animals↗

PubMed2000

Psychiatric disorders in juvenile patients with insulin-dependent diabetes mellitus.

The relationships of psychiatric characteristics to metabolic control and psychosocial functioning were examined in a group of 16 patients with insulin-dependent diabetes mellitus (IDDM) (mean age: 14.3+/-5.1 years, mean duration of follow-up: 5.0+/-2.3 years) and psychiatric disorders. The comparison is also made to 69 IDDM controls (mean age: 17.0+/-6.7 years) without psychiatric disorders. Metabolic control was evaluated in terms of glycosylated hemoglobin (HbA1c). Psychosocial functioning at both psychiatric treatment entry and discharge was assessed using the global assessment of functioning (GAF) scale. Subjects were divided into three subgroups - Somatoform Type (25%), Behavioral Type (50%) or Psychotic Type (25%) - according to the Diagnostic and Statistical Manual of Mental Disorders, third edition revised (DSM-III-R), based on semi-structured interviews. Four patients (25%) were diagnosed as having schizophrenia or schizoaffective disorder (Psychotic Type), which is rather rare. The mean HbA1c level in the Behavioral Type patients was significantly higher than in the other subgroups (P<0. 01). After psychiatric treatment a significant difference (P<0.0001) in the GAF Scale was observed in the Psychotic Type compared with the other subgroups. We conclude that the Behavioral Type is associated with poor metabolic control and that for the Psychotic Type, improved psychosocial functioning can be achieved through psychiatric treatment.

Adaptation, Psychological↗

PubMed2000

Marriage rate and number of children among young adults with insulin-dependent diabetes mellitus in Japan.

The main purpose of our study was to identify the social circumstances and lifestyle of IDDM patients in Japan. The present study focused on the marriage status of both men and women with IDDM as well as the number of children of women with IDDM. A questionnaire was sent to hospitals across the country. Doctors handed it or mailed it to IDDM patients aged 18 years or older. Unsigned answer sheets were returned directly by the patients. Data on the marriage rate and number of children were obtained, and possible factors affecting these indices were assessed. One thousand and thirteen patients (354 men and 659 women) answered the questionnaire. Both men and women with IDDM were less likely to be married in comparison with age-matched Japanese. The number of children of married IDDM women in various age groups was also lower in comparison with the general Japanese female population. Several factors other than diabetes complications including job discrimination, high medical costs, and psychological pressures, were thought to be responsible for these results.

Adult↗

PubMed2000

Effects of ketamine, MK-801, and amphetamine on regional brain 2-deoxyglucose uptake in freely moving mice.

Although the pathophysiology of schizophrenia remains unclear, behavioral effects in humans induced by N-methyl-D-aspartate (NMDA) antagonists, such as ketamine, provide direction for formulating new pharmacologic models of the illness. The purpose of the present study was to clarify the roles of NMDA receptor antagonism, as well as dopamine-releasing properties of ketamine, in regional brain metabolic activity and behavioral responses in mice. The effects of acute administration of ketamine (30 mg/kg, i.p.) were compared with those of the more selective non-competitive NMDA antagonist MK-801 (0.3 and 0.5 mg/kg, i.p.), and amphetamine (4 mg/kg, i.p.) on regional brain [14C]-2-deoxyglucose (2-DG) uptake, by using a high resolution autoradiographic technique in the freely moving mice. Both ketamine and MK-801 induced substantial and similar neuroanatomically selective alterations in regional 2-DG uptake. Remarkable increases in 2-DG uptake in response to the NMDA antagonists were seen in limbic cortical regions, hippocampal formation, nucleus accumbens, select thalamic nuclei, and basolateral amygdala. The behavior of mice given amphetamine was similar to that of mice given MK-801. However, the brain activity patterns induced by amphetamine were distinctly different from those observed after ketamine and MK-801 treatment. These results suggest that generalized behavioral activation and increased dopamine release are insufficient to account for the ketamine-induced alterations in regional brain metabolism, and that the effects of ketamine on 2-DG uptake are likely related to a reduction in NMDA receptor function. The data also suggest that ketamine-induced changes in 2-DG uptake may provide a useful paradigm for translational research to better understand the pathophysiology of schizophrenia.

Amphetamine↗

PubMed2000

Xestospongin C, a selective and membrane-permeable inhibitor of IP(3) receptor, attenuates the positive inotropic effect of alpha-adrenergic stimulation in guinea-pig papillary muscle.

We evaluated the role of the inositol 1,4,5-triphosphate (IP(3)) receptor-mediated Ca(2+) release on the positive inotropic effects of alpha-adrenergic stimulation using a novel, potent, selective membrane-permeable blocker of IP(3) receptor, xestospongin C. Guinea-pig papillary muscle permeabilized with saponin exhibited spontaneous oscillatory contractions in solution buffered with pCa(2+) 6.5 by a low concentration of EGTA. The oscillatory activity was increased by adding 100 microM IP(3) and abolished by 1 microM ryanodine or 30 microM cyclopiazonic acid. Xestospongin C (3 microM) inhibited the IP(3)-induced increase in the oscillatory contractions without affecting basal oscillations. In intact papillary muscle, xestospongin C (3 microM) inhibited the positive inotropic effects of phenylephrine, resulting in a rightward and downward shift of the concentration-response curve for phenylephrine. On the contrary, xestospongin C did not affect the concentration-response curve for phenylephrine obtained in the presence of ryanodine (1 microM). On the other hand, xestospongin C affected neither basal contractions nor the positive inotropic effects of a high extracellular Ca(2+) concentration (3.2 mM) or that of isoprenaline (1 and 10 nM). These results suggest that the IP(3)-mediated increase in Ca(2+) release is involved in the positive inotropic effects of alpha-adrenergic stimulation in the guinea-pig cardiac muscle.

Adrenergic alpha-Agonists↗

PubMed2000

Increased plasma level of soluble E-selectin in acute myocardial infarction.

BACKGROUND: E-selectin, also known as endothelial cell leukocyte adhesion molecule-1, is a member of the selectin family of adhesion molecules and is expressed on vascular endothelial cells in inflammatory reactions. The induction of surface E-selectin expression by endothelial cells is considered a marker of activation. METHODS AND RESULTS: We examined the plasma soluble E-selectin (sE-selectin) level in 41 patients within 6 hours after the onset of acute myocardial infarction (AMI) and in 37 patients with stable exertional angina and 27 control patients. Blood samples were obtained on admission, after reperfusion therapy, and at 4 hours, 8 hours, 12 hours, 24 hours, 48 hours, 3 days, 5 days, 1 week, and 2 weeks after admission in the AMI group. In this group, 21 patients had a history of prodromal unstable angina before infarction and 20 had sudden onset of infarction. The plasma sE-selectin level (ng/mL) on admission was higher in the AMI group than in the stable exertional angina group and control group (38.5 +/- 3.1 vs 28.5 +/- 1.5, P <.01, 26.0 +/- 1.8, P <.01, respectively). In addition, plasma sE-selectin levels were higher in the patients with AMI with prodromal unstable angina than in those with a sudden onset of infarction on admission (44.7 +/- 5.4 vs 32.0 +/- 2.1, P <.05). The plasma sE-selectin level decreased slowly during the chronic phase both in patients with AMI with prodromal unstable angina (from 44.7 +/- 5.4 to 33.8 +/- 3.4, P <.01) and those with a sudden onset of infarction (from 32.0 +/- 2.1 to 24.9 +/- 2.4, P <.01). CONCLUSIONS: These results suggest that an increase of sE-selectin may reflect enhanced endothelial cell activation in patients with AMI. The higher sE-selectin level in patients with AMI with prodromal unstable angina may have been associated with repeated episodes of myocardial ischemia and reperfusion.

Aged↗

PubMed2000

Role of primary sensorimotor cortices in generating inhibitory motor response in humans.

To clarify the mechanism by which inhibitory motor responses such as cortical negative myoclonus are generated in humans, three patients with medically intractable partial epilepsy (two with frontal lobe epilepsy and one with parietal lobe epilepsy) were studied by means of direct cortical stimulation with a single electric pulse through subdural electrodes. All underwent chronic long-term video/EEG monitoring, cortical mapping by 50 Hz electric cortical stimulation and recording of cortical somatosensory evoked potentials with chronically implanted subdural grid electrodes (3 mm in diameter and centre-to-centre distance of 1 cm) to map both epileptogenic and functional zones. After these clinical evaluations, cortical stimulation by single electric pulse (0.3 ms duration, 1 Hz) was carried out through pairs of subdural electrodes located at the primary sensorimotor area (MI-SI), pre-supplementary motor area (pre-SMA) and lateral negative motor area (lateral NMA), while surface EMG was recorded from the muscles of the contralateral hand. The results showed that (i) in all subjects, single pulse stimulation of MI-SI elicited a motor evoked potential (MEP) followed by a silent period (SP) in the contralateral distal hand muscles, the latter lasting 300 ms after the stimulus. The duration of SP was proportional to the size of the preceding MEP. In one subject, SP without any preceding MEP was elicited, and, in another subject, there was a short SP immediately before MEP in the contralateral thenar muscle. (ii) Following the stimulation of either pre-SMA or lateral NMA, no SP was observed. It is concluded that the inhibitory mechanism within the MI-SI, but probably not in the non-primary motor areas, either closely linked to or completely independent of excitation, most likely plays an important role in eliciting brief negative motor phenomena such as cortical negative myoclonus or SP.

Adult↗