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

Abstract

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.

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.

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.

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.