Kaoru Sakatani

Prof. Kaoru Sakatani

Department of Human and Engineered Environmental Studies, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan

Research Focus & Metrics

Academic Career Length

50Years (1977-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 July 1999 in Early Human Development
Verified
Journal Article
Closed access
KSKaoru Sakatani
Kaoru Sakatani
SCSaying Chen
Saying Chen
WLWemara Lichty
Wemara Lichty
HZHuancong Zuo
Huancong Zuo
YWYu-Ping Wang
Yu-Ping Wang

1 October 2004 in Neuroscience Letters
Verified
Journal Article
Closed access
MTMasahiro Tanida
Masahiro Tanida
KSKaoru Sakatani
Kaoru Sakatani
RTRuriko Takano
Ruriko Takano
KTKeiko Tagai
Keiko Tagai

1 May 1990 in Stroke
Verified
Journal Article
Closed access
HIH Iizuka
H Iizuka
KSKaoru Sakatani
Kaoru Sakatani
WYW Young
W Young
Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in Fink-Heimer sections. Rats with small lateral parietal cortical lesions had degenerating neurons limited to the medial ventroposteromedial nucleus. Large lesions involving the parasagittal sensorimotor cortex resulted in widespread neuronal damage in the ventroposteromedial, ventroposterolateral, intralaminar, and posterior nuclear regions but nowhere else. Immunoreactivity to laminin antibody decreased, and astrocytic proliferation was abundant in affected thalamic areas. These findings are consistent with retrograde neuronal degeneration due to thalamocortical fiber damage in ischemic cortical regions. Such lesions remote from the infarct may influence functional recovery in patients with stroke.

1 December 2007 in Brain Research
Verified
Journal Article
Closed access
MTMasahiro Tanida
Masahiro Tanida
MKMasako Katsuyama
Masako Katsuyama
KSKaoru Sakatani
Kaoru Sakatani

1 April 2004 in NeuroImage
Verified
Journal Article
Closed access
NFNorio Fujiwara
Norio Fujiwara
KSKaoru Sakatani
Kaoru Sakatani
YKYoichi Katayama
Yoichi Katayama
YMYoshihiro Murata
Yoshihiro Murata
THTetsuya Hoshino
Tetsuya Hoshino
TYTakamitsu Yamamoto
Takamitsu Yamamoto

1 July 1998 in Stroke
Verified
Journal Article
Closed access
KSKaoru Sakatani
Kaoru Sakatani
YXYuxiao Xie
Yuxiao Xie
WLWemara Lichty
Wemara Lichty
SLSunwei Li
Sunwei Li
HZHuancong Zuo
Huancong Zuo
Background and Purpose —In normal subjects, regional cerebral blood flow (rCBF) is greatly increased by neuronal activity, whereas the cerebral metabolic rate for O 2 is increased only slightly. However, it is not clear what kinds of cerebral blood oxygenation and hemodynamic changes can be induced by language activities in language-relevant areas of poststroke aphasics. In the present study, we investigated the difference in the changes of cerebral blood oxygenation and hemodynamics in the left prefrontal cortex induced by language activities between normal subjects, poststroke nonaphasic patients, and nonfluent aphasic patients using near-infrared spectroscopy (NIRS). Methods —Twenty-nine participants performed speech tasks, such as confrontational naming, to evaluate changes among poststroke nonfluent (Broca’s) aphasia patients (10 cases; mean±SEM, 56.9±2.2 years), age-matched normal subjects (13 cases; 50.7±2.2 years) and poststroke nonaphasic patients (6 cases; 52.5±3.9 years). The optodes of NIRS were placed over the left prefrontal cortex. We analyzed the NIRS parameter (oxyhemoglobin [oxy-Hb], deoxyhemoglobin [deoxy-Hb], and total hemoglobin [total-Hb]) changes by qualitative pattern analysis of the parameter changes and quantitative analysis of the parameter values among the groups. Results —The most common NIRS parameter change was an increase in oxy-Hb and total-Hb, with a slight decrease or no change in deoxy-Hb in the normal subjects (5 of 13 cases, 38.5%) and the nonaphasic cerebrovascular disease (CVD) patients (3 of 6 cases, 50.0%). In contrast, the most common pattern in the aphasic patients was an increase of deoxy-Hb, with an increase of oxy-Hb and total-Hb (5 of 10 cases, 50%). However, this pattern was observed in only 3 of 13 cases (23.1%) in the normal subjects and 1 of 6 cases (16.7%) in the nonaphasic CVD patients. The mean (±SEM) changes of deoxy-Hb of the aphasic patients, the normal subjects, and the nonaphasic CVD patients were 0.78±0.29, 0.06±0.16, and –0.18±0.22, respectively. The statistical analysis demonstrated a significant effect for deoxy-Hb ( P <0.05), with the aphasic patients differing significantly from the normal subjects and the nonaphasic CVD patients, while the 2 nonaphasic groups did not differ from each other. Conclusions —The present results demonstrate a multiplicity of language-activated cerebral blood oxygenation and hemodynamic changes in the left prefrontal cortex in the nonaphasic and aphasic groups. The increase of deoxy-Hb with increases of oxy-Hb and total-Hb in the aphasics during language tasks suggests that the left prefrontal cortex of the aphasics utilizes more oxygen than the nonaphasics during language tasks. Finally, functional MRI, which images the activation area in the brain by detecting the reduced concentration of deoxy-Hb during neuronal activation, should be performed on the patients with cerebral dysfunction, giving special consideration to the possible multiplicity of the rCBF and cerebral oxygen metabolism responses to functional tasks.