Introduction We previously reported centripetal propagation of vasoconstriction at the time of thunderclap headache remission in patients with reversible cerebral vasoconstriction syndrome. Here we examine the clinical significance of centripetal propagation of vasoconstriction. Methods Participants comprised 48 patients who underwent magnetic resonance angiography within 72 h of reversible cerebral vasoconstriction syndrome onset and within 48 h of thunderclap headache remission. Results In 24 of the 48 patients (50%), centripetal propagation of vasoconstriction occurred on magnetic resonance angiography at the time of thunderclap headache remission. The interval from first to last thunderclap headache in patients with centripetal propagation of vasoconstriction (14 ± 10 days) was significantly longer than that of patients without centripetal propagation of vasoconstriction (4 ± 2 days). In the patients with centripetal propagation of vasoconstriction at the time of thunderclap headache remission, the incidence of another cerebral lesion (38%, 9 of 24 cases) was significantly higher than in patients without centripetal propagation of vasoconstriction (0%). From findings of sequential magnetic resonance angiography before and after thunderclap headache remission, we observed tendencies in which centripetal propagation of vasoconstriction gradually progressed after the onset of reversible cerebral vasoconstriction syndrome and peaked at the time of thunderclap headache remission. The progress of centripetal propagation of vasoconstriction concluded with thunderclap headache remission. Conclusions Centripetal propagation of vasoconstriction has clinical significance as an indicator of the severity of reversible cerebral vasoconstriction syndrome. The presence of centripetal propagation of vasoconstriction is associated with an increased risk of brain lesions and a longer interval from first to last thunderclap headache. Moreover, repeat magnetic resonance angiography to assess centripetal propagation of vasoconstriction during the time from onset to thunderclap headache remission can help diagnose reversible cerebral vasoconstriction syndrome.

This study found evidence of centripetal propagation of vasoconstriction on MRA obtained at the time of thunderclap headache remission, compared with MRA obtained at the time of reversible cerebral vasoconstriction syndrome onset. If clinicians remain unsure of the diagnosis during early-stage reversible cerebral vasoconstriction syndrome, this time point represents the best opportunity to diagnose reversible cerebral vasoconstriction syndrome with confidence.

Patients with non-traumatic, non-aneurysmal, and non-perimesencephalic subarachnoid hemorrhage (SAH) tend to have clots circumscribed along the cortical convexity, a condition referred to as acute cortical SAH. Cerebral venous thrombosis (CVT) is a potential cause of cortical SAH. The study tried to establish the diagnosis and management of cortical SAH caused by CVT. Retrospective review of 145 patients with non-traumatic SAH identified 15 patients with no ruptured aneurysm. Clinical features were investigated with a specific focus on patients with SAH caused by CVT. Eight of the 15 patients had perimesencephalic SAH, and 7 had cortical SAH. SAH caused by CVT was diagnosed in 4 of the 7 patients with cortical SAH. The cortical SAH involved the unilateral convexity or sylvian cistern and spared the basal cistern on computed tomography in all 4 patients. CVT occurred in the transverse sinus and cortical vein (1 patient), insular vein (1 patient), and cortical vein (2 patients). Identification of thrombosed veins or sinuses was established directly by T 2 *-weighted and diffusion-weighted magnetic resonance (MR) imaging in the acute stage and diffusion-weighted and T 1 -weighted MR imaging in the subacute stage. All patients had cortical swelling without findings of venous hemorrhagic infarction on T 2 *-weighted MR imaging. None of the 4 patients received active treatment, and all had favorable outcomes. CVT in patients with non-traumatic cortical SAH should be first excluded as a potential hemorrhagic cause by MR imaging for thrombosed veins or sinuses before initiating antifibrinolytic therapy.

The diagnostic efficacy of fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging and computed tomography (CT) for acute subarachnoid hemorrhage (SAH) were compared and the problems with diagnosis were investigated in 81 patients with aneurysmal SAH within 24 hours after onset who underwent FLAIR imaging and CT on admission. The number of hematomas in the cisterns and ventricles were evaluated by clot scores. In addition, the frequency of undetected hematomas was calculated for the cisterns and ventricles. Clot scores were significantly higher for FLAIR imaging than for CT in the lateral sylvian, quadrigeminal, and convexity cisterns. On the other hand, clot scores were significantly higher for CT than for FLAIR imaging in the interhemispheric and medial sylvian cisterns. The overall frequency of undetected SAH was 2% for FLAIR imaging and 14% for CT. With the exception of the interhemispheric and medial sylvian cisterns, the frequency of undetected SAH was higher for CT than for FLAIR imaging. In this study, FLAIR imaging was more sensitive than CT for the detection of acute SAH within 24 hours after onset. However, the diagnostic efficacy of FLAIR imaging was reduced in comparatively tight cisterns.

In the present study, DWI-detected early infarction at the time of SAH onset was correlated with the occurrence of delayed extensive ischemic lesions. We believe that performing DWI at the time of admission is useful for evaluating the primary ischemic insult, which might play an important role in the pathogenesis of early brain injury and delayed vasospasm-related complications.