Williams Jennifer, Mullins Gerard, Delanty Norman, Bede Peter, Doherty Colin P
Department of Neurology, St. James's Hospital, James's Street, Dublin 8, Ireland; Academic Unit of Neurology, Trinity Biomedical Science Institute, Trinity College Dublin, 152-160 Pearse Street, Dublin 2, Ireland.
Department of Clinical Neurophysiology, Beaumont Hospital, Beaumont Road, Dublin 9, Ireland.
Seizure. 2017 Aug;50:189-193. doi: 10.1016/j.seizure.2017.06.024. Epub 2017 Jul 6.
Seizure induced neuronal hyperexcitability and increased unmet metabolic neuronal demand results in failure of the sodium/potassium ATP pump. Sodium and water accumulates intracellularly with cellular swelling and reduced extracellular volume demonstrating hyperintensity on DWI and reduced ADC. The aim of this study was to describe 4 clinical cases where we identified abnormalities in diffusion restriction in the acute peri-ictal period and followed them longitudinally.
Patients were recruited from the emergency department, clinical consultation service and epilepsy monitoring unit of two tertiary referral centres. Patients underwent either 1.5T or 3.0T MRI with DWI, ADC, T2-weighted and post contrast studies during their acute admission and again after a period of follow up.
Four patients were identified as having visible diffusion restriction and reduced ADC in one or both hippocampi and the splenium of the corpus callosum. These lesions either completely resolved, showed interval improvement or demonstrated atrophy on follow up imaging. The two patients with persisting abnormalities had presented with status epilepticus.
These acute ictal imaging changes give clinicians an important in-vivo look at the dynamic neuronal metabolic environment in the peri-ictal period. Areas that appear most susceptible include the mesial temporal structures and corpus callosum. Close imaging follow up to document resolution or evolution of long lasting sequelae is vital. There is no clear consensus as to why some patients develop ictal related imaging changes and others do not. Seizure length and time interval from ictus to scan appear to play a role but larger prospective studies are needed to confirm this.
癫痫发作诱导的神经元兴奋性过高以及未满足的代谢性神经元需求增加会导致钠/钾ATP酶泵功能衰竭。钠和水在细胞内蓄积，导致细胞肿胀，细胞外容积减少，在扩散加权成像（DWI）上表现为高信号，表观扩散系数（ADC）降低。本研究的目的是描述4例临床病例，我们在急性发作期发现了扩散受限异常，并对其进行了纵向随访。
从两家三级转诊中心的急诊科、临床咨询服务部和癫痫监测单元招募患者。患者在急性入院期间以及随访一段时间后分别接受1.5T或3.0T磁共振成像（MRI）检查，包括DWI、ADC、T2加权成像和增强扫描。
4例患者被确定在一个或双侧海马体以及胼胝体压部出现可见的扩散受限和ADC降低。这些病变在随访成像中要么完全消失，要么有间隔期改善，要么出现萎缩。两名病变持续存在的患者表现为癫痫持续状态。
这些急性发作期成像变化让临床医生能够在活体状态下重要地观察发作期神经元代谢环境的动态变化。最易受累的区域包括内侧颞叶结构和胼胝体。密切的成像随访以记录长期后遗症的消退或演变至关重要。对于为何有些患者出现发作期相关成像变化而其他患者未出现，目前尚无明确共识。发作时长以及从发作到扫描的时间间隔似乎起一定作用，但需要更大规模的前瞻性研究来证实这一点。
