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Hartmut Meierkord, MD
Universitätsklinikum Charité Neurologische Klinik Humboldt-Universität Berlin Schumannstrasse 20/21 10117 Berlin, Germany

Simon Shorvon, MD, FRCP
London, England

Arch Neurol. 1994;51(7):646.

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In reply

We are grateful for the comments of Bauer et al. However, details of the methods are not given and several other points can be made. First of all, our finding that frontal lobe partial seizures are less likely to generate prolactin discharge compared with temporal lobe seizures¹ is in keeping with the report by Sperling and Wilson,² in which electrical stimulations were delivered to the amygdala, hip-. pocampus, and frontal sites. Only stimulations producing a high-frequency regional limbic afterdischarge resulted in prolactin concentration elevations, but no stimulations without such discharges or of frontal regions including the orbitofrontal cortex, cingulate cortex, and supplementary motor cortex, suggesting that site and intensity of the stimulation are important factors in determining prolactin release.

A particular problem occurs when ictal discharges spread from the frontal to the temporal lobe. These two structures are richly connected, and prolactin levels may be elevated . . . [Full Text PDF of this Article]

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