[Epileptic activity of the occipital lobe. Clinico-electroencephalographic contribution]

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.