JaLCDOI 10.18926/AMO/56860
FullText URL 73_3_189.pdf
Author Sakamoto, Shinji| Kawai, Hiroki| Okahisa, Yuko| Tsutsui, Ko| Kanbayashi, Takashi| Tanaka, Keiko| Mizuki, Yutaka| Takaki, Manabu| Yamada, Norihito|
Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a recently-discovered autoimmune disorder in which antibodies target NMDAR in the brain. The number of reported cases of anti-NMDAR encephalitis has increased rapidly. Anti-NMDAR encephalitis can be mistakenly diagnosed as psychiatric disorders because many patients present with prominent psychiatric symptoms and visit psychiatric institutions first. Thus, psychiatrists should cultivate a better understanding of anti-NMDAR encephalitis. In this review, we present the mechanisms, epidemiology, symptoms and clinical course, diagnostic tests, treatment and outcomes of patients with anti-NMDAR encephalitis. Furthermore, we discuss the diversity of clinical spectra of anti-NMDAR encephalitis, and demonstrate a differential diagnosis of psychiatric disease from the perspective of psychiatry.
Keywords NMDAR encephalitis psychiatric symptom schizophrenia mood disorder
Amo Type Review
Published Date 2019-06
Publication Title Acta Medica Okayama
Volume volume73
Issue issue3
Publisher Okayama University Medical School
Start Page 189
End Page 195
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2019 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 31235965
JaLCDOI 10.18926/AMO/56066
FullText URL 72_3_211.pdf
Author Ikeda, Chikako| Yokota, Osamu| Miki, Tomoko| Takenoshita, Shintaro| Ishizu, Hideki| Terada, Seishi| Yamada, Norihito|
Abstract Neurodegenerative diseases in which tau accumulation plays a cardinal role in the pathogenic process are called tauopathies, and when tau isoforms having four repeats of the microtubule binding sites, four-repeat tau, are selectively accumulated as pathological hallmarks, the term four-repeat tauopathy is used. The major four-repeat tauopathies are progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and argyrophilic grain disease (AGD). Historically, neuronal cytopathologies, e.g., neurofibrillary tangles and ballooned neurons, were emphasized as characteristic lesions in PSP and CBD. Now, however, astrocytic tau pathologies, i.e., tufted astrocytes (TAs) and astrocytic plaques (APs), are considered to be highly disease-specific lesions. Although granular/fuzzy astrocytes (GFAs) frequently develop in the limbic system in AGD cases, the specificity is not conclusive yet. Some AGD cases have a few TAs, and to a lesser frequency, a few APs in the frontal cortex and subcortical nuclei. The number of astrocytic tau pathologies including TAs and GFAs increases with the progression of AGD. In this paper, histopathological features of astrocytic tau pathologies in PSP, CBD, and AGD are first reviewed. Then, recent findings regarding the coexistence of these tauopathies are summarized from a viewpoint of astrocytic tau pathologies. Further biochemical and pathological studies focusing tau-positive astrocytic lesions may be useful to increase understanding of the pathological process in four-repeat tauopathies and to develop novel therapeutic strategies for patients with these diseases.
Keywords astrocytic plaque four-repeat tau globular glial inclusion granular fuzzy astrocyte tufted astrocyte
Amo Type Review
Published Date 2018-06
Publication Title Acta Medica Okayama
Volume volume72
Issue issue3
Publisher Okayama University Medical School
Start Page 211
End Page 221
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2018 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 29925998
JaLCDOI 10.18926/AMO/32652
FullText URL fulltext.pdf
Author Inoue, Koutaro| Morimoto, Kiyoshi| Sato, Keiko| Yamada, Norihito| Otsuki, Saburo|
Abstract <p>A new model of status epilepticus (SE), which was induced by intermittent electrical stimulation (20 Hz for 20 sec every min for 180 min) of the deep prepyriform cortex, has been developed in the conscious rat. SE was induced in 9 of 16 rats in the drug-free group. The number of stimulation trains required to induce SE in this status subgroup was 125.6 +/- 12.7 (mean +/- SEM) and the mean duration of self-sustained seizure activity (SSSA) occurring after cessation of the stimulation session was 295.4 +/- 111.4 min. Some animals showed secondary generalized seizures. Significant cell loss was observed in the hippocampal CA3 pyramidal cell layer ipsilateral to the stimulation site and bilateral CA1 areas in the status subgroup compared with the group subjected to sham operation. In addition, there was a significant negative correlation between the duration of SSSA subsequent to the stimulation session and the total number of intact pyramidal neurons observed in the bilateral CA1 and ipsilateral CA3 subfields of the status subgroup. There were significant differences between the status and non-status subgroups with respect to the number of afterdischarges (ADs) and the total AD duration during the stimulation session. Pretreatment with phenobarbital (30 mg/kg) prevented the development of SE and hippocampal cell loss completely. Pretreatment with MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist (0.25 or 1 mg/kg), also prevented hippocampal cell loss, although it did not block SE generation completely, which suggests dissociation of the mechanisms underlying the development of SE and hippocampal damage. These results indicate that prolonged SSSA actually causes hippocampal damage and it is critically dependent upon NMDA receptor participation.</p>
Keywords status epilepticus deep prepyriform cortex electrical stimulation hippcampus N-methl-D-aspartate(NMDA) ??-aminobutyric acid(GABA)
Amo Type Article
Published Date 1992-04
Publication Title Acta Medica Okayama
Volume volume46
Issue issue2
Publisher Okayama University Medical School
Start Page 129
End Page 139
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 1533485
Web of Science KeyUT A1992HR48400010
JaLCDOI 10.18926/AMO/30752
FullText URL fulltext.pdf
Author Yamamoto, Shin| Kitamura, Yoshihiro| Yamada, Norihito| Nakashima, Yoshihiko| Kuroda, Shigetoshi|
Abstract <p>Previous EEG studies have shown that transcendental meditation (TM) increases frontal and central alpha activity. The present study was aimed at identifying the source of this alpha activity using magnetoencephalography (MEG) and electroencephalography (EEG) simultaneously on eight TM practitioners before, during, and after TM. The magnetic field potentials corresponding to TM-induced alpha activities on EEG recordings were extracted, and we attempted to localize the dipole sources using the multiple signal classification (MUSIC) algorithm, equivalent current dipole source analysis, and the multiple spatio-temporal dipole model. Since the dipoles were mapped to both the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC), it is suggested that the mPFC and ACC play an important role in brain activity induced by TM.</p>
Keywords transcendental meditation magnetoencephalography(MEG) source analysis medial prefrontal cortex anterior cingulate cortex
Amo Type Article
Published Date 2006-02
Publication Title Acta Medica Okayama
Volume volume60
Issue issue1
Publisher Okayama University Medical School
Start Page 51
End Page 58
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 16508689
Web of Science KeyUT 000235538900006