BACKGROUND AND PURPOSE: Conventional MR imaging techniques cannot produce optimal images of bone structures because bone has little water and a very short T2 life span. The aim of this study was to investigate the clinical feasibility of skull MR imaging using the zero TE sequence in patients with head trauma by assessing its diagnostic image quality and quantitative measurement compared with CT images. MATERIALS AND METHODS: Thirteen enrolled patients with head trauma were assessed using brain CT and skull MR imaging. Image quality was graded on a 5-point Likert scale to compare the 2 modalities. To evaluate quantitative analyses between the 2 imaging modalities, we measured skull thickness and normalized bone tissue signal. Interobserver reliability was assessed using weighted κ statistics and the intraclass correlation coefficient. RESULTS: Both imaging techniques clearly depicted skull fractures in all 13 patients. The mean scores for skull MR imaging and CT were 4.65 ± 0.56 and 4.73 ± 0.45 (P = .157), respectively, with substantial interobserver agreement (P < .05). The 2 imaging modalities showed no difference in skull thickness (P = .092) and had good correlation (r² = 0.997). The mean value of normalized bone tissue signal among the 3 layers of the skull was relatively consistent (P = .401) with high interobserver agreement (P < .001). CONCLUSIONS: Zero TE skull MR imaging has diagnostic image quality comparable with that of CT images. It also provides consistent results on the quantitative measurement of cortical bone with CT images.

Bow hunter's syndrome (BHS) is rare cause of vertebrobasilar insufficiency that arises from mechanical compression of the vertebral artery by head rotation. There is no standardized diagnostic regimen or treatment of BHS. Recently, we experienced 2 cases resisted continues medication and treated by surgical approach. In both cases, there were no complications after surgery and there were improvements in clinical symptoms. Thus, we describe our cases with surgical decompression with a review of the relevant medical literature.

Lee K, et al. J Cerebrovasc Endovasc Neurosurg. 2016 Dec;18(4):355-362. https://doi.org/10.7461/jcen.2016.18.4.355

Tandem pore domain weak inward rectifier potassium channel (TWIK)-related spinal cord K⁺ (TRESK; K_2P18.1) channel is the only member of the two-pore domain K⁺ (K_2P) channel family that is activated by an increase in intracellular Ca²⁺ concentration ([Ca²⁺]_i) and linked to migraines. This study was performed to identify the effect of verapamil, which is an L-type Ca²⁺ channel blocker and a prophylaxis for migraines, on the TRESK channel in trigeminal ganglion (TG) neurons, as well as in a heterologous system. Single-channel and whole-cell currents were recorded in TG neurons and HEK-293 cells transfected with mTRESK using patch-clamping techniques. In TG neurons, changes in [Ca²⁺]_i were measured using the fluo-3-AM Ca²⁺ indicator. Verapamil, nifedipine, and NiCl₂ inhibited the whole-cell currents in HEK-293 cells overexpressing mTRESK with IC₅₀ values of 5.2, 54.3, and >100 μM, respectively. The inhibitory effect of verapamil on TRESK channel was also observed in excised patches. In TG neurons, verapamil (10 μM) inhibited TRESK channel activity by approximately 76%. The TRESK channel activity was not dependent on the presence of extracellular Ca²⁺. In addition, the inhibitory effect of verapamil on the TRESK channel remained despite the absence of extracellular Ca²⁺. These findings show that verapamil inhibits the TRESK current independently of the blockade of Ca²⁺ influx in TG neurons. Verapamil will be able to exert its pharmacological effects by modulating TRESK, as well as Ca²⁺ influx, in TG neurons in vitro. We suggest that verapamil could be used as an inhibitor for identifying TRESK channel in TG neurons.

Lim S, et al. Korean J Neurotrauma. 2022 May;18:e27. https://doi.org/10.13004/kjnt.2022.18.e27

Background: Coil embolization is the mainstay treatment for carotid-cavernous fistulas (CCFs). However, few studies have reported entire occlusion of engorged veins to interrupt venous outflow. We report our experience with venous outflow-targeted coil embolization of direct CCFs. Methods: We retrospectively reviewed all the patients diagnosed with direct CCFs treated with venous outflow-targeted coil embolization between November 2013 and February 2020. Venous outflow-targeted coil embolization of the CCFs was performed as follows. First, transarterial stent-assisted coil embolization of CCFs was performed. If the venous outflow to the engorged veins persisted after transarterial stent-assisted coil embolization, entire occlusion of the engorged veins and additional coil packing within the cavernous sinus were performed to interrupt the venous outflow. Results: Ten patients had undergone venous outflow-targeted coil embolization, 6 women (60%) and 4 men (40%). Transfemoral cerebral angiography showed high-flow, direct CCFs in all the patients. Venous outflow occurred through the superior ophthalmic vein (SOV) in all the patients and was completely interrupted by the entire occlusion of the engorged veins with fibered coils. Three patients (30%) had undergone additional treatment in a supplementary manner because of recurrent symptoms (chemosis in 1 patient, faint tinnitus in 2 patients) in the early postprocedural period (1 to 4 weeks). All the symptoms were resolved on follow-up. No additional recurrence was found during follow-up (1–75 months). No peri-procedural complications were encountered. Conclusions: Venous outflow-targeted coil embolization of CCFs would be a safe and effective treatment method.