Changes In Serum Prolactin With Brain Stimulation
The first recognition of episodic hyperprolactinemia induced by seizures were the observations of investigators (11) who were seeking endocrine profiles to predict which patients would benefit from a full course of electrocon-vulsive therapy (ECT). Although endocrine changes did not predict the likelihood of successful ECT in women with depression, reproducible elevations in serum PRL followed ECT. ECT produces similar endocrine changes in schizophrenics (12,13).
Subsequent to the ECT reports, investigators studied the effects of other methods of brain stimulation on PRL secretion. Parra (14) demonstrated a transient elevation of serum PRL with the direct stimulation of the amygdala in humans, but a subsequent study (15) of limbic and extralimbic structures showed that elevations of serum PRL occur only when stimulation evokes high-frequency, widespread limbic discharges. Thus, it appears that stimulation within physiologic ranges control prolactin release via subcortical structures other than the amygdala. Gallagher (16) confirmed that the stimulation of the amygdala and hippocampus causes elevations of serum prolactin and ACTH, but not growth hormone, only when stimuli are sufficient to produce seizures or after-discharges that last 10 seconds or more.
Transcranial magnetic stimulation produces changes in serum PRL only when the stimulus induces a complex partial seizure (17). Transcutaneous stimulation of central motor pathways produces no changes in PRL (18), nor does an evoked photoconvulsive response alter serum PRL (19).
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