The Increasing Prevalence of REM Sleep Behavior Disorder with Parkinson's Disease Progression: A Polysomnography-Supported Study.

Objectives: Rapid eye movement (REM) sleep behavior disorder (RBD) is proposed as an early diagnostic marker in Parkinson's disease (PD). We investigated the frequency of RBD during the progression of PD in the advanced stages and identified potential risk factors for developing RBD earlier or later. Patients and Methods: We performed a retrospective analysis and determined the frequency of RBD in all PD in-patients (Hoehn and Yahr stages ≥3) with motor fluctuations who had undergone video-polysomnography (vPSG) for a sleep complaint or daytime sleepiness. To correct for selection bias, we analyzed the prevalence of RBD in PD patients from the DeNoPa cohort. PD patients with RBD were compared with PD without RBD. To identify potential risk factors, we performed multiple regression modeling. Results: A total of 504 PD patients had vPSG. 37 were excluded due to missing REM or artifacts during REM. RBD was present in 406/467 (86.9%) PD patients. PD + RBD patients were older than PDnonRBD (69 ± 7.7 vs. 64 ± 9.2 years, P < 0.01), were more likely to have postural instability [234 (59.1%) vs. 19 (33.9%), P < 0.01], and were treated more often with antidepressants (other than SSRIs) [141 (34.7%) vs. 7 (13%), P < 0.01]. Multiple regression modeling identified predictors of RBD with an AUC of 0.78. Conclusion: The prevalence of RBD in patients with advanced PD is high and increases with disease severity, motor deficits, postural instability, orthostatic symptoms, and age. This suggests RBD is a progression marker of PD in patients with sleep complaints.

Breach Rhythm May Be Suppressed as a Form of Todd's Paralysis.

This case report will provide further evidence for the fact that breach rhythm is not the effect of a bone abnormality only. We present the case of an 84-year-old woman, who had a craniotomy 14 month before admission to our emergency department with a focal inhibitory status epilepticus. Even after clinical recovery, electroencephalography revealed frequent subclinical seizure patterns. When seizure activity was suppressed by anticonvulsive medication with levetiracetam, breach rhythm appeared. Breach rhythm develops usually some months after craniotomy and therefore should have been established in our patient at the time of admission. Therefore, it is reasonable to assume that it was in some way suppressed by the seizure activity in our primary EEG recordings. The appearance of the breach rhythm after the complete suppression of seizure activity by antiepileptic drug treatment shows that breach rhythm is not purely the result of a skull defect but is related to the functional state of the brain tissue beneath.