Schäffler L, Karbowski K
Abteilung für Epileptologie und Elektroenzephalographie, Neurologischen Universitätsklinik Bern.
Fortschr Neurol Psychiatr. 1988 Sep;56(9):286-99. doi: 10.1055/s-2007-1001793.
Our analysis of the course of illness in 14 patients, whose common electroencephalographic characteristic was epileptogenic activity in the occipital area, showed very different clinical symptoms. The first group comprised patients who presented bilateral amaurosis. In four of these cases, the occipital hypersynchronous EEG activity was merely a secondary symptom of either ischaemic hypoxia or of a degenerative process in the occipital visual cortex and was not responsible for the genesis of the actual blindness. In two further cases of monosymptomatic temporary loss of vision, it was difficult to make a differential diagnosis between ictal blindness, respectively status epilepticus amauroticus occurring in a occipital lobe epilepsy and a migraine attack involving the basilar territory. The second group comprised five patients with paroxysmal visual hallucinations respectively illusions. Three of them suffered from hallucinations of the elementary type, respectively flickering fits in the hemianopic field, symptoms which are based on discharges in the visual cortex of the occipital lobe. In a case of one patient with complex visual hallucinations as well as in a further case with visual illusions, it was not possible to find out with certainty their place of origin. A study of these cases shows that the cortical or sub-cortical functional disturbance within the visual system causing the various optical deformations and visual hallucinations, form an inhomogeneous group with different etiology. In the only patient belonging to the third group, whose seizures were i.a. characterized through motor phenomena in the field of the ocular organs and the tonic lateral turning movement of the bulbi of the eyes and of the head, an occipital epileptic crisis with spread of discharges from the occipital pole to the frontomesial surface should be assumed. The occurrence of complex partial seizures, respectively generalized tonic-clonic attacks in two patients of the fourth group who have definite epileptogenic EEG-activity in the occipital area, can be explained by a propagation of paroxysmal activity to the temporal lobe or to the motor cortex. Because of the marked tendency to propagation of the hypersynchronous activity originating in the occipital lobe, many combinations of sensory and/or motor symptoms can occur within the frame-work of occipital epileptic seizures. On the basis of one scalp EEG finding, no final localizing conclusions may be drawn here.
我们对14例患者的病程进行了分析,这些患者共同的脑电图特征是枕叶存在致痫性活动,但其临床症状却大不相同。第一组患者表现为双侧黑矇。其中4例,枕叶脑电图活动超同步化仅仅是枕叶视觉皮层缺血缺氧或退行性病变的继发症状,并非导致实际失明的原因。另外2例单症状性短暂视力丧失患者,很难鉴别是发作性失明,即枕叶癫痫中出现的癫痫性黑矇状态癫痫,还是累及基底节区的偏头痛发作。第二组包括5例分别有阵发性视幻觉或错觉的患者。其中3例有基本类型的幻觉,即偏盲视野中的闪烁发作,这些症状基于枕叶视觉皮层的放电。在1例有复杂视幻觉的患者以及另1例有视错觉的患者中,无法确切查明其起源部位。对这些病例的研究表明,视觉系统内导致各种视觉变形和视幻觉的皮层或皮层下功能障碍,是一组病因不同的异质性疾病。在属于第三组的唯一1例患者中,其癫痫发作的特征是眼部区域出现运动现象以及眼球和头部的强直性侧转运动,应考虑为枕叶癫痫发作,放电从枕极扩散至额内侧表面。第四组的2例患者在枕叶有明确的致痫性脑电图活动,出现复杂部分性发作或全身性强直阵挛发作,可解释为阵发性活动扩散至颞叶或运动皮层。由于起源于枕叶的超同步活动有明显的扩散倾向,在枕叶癫痫发作的情况下可能会出现许多感觉和/或运动症状的组合。基于头皮脑电图的一项发现,在此无法得出最终的定位结论。