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Biomedical subjects

K Matsunaga

Publications and source records attributed to K Matsunaga.

At least 19 recordsLinked to original sources
PubMed1998

A novel unusual DNA structure formed in an inverted repeat sequence.

A potential to form a non-cruciform unusual DNA structure was shown at the inverted repeat DNA sequence of a fish satellite DNA. The recombinant plasmid harboring a member of the EcoRI satellite family of Sillago japonica (Percoidei, Sillaginidae) was subjected to S1 nuclease treatment, and the cutting sites were mapped by primer extension assay. The S1 nuclease attacked the 3'-half of the inverted repeat but not the middle part of symmetry under various salt conditions, suggesting that this unusual DNA structure is different from the DNA cruciform and a conventional intramolecular triplex structure. In the presence of 200 mM potassium chloride, the typical DNA cruciform has extruded, suggesting that certain purine-purine-pyrimidine base triads are involved in the formation of this unusual DNA structure. These results support the occurrence of a novel unusual DNA structure formed in the inverted repeat sequence.

Animals↗
PubMed1998

Modulation of actomyosin ATPase by goniodomin A differs in types of cardiac myosin.

Goniodomin A causes the conformational change of actin to modify actomyosin ATPase activity [Furukawa, K.-I., Sakai, K., Watanabe, S., Maruyama, K., Murakami, M., Yamaguchi, K., Ohizumi, Y., 1993. Goniodomin A induces modulation of actomyosin ATPase activity mediated through conformational change of actin. J. Biol. Chem. 268, 26026-26031]. Goniodomin A inhibited the ATPase activities of atrial myofibrils, myosin B and reconstituted actomyosin in a concentration-dependent manner. Interestingly, these ATPase activities of ventricular muscle were enhanced by goniodomin A (3 x 10(-8)-3 x 10(-7) M), but were decreased when the concentration was further raised. The stimulatory effect of goniodomin A was significantly inhibited by troponin tropomyosin complex. These results suggest that goniodomin A affects actin to modify cardiac actomyosin ATPase activity, and that this modulation differs in types of cardiac myosin.

Animals↗
PubMed1998

Induction of apoptosis in colonic epithelium treated with 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and its modulation by a P4501A2 inducer, beta-naphthoflavone, in male F344 rats.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is one of the mutagenic heterocyclic amines derived from cooked meat. In long-term experiments using rodents, carcinogenicity of PhIP in colon, mammary gland and prostate has been demonstrated. In this study, an experiment was designed to determine the apoptosis-inducing capacity of PhIP in colonic epithelium, a target organ for PhIP carcinogenicity, and possible modulating effects of beta-naphthoflavone (beta-NF), a P4501A2 inducer, on the apoptosis in rats. Out of eight groups of male F344 rats, four were given beta-NF in diet (1000 ppm) for a week beginning at 5 weeks of age. Four groups were given PhIP (100 mg/kg body weight) by gavage at 6 weeks of age. Twenty-four hours after the dosing of PhIP, cell death with typical morphology of apoptosis was apparent in the colon and the apoptotic index was significantly greater (P < 0.01) than of the control rats without exposure to PhIP. Prior administration of beta-NF caused significant acceleration of the induction of apoptosis by PhIP. Since PhIP requires metabolic activation by P4501A2 to exert genotoxic activities, the modulating effect of beta-NF on the PhIP-induced apoptosis will be through a P4501A2-dependent mechanism. Such assay of apoptotic indices in the colon may be useful not only for the evaluation of genotoxicity and/or the initiating capability of chemical agents with potentials for colorectal cancer, but also for the analysis of modifying agents on the carcinogenesis in the large bowel.

Animals↗
PubMed1998

Enhancement of serotonergic neural activity contributes to cyclosporine-induced tremors in mice.

A single cyclosporine injection (50 mg/kg, i.p.) significantly enhanced harmine- but not oxotremorine-induced tremors in mice. This potentiation became more apparent when cyclosporine (50 mg/kg, i.p.) was administered once a day for seven days. These findings suggest an involvement of monoaminergic mechanisms in cyclosporine-induced tremors. The effects of cyclosporine were examined on the dynamics of noradrenaline, dopamine and serotonin in the mouse brain. Both single and repeated treatment with cyclosporine significantly facilitated the serotonin turnover as estimated from the probenecid-induced accumulation of 5-hydroxyindoleacetic acid, but either mode of treatment failed to change the contents of monoamines and their metabolites or the turnover of noradrenaline and dopamine. Therefore, the cyclosporine-enhanced activity of serotonin neurons may be interpreted as producing adverse central effects, including tremors.

Animals↗
PubMed1998

Chemoprevention of 4-nitroquinoline 1-oxide-induced oral carcinogenesis by citrus auraptene in rats.

The modifying effects of citrus auraptene given during the initiation and post-initiation phases of oral carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. At 6 weeks of age, animals were divided into experimental and control groups, and fed the diets containing 100 ppm or 500 ppm auraptene. At 7 weeks of age, all animals except those treated with auraptene alone and control groups were given 4-NQO (20 ppm) in the drinking water for 8 weeks to induce tongue carcinoma. Starting 7 days before the 4-NQO exposure, groups of animals were fed the diets containing auraptene (100 and 500 ppm) for 10 weeks and then switched to the basal diet. Starting 1 week after the cessation of 4-NQO exposure, the groups given 4-NQO and a basal diet were switched to the diets mixed with auraptene (100 and 500 ppm), and maintained on these diets for 22 weeks. The other groups consisted of rats fed auraptene alone (500 ppm) or untreated rats. All rats were necropsied at the termination of the study (week 32). The incidences of tongue lesions (neoplasms and preneoplasms), polyamine levels in the tongue tissue and cell proliferation activity estimated by 5-bromodeoxyuridine (BrdU)-labelling index were compared among the groups. In addition, the activities of gluthathione S-transferase (GST) and quinone reductase (QR) in liver and tongue of rats gavaged various doses of auraptene (0, 200, 400 and 800 mg/kg body wt) for 5 days were assayed. Feeding of auraptene at both doses during the initiation phase caused a significant reduction in the frequency of tongue carcinoma (100 ppm auraptene, 91% reduction, P < 0.001; 500 ppm auraptene, 63% reduction, P < 0.05). When fed auraptene after 4-NQO exposure, the frequency of tongue carcinoma was also decreased (100 ppm auraptene, 100% reduction, P < 0.001; 500 ppm auraptene, 74% reduction, P < 0.01). The incidences of tongue severe dysplasia in these groups were significantly smaller than those in carcinogen controls (P < 0.05). There were no pathological alterations in rats treated with 500 ppm auraptene alone or those in an untreated control group. Dietary administration of auraptene significantly decreased BrdU-labelling index and polyamine concentrations in the oral mucosa (P < 0.05). In addition, auraptene administration significantly increased the activities of GST and QR in the liver and tongue. Although dose-dependent effect was not found, citrus auraptene is effective in inhibiting the development of oral neoplasms induced by 4-NQO. Thus, suppression by the initiation-feeding of auraptene might relate to elevation in the phase II enzymes GST and QR of the liver and tongue, and inhibition occurring during the post-initiation might be related to suppression of increased cell proliferation caused by 4-NQO in the oral mucosa.

4-Nitroquinoline-1-oxide↗
PubMed1998

The powerful stimulatory action of 6-O-acetyl-9-methyl-7-bromoeudistomin D on the contractile protein system of rabbit skeletal muscle.

6-O-Acetyl-9-methyl-7-bromoeudistomin D (AMBED) (> 10[-6] M), a derivative of eudistomin D, markedly enhanced the superprecipitation and the ATPase activity of skeletal muscle myosin B. In both the superprecipitation and ATPase activity of myosin B, the concentration-response curve for Ca2+ was shifted upwards by AMBED. AMBED did not affect the Ca2+-, K+-EDTA- or Mg2+-ATPase of myosin or the ATPase of actomyosin reconstituted from actin and myosin. These results suggest that AMBED causes an increase in the actomyosin ATPase activity mediated through the elevation of the maximum response to Ca2+, resulting in enhancement of the superprecipitation of skeletal muscle myosin B.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1998

Potent stimulation of myofilament force and ATPase activity of skeletal muscle by eudistomin M, a novel Ca(++)-sensitizing agent from a Caribbean tunicate.

In the course of our survey of biologically active compounds from natural sources, eudistomins were isolated from a Caribbean tunicate Eudistoma olivaceum. In the present experiments, eudistomin M (Eud-M, > 10(-5) M) caused a concentration-dependent increase in the contractile response of skinned fibers from guinea pig skeletal psoas muscles to Ca++. The superprecipitation and ATPase activity of myosin B from fast skeletal muscles of rabbit back and leg were potentiated by this compound (> 10(-5) M) in a concentration-dependent manner. In skinned fibers, superprecipitation and the ATPase activity of myosin B, Eud-M shifted the concentration-response curve for Ca++ to the upper direction. Ca(++)-, K(+)-EDTA- or Mg(++)-ATPase was not affected by Eud-M. This compound had no effect on the ATPase activity of actomyosin reconstituted from actin and myosin in the presence or absence of troponin. However, the ATPase activity of actin-myosin-troponin-tropomyosin reconstituted system was increased significantly by Eud-M. These results suggest that Eud-M increases the Ca++ sensitivity of the contractile apparatus in skeletal muscles at least partially mediated through troponin-tropomyosin system and thus enhances the ATPase activity of myosin B and the contractile force of myofilament.

Actin Cytoskeleton↗
PubMed1997

Oral administration of PSK can improve the impaired anti-tumor CD4+ T-cell response in gut-associated lymphoid tissue (GALT) of specific-pathogen-free mice.

We investigated both the effect and the mechanism of oral (p.o.) administration of PSK, a protein-bound polysaccharide derived from Basidiomycetes, on the anti-tumor T-cell response in gut-associated lymphoid tissue (GALT). The p.o. administration of PSK significantly suppressed the growth of colon 26 carcinoma (C-26) inoculated into the subserosal space of the cecum (i.c.), and augmented the tumor-neutralizing activity of the draining mesenteric lymph node (LN) cells. PSK treatment also significantly decreased the levels of immunosuppressive factors such as plasma transforming growth factor (TGF)-beta in the i.c. C-26-inoculated mice. We also evaluated the improving effect of PSK on the anti-tumor T-cell response in GALT by utilizing B7-transfected P815 mastocytoma (B7/P815). The PSK treatment promoted the rejection of i.c.-inoculated B7/P815 and restored the CD4+ T-cell-dependent proliferative response of the draining mesenteric LN cells against in vitro restimulation. Furthermore, the treatment also decreased the TGF-beta production but increased the IFN-gamma production of these cells. The p.o. administration of PSK, however, showed no effect in the CD8+ T-cell-dependent cytolytic activity of the draining mesenteric LN cells after in vitro restimulation. Overall, these results indicate that the p.o. administration of PSK can improve the impaired anti-tumor CD4+ T-cell response in GALT, mainly through a suppression of TGF-beta production and a restoration of IFN-gamma production.

Administration, Oral↗
PubMed1997

Immunomodulatory effects of a plasmid expressing B7-2 on human immunodeficiency virus-1-specific cell-mediated immunity induced by a plasmid encoding the viral antigen.

B7 co-stimulation is essential for activating resting T cells following antigen recognition by the T cell receptor. To determine whether B7 has adjuvant activities on human immunodeficiency virus type-1 (HIV-1)-specific immunity induced by inoculation of a plasmid encoding HIV-1 env and rev (DNA vaccine), B7-1 and B7-2 expression plasmids were co-inoculated with the DNA vaccine. The delayed-type hypersensitivity response and cytotoxic T lymphocyte (CTL) activity were significantly enhanced when B7-2 expression plasmid was co-inoculated with the DNA vaccine, but were unaffected when the B7-1 expression plasmid was used with the vaccine instead. The immunological response enhanced by B7-2 decreased below the level of mice immunized with the DNA vaccine in combination with CTLA4Ig, an inhibitor of the B7/CD28 co-stimulatory signal, suggesting that this signal is critical for the enhanced response induced by co-inoculation of the DNA vaccine and B7-2 expression plasmid. This enhancement appeared to occur via an interferon-gamma (IFN-gamma)-dependent mechanism, as combined administration of the B7-2 plasmid and neutralizing anti-IFN-gamma antibody abrogated the virus-specific cell-mediated immunity. These results suggest that this gene-based co-inoculation strategy using HIV-1 viral antigen and B7-2 co-stimulatory molecule could be a powerful means of combating HIV-1 infection.

AIDS Vaccines↗
PubMed1997

Inhibitory effect of NS-398, a selective cyclooxygenase-2 inhibitor, on azoxymethane-induced aberrant crypt foci in colon carcinogenesis of F344 rats.

Prostaglandin E2, which is produced by cyclooxygenase (COX) during arachidonic acid metabolism, is considered to be related to colon carcinogenesis. Therefore, the effect of NS-398 (N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide), a COX-2 inhibitor, was examined in azoxymethane (AOM)-induced colon carcinogenesis in rats in this study. In the first experiment, groups 1-3 were treated with AOM (15 mg/kg, s.c.) 3 times at intervals of a week from 5 weeks of age. Groups 2 and 3 were respectively given 1 mg/kg and 10 mg/kg of NS-398 in 5% gum arabic aqueous solution 3 times per week by oral gavage during the experiment. Six weeks after the first exposure to AOM, aberrant crypt foci (ACF) were counted in the colonic mucosa of all rats. The mean occurrence of ACF per length in rats given 1 mg/kg b.w. or 10 mg/kg b.w. of NS-398 was reduced to 65.7% or 52.8%, respectively, of that in rats treated with only AOM. Levels of COX-2 mRNA expression in groups treated with AOM, regardless of NS-398, were slightly higher than that in the group treated with NS-398 alone as judged from reverse transcription-polymerase chain reaction analysis. In the second experiment, the effect of NS-398 at different times, i.e., during initiation and post-initiation, was examined. Treatment with NS-398 in both phases significantly inhibited the appearance of ACF. The results imply that NS-398 might have a chemopreventive potential.

Animals↗
PubMed1997

Regressive effects of various chemopreventive agents on azoxymethane-induced aberrant crypt foci in the rat colon.

Regressive effects of four chemopreventive agents [5-hydroxy-4-(2-phenyl-(E)-ethenyl)-2(5H)-furanone (KYN-54), S-methyl methanethiosulfonate (MMTS), chlorogenic acid (CA), and piroxicam] on azoxymethane (AOM)-induced aberrant crypt foci (ACF) in the colon of male F344 rats were examined by dietary exposure. At six weeks of age, 60 rats of groups 1 through 5 received subcutaneous injections of AOM (15 mg/kg body weight) once a weeks. Twelve weeks after the first carcinogen injection, when the occurrence of ACF was maximal, the rats in groups 2 through 5 were started on diet containing the test chemicals as follows: group 2, KYN-54 (0.02%); group 3, MMTS (0.01%); group 4, CA (0.025%); and group 5, piroxicam (0.0125%). Group 1 (20 rats) was kept on the basal diet alone, and group 6 (12 rats) served as an untreated control. Rats in each group were killed at 6, 12, 18, or 24 weeks after the start of the experiment, and the yield of ACF in the colon of each group at 18 or 24 weeks was compared with that at 12 weeks. The number of ACF per rat colon of each group at 18 or 24 weeks was smaller than that at 12 weeks. The reduction rates at 18 weeks were 7% in group 1 (AOM alone), 11% in group 2 (AOM + KYN-54), 10% in group 3 (AOM + MMTS), 51% in group 4 (AOM + CA) (P < 0.01), and 33% in group 5 (AOM + piroxicam) (P < 0.02), while at 24 weeks they were 12%, 26%, 51% (P < 0.002), 43% (P < 0.05), and 70% (P < 0.001), respectively. These results indicate that chemopreventive agents for large bowel carcinogenesis, i.e., KYN-54, MMTS, CA, and piroxicam, are not only able to prevent the development of ACF, but also can regress ACF, which are regarded as precursor lesions of colorectal cancer.

4-Butyrolactone↗
PubMed1997

Chemoprevention of azoxymethane-induced rat colon carcinogenesis by a xanthine oxidase inhibitor, 1'-acetoxychavicol acetate.

In our studies to find natural compounds with chemopreventive efficacy in foods, using azoxymethane (AOM)-induced colonic aberrant crypt foci and colonic mucosal cell proliferation as biomarkers, a xanthine oxidase inhibitor, 1'-acetoxychavicol acetate (ACA), present in the edible plant Languas galanga from Thailand was found to be effective. This study was conducted to test the ability of ACA to inhibit AOM-induced colon tumorigenesis when it was fed to rats during the initiation or post-initiation phase. Male F344 rats were given three weekly s.c. injections of AOM (15 mg/kg body weight) to induce colonic neoplasms. They were fed diet containing 100 or 500 ppm ACA for 4 weeks, starting one week before the first dosing of AOM (the initiation feeding). The other groups were fed the ACA diet for 34 weeks, starting one week after the last AOM injection (the post-initiation feeding). At the termination of the study (week 38), AOM had induced 71% incidence of colonic adenocarcinoma (12/17 rats). The initiation feeding with ACA caused significant reduction in the incidence of colon carcinoma (54% inhibition by 100 ppm ACA feeding and 77% inhibition by 500 ppm ACA feeding, P = 0.03 and P = 0.001, respectively). The post-initiation feeding with ACA also suppressed the incidence of colonic carcinoma (45% inhibition by 100 ppm ACA feeding and 93% inhibition by 500 ppm ACA feeding, P = 0.06 and P = 0.00003, respectively). Such inhibition was dose-dependent and was associated with suppression of proliferation biomarkers, such as ornithine decarboxylase activity in the colonic mucosa, and blood and colonic mucosal polyamine contents. ACA also elevated the activities of phase II enzymes, glutathione S-transferase (GST) and quinone reductase (QR), in the liver and colon. These results indicate that ACA could inhibit the development of AOM-induced colon tumorigenesis through its suppression of cell proliferation in the colonic mucosa and its induction of GST and QR. The results confirm our previous finding that ACA feeding effectively suppressed the development of colonic aberrant crypt foci. These findings suggest possible chemopreventive ability of ACA against colon tumorigenesis.

Animal Feed↗
PubMed1997

[The diagnosis of amyotrophic lateral sclerosis supported by motor evoked potential and brain MRI studies].

A 57-year-old man developed severe muscle weakness and atrophy of the upper extremities within a five-month period. Neurological examination revealed severe weakness and atrophy in the scapular muscles and proximal and distal muscles of the upper extremities. Fasciculations were also observed in the various muscles of the upper extremities. There was neither muscle weakness, atrophy nor fasciculation in either his face, neck muscles or lower extremities. He had no pseudobulbar or bulbar signs. Tendon reflexes were mildly hyperactive in the jaw and lower extremities, and normal in the upper extremities. There were no pathological reflexes, spasticity or sensory disturbances. The needle EMG study revealed denervation potentials in all muscles of the upper extremities examined. The nerve conduction study revealed no findings of the conduction block. Cervical spine X-rays revealed the narrowing of the spinal foramens at the left C3/C4 and bilateral C4/C5, C5/C6, and C6/C7 intervertebral levels. In addition, magnetic resonance imaging (MRI) revealed compressions of the cervical cord at C4/C5 and C5/C6 intervertebral levels. These clinical and neuroradiological findings resembled those of the cervical spondylotic amyotrophy (CSA). However, the motor evoked potential (MEP) study revealed the pyramidal tract dysfunction above the levels of the pyramidal decussation. Furthermore, brain MRI revealed abnormal foci in both internal capsules which were characterized by hyperintense relative to cortical gray matter on T2-weighted images and still hyperintense to white matter on proton-density-weighted images. In addition, T2-weighted images demonstrated a low signal within the motor cortex and hyperintense lesions in the white matter of the precentral gyri. These MRI findings indicated the degeneration of the pyramidal tract and corresponded to those found in the patients with amyotrophic lateral sclerosis (ALS) which have been recently reported. It has been difficult to distinguish ALS from CSA. However, MEP and brain MRI studies were useful for distinguishing these two diseases in this patient. In addition, this patient showed typical MRI findings suggesting the degeneration of the pyramidal tract, although this patient had a relatively short course of illness and did not show obvious physical findings suggesting pyramidal tract dysfunction.

Amyotrophic Lateral Sclerosis↗
PubMed1997

[A 10-year-old case with idiopathic oculomotor nerve palsy].

We reported a 10-year-old girl with acquired left oculomotor nerve palsy. Neurologic and radiological examinations failed to reveal the etiology. Following administration of corticosteroid and vitamin B6, diplopia improved within 6 weeks, and mydriasis has been improving over the past 9 months. Idiopathic acquired oculomotor nerve palsy is a very rare condition in childhood, and prognosis of the disease is sometimes good.

Child↗
PubMed1997

[Successful eradication of H. pylori in an elderly patient with gastric cancer after effective UFT-E therapy].

The patient was a 83-year-old female with 2' T2-type gastric cancer associated with positive H. pylori in the lesser curvature of the stomach. The patient was treated with oral UFT-E alone in a daily dose of 400 mg. The tumor exhibited an O' IIa + IIc-like appearance 4 weeks after the start of administration and became scarred 8 weeks later, revealing marked tumor reduction in a short period of time. At 8 weeks, biopsy showed marked polymorphonuclear cells infiltration of gastric mucosa with no evidence of malignancy. In an attempt to eradicate H. pylori, 30 mg of lansoprazole, 400 mg of clarithromycin, and 2.0 g of ecabet-Na (3.0 g of Gastrom) were administered for 2 weeks. H. pylori was found to have been successfully eradicated, and the inflammatory lesions were no longer visible histologically. UFT-E was highly effective in this patient, and the eradication of H. pylori may contribute to the prevention of cancer recurrence.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

[The diagnosis and follow-up evaluation of acute cerebellar ataxia supported by a cerebellar stimulation study].

A 70-year-old woman who has been suffering from diabetes mellitus since 67 years of age rapidly developed severe truncal ataxia. Neurological examination showed severe truncal ataxia, incoordination and decreased deep sensations in the bilateral lower extremities. A CSF study revealed a moderately elevated total protein (125 mg/dl) without any elevation of the cell count. A nerve conduction study supported the diagnosis of polyneuropathy. Lumbar MRI revealed spinal canal stenosis at the L3/L4-L5/S1 intervertebral levels due to disk herniations and ossification of the yellow ligaments. We examined cerebellar stimulation in order to determine whether the ataxia was due to dysfunction of the cerebellum or peripheral nervous system. Conditioning electrical stimulation over the cerebellum did not change the size of motor potentials evoked by magnetic cortical stimulation in the right first dorsal interosseous muscle. Her clinical course was good, and the limb and truncal ataxia became very mild about 4 months after the onset, although there was little change in the decreased deep sensations. The cerebellar stimulation in the second study was normal. We diagnosed her as having acute cerebellar ataxia and thought that the decreased deep sensations were due to diabetic polyneuropathy and lumbosacral radiculopathies. A cerebellar stimulation study was useful for the diagnosis and follow-up evaluation of acute cerebellar ataxia in this patient.

Acute Disease↗
PubMed1997

[A case of cortical reflex positive-negative myoclonus--electrophysiological study].

An 11-year-old girl who had the positive-negative myoclonus and the history of the generalized tonic clonic seizure was electrophysiologically studied. She had no siblings with either myoclonus or epilepsy, and her intellectual level was normal. She had no other neurological deficits including ataxia, pyramidal and extrapyramidal signs. Surface EMG showed a brief increase in the EMG activity followed by the silent period associated with positive and negative myoclonus during sustained wrist extension. Giant SEP and C reflex (38.6 ms) following electric stimulation of the median nerve at the wrist were obtained in the resting condition and the silent period (about 180 ms) following C reflex was obtained during voluntary contraction. Jerk-locked back averaging of the EEG time-locked to the onset of the myoclonic discharge recorded from the right biceps muscle showed a cortical spike at the left central region preceding the myoclonus onset by 12.6 ms. The latency of C reflex in this case was very short compared with that of previously reported cortical reflex myoclonus. The estimated cortical delay between the arrival of the somatosensory volley and the motor cortex discharge responsible for the C reflex was -1.0 ms and this value was shorter than that in patients with typical cortical reflex myoclonus (mean 3.7 +/- 1.1 ms). Conditioning stimuli (C) of the right median nerve at the wrist started to facilitate the amplitude of the motor evoked potential recorded from the right abductor pollicis brevis muscle after magnetic test stimuli (T) of the left motor cortex at 20 ms of the C-T interval. This C-T interval was shorter than that (24.6 +/- 1.6 ms) in patients with the typical cortical myoclonus. These electrophysiological findings suggested the shorter reflex pathway of the cortical reflex myoclonus in this case than in typical cortical reflex myoclonus. We speculated that the myoclonus was based upon the direct sensory projection from the thalamus to the motor cortex in this case.

Child↗