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1. Temporal Changes on 123I-Iomazenil and Cerebral Blood Flow Single-photon Emission Computed Tomography in a Patient with Anti-N-methyl-D-aspartate Receptor Encephalitis

Author

Kasahara, Hiroo, Sato, Masayuki, Nagamine, Shun, Makioka, Kouki, Tanaka, Keiko, and Ikeda, Yoshio

Subjects
cerebral blood flow SPECT, Anti-N-Methyl-D-Aspartate Receptor Encephalitis, Flumazenil, Male, Case Report, anti-NMDA receptor encephalitis, Hashimoto Disease, Middle Aged, Immunomodulation, Treatment Outcome, Asian People, Cerebrovascular Circulation, Encephalitis, Humans, 123I-Iomazenil SPECT, Autoantibodies
Abstract

A 45-year-old man was admitted due to tonic seizures, aphasia, disturbance of consciousness, and abnormal behavior. Because cerebral magnetic resonance imaging findings were normal and mild cerebrospinal fluid (CSF) pleocytosis was observed, autoimmune encephalitis was suspected. The presence of anti-N-methyl-D-aspartate (NMDA) receptor antibodies in the CSF was subsequently confirmed. 123I-Iomazenil and cerebral blood flow single photon emission computed tomography (SPECT) revealed an abnormal uptake in the left frontotemporal region. Multimodal immunotherapy was administered, which remarkably improved the level of consciousness. Progressive reversibility of SPECT findings with clinical improvement suggested that the disorder-related functional deficits had been caused by anti-NMDA receptor antibodies.

Published
2019

2. Recurrent Lobar Hemorrhages and Multiple Cortical Superficial Siderosis in a Patient of Alzheimer's Disease With Homozygous APOE ε2 Allele Presenting Hypobetalipoproteinemia and Pathological Findings of 18F-THK5351 Positron Emission Tomography: A Case Report

Author

Ikeda, Masaki, primary, Okamoto, Koichi, additional, Suzuki, Keiji, additional, Takai, Eriko, additional, Kasahara, Hiroo, additional, Furuta, Natsumi, additional, Furuta, Minori, additional, Tashiro, Yuichi, additional, Shimizu, Chisato, additional, Takatama, Shin, additional, Naito, Isao, additional, Sato, Mie, additional, Sakai, Yasujiro, additional, Takahashi, Manabu, additional, Amari, Masakuni, additional, Takatama, Masamitsu, additional, Higuchi, Tetsuya, additional, Tsushima, Yoshito, additional, Yokoo, Hideaki, additional, Kurabayashi, Masahiko, additional, Ishibashi, Shun, additional, Ishii, Kenji, additional, and Ikeda, Yoshio, additional

Published
2021
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3. Cerebral Microbleeds, Cerebrospinal Fluid, and Neuroimaging Markers in Clinical Subtypes of Alzheimer's Disease

Author

Ikeda, Masaki, primary, Kodaira, Sayaka, additional, Kasahara, Hiroo, additional, Takai, Eriko, additional, Nagashima, Kazuaki, additional, Fujita, Yukio, additional, Makioka, Kouki, additional, Hirayanagi, Kimitoshi, additional, Furuta, Natsumi, additional, Furuta, Minori, additional, Sanada, Etsuko, additional, Kobayashi, Ayumi, additional, Harigaya, Yasuo, additional, Nagamine, Shun, additional, Hattori, Noriaki, additional, Tashiro, Yuichi, additional, Kishi, Kazuhiro, additional, Shimada, Hirotaka, additional, Suto, Takayuki, additional, Tanaka, Hisashi, additional, Sakai, Yasujiro, additional, Yamazaki, Tsuneo, additional, Tanaka, Yukiko, additional, Aihara, Yuko, additional, Amari, Masakuni, additional, Yamaguchi, Haruyasu, additional, Okamoto, Koichi, additional, Takatama, Masamitsu, additional, Ishii, Kenji, additional, Higuchi, Tetsuya, additional, Tsushima, Yoshito, additional, and Ikeda, Yoshio, additional

Published
2021
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5. Increased Neurofilament Light Chain and YKL-40 CSF Levels in One Japanese IBMPFD Patient With VCP R155C Mutation: A Clinical Case Report With CSF Biomarker Analyses

Author

Ikeda, Masaki, primary, Kuwabara, Takeo, additional, Takai, Eriko, additional, Kasahara, Hiroo, additional, Furuta, Minori, additional, Sekine, Akiko, additional, Makioka, Kouki, additional, Yamazaki, Tsuneo, additional, Fujita, Yukio, additional, Nagashima, Kazuaki, additional, Higuchi, Tetsuya, additional, Tsushima, Yoshito, additional, and Ikeda, Yoshio, additional

Published
2020
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8. Recurrent Lobar Hemorrhages and Multiple Cortical Superficial Siderosis in a Patient of Alzheimer's Disease With Homozygous APOE ε2 Allele Presenting Hypobetalipoproteinemia and Pathological Findings of 18F-THK5351 Positron Emission Tomography: A Case Report

Author

Ikeda, Masaki, Okamoto, Koichi, Suzuki, Keiji, Takai, Eriko, Kasahara, Hiroo, Furuta, Natsumi, Furuta, Minori, Tashiro, Yuichi, Shimizu, Chisato, Takatama, Shin, Naito, Isao, Sato, Mie, Sakai, Yasujiro, Takahashi, Manabu, Amari, Masakuni, Takatama, Masamitsu, Higuchi, Tetsuya, Tsushima, Yoshito, Yokoo, Hideaki, and Kurabayashi, Masahiko

Subjects
CEREBRAL amyloid angiopathy, APOLIPOPROTEIN E, POSITRON emission tomography, ALZHEIMER'S patients, ALLELES, CEREBRAL hemorrhage, ALZHEIMER'S disease
Abstract

In Alzheimer's disease, the apolipoprotein E gene (APOE) ε2 allele is a protective genetic factor, whereas the APOE ε4 allele is a genetic risk factor. However, both the APOE ε2 and the APOE ε4 alleles are genetic risk factors for lobar intracerebral hemorrhage. The reasons for the high prevalence of lobar intracerebral hemorrhage and the low prevalence of Alzheimer's disease with the APOE ε2 allele remains unknown. Here, we describe the case of a 79-year-old Japanese female with Alzheimer's disease, homozygous for the APOE ε2 allele. This patient presented with recurrent lobar hemorrhages and multiple cortical superficial siderosis. The findings on the 11C-labeled Pittsburgh Compound B-positron emission tomography (PET) were characteristic of Alzheimer's disease. 18F-THK5351 PET revealed that the accumulation of 18F-THK 5351 in the right pyramidal tract at the pontine level, the cerebral peduncle of the midbrain, and the internal capsule, reflecting the lesions of the previous lobar intracerebral hemorrhage in the right frontal lobe. Moreover, 18F-THK5351 accumulated in the bilateral globus pallidum, amygdala, caudate nuclei, and the substantia nigra of the midbrain, which were probably off-target reaction, by binding to monoamine oxidase B (MAO-B). 18F-THK5351 were also detected in the periphery of prior lobar hemorrhages and a cortical subarachnoid hemorrhage, as well as in some, but not all, areas affected by cortical siderosis. Besides, 18F-THK5351 retentions were observed in the bilateral medial temporal cortices and several cortical areas without cerebral amyloid angiopathy or prior hemorrhages, possibly where tau might accumulate. This is the first report of a patient with Alzheimer's disease, carrying homozygous APOE ε2 allele and presenting with recurrent lobar hemorrhages, multiple cortical superficial siderosis, and immunohistochemically vascular amyloid β. The 18F-THK5351 PET findings suggested MAO-B concentrated regions, astroglial activation, Waller degeneration of the pyramidal tract, neuroinflammation due to CAA related hemorrhages, and possible tau accumulation. [ABSTRACT FROM AUTHOR]

Published
2021
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31. Recurrent Lobar Hemorrhages and Multiple Cortical Superficial Siderosis in a Patient of Alzheimer's Disease With Homozygous APOE ε2 Allele Presenting Hypobetalipoproteinemia and Pathological Findings of 18 F-THK5351 Positron Emission Tomography: A Case Report.

Author

Ikeda M, Okamoto K, Suzuki K, Takai E, Kasahara H, Furuta N, Furuta M, Tashiro Y, Shimizu C, Takatama S, Naito I, Sato M, Sakai Y, Takahashi M, Amari M, Takatama M, Higuchi T, Tsushima Y, Yokoo H, Kurabayashi M, Ishibashi S, Ishii K, and Ikeda Y

Abstract

In Alzheimer's disease, the apolipoprotein E gene (APOE) ε2 allele is a protective genetic factor, whereas the APOE ε4 allele is a genetic risk factor. However, both the APOE ε2 and the APOE ε4 alleles are genetic risk factors for lobar intracerebral hemorrhage. The reasons for the high prevalence of lobar intracerebral hemorrhage and the low prevalence of Alzheimer's disease with the APOE ε2 allele remains unknown. Here, we describe the case of a 79-year-old Japanese female with Alzheimer's disease, homozygous for the APOE ε2 allele. This patient presented with recurrent lobar hemorrhages and multiple cortical superficial siderosis. The findings on the 11 C-labeled Pittsburgh Compound B-positron emission tomography (PET) were characteristic of Alzheimer's disease. 18 F-THK5351 PET revealed that the accumulation of 18 F-THK 5351 in the right pyramidal tract at the pontine level, the cerebral peduncle of the midbrain, and the internal capsule, reflecting the lesions of the previous lobar intracerebral hemorrhage in the right frontal lobe. Moreover, 18 F-THK5351 accumulated in the bilateral globus pallidum, amygdala, caudate nuclei, and the substantia nigra of the midbrain, which were probably off-target reaction, by binding to monoamine oxidase B (MAO-B). 18 F-THK5351 were also detected in the periphery of prior lobar hemorrhages and a cortical subarachnoid hemorrhage, as well as in some, but not all, areas affected by cortical siderosis. Besides, 18 F-THK5351 retentions were observed in the bilateral medial temporal cortices and several cortical areas without cerebral amyloid angiopathy or prior hemorrhages, possibly where tau might accumulate. This is the first report of a patient with Alzheimer's disease, carrying homozygous APOE ε2 allele and presenting with recurrent lobar hemorrhages, multiple cortical superficial siderosis, and immunohistochemically vascular amyloid β. The 18 F-THK5351 PET findings suggested MAO-B concentrated regions, astroglial activation, Waller degeneration of the pyramidal tract, neuroinflammation due to CAA related hemorrhages, and possible tau accumulation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Ikeda, Okamoto, Suzuki, Takai, Kasahara, Furuta, Furuta, Tashiro, Shimizu, Takatama, Naito, Sato, Sakai, Takahashi, Amari, Takatama, Higuchi, Tsushima, Yokoo, Kurabayashi, Ishibashi, Ishii and Ikeda.)

Published
2021
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32. Temporal Changes on 123 I-Iomazenil and Cerebral Blood Flow Single-photon Emission Computed Tomography in a Patient with Anti-N-methyl-D-aspartate Receptor Encephalitis.

Author

Kasahara H, Sato M, Nagamine S, Makioka K, Tanaka K, and Ikeda Y

Subjects
Anti-N-Methyl-D-Aspartate Receptor Encephalitis pathology, Asian People, Autoantibodies blood, Humans, Male, Middle Aged, Treatment Outcome, Anti-N-Methyl-D-Aspartate Receptor Encephalitis diagnosis, Anti-N-Methyl-D-Aspartate Receptor Encephalitis therapy, Cerebrovascular Circulation drug effects, Encephalitis diagnosis, Encephalitis therapy, Flumazenil metabolism, Hashimoto Disease diagnosis, Hashimoto Disease therapy, Immunomodulation
Abstract

A 45-year-old man was admitted due to tonic seizures, aphasia, disturbance of consciousness, and abnormal behavior. Because cerebral magnetic resonance imaging findings were normal and mild cerebrospinal fluid (CSF) pleocytosis was observed, autoimmune encephalitis was suspected. The presence of anti-N-methyl-D-aspartate (NMDA) receptor antibodies in the CSF was subsequently confirmed. 123 I-Iomazenil and cerebral blood flow single photon emission computed tomography (SPECT) revealed an abnormal uptake in the left frontotemporal region. Multimodal immunotherapy was administered, which remarkably improved the level of consciousness. Progressive reversibility of SPECT findings with clinical improvement suggested that the disorder-related functional deficits had been caused by anti-NMDA receptor antibodies.

Published
2019
Full Text
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