Pathophysiological mechanisms of sulcal hyperintensity on magnetic resonance imaging with fluid-attenuated inversion recovery sequence and the relationship with seizure in patients with chronic subdural hematoma revealed by 1.5-Tesla arterial spin labeling perfusion imaging

  • Mugita Fumihito
    Department of Neurosurgery, Hachisuga Hospital, Munakata, Fukuoka, Japan
  • Morioka Takato
    Department of Neurosurgery, Hachisuga Hospital, Munakata, Fukuoka, Japan
  • Inoha Satoshi
    Department of Neurosurgery, Hachisuga Hospital, Munakata, Fukuoka, Japan
  • Oketani Hiroshi
    Department of Neurosurgery, Hachisuga Hospital, Munakata, Fukuoka, Japan Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan
  • Akiyama Tomoaki
    Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan
  • Shimogawa Takafumi
    Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan
  • Mukae Nobutaka
    Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan
  • Sakata Ayumi
    Department of Clinical Laboratory, Kyushu University Hospital, Fukuoka, Fukuoka, Japan Division of Medical Technology, Department of Health Sciences, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan
  • Shigeto Hiroshi
    Division of Medical Technology, Department of Health Sciences, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan Department of Neurology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan
  • Yoshimoto Koji
    Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan

説明

<p>Purpose: The mechanism underlying sulcal hyperintensity observed on fluid-attenuated inversion recovery magnetic resonance imaging (MRI) (sulcal FLAIR hyperintensity [S-FLAIR-HI]) without apparent abnormalities in the cerebrospinal fluid (CSF) is believed to involve alterations in regional hemodynamics, including venous congestion caused by mass effect, leading to a pathological increase in the blood pool-to-CSF ​​ratio. While S-FLAIR-HI is observed in chronic subdural hematoma (CSDH), its exact incidence, mechanism of occurrence, and relationship with seizures remain unclear.</p><p> Methods: Clinical data and MRI findings, including FLAIR and 1.5-Tesla pseudo-continuous arterial spin labeling perfusion imaging performed within 1 day before surgery in 34 patients with CSDH, were retrospectively reviewed. The focus was on the laterality of arterial transit artifact(s) in the sulcus (sulcal ATA [S-ATA]), which are intravascular signals that increase with a delay in arterial transit time, and (peri-)ictal hyperperfusion linked to seizure activity by neurovascular coupling.</p><p> Results: S-FLAIR-HI was observed in 12 (35.3%) of the 34 patients with CSDH, 11 of whom exhibited an increase in S-ATA on the ipsilateral side. Increased S-ATA levels were also observed in 10 of the 22 patients without S-FLAIR-HI. However, none of the 12 patients with S-FLAIR-HI developed seizures. In addition, 2 patients who exhibited perioperative seizures did not undergo S-FLAIR-HI. </p><p>Discussion: S-FLAIR-HI, observed preoperatively in approximately one-third of patients with CSDH, is a nonspecific finding caused by alterations in regional hemodynamics. Furthermore, there is no evidence supporting the direct involvement of S-FLAIR-HI in the development of seizures. </p>

収録刊行物

  • Epilepsy & Seizure

    Epilepsy & Seizure 17 (0), n/a-, 2025

    一般社団法人 日本てんかん学会

詳細情報 詳細情報について

  • CRID
    1390586057019063040
  • DOI
    10.3805/eands.a000166
  • ISSN
    18825567
  • 本文言語コード
    en
  • データソース種別
    • JaLC
  • 抄録ライセンスフラグ
    使用不可

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