Osaka Neurological Institute

Neoplastic cerebral aneurysms (NCAs) are rare. This study reported a case of an NCA secondary to a poorly differentiated carcinoma of the parotid gland. An 84-year-old Japanese woman undergoing treatment for parotid gland cancer was admitted to our hospital with headache and progressive loss of consciousness. Based on computed tomography (CT) and CT angiography (CTA), a diagnosis of subarachnoid hemorrhage due to rupture of a left posterior inferior cerebellar artery aneurysm was made, and emergency aneurysmectomy was performed. Pathological examination of the resected aneurysm showed an NCA secondary to parotid carcinoma. After the aneurysmectomy, her condition stabilized; however, 33 days later, the patient developed an intracerebral hemorrhage, and a new aneurysm was confirmed in the right middle cerebral artery. To the best of our knowledge, there have been no previous reports on cases of NCAs secondary to parotid carcinoma. The pathology and clinical course strongly suggest that NCAs derived from malignant tumors may have an aggressive course.

N-butyl cyanoacrylate (n-BCA) is often utilized for preoperative transarterial embolization (TAE) of meningiomas. However, factors affecting the embolization effect with n-BCA remain unclear. This study aimed to clarify the factors associated with the embolization rate after TAE using n-BCA in meningioma, from the aspect of feeder architecture.

We retrospectively analyzed 62 patients with meningioma who underwent preoperative TAE with n-BCA between 2016 and 2021. Patient variables, including characteristics, intraoperative findings, and outcomes, were collected. Feeder architecture was classified into seven groups: 1) internal maxillary artery, 2) occipital artery, 3) ascending pharyngeal artery, 4) posterior meningeal artery, 5) infraclinoidal internal carotid artery, 6) ophthalmic artery (OphA), and 7) pial feeder group, based on preoperative angiography. We set primary outcome as the embolization rate, representing the reduction rate of the gadolinium-enhanced lesion volume observed on contrast-enhanced magnetic resonance imaging. Angiographic findings following n-BCA injection were classified as feeder occlusion (FO) or intratumoral embolization (IE). We analyzed the factors associated with the embolization rate.

The OphA feeder group showed a decrease in the embolization rate (P = 0.008). The number of feeder groups with IE showed a robust positive correlation (r = 0.557). The OphA feeder group showed an increase in the number of feeder groups (P < 0.001) and larger tumor volume (P = 0.005).

The OphA feeder group was associated with a lower embolization rate. Our study suggested that the vascular architecture in meningioma affected the efficacy of TAE with n-BCA.

Restenosis after carotid artery stenting (CAS) is associated with the risk of developing ischemic stroke. We aimed to evaluate the inhibitory effect of cilostazol addition on in-stent restenosis (ISR) in patients treated with CAS.

In a randomized, open-label, blind-end point trial, patients with symptomatic and asymptomatic carotid artery stenosis and scheduled for CAS were randomly assigned to adding cilostazol (50 or 100 mg, twice per day) on other antiplatelets from 3 days before CAS or not adding cilostazol. Concomitant use of other antiplatelets was unrestricted. ISR was diagnosed by a peak systolic velocity of at least 1.75 m/s on duplex ultrasonography. The primary outcome was incidence of ISR within 2 years after CAS. Secondary outcomes included occurrences of cardiovascular events or any death and hemorrhagic events.

Participants were recruited from December 2010 to September 2015. Although the sample size was initially set to be 900 (450 in each group), 631 patients (mean age 69.9 years, 558 men, 325 in the cilostazol, and 306 in the noncilostazol group) were included in the primary analysis. Within 2 years’ follow-up, ISR occurred in 31 of 325 patients (cumulative incidence 10.8%) in the cilostazol group and 46 of 306 patients (19.6%) in the noncilostazol group (hazard ratio, 0.64 [95% CI, 0.41–1.0]; P =0.056). In the exploratory analysis, incidence of ISR beyond 30 days after CAS was lower in the cilostazol group than in the noncilostazol group (10.3% versus 19.3%; P =0.040). Incidences of cardiovascular events or any death and hemorrhagic events were similar between the groups (6.2% versus 6.7% and 2.3% versus 1.4%, respectively).

The addition of cilostazol to other antiplatelet agents could contribute to the reduction of ISR in the chronic stage of patients who underwent CAS, the authenticity of which depends on further studies with sufficient statistical power.

URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01261234.