Details

Autor(en) / Beteiligte

• Tashiro, Kota
• Haga, Sei
• Tanaka, Shunya
• Tokunaga, So
• Inoue, Daisuke
• Shimogawa, Takafumi
• Mukae, Nobutaka
• Shono, Tadahisa
• Yoshimoto, Koji
• Morioka, Takato

Titel

Sulcal hyperintensity on magnetic resonance imaging with fluid-attenuated inversion recovery sequence in patients with chronic subdural hematoma

Ist Teil von

• Interdisciplinary neurosurgery : Advanced techniques and case management, 2022-09, Vol.29, p.101571, Article 101571

Ort / Verlag

Elsevier B.V

Erscheinungsjahr

2022

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• •ASL with dual PLDs revealing the mechanism of sulcal hyperintensity on FLAIR image in CSDH patient.•Prolonged arterial transit time causing increase in the blood pool to CSF within the sulcus.•Sulcal hyperintensity having relationship with the development of epilepsy. Sulcal hyperintensity on magnetic resonance images with fluid-attenuated inversion recovery sequences (FLAIR) can occur in patients without apparent cerebrospinal fluid (CSF) abnormalities. Taoka et al. speculated that pathological increases of the blood pool to CSF ratio within the sulcus, which could be caused by alterations in regional hemodynamics including venous congestion, do not suppress water signals on FLAIR images. However, few previous reports have described sulcal hyperintensity in patients with chronic subdural hematoma (CSDH). To demonstrate the pathophysiological mechanism and clinical significance of sulcal hyperintensity in CSDH, we retrospectively reviewed the chronological changes in clinical, electroencephalographic (EEG), and neuroradiological findings, including arterial spin labeling perfusion magnetic resonance imaging (ASL) with dual post-labeling delays (PLDs) of 1.5 and 2.5 s, of three patients who had sulcal hyperintensity. In all three cases, sulcal hyperintensity was observed just below the CSDH with mass effect, and became more prominent as it went to the vertex. In patients 1 and 2, ASL with dual PLDs showed a prolonged arterial transit time (ATT) in the region with sulcal hyperintensity, and the sulcal hyperintensity disappeared along with the improvement of the prolonged ATT. In patient 3, in whom the degree of sulcal hyperintensity was mild, the prolongation of ATT was also very mild. In patient 2, a coinciding ictal EEG and ASL hyperperfusion findings were present in the cortex showing sulcal hyperintensity. In patients 1 and 3, the laterality of the sulcal hyperintensity was consistent with that of the epileptic symptoms, which were controlled by the administration of antiepileptic drugs. Although further studies with a larger number of patients are needed, the pathophysiological mechanism of sulcal hyperintensity in CSDH could be explained by the idea proposed by Taoka et al. Our findings also indicate that sulcal hyperintensity has a possible relationship with the development of epilepsy in the perioperative period of CSDH.