Watson C, Cendes F, Fuerst D, Dubeau F, Williamson B, Evans A, Andermann F
Department of Neurology, Wayne State University School of Medicine, Detroit, Mich, USA.
Arch Neurol. 1997 Jan;54(1):67-73. doi: 10.1001/archneur.1997.00550130049015.
Magnetic resonance imaging (MRI)-based volumetric measurements of the hippocampal formation are useful in detecting unilateral hippocampal sclerosis (HS) in patients with temporal lobe epilepsy. In this pathologic entity, volumetric MRI analysis shows the epileptogenic structure to be atrophic when compared with the normal, nonepileptogenic side. Some authors have suggested that the radiological features of atrophy of medial temporal lobe structures are common in patients with complex partial seizures, but also are seen frequently in other seizure types and can occur even in patients without epilepsy.
To determine if seizures originating in extrahippocampal sites cause gliosis, cell loss, and atrophy of medial temporal lobe structures (i.e., HS).
We studied 110 patients with chronic epilepsy using volumetric MRI measurements of the hippocampal formation. Seventeen patients had pathologically proven HS, 27 patients had seizures due to extratemporal structural lesions, 15 patients had seizures caused by extrahippocampal temporal lobe lesions, 29 patients had primary generalized epilepsy, and 22 patients had secondary generalized epilepsy.
All 17 patients with HS showed significantly reduced absolute hippocampal formation volumes of greater than 2 SDs below the mean of the control groups. The preoperative hippocampal formation volume measurements correlated well with the severity of HS on pathological examination. Hippocampal volumes were within the normal range in all patients with primary generalized epilepsy, secondary generalized epilepsy, extratemporal structural lesions, and extrahippocampal temporal lobe lesions.
Seizures originating at extrahippocampal sites do not cause gliosis, cell loss, or atrophy of medial temporal structures. Significant reduction in hippocampal volumes is a specific marker for HS.
基于磁共振成像（MRI）对海马结构进行体积测量，有助于检测颞叶癫痫患者的单侧海马硬化（HS）。在这种病理情况下，与正常的、非致痫侧相比，MRI体积分析显示致痫结构萎缩。一些作者认为，内侧颞叶结构萎缩的影像学特征在复杂部分性发作患者中很常见，但在其他发作类型中也经常出现，甚至在无癫痫的患者中也可能发生。
确定起源于海马外部位的癫痫发作是否会导致内侧颞叶结构（即HS）的胶质增生、细胞丢失和萎缩。
我们使用MRI对海马结构进行体积测量，研究了110例慢性癫痫患者。17例患者经病理证实为HS，27例患者因颞叶外结构病变导致癫痫发作，15例患者由海马外颞叶病变引起癫痫发作，29例患者为原发性全身性癫痫，22例患者为继发性全身性癫痫。
所有17例HS患者的海马结构绝对体积均显著减小，比对照组平均值低2个标准差以上。术前海马结构体积测量结果与病理检查中HS的严重程度密切相关。所有原发性全身性癫痫、继发性全身性癫痫、颞叶外结构病变和海马外颞叶病变患者的海马体积均在正常范围内。
起源于海马外部位的癫痫发作不会导致内侧颞叶结构的胶质增生、细胞丢失或萎缩。海马体积显著减小是HS的特异性标志。
