Faculty Profiles - Ishiura Hiroyuki

Papers - Ishiura Hiroyuki

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A novel de novo disease-causing variant in ATL1 in a pediatric patient with spastic paraplegia

Ayumi Nakamura, Hiroya Naruse, Akihiko Mitsutake, Jun Mitsui, Shinichi Morishita, Mie Iwakoshi, Hiroyuki Ishiura, Shoji Tsuji, Tatsushi Toda

Neurology and Clinical Neuroscience 2024

神経伝導検査と免疫固定電気泳動法からPOEMS症候群と診断し得た59歳男性例 Reviewed

時村瞭, 原涼, 久保田暁, 石浦浩之, 小玉聡, 代田悠一郎, 濱田雅, 戸田達史

臨床神経生理学 51 ( 6 ) 651 - 657 2023.12

Language：Japanese Publisher：(一社)日本臨床神経生理学会

症例は59歳男性。4ヵ月の経過で進行する歩行障害と両下肢遠位の異常感覚を主訴に受診した。診察上,両下肢遠位筋筋力低下,四肢腱反射減弱,両下腿以遠の全感覚鈍麻,異常感覚を認めた。血清蛋白電気泳動法ではM蛋白は検出されなかった。神経伝導検査では尺骨神経前腕部での脱髄性所見と下肢にアクセントのある神経障害を認めた。この結果から追加検査を行ったところ,血清免疫固定電気泳動法でIgA-λ型のM蛋白を認め,血清VEGFが1526pg/mlと上昇していた。以上からPOEMS症候群と診断した。サリドマイド・デキサメタゾン療法と自家末梢血幹細胞移植を行い,下肢筋力が僅かに改善した。神経遠位部より中間部に伝導速度の低下が目立ち,下肢にアクセントのある神経障害の合併はPOEMS症候群と他の脱髄性ニューロパチーとの鑑別に有用である。POEMS症候群を疑った場合は免疫固定電気泳動法によるM蛋白測定が必要である。(著者抄録)

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2023&ichushi_jid=J03414&link_issn=&doc_id=20240111330005&doc_link_id=10.11422%2Fjscn.51.651&url=https%3A%2F%2Fdoi.org%2F10.11422%2Fjscn.51.651&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

Case Report: Intraventricular Cerliponase Alfa Treatment in a Patient with Advanced Neuronal Ceroid Lipofuscinosis Type 2. Reviewed

Saki Nakashima, Masashi Hamada, Tomohiko Kimura, Shuichi Tanifuji, Akiko Takahashi, Daiki Yashita, Yu Kakimoto, Takashi Matsukawa, Hiroyuki Ishiura, Tatsushi Toda

Internal medicine (Tokyo, Japan) 63 ( 12 ) 1807 - 1812 2023.11

Language：English Publishing type：Research paper (scientific journal)

Neuronal ceroid lipofuscinosis type 2 (CLN2) is an autosomal recessive lysosomal disease caused by decreased activity of the enzyme tripeptidyl peptidase 1 (TPP1) due to pathogenic variants in the TPP1 gene. Cerliponase alfa, a recombinant proenzyme form of TPP1, has shown efficacy in preventing motor and language function decline in early-stage CLN2. However, the safety and effects of this therapy in advanced-stage CLN2 are unclear. We herein report a case of intraventricular cerliponase alfa treatment for over a year in a patient with advanced-stage CLN2. The results suggest the safety and potential efficacy of treatment at an advanced stage of CLN2.

DOI： 10.2169/internalmedicine.2563-23

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Protective Effects of Rivaroxaban on White Matter Integrity and Remyelination in a Mouse Model of Alzheimer's Disease Combined with Cerebral Hypoperfusion. Reviewed International journal

Zhihong Bian, Xinran Hu, Xia Liu, Haibo Yu, Yuting Bian, Hongming Sun, Yusuke Fukui, Ryuta Morihara, Hiroyuki Ishiura, Toru Yamashita

Journal of Alzheimer's disease : JAD 96 ( 2 ) 609 - 622 2023.10

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Alzheimer's disease (AD) is characterized by cognitive dysfunction and memory loss that is accompanied by pathological changes to white matter. Some clinical and animal research revealed that AD combined with chronic cerebral hypoperfusion (CCH) exacerbates AD progression by inducing blood-brain barrier dysfunction and fibrinogen deposition. Rivaroxaban, an anticoagulant, has been shown to reduce the rates of dementia in atrial fibrillation patients, but its effects on white matter and the underlying mechanisms are unclear. OBJECTIVE: The main purpose of this study was to explore the therapeutic effect of rivaroxaban on the white matter of AD+CCH mice. METHODS: In this study, the therapeutic effects of rivaroxaban on white matter in a mouse AD+CCH model were investigated to explore the potential mechanisms involving fibrinogen deposition, inflammation, and oxidative stress on remyelination in white matter. RESULTS: The results indicate that rivaroxaban significantly attenuated fibrinogen deposition, fibrinogen-related microglia activation, oxidative stress, and enhanced demyelination in AD+CCH mice, leading to improved white matter integrity, reduced axonal damage, and restored myelin loss. CONCLUSIONS: These findings suggest that long-term administration of rivaroxaban might reduce the risk of dementia.

DOI： 10.3233/JAD-230413

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脊髄性筋萎縮症患者7名に対するリスジプラムの治療効果

山下徹, 柚木太淳, 中田有美, 松岡千加, 佐々木涼, 田所功, 中野由美子, 武本麻美, 森原隆太, 石浦浩之

臨床神経学 63 ( Suppl. ) S215 - S215 2023.9

Foix-Chavany-Marie症候群を呈した持続性部分てんかんの一例

佐々木諒, 柚木太淳, 中田有美, 松岡千加, 田所功, 中野由美子, 武本麻美, 森原隆太, 山下徹, 石浦浩之

臨床神経学 63 ( 9 ) 620 - 620 2023.9

抗AQP4抗体陽性のNMOsd患者の髄液におけるIL-6測定の有用性の検討

柚木太淳, 中田有美, 松岡千加, 田所功, 佐々木諒, 中野由美子, 武本麻実, 森原隆太, 山下徹, 石浦浩之

臨床神経学 63 ( Suppl. ) S298 - S298 2023.9

70代以降意識減損・消失発作が増悪し,抗てんかん薬の調整に難渋した良性成人型家族性ミオクローヌスてんかん1型の80歳女性例

高橋健祐, 栗原正典, 東原真奈, 松平敬史, 広吉祐子, 松川美穂, 石浦浩之, 岩田淳

臨床神経学 63 ( 9 ) 604 - 604 2023.9

当院で経験した脊髄小脳変性症7型2家系の臨床的検討

吉田千晴, 小松大樹, 馬場智也, 後藤良司, 首藤篤史, 松川敬志, 石浦浩之, 三井純, 中森知毅, 市川弥生子, 後藤順, 中村奈津子, 角田和繁, 小畑亮, 澤村裕正, 戸田達史

臨床神経学 63 ( Suppl. ) S298 - S298 2023.9

A Case of Adrenomyeloneuropathy with Later Development of Cerebral Form Caused by a Hemizygous Splice-site Variant in ABCD1. Reviewed

Naoki Takegami, Takashi Matsukawa, Masashi Hamada, Shuichi Tanifuji, Takayuki Tamura, Nanaka Yamaguchi-Takegami, Hiroyuki Ishiura, Jun Mitsui, Kaori Sakuishi, Shoji Tsuji, Tatsushi Toda

Internal medicine (Tokyo, Japan) 63 ( 7 ) 999 - 1004 2023.8

Language：English Publishing type：Research paper (scientific journal)

Adrenomyeloneuropathy (AMN)/adrenoleukodystrophy (ALD) is an X-linked genetic disorder caused by pathogenic variants in ABCD1. We treated a 54-year-old man with slowly progressive spastic paraparesis with later development of the cerebral form. A pathogenic splice-site variant of ABCD1 (c.1489-1G>A, p. Val497Alafs*51) and elevated levels of very long-chain fatty acids were found, leading to the diagnosis of AMN. Detailed ABCD1 mRNA expression analyses revealed decreased levels of ABCD1 mRNA accompanied by deletion of the first 31 bp in exon 6. The altered mRNA transcriptional patterns associated with splice site variants are diverse and may provide important insights into ALD pathogenesis.

DOI： 10.2169/internalmedicine.2240-23

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Late-onset Myoclonic Seizure in a 78-year-old Woman with Gaucher Disease. Reviewed

Nanaka Yamaguchi-Takegami, Akiko Takahashi, Jun Mitsui, Yusuke Sugiyama, Ayaka Chikada, Kristine Joyce L Porto, Naoki Takegami, Kaori Sakuishi, Hiroyuki Ishiura, Kaoru Yamada, Jun Shimizu, Shoji Tsuji, Tatsushi Toda

Internal medicine (Tokyo, Japan) 63 ( 6 ) 861 - 865 2023.8

Language：English Publishing type：Research paper (scientific journal)

We herein report a 78-year-old woman with Gaucher disease (GD) who was initially diagnosed with GD type 1, had been receiving long-term enzyme replacement therapy since 58 years old, and developed neurological manifestations in her 70s. The neurological manifestations included myoclonic seizures and progressive cognitive decline. Although it is rare for GD patients to first develop neurologic manifestations at such an advanced age, physicians engaged in long-term care for GD patients should be alert for this possibility.

DOI： 10.2169/internalmedicine.1699-23

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A Japanese family with idiopathic basal ganglia calcification carrying a novel XPR1 variant Reviewed International journal

Kenta Orimo, Toshiyuki Kakumoto, Ryo Hara, Ryoji Goto, Hiroyuki Ishiura, Jun Mitsui, Chiharu Yoshida, Yoshikazu Uesaka, Yuta Suzuki, Shinichi Morishita, Wataru Satake, Shoji Tsuji, Tatsushi Toda

Journal of the Neurological Sciences 451 120732 - 120732 2023.7

Anti-neurofascin 155 Antibody-positive Neuropathy in a Human Immunodeficiency Virus-infected Patient. Reviewed

So Okubo, Tatsuo Mano, Atsushi Sudo, Ryoji Goto, Satoka Yano, Manato Hara, Hiroyuki Ishiura, Wataru Satake, Shintaro Yanagimoto, Hidenori Ogata, Tatsushi Toda

Internal medicine (Tokyo, Japan) 63 ( 4 ) 565 - 569 2023.6

Language：English Publishing type：Research paper (scientific journal)

Human immunodeficiency virus (HIV)-associated neuropathy is a common complication of HIV infection and has several clinical subtypes. HIV-associated chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a demyelinating neuropathy whose clinical features are known to differ from those of CIDP in the HIV-uninfected population. We herein report a case of CIDP in an HIV-infected patient who was finally diagnosed with anti-neurofascin 155 (NF155) antibody-positive neuropathy. The clinical features, including clinical findings and therapeutic responses, were typical of paranodal antibody-mediated neuropathy. To our knowledge, this is the first case of anti-NF155 antibody-associated neuropathy in an HIV-infected patient.

DOI： 10.2169/internalmedicine.1919-23

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Nine Hereditary Movement Disorders First Described in Asia: Their History and Evolution. Reviewed International journal

Priya Jagota, Yoshikazu Ugawa, Zakiyah Aldaajani, Norlinah Mohamed Ibrahim, Hiroyuki Ishiura, Yoshiko Nomura, Shoji Tsuji, Cid Diesta, Nobutaka Hattori, Osamu Onodera, Saeed Bohlega, Amir S N AlDin, Shen-Yang Lim, Jee-Young Lee, Beomseok Jeon, Pramod Kumar Pal, Huifang Shang, Shinsuke Fujioka, Prashanth Lingappa Kukkle, Onanong Phokaewvarangkul, Chin-Hsien Lin, Cholpon Shambetova, Roongroj Bhidayasiri

Journal of movement disorders 16 ( 3 ) 231 - 247 2023.6

Language：English Publishing type：Research paper (scientific journal)

Clinical case studies and reporting are important to the discovery of new disorders and the advancement of medical sciences. Both clinicians and basic scientists play equally important roles leading to treatment discoveries for both cures and symptoms. In the field of movement disorders, exceptional observation of patients from clinicians is imperative, not just for phenomenology but also for the variable occurrences of these disorders, along with other signs and symptoms, throughout the day and the disease course. The Movement Disorders in Asia Task Force (TF) was formed to help enhance and promote collaboration and research on movement disorders within the region. As a start, the TF has reviewed the original studies of the movement disorders that were preliminarily described in the region. These include nine disorders that were first described in Asia - Segawa disease, PARK-Parkin, X-linked dystonia-parkinsonism (XDP), dentatorubral-pallidoluysian atrophy (DRPLA), Woodhouse-Sakati syndrome, benign adult familial myoclonic epilepsy (BAFME), Kufor-Rakeb disease, tremulous dystonia associated with mutation of the calmodulin-binding transcription activator 2 (CAMTA2) gene, and paroxysmal kinesigenic dyskinesia (PKD). We hope that the information provided will honor the original researchers and help us learn and understand how earlier neurologists and basic scientists together discovered new disorders and made advances in the field, which impact us all to this day.

DOI： 10.14802/jmd.23065

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Insights into familial adult myoclonus epilepsy pathogenesis: How the same repeat expansion in six unrelated genes may lead to cortical excitability. Reviewed International journal

Christel Depienne, Arn M J M van den Maagdenberg, Theresa Kühnel, Hiroyuki Ishiura, Mark A Corbett, Shoji Tsuji

Epilepsia 64 Suppl 1 S31-S38 2023.6

Language：English Publishing type：Research paper (scientific journal)

Familial adult myoclonus epilepsy (FAME) results from the same pathogenic TTTTA/TTTCA pentanucleotide repeat expansion in six distinct genes encoding proteins with different subcellular localizations and very different functions, which poses the issue of what causes the neurobiological disturbances that lead to the clinical phenotype. Postmortem and electrophysiological studies have pointed to cortical hyperexcitability as well as dysfunction and neurodegeneration of both the cortex and cerebellum of FAME subjects. FAME expansions, contrary to the same expansion in DAB1 causing spinocerebellar ataxia type 37, seem to have no or limited impact on their recipient gene expression, which suggests a pathophysiological mechanism independent of the gene and its function. Current hypotheses include toxicity of the RNA molecules carrying UUUCA repeats, or toxicity of polypeptides encoded by the repeats, a mechanism known as repeat-associated non-AUG translation. The analysis of postmortem brains of FAME1 expansion (in SAMD12) carriers has revealed the presence of RNA foci that could be formed by the aggregation of RNA molecules with abnormal UUUCA repeats, but evidence is still lacking for other FAME subtypes. Even when the expansion is located in a gene ubiquitously expressed, expression of repeats remains undetectable in peripheral tissues (blood, skin). Therefore, the development of appropriate cellular models (induced pluripotent stem cell-derived neurons) or the study of affected tissues in patients is required to elucidate how FAME repeat expansions located in unrelated genes lead to disease.

DOI： 10.1111/epi.17504

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Neurofilament light chain levels in cerebrospinal fluid as a sensitive biomarker for cerebral adrenoleukodystrophy. Reviewed International journal

Toshiyuki Kakumoto, Takashi Matsukawa, Hiroyuki Ishiura, Harushi Mori, Shoji Tsuji, Tatsushi Toda

Annals of clinical and translational neurology 10 ( 7 ) 1230 - 1238 2023.5

Language：English Publishing type：Research paper (scientific journal)

OBJECTIVE: Adrenoleukodystrophy (ALD) has a poor prognosis when it progresses to the cerebral form (CALD). The aim of this study is to investigate whether cerebrospinal fluid (CSF) neurofilament light chain (cNfL) is a sensitive biomarker for detecting CALD and assessing response to hematopoietic stem cell transplantation (HSCT). METHODS: We conducted a cross-sectional study of 41 male ALD patients. The cNfL levels in patients with the cerebral form of ALD (CALD) or the cerebello-brainstem form of ALD were compared with those in patients with adrenomyeloneuropathy (AMN). The correlation between cNfL levels and MRI-based Loes severity scores was investigated. A longitudinal analysis was performed on patients who underwent multiple CSF examinations. RESULTS: The cNfL levels in 22 patients with CALD were significantly higher than those in 14 patients with AMN (median, 5545 vs. 1490 pg/mL; p < 0.001). The cutoff cNfL level of 1930 pg/mL showed good sensitivity (95.5%) and specificity (85.7%) for distinguishing CALD from AMN. The cNfL levels were positively correlated with Loes scores (p < 0.001). The cNfL levels in three AMN patients who later converted to CALD increased above the cutoff level during the conversion period, while the cNfL levels in four patients who remained in AMN were consistently below the cutoff. In 10 ALD patients who underwent HSCT, their cNfL levels decreased 3-24 months after HSCT. Two patients whose cNfL increased after HSCT showed deterioration in cognitive functions. INTERPRETATION: The cNfL level is useful for evaluating the disease activities of ALD and the response to HSCT.

DOI： 10.1002/acn3.51818

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Clinical features of a family with late-onset distal hereditary motor neuropathy harboring p.Pro39Leu variant of HSPB1. Reviewed International journal

Hiroya Naruse, So Okubo, Atsushi Sudo, Jun Mitsui, Takashi Mikata, Hiroyuki Ishiura, Shinichi Morishita, Shoji Tsuji, Tatsushi Toda

Journal of the peripheral nervous system : JPNS 28 ( 3 ) 518 - 521 2023.5

Language：English

BACKGROUND AND AIMS: Pathogenic variants of HSPB1, the gene encoding the small heat shock protein 27, have been reported to cause autosomal dominant distal hereditary motor neuropathy (dHMN) type II and autosomal dominant Charcot-Marie-Tooth (CMT) disease with minimal sensory involvement (CMT2F). This study aimed to describe the clinical features of patients in a family with late-onset dHMN carrying the Pro39Leu variant of HSPB1. METHODS: Whole-exome sequence analysis identified a heterozygous pathogenic variant (Pro39Leu) of HSPB1 in the proband. The presence of the HSPB1 Pro39Leu variant in two affected individuals was confirmed using direct nucleotide sequence analysis. RESULTS: Both patients exhibited distal muscle weakness with lower extremity predominance and no obvious sensory deficits, leading to a clinical diagnosis of late-onset dHMN. Nerve conduction studies (NCSs) revealed a subclinical complication of sensory disturbance in one of the patients. The clinical and electrophysiological findings of patients with the HSPB1 Pro39Leu variant in this study and previous reports are summarized. INTERPRETATION: This study suggests that the clinical spectrum of patients carrying HSPB1 Pro39Leu variants, especially the disease onset, might be broader than expected, and HSPB1 variants should be considered in patients diagnosed with late-onset dHMN. Furthermore, patients with dHMN may have concomitant sensory deficits that should be evaluated using NCSs.

DOI： 10.1111/jns.12567

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Noncanonical splice-site variant in peripheral myelin protein 22 gene (PMP22) in a patient with hereditary neuropathy with liability to pressure palsies. Reviewed International journal

Norifumi Kawamoto, Yuichi Hamada, Shunsuke Kobayashi, Hiroya Naruse, Hiroyuki Ishiura, Takashi Matsukawa, Jun Mitsui, Shoji Tsuji, Masahiro Sonoo, Tatsushi Toda

Journal of the peripheral nervous system : JPNS 28 ( 3 ) 513 - 517 2023.5

Authorship：Corresponding author Language：English

AIM: Hereditary neuropathy with liability to pressure palsies (HNPP) is a peripheral neuropathy with autosomal dominant inheritance. Diagnosis can be made from the characteristic abnormalities determined by nerve conduction studies (NCS), including subclinical deficits at physiological compression sites. Heterozygous deletion of the chromosome 17p11.2-p12 region including the peripheral myelin protein 22 gene (PMP22) is the cause in the majority of cases. However, the loss of function of PMP22 due to frameshift-causing insertion/deletion, missense, nonsense, or splice-site disrupting variants cause HNPP in some patients. We report a case of a patient diagnosed with HNPP on the basis of clinical features and the results of NCS. No deletions of PMP22 were detected by fluorescence in situ hybridization. METHODS: We performed direct nucleotide sequence analysis and identified a heterozygous variant, c.78 + 3G > T, in PMP22. Since this variant is located outside the canonical splice site at the exon 2-intron 2 junction, we investigated whether the variant causes aberrant splicing and leads to the skipping of exon 2 of PMP22 by in vitro minigene splicing assay. RESULTS: We demonstrated that the c.78 + 3G > T variant causes the skipping of exon 2 and leads to loss of function of the mutant allele. CONCLUSION: Searching for sequence variants located outside the canonical splice sites should also be considered even when deletion of PMP22 is not found in a patient with a clinical diagnosis suggesting HNPP.

DOI： 10.1111/jns.12558

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Genome-wide association study identifies a new susceptibility locus in PLA2G4C for Multiple System Atrophy. International journal

Yasuo Nakahara, Jun Mitsui, Hidetoshi Date, Kristine Joyce Porto, Yasuhiro Hayashi, Atsushi Yamashita, Yoshio Kusakabe, Takashi Matsukawa, Hiroyuki Ishiura, Tsutomu Yasuda, Atsushi Iwata, Jun Goto, Yaeko Ichikawa, Yoshio Momose, Yuji Takahashi, Tatsushi Toda, Rikifumi Ohta, Jun Yoshimura, Shinichi Morishita, Emil K Gustavsson, Darren Christy, Melissa Maczis, Matthew J Farrer, Han-Joon Kim, Sung-Sup Park, Beomseok Jeon, Jin Zhang, Weihong Gu, Sonja W Scholz, Andrew B Singleton, Henry Houlden, Ichiro Yabe, Hidenao Sasaki, Masaaki Matsushima, Hiroshi Takashima, Akio Kikuchi, Masashi Aoki, Kenju Hara, Akiyoshi Kakita, Mitsunori Yamada, Hitoshi Takahashi, Osamu Onodera, Masatoyo Nishizawa, Hirohisa Watanabe, Mizuki Ito, Gen Sobue, Kinya Ishikawa, Hidehiro Mizusawa, Kazuaki Kanai, Satoshi Kuwabara, Kimihito Arai, Shigeru Koyano, Yoshiyuki Kuroiwa, Kazuko Hasegawa, Tatsuhiko Yuasa, Kenichi Yasui, Kenji Nakashima, Hijiri Ito, Yuishin Izumi, Ryuji Kaji, Takeo Kato, Susumu Kusunoki, Yasushi Osaki, Masahiro Horiuchi, Ken Yamamoto, Mihoko Shimada, Taku Miyagawa, Yosuke Kawai, Nao Nishida, Katsushi Tokunaga, Alexandra Dürr, Alexis Brice, Alessandro Filla, Thomas Klockgether, Ullrich Wüllner, Caroline M Tanner, Walter A Kukull, Virginia M-Y Lee, Eliezer Masliah, Phillip A Low, Paola Sandroni, Laurie Ozelius, Tatiana Foroud, Shoji Tsuji

medRxiv : the preprint server for health sciences 2023.5

Language：English

To elucidate the molecular basis of multiple system atrophy (MSA), a neurodegenerative disease, we conducted a genome-wide association study (GWAS) in a Japanese MSA case/control series followed by replication studies in Japanese, Korean, Chinese, European and North American samples. In the GWAS stage rs2303744 on chromosome 19 showed a suggestive association ( P = 6.5 × 10 -7 ) that was replicated in additional Japanese samples ( P = 2.9 × 10 -6 . OR = 1.58; 95% confidence interval, 1.30 to 1.91), and then confirmed as highly significant in a meta-analysis of East Asian population data ( P = 5.0 × 10 -15 . Odds ratio= 1.49; 95% CI 1.35 to 1.72). The association of rs2303744 with MSA remained significant in combined European/North American samples ( P =0.023. Odds ratio=1.14; 95% CI 1.02 to 1.28) despite allele frequencies being quite different between these populations. rs2303744 leads to an amino acid substitution in PLA2G4C that encodes the cPLA2γ lysophospholipase/transacylase. The cPLA2γ-Ile143 isoform encoded by the MSA risk allele has significantly decreased transacylase activity compared with the alternate cPLA2γ-Val143 isoform that may perturb membrane phospholipids and α-synuclein biology.

DOI： 10.1101/2023.05.02.23289328

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A case of intravascular lymphoma presenting with a lesion in the splenium of the corpus callosum. Reviewed International journal

Haruka Masuzawa, Fumio Suzuki, Shiori Amemiya, Kenta Orimo, Hiroyuki Ishiura, Ryo Hara, Tatsushi Toda, Teruo Nakazawa, Akira Honda, Mariko Tanaka, Munetoshi Hinata, Osamu Abe

Radiology case reports 18 ( 5 ) 1929 - 1932 2023.5

Language：English

Intravascular lymphoma (IVL) is difficult to diagnose because its clinical presentation and laboratory and imaging findings are nonspecific. Herein, we report a case of IVL presenting as a lesion in the splenium of the corpus callosum. A 52-year-old man attended the emergency department with a 2-week history of progressively worsening abnormal behavior and gait disturbance. Magnetic resonance imaging on admission revealed an oval lesion in the splenium of the corpus callosum. The follow-up magnetic resonance imaging performed 2 months after disease onset revealed multiple high-signal areas in the bilateral cerebral white matter on T2-weighted images and diffusion-weighted images. The blood test results showed an elevated level of lactate dehydrogenase and serum-soluble interleukin-2 receptor. These findings were compatible with the diagnosis of IVL. IVL is often difficult to diagnose due to a wide variety of clinical presentations and imaging findings.

DOI： 10.1016/j.radcr.2023.02.025

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Papers - Ishiura Hiroyuki