Abstract
The objectives of this study were: (1) to identify subjects with hyperprolactinemia in a clinical sample of patients; (2) to compare the neurologic, psychiatric, and sleep conditions found in patients subgrouped by excessive daytime sleepiness (EDS) and hyperprolactinemia; and (3) to identify patients with hyperprolactinemia and EDS not supported by the presence of any other neurologic, psychiatric, or sleep disorder, or substance/medication use. A retrospective chart review of inpatients was carried out in order to identify all patients in whom the prolactin (PRL) serum levels were determined. A total of 130 subjects were retrieved: 55 had increased levels of PRL, while the remaining 75 participants had normal PRL levels. EDS was reported by 32 (58.2%) participants with increased PRL and 34 (45.3%) with normal PRL. Obstructive sleep apnea or other sleep or neurologic/psychiatric conditions could explain EDS in all participants with normal PRL. Among subjects with increased PRL, eight had no other neurologic/psychiatric or sleep disorder (or drug) potentially causing EDS; these participants, at polysomnography, had time in bed, sleep period time, and total sleep time longer than those with EDS associated to another condition. These findings can be considered as a preliminary indication of a role of hyperprolactinemia in EDS and represent a basis for future controlled studies able to test this hypothesis in a reliable, objective, and methodologically more appropriate way.
Highlights
A total of 249 files were selected in this way, but we excluded from this sample all subjects with a significant cognitive impairment that would have interfered with their capacity to reliably report their subjective excessive daytime sleepiness (EDS), as reflected by a score of
For each patient included in this analysis, the following data were routinely collected: sex, age, neurologic and psychiatric diagnosis, presence and type of sleep disorder, MMSE, serum PRL level, use of any drug acting at the central nervous system (CNS) level, complaint of subjective EDS and, whenever available, Epworth sleepiness scale (ESS) score, hypocretin dosage in the cerebrospinal fluid (CSF), polysomnographically measured total sleep time, index of periodic leg movements during sleep (PLMS), apnea/hypopnea index (AHI), mean sleep latency and number of sleep-onset REM periods at the multiple sleep latency test (MSLT), brain imaging, and presence/absence of narcolepsy-like symptoms
Among the narcolepsy-like symptoms collected from all subjects, we found a marginally statistically significant difference for the frequency of sleep attack, which was reported by 10 hPRL participants and five nPRL patients, while no statistically significant difference was found for the very few reports of cataplexy, hypnagogic/hypnopompic hallucinations, sleep paralysis, or automatic behaviors
Summary
Experimental Rationale for a Possible Role of Prolactin in Sleep Regulation. Prolactin (PRL) is a peptide hormone mainly synthesized and secreted by the anterior pituitary gland; it can be produced by the mammary gland, deciduous, prostate, skin, and possibly brain. The PRL receptor has been detected in different regions of the brain, such as the cerebral cortex, the olfactory bulb, the hypothalamus, the hippocampus, and the amygdala [1]. New roles have been described for PRL, such as in neurogenesis, neurodevelopment and neuronal plasticity, sleep, learning, memory, and neuroprotection [2]. PRL is involved in glial responses to cortical lesions caused by hypoxia; the number of oligodendrocytes of the corpus callosum seems to increase in relation to the levels of PRL [2]
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