論文

BACKGROUND Microvascular decompression (MVD) for trigeminal neuralgia (TN) caused by vertebrobasilar dolichoectasia (VBD) is technically challenging due to the vessel’s size and stiffness. While ipsilateral abducens nerve (cranial nerve [CN] VI) palsy is a known complication, contralateral palsy resulting from force transmission remains unreported. OBSERVATIONS The authors describe 2 cases of CN VI palsy following MVD for VBD-associated TN. Case 1 developed ipsilateral palsy after caudal transposition of the vertebral artery, resulting from a paradoxical medial shift of the proximal vessel segment. Case 2 presented with a rare contralateral CN VI palsy. Postoperative imaging indicated that mobilizing the rigid VBD caused an “en bloc” shift of the entire vertebrobasilar system, resulting in secondary compression of the contralateral CN VI. Both patients achieved immediate pain relief, and the palsies recovered with conservative management. LESSONS Mobilizing a dolichoectatic VBD transmits mechanical force to distant segments via an en bloc shift, potentially injuring CN VI on either the operative or contralateral side. Preoperative identification of risk factors—specifically severe calcification, preexisting contralateral deviation, and minimal contralateral CSF space—is crucial. Surgeons should recognize that vascular transposition can transmit force bilaterally and must counsel patients regarding these risks.

Cerebrospinal fluid (CSF) leakage is a common complication associated with endoscopic endonasal skull-base surgery (EESBS). Postoperative mobilization-associated postural changes are considered to cause CSF leakage. However, no study has demonstrated a robust relationship between postural changes and CSF leakage. We used upright computed tomography (CT) to clarify the effects of postural changes on the reconstructed skull base (RSB) after EESBS. Thirty patients who underwent EESBS at our institution were prospectively included, and their upright and supine CTs were compared to measure morphological changes in the RSB. Patient clinical data were also collected from medical charts and surgical videos, and their relationships with morphological changes were assessed. In upright CTs, the RSB shifted intracranially by 0.94 (0.0–2.9) mm on average. This shift was larger in cases with lesions extending to the sphenoid sinus, dural defects, intraoperative pulsation of the RSB, and large bone windows. The direction of the change was opposite to intuitive movement driven by gravity because of reduced intracranial pressure in the sitting position. Thus, these shifts can be directly associated with postoperative CSF leakage caused by reconstruction material displacement. Skull-base reconstruction and postoperative postural management accounting for these morphological changes may be necessary for preventing CSF leakage.

Background: Vagus nerve stimulation (VNS) is an established therapy for refractory epilepsy, indicating that enhanced vagal activity can suppress excessive brain excitability. However, whether endogenous vagal tone itself serves as an intrinsic antiepileptic mechanism remains unclear. We aimed to determine if endogenous vagal activity restrains epileptic dynamics and to elucidate the neural pathways involved. Methods: We employed an intrahippocampal kainate-induced mouse model of temporal lobe epilepsy and an optogenetic model of hippocampal excitability. We performed gain-of-function studies using cervical VNS (30 Hz) and loss-of-function studies using bilateral subdiaphragmatic vagotomy and selective ablation of VGluT2-positive vagal afferents. Results: Cervical VNS attenuated network hyperexcitability, significantly reducing delta power and root mean square (RMS) amplitude, consistent with its clinical efficacy. By contrast, bilateral subdiaphragmatic vagotomy increased delta power, RMS amplitude, and mortality, demonstrating that endogenous vagal activity restrains epileptic dynamics. In the optogenetic model, VNS suppressed, whereas vagotomy exacerbated, light-evoked after-discharges. Crucially, selective ablation of VGluT2-positive vagal afferents largely abolished the electrophysiological signatures of VNS, including power suppression and network desynchronization, establishing that the antiseizure action of VNS depends on intact afferent pathways. Conclusions: These findings identify endogenous vagal afferent signaling as a tonic brake on epileptic network activity and provide mechanistic evidence that cervical VNS suppresses seizures by amplifying this endogenous pathway. This work presents a conceptual and mechanistic framework for afferent-targeted neuromodulation strategies aimed at improving therapeutic precision in epilepsy.

Developmental and epileptic encephalopathies (DEEs) are devastating syndromes characterized by early-onset, treatment-resistant seizures, and significant developmental delays. KCNB1-related DEE, arising from pathogenic variants in the KCNB1 gene, presents with profound cognitive impairment and persistent seizures despite multiple antiseizure medications (ASMs). Vagus nerve stimulation (VNS) has emerged as a valuable adjunctive therapy for medically intractable epilepsy, yet its effectiveness in rare genetic DEEs remains unknown. We report the first case of VNS in a 5-year-old child with KCNB1-related DEE, achieving about 90% seizure reduction after one year. Prior treatments with multiple ASMs had minimal effect. After VNS implantation, optimized stimulation parameters combined with fenfluramine markedly improved seizure control. Although concurrent medication adjustments and transient seizure cessation during infection complicated interpretation, the sustained seizure improvement strongly suggests VNS's efficacy in this genetic epilepsy. This case illustrates VNS's potential benefit and possible synergy with fenfluramine in KCNB1-related DEE. Further accumulation of case reports is necessary to confirm these findings.

BACKGROUND: Stereotactic ablation surgeries including radiofrequency thermocoagulation (RFTC) and laser interstitial thermal therapy are recent less invasive treatment methods for insular epilepsy. Volume-based RFTC after stereoelectroencephalography was first proposed by a French group as a more effective method for seizure relief in insular epilepsy patients than stereoelectroencephalography-guided RFTC. OBJECTIVE: To describe the feasibility and technical details about volume-based RFTC in patients with insulo-opercular epilepsy. METHODS: We successfully treated 3- and 6-year-old patients with medically refractory insulo-opercular epilepsy with volume-based RFTC, in which the target volume of coagulation was flexibly designed by combining multiple spherical models of 5-mm diameter which is smaller than reported previously. RESULTS: The insula was targeted by oblique trajectory from the frontoparietal area in one case, and the opercular cortex was targeted by perpendicular trajectories from the perisylvian cortex in the other case. The use of the small sphere model required more trajectories and manipulations but enabled more exhaustive coagulation of the epileptogenic zone, with 70% to 78% of the planned target volume coagulated without complications, and daily seizures disappeared after RFTC in both patients. CONCLUSION: Volume-based RFTC planned with small multiple sphere models may improve the completeness of lesioning for patients with insulo-opercular epilepsy. Careful planning is necessary to reduce the risks of vascular injuries.