Morphological changes in chronic subdural hematomas following upfront middle meningeal artery embolization: sequence, timing, and association with outcomes.

OBJECTIVE: Middle meningeal artery embolization (MMAE) is an increasingly utilized approach for the treatment of chronic subdural hematomas (CSDHs). The course of morphological progression of CSDHs following MMAE is poorly understood. Herein, the authors aimed to describe these morphological changes and assess their prognostic significance for the outcomes on follow-up. METHODS: A single-institution retrospective cohort study of CSDH cases treated by upfront MMAE, without prior or adjunctive surgical evacuation, was performed. Clinical outcomes, complications, and the need for rescue surgery on follow-up were recorded. Hematomas were categorized into 6 morphological subtypes. All baseline and follow-up head CT scans were assessed for CSDH structural appearance, density, and loculation. Changes in CSDH size were quantified via 3D reconstruction for volumetric measurement. RESULTS: Overall, 52 CSDHs in 45 patients treated with upfront MMAE were identified. Hematomas were followed for a mean of 92.9 days. Volume decreased by ≥ 50% in 79.6% of the CSDHs. The overall rescue surgery rate was 9.6%. A sequence of morphological changes after MMAE was identified. Hematomas that diverged from this sequence (5.4%) all progressed toward treatment failure and required rescue surgery. The CSDHs were categorized into early, intermediate, and late stages based on the baseline morphological appearance. Progression from early to intermediate and then to late stage took 12.7 and 30.0 days, respectively, on average. The volume of early/intermediate- and late-stage hematomas decreased by ≥ 50%, a mean of 78.2 and 47.6 days after MMAE, respectively. Early- and intermediate-stage hematomas showed a trend toward more favorable outcomes compared with late-stage hematomas. The density of homogeneous hypodense hematomas (HSDHs) transiently increased immediately after MMAE (p < 0.001). A marked decrease in density and volume 1 to 3 weeks after MMAE in HSDHs was detected, the lack of which indicated an eventual need for rescue surgery. In HSDHs, a baseline mean density of < 20 HU, and a lower density than baseline by 1 month post-MMAE were predictors of favorable outcomes. The baseline hematoma volume, axial thickness, midline shift, and loculation were not correlated with MMAE outcomes. Loculated, trabecular, and laminar hematomas, which are known to have unfavorable surgical outcomes, had MMAE outcomes similar to those of other "surgical" hematomas. CONCLUSIONS: The current study was the first to describe the nature, sequence, and timing of morphological changes of CSDHs after MMAE treatment and has identified structural features that can predict treatment outcomes.

Successful balloon-assisted coil embolization for a diagnostically difficult case of spontaneous vertebrovertebral arteriovenous fistula.

BACKGROUND: We describe a rare case of idiopathic lower cervical vertebro-vertebral arteriovenous fistula (VVAVF) with compression of the nerve roots and spinal cord, successfully treated with detachable coils utilizing the transarterial balloon-assisted technique without complication of coil mass. CASE DESCRIPTION: A 68-year-old woman was admitted for numbness of the left upper limb and pain in the left neck. Cervical magnetic resonance imaging (MRI) revealed compression of nerve roots and spinal cord by a large vascular lesion. The left vertebral angiography demonstrated a VVAVF draining into the vertebral venous plexus at C5 level. Under general anesthesia, the fistula site was accessed with a microcatheter through the right femoral artery, and successful embolization performed by compactly placing several detachable coils using balloon-assisted technique. The patient made a full recovery, with long-term MRI-documented left vertebral artery patency and no fistular leakage, and without postoperative complications. CONCLUSION: Target occlusion utilizing the balloon-assisted technique in this case of VVAVF with compression of nerve roots and spinal cord, was effective in improving neurological symptoms, and achieved long-term occlusion when preservation of the VA was desired.

Endovascular Treatment of Intracranial Hypertension Associated with Venous Sinus Stenosis due to Tumor Compression.

Objective: We report a patient with intracranial hypertension associated with venous sinus stenosis due to tumor compression. Embolization of tumor feeding blood vessels reduced the tumor volume, improved venous sinus stenosis, and alleviated the symptoms of intracranial hypertension. Case Presentation: The patient was a 46-year-old woman with chronic headache and blurred vision. Magnetic resonance venography (MRV) revealed stenosis of the right transverse-sigmoid sinus. Intracranial hypertension was diagnosed by lumbar puncture. A high-intensity 2-cm tumor was detected on T2-weighted magnetic resonance imaging (MRI), and the homogenously enhanced tumor was adjacent to the right transverse-sigmoid sinus. Cerebral angiography demonstrated tumor staining mainly from the right occipital artery (OA). Collateral venous flow was minimal. In such cases, resection and reconstruction of the involved sinus segment have a high risk of venous infarction. Accordingly, percutaneous transluminal angioplasty (PTA) was performed, but dilation of the stenosis was poor. Thus, feeder occlusion of the tumor was added and lumboperitoneal (LP) shunt was placed, alleviating the headache and blurred vision. Ten months later, reduction of the tumor volume and improvement of sinus stenosis were observed, and the LP-shunt system was removed. A decrease in tumor volume via feeder occlusion may lead to partial sinus decompression and increased venous flow, resulting in long-term clinical remission. Conclusion: Transverse-sigmoid sinus stenosis can be a cause of intracranial hypertension, albeit rare. Embolization of the tumor is considered to be a treatment option for patients who cannot undergo resection.

Impact of diabetes mellitus on characteristics of carotid plaques and outcomes after carotid endarterectomy.

BACKGROUND: Published results for carotid endarterectomy (CEA) in symptomatic and asymptomatic severe carotid stenosis with diabetes mellitus (DM) are contradictory. To evaluate perioperative and long-term results of CEA in patients with DM, we retrospectively analyzed data of patients with or without DM who underwent CEA in our institute. METHODS: Between January 2005 and December 2010, 281 consecutive CEAs were performed in 268 patients under general anesthesia. All patients were subject to cardiac work-ups before surgery, and coronary revascularization was performed prior to CEA if patients were diagnosed with significant coronary artery stenosis. Lesion characteristics were assessed by a duplex ultrasound scan, computed tomography angiography (CTA), and plaque imaging on magnetic resonance imaging (MRI) before surgery, and patients were followed-up by a duplex ultrasound scan at three, six, and 12 months, then yearly, after surgery. RESULTS: Of 281 cases, 136 had DM (48 %). Diabetic patients more frequently had a history of coronary artery disease than non-diabetic patients (48.5 % vs. 36.6 %, P = 0.042). Coronary intervention prior to CEA was more frequently performed in diabetic patients than in non-diabetic patients (22.1 % vs. 11.0 %, P = 0.013). The incidence of perioperative (30 day) stroke (P = 1.000), death (P = 1.000), and cardiac complications (P = 0.484) did not differ among groups. Follow-up was available in 77.2 % of patients, with a median duration of 50 months (interquartile range, 32.1-67.2 months). The incidence of ipsilateral stroke (P = 0.720), death (P = 0.351), and severe restenosis (peak systolic velocity > 230 cm/sec) (P = 0.905) were not different between groups. CONCLUSIONS: DM does not increase the risk of perioperative complications and does not influence long-term outcomes after CEA if preexisting vascular risk factors and cardiac diseases are appropriately evaluated and treated before surgery.

Involvement of p38alpha in kainate-induced seizure and neuronal cell damage.

We investigated how p38alpha mitogen-activated protein kinase (p38) is related to kainate-induced epilepsy and neuronal damages, by using the mice with a single copy disruption of the p38 alpha gene (p38alpha(+/-)). Mortality rate and seizure score of p38alpha(+/-) mice administered with kainate were significantly reduced compared with the case of wild-type (WT) mice. This was clearly supported by the electroencephalography data in which kainate-induced seizure duration and frequency in the brain of p38alpha(+/-) mice were significantly suppressed compared to those of WT mice. As a consequence of seizure, kainate induced delayed neuronal damages in parallel with astrocytic growth in the hippocampus and ectopic innervation of the mossy fibers into the stratum oriens in the CA3 region of hippocampus in WT mice, whose changes were moderate in p38alpha(+/-) mice. Likewise, kainate-induced phosphorylation of calcium/calmodulin-dependent kinase II in the hippocampus of p38alpha (+/-) mice was significantly decreased compared to that of WT mice. These results suggest that p38alpha signaling pathway plays an important role in epileptic seizure and excitotoxicity.