Is there a relation between the physiopathological mechanism of prostate cancer and REM sleep behavior disorder?

Abstract

Rapid eye movement (REM) sleep behavior disorder (RBD) is a clinical picture with the intermittent loss of REM sleep without atonia but with vivid dreams. There are numerous diseases accompanying RBD that are of vascular, neoplastic, toxic, metabolic, infectious, degenerative, traumatic, or congenital origin. Patient #1: A 60-year-oldmanwas beating and kicking his wife during sleep for the last 5-6months. Hewas in embarrassment due to the situation. Based on the subjects self report, his complaints over sleep began 10 years ago with sleeplessness, insomnia at night and increasing drowsiness throughout the day. His neurological examination and blood, urine andMRI tests were found to be normal. VPSG revealed REM episodes without atony. Patient #2: A 76-year-old man underwent a radical prostatectomy because of prostatic adenocarcinoma in 2003. Four years after the operation he once started to dance and then became abusive during his sleep. After 15 days during night time he danced and sang songs again and tried to move out of the bedroom. His wife stopped him. The two episodes happened in the very early morning. His MRI and VPSG were normal. This study represents the first case of RBD accompanied by Prostate cancer (PCa). The fact that PCa developed 1 year after RBD in patient #1 and four years before in patient #2 is of clinical significance. It has been well established that cases of Limbic Encephalitis (LE) are associated with paraneoplastic antibody. The RBD-associated cases were voltage-gated K tract antibody positive. Pathologies of limbic structures were reported in cases with Parkinson's disease, multi-system atrophy and Lewy Body dementia. The most striking fact was that the limbic system might play a role in the occurrence of unpleasant and dreadful dreams. The possible contribution of voltage-gated K channel activity in the metastatic process was emphasized in a PCa model in rats. This view is also affirmed by studies concerning the relationship between human PCa and K channels and the fact that K channel blockers inhibit PCa. Although our hypotheses can be explained by voltagegated K channel activity, there are still a number of ambiguities. Then again, these cases make us ask unexpected questions during the process of RBD development.