Pathophysiological relevance of EEG slowing: An EEG/fMRI/MR-spectroscopy study in patients with borderline personality disorder and autoimmune psychosis

边缘型人格障碍（BPD）和自身免疫性精神病（AP）患者脑电图（EEG）减慢的患病率很高。特别是，这些患者表现出可识别的、全身性的、间歇性的节律性δ和θ活动（IRDA和IRTA）。在早期研究中，我们在15%的BPD患者中发现了这些现象。脑电图减慢如irda / irta在自身免疫性精神病患者中更为常见（80-90%）。irda / irta的确切病理生理和鉴别诊断意义尚不清楚。它们被解释为不同神经精神疾病的癫痫性成分，可以是神经网络不稳定的一种表达。有了新的功能和神经化学成像方法，进一步的科学见解是可能的。在初步研究中，我们能够通过同时进行的EEG/fMRI成像显示irda / irta的产生区域的有效定位。在计划的项目中，同时静息状态EEG- fMRI成像将用于显示BPD和AP患者的irda / irta的血流动力学相关性。在体积和磁共振光谱（MRS）测量中，应分析产生区域的体积和神经化学完整性，并与对照组进行比较。本研究的目的是为这些脑电图现象建立一个更好的跨诊断病理生理分类。因此，在脑电图改变的患者组中，应明确BPD和AP的病理生理学。在BPD和AP患者中，我们计划首次使用全脑MRS来量化GABA和谷氨酸的浓度。这项研究具有临床意义，因为抗惊厥药（例如，GABA激动剂和NMDA拮抗剂丙戊酸钠）已经在BPD和AP患者的适应症外使用。这项研究应该能够为部分成功使用此类抗惊厥药提供解释方法。

Patients with borderline personality disorder (BPD) and autoimmune psychosis (AP) show a high prevalence of electroencephalography (EEG) slowing. In particular, these patients display identifiable, generalized, and intermittent rhythmic delta- and theta activity (IRDA and IRTA). In earlier studies, we found these phenomena in 15% of patients with BPD. EEG slowing such as IRDAs/IRTAs was found even more frequently in patients with autoimmune psychoses (in 80-90%). The exact pathogenetic-pathophysiological and differential diagnostic importance of IRDAs/IRTAs is still unclear. They have been interpreted as paraepileptic components in different neuropsychiatric disorders and can be an expression of neuronal network instability. With new functional and neurochemical imaging methods, further scientific insights are possible. In preliminary investigations, we were able to show valid localization of the generator areas of IRDAs/IRTAs with simultaneous EEG/fMRI imaging. In the planned project, simultaneous resting state EEG- fMRI imaging will be used to show hemodynamic correlates of IRDAs/IRTAs in patients with BPD and AP. In volumetric and MR-spectroscopic (MRS) measurements, the generator areas should be analyzed regarding their volume and neurochemical integrity and compared with a control group. The aim of this study is to create a better trans-diagnostic pathophysiological classification of these EEG phenomena. Therefore, the pathophysiology of BPD and AP should be clarified in the patient group with these EEG alterations. For the first time in patients with BPD and AP, we plan to use the whole brain MRS to quantify GABA and glutamate concentrations. The study is clinically relevant because anticonvulsants (e.g., the GABA agonist and NMDA antagonist valproate) were already used off-label in patients with BPD and AP. This study should be able to provide explanatory approaches for the partially successful use of such anticonvulsants.