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Y Terao

Publications and source records attributed to Y Terao.

At least 91 records · Page 5Linked to original sources
PubMed1995

Altered motor cortical excitability to magnetic stimulation in a patient with a lesion in globus pallidus.

A 27-year-old man with Behçet's disease presented with dyskinesia of the right hand and leg, but without paresis. MRI showed a discrete lesion in the internal segment of the left globus pallidus. SPECT (single photon emission tomography) disclosed increased perfusion in the hand and leg area of the left motor cortex and ipsilateral thalamus compared to that of the corresponding regions on the right. The dyskinesia was considered to be produced by disinhibition of the motor cortex due to loss of inhibitory inputs from the ipsilateral pallidum via the thalamus. Double transcranial magnetic stimulation revealed loss of suppression (loss of intracortical inhibition) of the left motor cortex while it showed normal suppression on the right, even though conventional techniques of magnetic stimulation failed to show any changes in excitability of the left motor cortex. We conclude that it is possible to detect changes of motor cortical excitability caused by dysfunction of some inputs from the basal ganglia by using the double cortical stimulation technique here described.

Adult↗
PubMed1995

Mutagenic activity of 6-aminoquinoxalines in Salmonella typhimurium.

Mutagenicity of 6-aminoquinoxaline derivatives was tested with Salmonella typhimurium strains TA98 and TA100 in the presence and absence of S9 mix from the viewpoint that the 6-aminoquinoxaline skeleton is a common unit of mutagenic imidazoquinoxalines. We tested nine compounds: 5-methyl-6-methylaminoquinoxaline (1), 3,5-dimethyl-6-methylaminoquinoxaline (2), 2,5-dimethyl-6-methylaminoquinoxaline (3), 6-methylamino-2,3,5-trimethylquinoxaline (4), 2,3-diethyl-5-methyl-6-methylaminoquinoxaline (5), 5-methyl-6-methylamino 3-phenylquinoxaline (6), 6-amino-2,3,5-trimethylquinoxaline (7), 6-dimethylamino-2,3,5- trimethylaminoquinoxaline (8), 6-amino-2,3-dimethylquinoxaline (9). These compounds showed the mutagenic activity for both TA98 and TA100 in the presence of S9 mix, where they were more sensitive for TA100 strain. Methyl groups at the 2, 3 and/or 5 positions increased the potency of mutagenicity (1 < 2 < 3 << 4, 9 < 7). However, ethyl groups at the 2 and 3 positions lowered the mutagenicity of the methyl substitute but elevated it of the parental compound (1 < 5 < 4). A methyl group at the N6 position decreased the mutagenicity (7 > 4 > 8).

Amines↗
PubMed1995

Input-output organization in the hand area of the human motor cortex.

The primate motor cortex consists of efferent zones which receive sensory information from a portion of limb in close anatomical relation to the muscle to which they project. To investigate a similar input-output relation in humans, we studied the effect of tactile stimuli on the size of motor evoked potentials (MEPs) elicited by transcranial magnetic and electrical stimulation. For tactile stimuli we applied air to the skin. The sizes of MEP of 3 finger muscles (flexor pollicis brevis, first dorsal interosseous, and abductor digiti minimi) with and without air stimuli were compared. Air stimuli applied to the tip of one finger facilitated mainly the magnetically evoked MEP of a muscle attached to that finger. A less obvious facilitatory effect was observed when giving stimuli on the dorsal aspect of the hand. Air stimuli had no facilitatory effect on electrically evoked MEPs. In one subject, there was no facilitatory effect even to magnetically evoked MEPs. In this subject, D-waves had the lowest threshold for magnetic and electrical stimulation. These results suggested that the effect was produced at the cortical level. This effect may correspond to the input-output relation found in the primate motor cortex.

Electric Stimulation↗
PubMed1995

Facilitatory effect of tonic voluntary contraction on responses to motor cortex stimulation.

To investigate the mechanisms underlying the facilitation of responses to motor cortical stimulation produced by tonic voluntary contraction, we studied the facilitatory effects in 7 normal volunteers during different levels of muscle contraction. Responses were similarly facilitated by voluntary contraction with 3 forms of stimulation: magnetic cortical, electrical cortical, and foramen magnum level stimulation. At a high level of contraction, however, only magnetic responses were markedly facilitated. We conclude that the facilitation of responses to cortical stimulation induced by tonic voluntary contraction occurs mainly at the spinal level, but that cortical excitability changes also contribute to the enlargement of magnetic responses in the case of a high level of contraction.

Adult↗
PubMed1995

Mutagenicity of alkyl azides.

Alkyl azides showed mutagenicity for S. typhimurium TA100 strain with S9 mix. However, no significant activity was observed for TA98 either with or without S9 mix or for TA100 without S9 mix. On the other hand, 3-azido-1,2-propanediol showed the enantioselective activity regardless of S9 mix. Two aryl azides tested were not mutagenic, and trimethylsilyl azide exhibited potent activity for TA100. Their structure-activity relationships are discussed.

Azides↗
PubMed1994

Magnetic stimulation of corticospinal pathways at the foramen magnum level in humans.

Magnetic stimulation done with a double cone coil placed over the back of the head activated descending motor pathways and produced electromyographic responses in muscles of the arms and legs. The latencies of these responses were the same as those of responses to electrical brainstem stimulation. The threshold was lowest when the coil was placed over the inion or below it on the median line. Placement of the coil on the side ipsilateral to the muscle was more effective than placement on the contralateral side. These results indicate that activation occurs at the foramen magnum level (just below the pyramidal decussation). Collision experiments that used cortical and magnetic brainstem stimulation indicated that the major part of the responses to the latter stimulation were conducted via the large diameter component of the corticospinal tract. Collision experiments done with the peripheral nerve and magnetic brainstem stimulation showed that this stimulation produced a single descending volley in the descending tract. We conclude that magnetic brainstem stimulation produces a single descending volley in the corticospinal tract at the foramen magnum level with less discomfort.

Adult↗
PubMed1994

Transcranial stimulation of the leg area of the motor cortex in humans.

We used transcranial magnetic stimulation on nine normal volunteers to establish an effective way to stimulate the leg area of the motor cortex. Three types of coils: a large figure-eight coil, small figure-eight coil, and a round coil were used. Surface electromyographic activities were recorded from the left tibialis anterior muscle, and the latencies and amplitudes compared with those obtained by anodal electrical stimulation. The most stable responses were obtained when the large figure-eight coil was centered over the vertex and backward current was run through it or when the round coil was centered two to three centimeters anterior to the vertex with left-flowing current in it at the posterior widening. The latencies obtained under these stimulation conditions were the same as those obtained by electrical stimulation. We conclude that direct activation of the pyramidal cells occurs in the leg area of the motor cortex in all forms of magnetic and electrical stimulation.

Electric Stimulation↗
PubMed1994

Synthesis and mutagenicity of a new mutagen, 2-amino-1,7,9-trimethylimidazo[4,5-g]quinoxaline, and its analog.

A new mutagen, 2-amino-1,7,9-trimethylimidazo[4,5-g]quinoxaline (1), isolated from beef extract, was synthesized from 3-fluoro-2-methylaniline via an intermediate, 2,8-dimethyl-7-methylaminoquinoxaline (7a). Its 2-methylanalog (2) was also synthesized from the same intermediate. The synthetic 1 showed the same mutagenic activity as the isolated mutagen. However, 2 was non-mutagenic.

Mutagenicity Tests↗
PubMed1994

[Gastric acid secretion and absorption of levodopa in patients with Parkinson's disease--the effect of supplement therapy to gastric acid].

Since an oral regimen of levodopa has been instituted for treatment of Parkinson's disease, its absorption and metabolism has been well demonstrated. However, its chemical characteristics of high solubility in acid solution and low solubility in water have not been well known. We paid attention to this characteristic and studied the relationship between its absorption and gastric acid secretion in 38 patients with Parkinson's disease who became refractory to therapy of levodopa. We measured the pH and amount of collected fasting gastric juice. Gastric acid secretion was decreased in 22 patients (58%). In ten of these 22 patients, 30 ml of lemon juice was prescribed in every administration of levodopa as a supplement to gastric acid for two weeks. Increases of L-dopa concentration after 60 min. and 180 min. were observed after lemon juice supplement therapy. Among the Parkinson symptoms, rigidity, akinesia, and small step gait were improved in every case except one patient who showed decrease of L-dopa concentration at 180 minutes. However, improvement of tremor was less remarkable. We consider this supplement therapy to gastric acid is one of the effective and useful methods in the management of Parkinson's disease.

Aged↗
PubMed1993

Novel missense variants of prion protein in Creutzfeldt-Jakob disease or Gerstmann-Sträussler syndrome.

We found 3 novel missense variants in the open reading frame of the prion protein (PrP) gene. The codon 105 point mutation (proline to leucine) was found on a codon 129 (Valine) PrP allele in 4 patients from 3 different Japanese families with Gerstmann-Sträussler syndrome. The codon 180 variant PrP (valine to isoleucine) was found in Creutzfeldt-Jakob disease (CJD) patients with a similar clinical course to that of codon 178 mutation. The codon 232 variant PrP (methionine to arginine) was documented in the CJD patients with typical clinical and pathological findings. These variant PrP molecules were not detected in 200 normal Japanese PrP alleles. PrP has a large repertoire of variant forms, and each primary structure of PrP corresponds to the distinct phenotype of prion diseases.

Base Sequence↗
PubMed1993

A new inherited prion disease (PrP-P105L mutation) showing spastic paraparesis.

We report the clinicopathological findings of 5 patients with an inherited prion disease with a codon 105 (Pro to Leu) mutation. All of the patients had a spastic gait disturbance and progressive dementia without either cerebellar signs, myoclonus, or periodic synchronous discharges. Autopsy of 3 patients revealed numerous amyloid plaques in the cerebral cortex, especially in the motor cortex and the frontal lobe where neuronal loss and severe gliosis were observed in the absence of spongiform changes. The cerebellum was preserved histologically except for only a few amyloid plaques. The pyramidal tracts in the brainstem and spinal cord showed vacuolated changes and a loss of myelin, but no prion protein accumulations. Thus, the prion protein codon 105 mutation is considered to correspond to a new variant of the Gerstmann-Sträussler syndrome with spastic paraparesis.

Adult↗
PubMed1993

Pure progressive autonomic failure: a clinicopathological study.

Two cases of pure progressive autonomic failure (PAF) are presented. A postmortem study of one case (case 2) showed a pathology resembling that of Parkinson's disease. Marked cell loss was noted in the substantia nigra, nucleus ceruleus, and intermediolateral column of the spinal cord, while cell loss in the sympathetic ganglion was not remarkable. This case may be an exceptionally rare case of late-onset PAF in which autonomic failure was mainly ascribed to preganglionic (and central) pathology, although autonomic function tests suggested postganglionic sympathetic disorder in both cases.

Aged↗
PubMed1993

Discrete cortical infarction with prominent impairment of thumb flexion.

BACKGROUND: Intracortical efferent zones in the primary motor cortex for thumb movements, namely thumb flexion, extension, adduction, and abduction, have been described in Macaca mulatta monkeys but not in humans. Even recent cortical mapping based on intraoperative monitoring does not provide information about intracortical efferent zones as it is not ethically possible to search the human motor cortex extensively by punctate electrodes. CASE DESCRIPTION: A 78-year-old man with discrete cortical embolism over the left central sulcus is described. Only a mild weakness of his right thumb was observed. Thumb flexion was affected to a greater degree than thumb extension, adduction, and abduction. The lesion ran along the bottom of the central sulcus and affected part of the precentral and postcentral gyri on both sides of it. Animal studies in Macaca mulatta monkeys have shown that the intracortical efferent zones for thumb movement, especially for thumb flexion, are located in the part of the motor cortex just adjoining the central sulcus that folds down from the "bank" to the depth of the central sulcus. It was possible to explain the prominent weakness of thumb flexion if we applied the results of the animal studies. CONCLUSIONS: Our case suggests that the same arrangement of intracortical efferent zones found in monkeys may also exist in human beings.

Aged↗
PubMed1993

Portal-systemic encephalopathy and hypothalamic hypothyroidism: effect of thyroid hormone on ammonia metabolism.

We describe a 53-year-old woman with portal-systemic encephalopathy and altered thyroid function. Endocrinological studies revealed low levels of free thyroid hormone with an inappropriately low level of thyroid-stimulating hormone that responded to bolus injection of thyrotropin-releasing hormone with a normal but somewhat delayed pattern. On the diagnosis of hypothalamic hypothyroidism, she was treated with levothyroxine sodium. Thyroid hormone replacement improved not only the symptoms of hypothyroidism but the hyperammonemia and consciousness disturbance, which suggested a hitherto undescribed possibility that hypothyroidism may be an exacerbation factor of hyperammonemia and portal-systemic encephalopathy.

Ammonia↗
PubMed1993

[FDG-PET in an amnestic and hypersomnic patient with bilateral paramedian thalamic infarction].

A 67-year-old patient was admitted to our hospital owing to coma and tetraplegia. MRI showed T2 weighed high intensity areas in the pontine tegmentum, lower aspect of the right cerebellar hemisphere, left half of medulla oblongata, and bilateral paramedian thalamus. He showed marked recovery by urokinase injection becoming able to walk in a few months, but severe amnesia and hypersomnia persisted even 5 months after onset. EEG showed diffuse alpha activity with occasional delta waves in frontal leads. Intelligence was considered normal (WAIS score; verbal IQ 97, performance IQ 102, total IQ 99), through performance on Wechsler memory Scale-R (Revised Japanese edition, WMS-R) and Benton Visual Retention Test indicated impairment of both verbal and visual memory. Verbal memory was impaired to a greater degree than visual memory (Scores of WMS-R: verbal memory index 60, visual memory index 98, index of general memory 72, attention index 95, index of delayed memory 71). He was able to finish only 0 and 1 categories on two trials of the Wisconsin Card Sorting Test. FDG (18F-fluorodeoxyglucose)-PET showed diffuse areas of decreased metabolism in bilateral thalami, frontal lobes, cingulate gyri and medial temporal lobes. The bilateral thalamic lesion seemed to affect the following structures, as judged from MRI: 1) The anterior thalamic peduncle including most of the reciprocal connections between dorsomedial nucleus of thalamus (MD nucleus) and the frontal lobe, 2) The inferior thalamic peduncle which serves as the reciprocal pathway between MD nucleus and medial temporal lobe, especially the amygdala (component of Yakovlev circuit), and 3) The inferior part of mammillothalamic tract (component of Papez circuit).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗