Quan Wan, Daying Zhang, Xintian Cao, Yong Zhang, Mengye Zhu and Wei Zuo
Although CT-guided selective percutaneous radiofrequency thermocoagulation (PRFT) via the foramen rotundum (FR) has been used in the clinic as a novel successful treatment for isolated, second division (maxillary nerve [V2]), idiopathic trigeminal neuralgia (ITN), there is only very limited related literature published to date. This report aims to provide more detail for physicians about this technique.
Between March 2013 and April 2014, 20 patients with isolated V2 ITN refractory to or intolerant of drug treatment were treated by CT-guided selective PRFT via the FR at the First Affiliated Hospital of Nanchang University. The outcome of pain relief was assessed using the Barrow Neurological Institute (BNI) pain score, and grouped as good (BNI Class I or II, no medication required) and bad (BNI Class III–V, medication required or failed). Recurrence was defined as a relapse to a previous lower level after attainment of any higher level of pain relief. Adverse effects and complications were also monitored and recorded.
All patients (100%) obtained good pain relief including BNI Class I in 17 patients (85%) and BNI Class II in 3 patients (15%) immediately postoperatively. None of the patients were lost to follow-up. During the mean follow-up period of 24.3 months (range 18–30 months), 2 patients (10%) experienced recurring pain and the mean time until recurrence was 10.5 months (range 8–13 months). No adverse effects or complications occurred except for transient numbness restricted to the V2 dermatome in all patients (100%) and facial hematoma in 3 patients (15%).
In the current study, CT-guided selective PRFT via the FR not only achieved absolute selective lesioning to V2, but also helped patients attain successful pain relief with few adverse effects. These limited data suggest that CT-guided selective PRFT via the FR appears to be a feasible, safe, effective, and even relatively ideal treatment for isolated V2 ITN, but these findings need confirmation from further studies.
Philip Cheng, Li Ma, Sonali Shaligram, Espen J. Walker, Shun-Tai Yang, Chaoliang Tang, Wan Zhu, Lei Zhan, Qiang Li, Xiaonan Zhu, Michael T. Lawton and Hua Su
A high level of vascular endothelial growth factor (VEGF) has been implicated in brain arteriovenous malformation (bAVM) bleeding and rupture. However, direct evidence is missing. In this study the authors used a mouse bAVM model to test the hypothesis that elevation of focal VEGF levels in bAVMs exacerbates the severity of bAVM hemorrhage.
Brain AVMs were induced in adult mice in which activin receptor–like kinase 1 (Alk1, a gene that causes AVM) gene exons 4–6 were floxed by intrabasal ganglia injection of an adenoviral vector expressing Cre recombinase to induce Alk1 mutation and an adeno-associated viral vector expressing human VEGF (AAV-VEGF) to induce angiogenesis. Two doses of AAV-VEGF (5 × 109 [high] or 2 × 109 [low]) viral genomes were used. In addition, the common carotid artery and external jugular vein were anastomosed in a group of mice treated with low-dose AAV-VEGF 6 weeks after the model induction to induce cerebral venous hypertension (VH), because VH increases the VEGF level in the brain. Brain samples were collected 8 weeks after the model induction. Hemorrhages in the bAVM lesions were quantified on brain sections stained with Prussian blue, which detects iron deposition. VEGF levels were quantified in bAVM tissue by enzyme-linked immunosorbent assay.
Compared to mice injected with a low dose of AAV-VEGF, the mice injected with a high dose had higher levels of VEGF (p = 0.003) and larger Prussian blue–positive areas in the bAVM lesion at 8 or 9 weeks after model induction (p = 0.002). VH increased bAVM hemorrhage in the low-dose AAV-VEGF group. The overall mortality in the high-dose AAV-VEGF group was 26.7%, whereas no mouse died in the low-dose AAV-VEGF group without VH. In contrast, VH caused a mortality of 50% in the low-dose AAV-VEGF group.
Using mouse bAVM models, the authors provided direct evidence that elevation of the VEGF level increases bAVM hemorrhage and mouse mortality.