REM sleep behavior disorder in Parkinson's disease: A case from India confirmed with polysomnographic data
A 55-year-old male presented with the complaints of non-refreshing sleep, excessive drowsiness during the day but, without experiencing irresistible sleepiness. He also had a history of nocturnal symptoms for the past 2.5 years manifesting as somniloquy and abnormal sleep behavior. On a recent visit to his attending neurologist (DG), his wife complained of increasing frequency of abnormal activity during sleep after which he was referred to a sleep specialist (RG).\nAccording to his wife, he followed a regular sleep schedule (bedtime: 11:00 pm and wake-time: 5:00 am). His wife reported that he used to have episodes of sleep talking (4-5 times/night), each lasting 10-15 minutes on most of the nights. At times, he also appeared enacting his dreams. During night-time acts his movements used to be a combination of sitting up in bed, kicking, searching, and picking. He had occasionally struck his wife and also fallen out of bed during these episodes. He himself reported having violent dreams during the night in which he was fighting with somebody. Content of the dreams varied and he reported being engaged in searching activity after losing some belongings in dreams. On few occasions, he woke up during these dreams and found that he was acting on his dreams. He snored (Grade II) but apneas were never witnessed by the bed-partner. Any kind of behavioral abnormality was never noticed during daytime. His Epworth Sleepiness score was 6 (normal < 10).\nHe had developed resting tremor in the right hand 8 years earlier back subsequent to an alleged insecticide exposure. He was then diagnosed as PD by a neurologist. Presently, the patient was suffering from stage-II (Hoehn and Yahr Staging). Since then he had been on treatment with a combination of drugs that included carbidopa/levodopa 10/100 mg bid, amantadine 100 mg bid and pramipexole 0.25 mg bid. He responded well to these drugs and symptoms of PD improved. It must be noted here that he changed the dose of levodopa/carbidopa on his own in spite of counseling and efforts by doctor and family members. In addition, many a times he had presented with dyskinesia. Hence, the dose of levodopa was kept low, but it is difficult to comment whether he was taking the prescribed doses or higher doses.\nThere was no history to suggest childhood parasomnias, restless leg syndrome, sleep-terrors, narcolepsy, closed head injury, seizures, alcohol use, consumption or therapy with antidepressants. Also, there was no history of PD or RBD in the family members.\nPhysical examination revealed that he weighed 65 kgs, was 165 cms tall (BMI = 23.9). He had Mallampatti grade III airway with neck circumference of 38 cms. Neurological examination was unremarkable except for postural tremors in his hands. MRI scan of brain was non-diagnostic. Diagnostic polysomnography was performed (see below) confirming the diagnosis of RBD after which he was treated with clonazepam 1.0 mg at bedtime. One week later, his wife reported a significant reduction in frequency of these episodes. The dose was escalated to 1.5 mg for optimal suppression of the behavior.\nStandard attended 17-channel polysomnography with video monitoring using Cadwell III Sleep Easy acquisition system (Cadwell Laboratories, Inc., Kennewick, WA.) was performed. Electrophysiologic sleep parameters included frontal, central, and occipital electroencephalogram, right and left electrooculogram, and submentalis electromyogram. Anterior tibialis electromyogram was recorded to assess limb movement activity. Airflow was detected by thermistors and respiratory effort was determined by measurement of chest and abdomen motion with piezoelectric sensors. The arterial oxygen saturation was measured by the Cadwell oximeter with a 4-beat averaging mode. Raw data was manually scored in 30-second epochs for sleep stages using standard criteria.[]\nResults of sleep measurements are shown in the . The hypnogram [] showed poor sleep continuity but total sleep time and REM duration that were adequate for evaluation. REM latency was longer than usual (170 minutes compared to normal approximately 90 minutes) but the amount of REM sleep was within normal limits (22% total sleep time; normal approximately 20-25%). Periodic limb movement index (PLMS) was mildly increased (12/hr; normal approximately 5/hr). Respiratory parameters were normal. The AHI measured 1/hr (normal < 5/hr) and there was no hypoxemia. Video monitoring depicted periods of frequent movements of the arms and legs associated with vocalizations and sitting up in bed developing strictly out of REM sleep []. In addition, excessive phasic activity was noted in the submentalis and anterior tibialis recordings with movement artifacts during REM sleep [].