Bunyamin Jacob, Sinclair Benjamin, Wittayacharoenpong Thanomporn, Sagar Parveen, Pham William, Chen Zhibin, Bosak Noam, Laing Joshua, Gutman Matthew, Hunn Martin, Kwan Patrick, O'Brien Terence J, Law Meng, Neal Andrew
Department of Neuroscience, School of Translational Medicine, Monash University, Melbourne, Victoria, Australia.
Department of Neurology, Alfred Health, Melbourne, Victoria, Australia.
Epilepsia. 2025 Aug 26. doi: 10.1111/epi.18614.
We aim to explore the association between enlarged perivascular space (ePVS) density and stereo-electroencephalography (SEEG) biomarkers of epileptogenicity.
We retrospectively analyzed consecutive SEEG patients from an Australian site. We automatically segmented ePVSs from 3T pre-SEEG T1-weighted magnetic resonance imaging (MRI) scans and calculated ePVS (1) hemispheric, (2) sub-lobar, and (3) contact-level density. We defined the epileptogenic zone (EZ) SEEG contacts as those identified as the primary EZ and then selected for radiofrequency thermocoagulation (RF-TC). We classified contacts generating the top 10% of interictal epileptogenicity biomarkers (spikes, fast ripples, and cross-rates of high-frequency oscillations [HFO]*spikes). We assessed the relationship at each level for the whole cohort and its subgroups: MRI-negative-only, different voxel sizes (.9 mm/1.0 mm), contact locations (mesial temporal/neocortical), and seizure-free patients.
From 53 RF-TC patients, ePVS density was not associated with the EZ at the hemispheric (p = .995), sub-lobar (p = .090), or contact (p = .999) level in the whole cohort. In the MRI-negative-only subgroup and 1.0 mm isotropic subgroup, ePVS density was inversely associated with EZ (odds ratio [OR] .76, 95% confidence interval [CI]: .61-.93, p = .009 and OR .83, 95% CI: .69-.99, p = .036, respectively). There was no association between ePVSs and the interictal epileptogenic biomarkers at all levels in the whole cohort. At the subgroup level, mesial temporal ePVS density was inversely associated with the top 10% of fast ripples (OR .09, 95% CI: .04-.24, p < .001) and cross-rates of HFO*spikes (OR .22, 95%CI: .11-.44, p < .001), whereas in the neocortex, ePVSs were positively associated with fast ripples (OR 1.10, 95% CI: 1.01-1.18, p = .018), which may be driven by the interictal biomarker organization rather than epileptogenicity.
ePVS density may not be a consistent biomarker of SEEG-defined epileptogenicity. The relationship between reduced ePVS and epileptogenicity in MRI-negative cases warrants further study, as this may shed light on underlying pathobiology and EZ biomarkers. Different imaging techniques may be able to capture the relationship between the glymphatic system disruption and epileptogenicity.
我们旨在探讨血管周围间隙增宽（ePVS）密度与癫痫致痫性的立体定向脑电图（SEEG）生物标志物之间的关联。
我们回顾性分析了来自澳大利亚某研究点的连续SEEG患者。我们从3T的SEEG前T1加权磁共振成像（MRI）扫描中自动分割出ePVS，并计算ePVS（1）半球、（2）脑叶下和（3）接触层面的密度。我们将致痫区（EZ）的SEEG接触点定义为那些被确定为主要EZ并随后被选作射频热凝（RF-TC）的接触点。我们对产生发作间期癫痫致痫性生物标志物（棘波、快波以及高频振荡[HFO]*棘波的交叉发生率）前10%的接触点进行分类。我们评估了整个队列及其亚组在每个层面的关系：仅MRI阴性患者组、不同体素大小（0.9毫米/1.0毫米）、接触点位置（内侧颞叶/新皮质）以及无癫痫发作患者组。
在53例接受RF-TC的患者中，整个队列在半球层面（p = 0.995）、脑叶下层面（p = 0.090）或接触层面（p = 0.999），ePVS密度与EZ均无关联。在仅MRI阴性亚组和1.0毫米各向同性亚组中，ePVS密度与EZ呈负相关（优势比[OR]分别为0.76，95%置信区间[CI]：0.61 - 0.93，p = 0.009；以及OR 0.83，95% CI：0.69 - 0.99，p = 0.036）。在整个队列的所有层面，ePVS与发作间期癫痫致痫生物标志物之间均无关联。在亚组层面，内侧颞叶的ePVS密度与前10%的快波（OR 0.09，95% CI：0.04 - 0.24，p < 0.001）以及HFO*棘波的交叉发生率（OR 0.22，95% CI：0.11 - 0.44，p < 0.001）呈负相关，而在新皮质中，ePVS与快波呈正相关（OR 1.10，95% CI：1.01 - 1.18，p = 0.018），这可能是由发作间期生物标志物的组织情况而非癫痫致痫性所驱动。
ePVS密度可能并非SEEG定义的癫痫致痫性的一致生物标志物。MRI阴性病例中ePVS减少与癫痫致痫性之间的关系值得进一步研究，因为这可能有助于揭示潜在的病理生物学和EZ生物标志物。不同的成像技术或许能够捕捉到淋巴系统功能障碍与癫痫致痫性之间的关系。
