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S Terao

Publications and source records attributed to S Terao.

At least 19 recordsLinked to original sources
PubMed2000

Course and distribution of facial corticobulbar tract fibres in the lower brain stem.

The course and distribution of the facial corticobulbar tract (CBT) was examined by correlating MRI of brain stem lesions with neurological symptoms and signs including central (C-FP) or peripheral facial paresis (P-FP) in 70 patients with localised infarction of the lower brain stem. C-FP occurred more often in patients with lesions of the lower pons or upper medulla of the ventromedial brain stem. Some patients with dorsolateral infarcts of the upper medulla to the lower pons showed C-FP, mostly on the lesion side. P-FP on the side of the lesion was also seen in patients with dorsolateral involvement of the lower pons. Patients with ventromedial infarction of the brain stem showed paresis of extremities contralateral to the lesion. Specific neurological symptoms and signs such as dysphagia, vertigo, nystagmus, Horner's syndrome, ipsilateral cerebellar ataxia, and contralateral superficial sensory impairment were seen in patients with dorsolateral infarcts of the brain stem. It is hypothesised that the facial CBT descends at the ventromedial lower pons, near the corticospinal tract, mainly to the level of the upper medulla, where the fibres then decussate and ascend in the dorsolateral medulla to synapse in the contralateral facial nucleus.

Adult↗
PubMed2000

Clinical and pathophysiological features of amaurosis fugax in Japanese stroke patients.

OBJECTIVE: It has been emphasized that amaurosis fugax (AmF) is caused by thromboembolism due to atheromatous lesions of the extracranial carotid artery (EC-CA) in Caucasian populations. However, there have been few studies of AmF in Japan. We analyzed the clinical and pathophysiologic features of AmF in 43 Japanese AmF patients. SUBJECTS AND METHODS: Forty-three patients presented with AmF from a group of 2,056 Japanese patients with acute ischemic stroke. We investigated angiographic and transcranial Doppler findings, precipitating factors, medical treatment and prognosis, to elucidate the pathogenetic mechanism of AmF. RESULTS: Angiographic findings revealed an intracranial lesion in 22 patients (51%), extracranial lesion in 16 (37%), and no abnormality in 5 (12%). Blood flow in the ophthalmic artery (OA) examined by the transcranial Doppler ultrasonography (TCD) showed normal antegrade flow in 24 patients and reversed flow in 7. Precipitating factors for AmF were seen in 7 out of 43 patients. Regarding the pathogenesis of AmF, the micro-thromboembolism originated from the internal carotid artery (ICA) in 25 patients, the thromboembolism was via the external carotid artery (ECA) in 7, the hemodynamic retinal vascular insufficiency in 6 patients showed various atheromatous changes in the intracranial carotid artery (IC-CA) or EC-CA, and the cause was unknown in 5. CONCLUSION: In this series of patients, AmF was mainly caused by thromboembolism from IC-CA atheromatous lesions. Micro-thromboemboli from the ECA or hemodynamic retinal vascular insufficiency, although less frequent, should also be considered as possible etiologies for AmF.

Adolescent↗
PubMed2000

[Thromboxane A2].

Explore the source record for details and available documents.

Anti-Asthmatic Agents↗
PubMed1999

Tissue-specific somatic mosaicism in spinal and bulbar muscular atrophy is dependent on CAG-repeat length and androgen receptor--gene expression level.

The factors influencing the tissue-specific pattern of somatic mosaicism in CAG-repeat diseases have not yet been fully resolved. We performed a detailed analysis of the degree of somatic mosaicism in various tissues from 20 patients with spinal and bulbar muscular atrophy (SBMA), including 4 who were deceased. The most outstanding feature was the prominent somatic mosaicism observed in the cardiac and skeletal muscles, composed predominantly of postmitotic cells, and in the skin, prostate, and testis. The CNS tissues, liver, and spleen showed the least mosaicism. The tissue distribution of somatic mosaicism in patients with SBMA was markedly different from that in patients with Huntington disease (HD) and from that in patients with dentatorubral-pallidoluysian atrophy (DRPLA). The degree of somatic mosaicism correlated with the CAG-repeat number but not with age at examination. Furthermore, tissues with a higher mosaicism level corresponded well to those with a higher expression level of androgen receptor protein. The tissue-specific pattern of somatic mosaicism related not only to cell composition with different cell turnover rates but to repeat size and gene expression levels, and postnatal cell division is unlikely to be a major cause of somatic mosaicism probably because of the relative stability of CAG repeat in SBMA.

Adult↗
PubMed1999

Axonal and perikaryal involvement in chronic inflammatory demyelinating polyneuropathy.

OBJECTIVES: To assess the extent of loss of myelinated nerve fibres and spinal motor neuron loss in chronic inflammatory demyelinating polyneuropathy (CIDP), a clinicopathological study was conducted on biopsied sural nerves and necropsied spinal cords from patients with CIDP. METHODS: The myelinated fibre pathology of 71 biopsied sural nerves and motor neuron pathology of nine necropsied spinal cords at L4 levels in patients with CIDP were quantitatively and immunohistochemically assessed. RESULTS: Myelinated nerve fibre density was significantly diminished to 65.4% of the control values (p <0.0001), correlating inversely with the extent of segmental demyelination and remyelination (r = -0.43, p < 0.0005) and duration of illness (r = -0.31, p < 0.01). Numbers of large spinal motor neurons in CIDP were variably but significantly diminished (range from 46.0 to 97.6% of the age matched control value (p < 0.005)), and reactive astrogliosis was evident in the ventral horn in CIDP. The frequency of ventral horn neurons exhibiting central chromatolysis and the accumulation of phosphorylated high molecular weight neurofilament protein was significantly higher in CIDP than in controls (p<0.01 and p<0.05). CONCLUSIONS: The loss of nerve axons and spinal motor neurons is common in CIDP, and extensive in some cases. These neuronal and axonal losses may influence the functional prognosis in CIDP.

Adolescent↗
PubMed1999

[Thromboxane A2 antagonist--discovery of seratrodast].

We were interested in RCS (rabbit aorta contracting substance) and SRS-A (slow reacting substance of anaphylaxis) and their involvement in human bronchial asthma. When we started our anti-asthmatic drug research in the 1970's. We synthesized a lot of chemical compounds and eventually discovered that AA-861 inhibited the generation of SRS-A from the lung tissue of actively sensitized guinea pigs. AA-861 was found to be a potent 5-lipoxygenase inhibitor. This compound reduced experimental allergic asthma in guinea pigs, but it is easily metabolized in the body. More recently, we found a novel compound, AA-2414 (seratrodast), which is not metabolized in the body. AA-2414 proved to be not a 5-lipoxygenase inhibitor, but a thromboxane A2 (TXA2) receptor antagonist. Seratrodast is the first receptor antagonist that is being developed as an anti-asthmatic drug. Seratrodast inhibits both immediate-, late asthmatic responses in guinea pigs, and also reduces airway hyperresponsiveness in dogs. The anti-asthmatic action of seratrodast in animal models indicates that the drug should be of use in the treatment of human asthmatics. In clinical studies, seratrodast showed a marked effect to improve clinical parameters in bronchial asthma. It is also reported that seratrodast is free from harmful aftereffects. Clinical trials are under way in the US.

Animals↗
PubMed1998

Slow intrinsic optical signals in the rat spinal dorsal horn in slice.

Tetanic stimulation of high-threshold primary afferent fibers in the dorsal root was found to elicit intrinsic optical signals (IOSs) in transverse slices of 11- to 20-day-old rat spinal cords. The IOS, lasting for 30 s or longer, was most prominent in the lamina II of the dorsal horn. Treatment with a Na+-K+-2Cl- co-transport blocker, furosemide, abolished the IOS, suggesting that the origin of the IOS is the cellular swelling due to an activity-dependent rise in extracellular K+. Substance P antagonist spantide, glutamate antagonists 2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2,3-dione, and the mu-opioid agonist [d-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin suppressed IOSs. Thus, IOSs represent at least in part the slow excitatory response that is known to be generated in dorsal horn neurons after tetanic activation of unmyelinated afferent fibers.

2-Amino-5-phosphonovalerate↗
PubMed1998

[Serial MRI findings in patients with CNS cryptococcosis].

We reported the serial magnetic resonance imaging (MRI) findings of two patients with central nervous system (CNS) cryptococcal infection without AIDS. The diagnosis of CNS cryptococcosis was made by visualizing the fungi in the CSF with the India ink test, detecting cryptococcal antigens, and culturing the fungus. Both patients had dilated perivascular Virchow-Robin (V-R) spaces, which were defined as small rounded lesions greater less than 3mm diameter that were hyperintense on T2-weighted images. They were present in the basal ganglia, brainstem and cerebral white matter. Case 1 had bilateral parietal arachnoid cyst which was thought to represent a focal collection of organisms and mucoid material within subarachnoid space. Abnormal optochiasmatic arachnoid enhancement detected in case 2, who had complete loss of vision. With disease progression perivascular V-R increased in size, resulting in the developing cryptococomas which were defined as rounded lesions greater than 3mm diameter, and were hyperintense on T2-weighted images in the basal ganglia, cerebellum and cerebral white matter. In follow-up MRI of those patients, radiological progression was seen despite appropriate treatment and falling CSF cryptococcal antigens. In conclusion, this spectrum of MRI appearances in CNS cryptococcosis reflects the pathological mechanism of invasion by the fungus, and may be relatively specific for cryptococcosis.

Aged↗
PubMed1998

[Cerebral infarction associated with nephrotic syndrome in a young adult: a case report].

We report a 19-year-old man who developed a cerebral infarction in the territory of the anterior choroidal artery and showed a hypercoagulable state and nephrotic syndrome after diarrhea and appetite loss. He had suffered from nephrotic syndrome from the age of three and had been treated for five years. MR-angiography showed an occlusion originating in the right internal carotid artery. The right anterior and middle cerebral arteries were imaged from the left internal carotid artery via the anterior communication artery. He showed symptoms of left hemiparesis, agnosia, loss of activity, anasarca and left hypacusis following his clinical course, but had recovered from all but left hemiparesis following medical treatments including steroid therapy. The histologic finding by a renal biopsy revealed focal glomerulosclerosis. In this case, we considered that when he was in a hypercoagulable state and had a second attack of nephrotic syndrome because of inflammation and dehydration due to diarrhea and appetite loss, his hypercoagulable state grew worse, and he then developed a cerebral infarction. When one see a patient with nephrotic syndrome, one should be attentive to the possibility of a complication of cerebral infarction.

Adult↗
PubMed1997

The lateral corticospinal tract and spinal ventral horn in X-linked recessive spinal and bulbar muscular atrophy: a quantitative study.

A quantitative study was performed on spinal cord lesions in seven patients with X-linked recessive spinal and bulbar muscular atrophy. The myelinated fiber density of the lateral corticospinal tracts at the T7 cord level was well preserved for both large and small myelinated fibers. On the other hand, neurons in the L4 ventral horn were markedly depleted; marked loss was noted of the large alpha and medium-sized gamma motor neurons located in the lateral and medial nuclei as well as the small neurons in the intermediate zones of the ventral horn. These results suggest that myelinated fiber density and fiber-size distribution in the corticospinal tract are well preserved and that neuronal loss in the ventral horns is not restricted to alpha and gamma motoneurons but also involves small interneurons.

Aged↗
PubMed1997

Central facial weakness due to medial medullary infarction: the course of facial corticobulbar fibres.

Two patients are reported with contralateral hemiparesis including a face of supranuclear type, caused by an infarct of the unilateral ventromedial part of the upper medulla. Data from these patients support the hypothesis that part of the corticobulbar fibres supplying the lower facial muscles descend ipsilaterally in the ventromedial part of the upper medulla and then, after decussation, ascend rostrally to the contralateral facial nucleus.

Adult↗
PubMed1997

Upper motor neuron lesions in stroke patients do not induce anterograde transneuronal degeneration in spinal anterior horn cells.

BACKGROUND AND PURPOSE: To determine whether upper motor neuron lesions in stroke can cause transneuronal degeneration of lower motor neurons, we assessed spinal anterior horn cells in patients dying with poststroke hemiplegia. METHODS: Subjects were four stroke patients with severe left hemiplegia and four age-matched control subjects who died of nonneurological disease. After histological processing and staining, cytoarchitectonic assessment was made of all neurons in the ventral horns of the 4th lumbar segment of the spinal cord according to cell diameter and topography. RESULTS: In the four stroke patients, no differences were seen in anterior horn cell populations or diameter and size distribution patterns between affected and unaffected sides or between these patients and the control subjects. CONCLUSIONS: The present quantitative analysis provides no evidence of anterograde transneuronal degeneration of lower motor neurons after upper motor neuron damage in stroke patients.

Adult↗
PubMed1997

Axonal pathology in Japanese Guillain-Barré syndrome: a study of 15 autopsied cases.

We assessed the frequency and extent of axonal involvement in the ventral spinal roots in 15 Japanese autopsied patients with Guillain-Barré syndrome (GBS). Teased-fiber preparation revealed that five had predominantly axonal pathology with minimal segmental demyelination, seven had predominantly segmental demyelination with minimal axonal changes, two patients showed a mixture of both conditions, and one patient did not show any particular pathologic changes. We confirmed axon loss by immunohistochemical analysis of high-molecular-weight neurofilament protein. Macrophage invasion was a prominent feature in nerves with predominantly axonal changes. Two patients with severe axonal involvement and prolonged clinical courses exhibited motor neuron loss with astrogliosis in the ventral horns. These results suggest that autopsy-verified axonal involvement is more frequent among Japanese GBS patients than in Caucasian populations but less frequent than that reported from northern China.

Adult↗
PubMed1996

Expression of glial cell line-derived growth factor mRNA in the spinal cord and muscle in amyotrophic lateral sclerosis.

The steady-state expression levels of glial cell line-derived growth factor (GDNF) mRNA was studied in the post mortem spinal cord and muscle of patients with amyotrophic lateral sclerosis (ALS), by reverse transcription followed by polymerase chain reaction (RT-PCR). GDNF mRNA levels in the lumbar cord were significantly increased in ALS as compared with controls. On the other hand, GDNF mRNA levels were significantly lower in the muscle in ALS patients. The increase of GDNF mRNA in the spinal cord mostly reflected an increase in the anterior horn, anterior and lateral columns, where the pathological involvement was severe. In the posterior column and posterior horn with less pathological involvement, the increase was less. These results suggest that GDNF mRNA levels are inversely regulated between the spinal cord and muscle in ALS, increased in the spinal cord and lowered in the muscle, in correlation with the pathological severity.

Aged↗
PubMed1996

Expression of mRNAs for neurotrophic factors (NGF, BDNF, NT-3, and GDNF) and their receptors (p75NGFR, trkA, trkB, and trkC) in the adult human peripheral nervous system and nonneural tissues.

The steady-state mRNA levels of the four neurotrophic factors of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and glial cell line-derived neurotrophic factor (GDNF) and their receptors (p75NGFR, trkA, trkB and trkC) in the adult human peripheral nervous system (PNS) as well as nonneural tissues were examined using quantitative reverse transcription-polymerase chain reaction (RT-PCR). NGF and BDNF mRNA levels were high in the heart and spleen as well as in the dorsal root ganglia (DRG) and spinal cord, showing similar spatial expression patterns, while NT-3 mRNA levels were more pronounced in the liver and spleen. In contrast to these neurotrophins, GDNF mRNA expression occurred at the highest levels in the muscle, and it was also comparatively high in the spinal cord. p75NGFR mRNA was expressed extensively throughout the PNS tissues and in the spleen. The spatial expression patterns differed among trkA, and trkB and trkC mRNAs. trkA mRNA was greatly expressed in the DRG, sympathetic ganglia and spleen, while the trkB and trkC mRNA levels were high in the DRG, spinal cord and brain. The levels of trkB and trkC mRNAs with tyrosine kinase domain, compared to those with extracellular domain, were relatively high in the DRG, whereas they were low in the spinal cord and brain. The spatial patterns of the distributions of neurotrophic factors and their receptors mRNA levels in the adult human PNS and nonneural tissues are largely similar to those reported in other mammals, but these findings provide further, more specific, understanding relevant to the therapeutic approach to human diseases.

Adult↗