EEG Studies of Cortical Blindness in a Case of Salicylate Poisoning

Salicylate poisoning and an episode of water retention during the procedure of flushing out the poison caused temporary hyponatremia and cerebral edema followed by cortical blindness. Recovery was slow and cortical malfunction in the occipital area can still be demonstrated.

The first EEG on this 5œ year old girl taken after she came out of her coma was still compatible with a comatous state. The tracing consisted of high voltage slow waves. Four days later the abnormal slow wave activity was limited to the occipital areas, occasionally mixed with spikes. Short paroxysmal bursts were seen during subsequent examination without concurrent clinical manifestations. Visual acuity improved very slowly during the course of the year to 20/40 on each side. Optic atrophy developed r > 1. The present EEG shows frequent occipital spikes followed by irregular slow waves, most marked over the right occipital area.

Abnormal visual evoked potentials during the first tracing showed an N₁₀₀ (first negative peak) followed by a P₂₄₃ with intermediate waves missing. The VER now has a normal pattern with N₈₇ and P₁₁₈ (the numbers indicate peak latencies from stimulus onset in msec).