BACKGROUND AND PURPOSE:CBV is a key parameter in distinguishing penumbra from ischemic core. The purpose of this study was to compare CBV measurements acquired with standard PCT with ones obtained with C-arm CT in a canine stroke model.

ObjectiveThis study aimed to predict recurrence after coil embolization of unruptured cerebral aneurysms with computational fluid dynamics (CFD) using porous media modeling (porous media CFD).MethodA total of 37 unruptured cerebral aneurysms treated with coiling were analyzed using follow-up angiograms, simulated CFD prior to coiling (control CFD), and porous media CFD. Coiled aneurysms were classified into stable or recurrence groups according to follow-up angiogram findings. Morphological parameters, coil packing density, and hemodynamic variables were evaluated for their correlations with aneurysmal recurrence. We also calculated residual flow volumes (RFVs), a novel hemodynamic parameter used to quantify the residual aneurysm volume after simulated coiling, which has a mean fluid domain > 1.0 cm/s.ResultFollow-up angiograms showed 24 aneurysms in the stable group and 13 in the recurrence group. Mann-Whitney U test demonstrated that maximum size, dome volume, neck width, neck area, and coil packing density were significantly different between the two groups (P < 0.05). Among the hemodynamic parameters, aneurysms in the recurrence group had significantly larger inflow and outflow areas in the control CFD and larger RFVs in the porous media CFD. Multivariate logistic regression analyses demonstrated that RFV was the only independently significant factor (odds ratio, 1.06; 95% confidence interval, 1.01–1.11; P = 0.016).ConclusionThe study findings suggest that RFV collected under porous media modeling predicts the recurrence of coiled aneurysms.

OBJECTIVE Chronic hydrocephalus develops in association with the induction of tenascin-C (TNC), a matricellular protein, after aneurysmal subarachnoid hemorrhage (SAH). The aim of this study was to examine if cilostazol, a selective inhibitor of phosphodiesterase Type III, suppresses the development of chronic hydrocephalus by inhibiting TNC induction in aneurysmal SAH patients. METHODS The authors retrospectively reviewed the factors influencing the development of chronic shunt-dependent hydrocephalus in 87 patients with Fisher Grade 3 SAH using multivariate logistic regression analyses. Cilostazol (50 or 100 mg administered 2 or 3 times per day) was administered from the day following aneurysmal obliteration according to the preference of the attending neurosurgeon. As a separate study, the effects of different dosages of cilostazol on the serum TNC levels were chronologically examined from Days 1 to 12 in 38 SAH patients with Fisher Grade 3 SAH. RESULTS Chronic hydrocephalus occurred in 12 of 36 (33.3%), 5 of 39 (12.8%), and 1 of 12 (8.3%) patients in the 0 mg/day, 100 to 200 mg/day, and 300 mg/day cilostazol groups, respectively. The multivariate analyses showed that older age (OR 1.10, 95% CI 1.13-1.24; p = 0.012), acute hydrocephalus (OR 23.28, 95% CI 1.75-729.83; p = 0.016), and cilostazol (OR 0.23, 95% CI 0.05-0.93; p = 0.038) independently affected the development of chronic hydrocephalus. Higher dosages of cilostazol more effectively suppressed the serum TNC levels through Days 1 to 12 post-SAH. CONCLUSIONS Cilostazol may prevent the development of chronic hydrocephalus and reduce shunt surgery, possibly by the inhibition of TNC induction after SAH.

Background & purposeHyperplastic remodeling (HR) lesions are sometimes found on cerebral aneurysm walls. Atherosclerosis is the results of HR, which may cause an adverse effect on surgical treatment for cerebral aneurysms. Previous studies have demonstrated that atherosclerotic changes had a correlation with certain hemodynamic characteristics. Therefore, we investigated local hemodynamic characteristics of HR lesions of cerebral aneurysms using computational fluid dynamics (CFD).MethodsTwenty-four cerebral aneurysms were investigated using CFD and intraoperative video recordings. HR lesions and red walls were confirmed on the intraoperative images, and the qualification points were determined on the center of the HR lesions and the red walls. The qualification points were set on the virtual operative images for evaluation of wall shear stress (WSS), normalized WSS (NWSS), oscillatory shear index (OSI), relative residence time (RRT), and aneurysm formation indicator (AFI). These hemodynamic parameters at the qualification points were compared between HR lesions and red walls.ResultsHR lesions had lower NWSS, lower AFI, higher OSI and prolonged RRT compared with red walls. From analysis of the receiver-operating characteristic curve for hemodynamic parameters, OSI was the most optimal hemodynamic parameter to predict HR lesions (area under the curve, 0.745; 95% confidence interval, 0.603–0.887; cutoff value, 0.00917; sensitivity, 0.643; specificity, 0.893; P<0.01). With multivariate logistic regression analyses using stepwise method, NWSS was significantly associated with the HR lesions.ConclusionsAlthough low NWSS was independently associated with HR lesions, OSI is the most valuable hemodynamic parameter to distinguish HR lesions from red walls.

Cilostazol is a selective inhibitor of phosphodiesterase type III that downregulates tenascin-C (TNC), a matricellular protein, which may cause delayed cerebral infarction after aneurysmal subarachnoid hemorrhage (SAH). The authors increased the dosage and evaluated the dose-dependent effects of cilostazol on delayed cerebral infarction and outcomes in SAH patients. This was a retrospective cohort study in a single center. One hundred fifty-six consecutive SAH patients including 67 patients of admission World Federation of Neurological Surgeons grades IV-V who underwent aneurysmal obliteration within 48 h post-SAH from 2007 to 2017 were analyzed. Cilostazol (0 to 300 mg/day) was administered from 1-day post-clipping or post-coiling to day 14 or later. Cilostazol treatment dose-dependently decreased delayed cerebral infarction and tended to improve outcomes, although cilostazol did not affect other outcome measures including angiographic vasospasm. On multivariate analyses, 300 mg/day (100 mg three times) cilostazol independently decreased delayed cerebral infarction and improved 3-month outcomes, but other regimens including 200 mg/day (100 mg twice) cilostazol were not independent prognostic factors. Propensity score-matched analyses showed that the 300 mg/day cilostazol cohort had lower plasma TNC levels and a lower incidence of delayed cerebral infarction associated with better outcomes compared with the non-cilostazol cohort. The 300 mg/day cilostazol may improve post-SAH outcomes by reducing plasma TNC levels and delayed cerebral infarction, but not vasospasm. Further studies are warranted to investigate if 300 mg/day cilostazol is more beneficial to post-SAH outcomes than a usual dose of 200 mg/day cilostazol that was demonstrated to be effective in randomized controlled trials.