Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Hiroyuki Nakayasu is active.

Publication


Featured researches published by Hiroyuki Nakayasu.


Acta Neurologica Scandinavica | 2004

Stroke recurrence within the first year following cerebral infarction: Tottori University Lacunar Infarction Prognosis Study (TULIPS)

Takao Soda; Hiroyuki Nakayasu; Masanobu Maeda; Masayoshi Kusumi; Hisanori Kowa; Etsuko Awaki; Jun Saito; Kenji Nakashima

Objectives – To identify determinants of recurrence after ischemic stroke in the Japanese population.


Journal of Clinical Neuroscience | 2006

Anterior and posterior inferior cerebellar artery infarction with sudden deafness and vertigo

Takenobu Murakami; Hiroyuki Nakayasu; Mitsuru Doi; Yasuyo Fukada; Miwa Hayashi; Takeo Suzuki; Yuichi Takeuchi; Kenji Nakashima

We report a patient with anterior and posterior inferior cerebellar artery infarction, which manifested as profound deafness, transient vertigo, and minimal cerebellar signs. We suspect that ischaemia of the left internal auditory artery, which originates from the anterior inferior cerebellar artery, caused the deafness and transient vertigo. A small lesion in the middle cerebellar peduncle in the anterior inferior cerebellar artery territory and no lesion in the dentate nucleus in the posterior inferior cerebellar artery territory are thought to explain the minimal cerebellar signs despite the relatively large size of the infarction. Thus a relatively large infarction of the vertebral-basilar territory can manifest as sudden deafness with vertigo. Neuroimaging, including magnetic resonance imaging, is strongly recommended for patients with sudden deafness and vertigo to exclude infarction of the vertebral-basilar artery territory.


European Neurology | 2009

Long-Term Prognosis of Patients with Large Subcortical Infarctions

Yutaka Suto; Hiroyuki Nakayasu; Masanobu Maeda; Masayoshi Kusumi; Hisanori Kowa; Etsuko Awaki; Jun Saito; Kenji Nakashima

Aim: We assessed the long-term prognosis of patients with large subcortical infarctions (LSCI). Methods: We defined LSCI as lesions ≥15 mm confined to deep penetrating arteries without a cardioembolic or atherothrombotic source. Patients with acute ischemic strokes were consecutively registered and followed for 751 ± 441 days. The clinical characteristics and long-term prognoses of patients with LSCI were compared to those of patients with lacunar (LACI), atherothrombotic (ATI) and cardioembolic infarctions (CEI). Results: At discharge from the hospital, the proportion of good outcomes (modified Rankin Scale ≤2) for patients with LSCI (52.1%) was similar to that for ATIs (47.2%), but worse than that for LACIs (73.2%). After a 3-year follow-up period, the mortality rates from LSCI, LACIs, ATIs and CEIs were 8.4, 8.2, 22.3 and 41.1%, respectively; the recurrence rates were 9.3, 14.1, 16.6 and 23.8%, respectively. Conclusions: The short-term prognosis of functional outcomes for LSCI was worse than that for LACIs, but similar to acute-phase ATI outcomes. The long-term prognosis after a LSCI is good, and recurrence tends to be lower than for LACIs.


Neurogenetics | 2004

Mutations of the MTHFR gene (428C>T and [458G>T+459C>T]) markedly decrease MTHFR enzyme activity

Hidetaka Yano; Kazuhiro Nakaso; Kenichi Yasui; Yosuke Wakutani; Hiroyuki Nakayasu; Hisanori Kowa; Yoshiki Adachi; Kenji Nakashima

Methylenetetrahydrofolate reductase (MTHFR) is the only route for the synthesis of 5-methyltetrahydrofolate, which is utilized to convert homocysteine to methionine. In this study, we measured the enzyme activity of a mutant MTHFR that was detected in a patient with hyperhomocysteinemia. The 428C>T mutation in exon 2 of the MTHFR gene is a novel mutation, while the [458G>T+459C>T] mutation in exon 2 is a previously reported mutation. The activity of mutant enzymes containing the 428C>T, [458G>T+459C>T] and 677C>T mutations was 12.7±4.7%, 48.1±18.8%, and 43.6±14.4%, respectively, of that of the wild type enzyme. Our results suggest that these two variants each result in a severe MTHFR deficiency, which causes a developmental delay and cerebral vascular disease.


Cerebrovascular Diseases | 2003

The Antiplatelet Aggregation Effects of Aspirin Suppositories

Hiroyuki Nakayasu; Masanobu Maeda; Takao Soda; Kenji Iijima; Manabu Ishimoto; Ichiro Ieiri; Fumie Tabuchi; Kenji Otsubo; Kenji Nakashima

To confirm that aspirin suppositories are an effective treatment for acute ischemic stroke, we examined the suppressive effects of 200-mg aspirin suppositories on platelet aggregation. Aspirin suppositories suppressed platelet aggregation induced by ADP or collagen, and the suppression continued for 24 h. There was no significant difference in suppression of platelet aggregation between aspirin administered by suppository and orally given aspirin. These results suggest that aspirin suppositories are a useful treatment for acute ischemic stroke.


Geriatrics & Gerontology International | 2017

Association between body mass index and outcome in Japanese ischemic stroke patients

Shinya Kawase; Hisanori Kowa; Yutaka Suto; Hiroki Fukuda; Masayoshi Kusumi; Hiroyuki Nakayasu; Kenji Nakashima

An association between body mass index (BMI) and stroke outcome have been reported, but the results are controversial. The aim of the present study was to evaluate whether BMI is associated with ischemic stroke outcome.


Journal of Stroke & Cerebrovascular Diseases | 2012

Heparin-induced Thrombocytopenia in Essential Thrombocytosis

Ayumi Murawaki; Hiroyuki Nakayasu; Mitsuru Doi; Kaori Suzuki-Kinoshita; Yasumasa Asai; Hiromi Omura; Kenji Nakashima

We report a 67-year-old woman with essential thrombocytosis who developed cerebral infarction and heparin-induced thrombocytopenia during treatment for the cerebral infarction. She developed additional cerebral infarcts, acute femoral artery occlusion, and thrombophlebitis of her lower extremities. She was successfully treated with argatroban. This is the first report of a patient with essential thrombocytosis who developed heparin-induced thrombocytopenia and serious conditions, which included multiple thromboembolisms and coagulation disorders mimicking disseminated intravascular coagulation.


Journal of Stroke & Cerebrovascular Diseases | 2012

Moyamoya Disease Presenting as Thalamic Hemorrhage in A Patient With Neuromyelitis Optica and Sjögren's Syndrome

Yasumasa Asai; Hiroyuki Nakayasu; Emi Fusayasu; Kenji Nakashima

A 52-year-old woman was admitted to the hospital with right thalamic hemorrhage. A carotid angiogram revealed occlusion of the terminal portions of the bilateral internal carotid arteries with basal moyamoya vessels, which was diagnosed as moyamoya disease (MMD). At 31 years of age, she was diagnosed with multiple sclerosis because of optic neuritis and myelitis. Paraplegia appeared 14 days after admission. T2-weighted thoracic magnetic resonance imaging revealed a high intensity lesion extending from T4 to T6. Her left upper limb was partially paralytic and her lower limbs exhibited paraplegia and dysesthesia. Anti-aquaporin 4 and anti-Sjögrens syndrome-A and -B antibodies were positive. The pathogenesis of neuromyelitis optica may be associated with such immunologic factors, but there are no reports of simultaneous presentations of neuromyelitis optica and MMD. Autoimmunity may be associated with the etiology of MMD.


Journal of Neuroimmunology | 1990

Suppression of actively induced and passively transferred experimental allergic neurities by cyclosporin A

Hiroyuki Nakayasu; Kiyoshi Ota; Hiromichi Tanaka; Hideki Irie; Kazuro Takahashi

The effect of cyclosporin A (CyA) on experimental allergic neuritis (EAN) was examined. CyA suppressed the development of actively induced EAN. The earlier treatment with CyA was begun, the more effective was its effect. CyA was effective even after the development of clinical signs. In actively induced EAN, cessation of CyA treatment lead to the development of EAN. However, in passively induced EAN, it did not. We could not find any differences in the distribution of infiltrating T cell subsets between the control group and the CyA-treated group.


Acta Neurologica Scandinavica | 2001

Alpha‐like activity in terminal stage of Creutzfeldt–Jakob disease

Y. Asai; M. Shimoda; K. Sasaki; Hiroyuki Nakayasu; T. Takeshima; H. Miyata; Eisaku Ohama; Kenji Nakashima

We report a case of Creutzfeldt–Jakob disease showing various changes in electroencephalogram (EEG) throughout the course of the disease. The patients EEG patterns showed periodic synchronous discharge in the intermediate stage of the disease, delta activity in the advanced stage and alpha‐like activity in the terminal stage. The mechanism generating alpha‐like activity may resemble, at least in part, that of an alpha coma.

Collaboration


Dive into the Hiroyuki Nakayasu's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge