Occipital Seizures and Visual Evoked Potentials

To the Editor: We read with interest the article of Wang et al. (1), reporting on visual evoked potential (VEP) findings in a patient with left occipital status epilepticus (SE) and a right hemianopsia. Using full-field pattern-reversal VEP testing, P100 amplitudes during SE were higher contralateral to the seizure focus, whereas P100 amplitudes were higher ipsilateral to the afflicted occipital lobe 6 months later, after cessation of SE. The findings are described to be consistent with the literature with respect to the normal paradoxical lateralization of the P100 component of VEPs and also with the earlier case study of Hughes et al. (2), who likewise found increased P100 amplitudes contralateral to the seizure focus in a patient with occipital seizures. We also have recorded altered VEPs in a patient during occipital lobe SE and have been puzzled by the pathophysiologic implications of the findings. Although they do not state it explicitly, Wang et al. (1) are presumably suggesting an ictal “activation” or “disinhibition” of the seizure-generating occipital lobe in their patient. In other words, if the normal contribution to the full-field VEP represents a summation of the responses to bilateral hemifield stimulation, with the right hemifield stimulation producing a VEP generated by the left occipital lobe that appears “paradoxically” with highest amplitude over the right posterior hemisphere (and vice versa for the left hemifield stimulation response), then the findings in this case might suggest that the occipital cortex during SE responds to pattern-reversal stimulation to a greater extent than it would do in its normal (interictal or nonepileptic) state. However, this becomes somewhat counterintuitive when one considers the clinical hemianopsia colocalized to the same occipital lobe that is presumed to be “activated” or “disinhibited” in its response to pattern-reversal visual input. Our patient also had a left occipital simple partial SE and a corresponding right hemianopsia, and had an ictal H215O PET study showing increased left mesial occipital and lateral occipitotemporal perfusion in cortical areas virtually identical to those shown in Fig. 2 of Wang et al. (1). Rather than full-field VEP testing, we performed a hemifield VEP study and recorded over the occipitotemporal areas (Fig. 1). In this case, we found, during SE, a normal P100 with left hemifield stimulation to the unaffected right occipital lobe. However, right hemifield stimulation to the seizure-generating left occipital lobe produced only a grossly distorted VEP topographically restricted to the ipsilateral left occipitotemporal region. VEPs were normal 2 days later after cessation of the SE. Hemifield pattern-reversal visual evoked potential study during (A) and after cessation (B, normal) of left occipital status epilepticus 2 days later. A normal P100 (*) was found with stimulation of the unaffected right occipital lobe but a clear distortion of the VEP topography with stimulation of the epileptic left occipital lobe: Whereas the normal P100 is abolished (**), a pronounced positive deflection with a latency of ∼120 ms (***) was found ipsilateral to the epileptic lobe, extending into the midline occipital structures (Oz). As mentioned earlier, we remain somewhat puzzled by these findings, but believe they underscore the complicated nature of the multiple sources underlying VEP generation, as well as the need for hemifield-stimulation studies to understand the effects of lateralized epileptic interference on VEP generation. In this context, we suggest that the VEP findings of Wang et al. (1) might equally well represent a complicated seizure-related distortion of VEP topography as an epileptic “activation” or “disinhibition” of the involved cortical structures.

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