Medline ® Abstracts for References 109-112
of 'Rapid eye movement sleep behavior disorder'
109
TI
Hallucinations, REM sleep, and Parkinson's disease: a medical hypothesis.
AU
Arnulf I, Bonnet AM, Damier P, Bejjani BP, Seilhean D, Derenne JP, Agid Y
SO
Neurology. 2000;55(2):281.
BACKGROUND:
Patients with PD can have disabling visual hallucinations associated with dopaminergic therapy. Sleep disorders, including vivid dreams and REM sleep with motor behaviors (RBD), are frequent in these patients.
METHODS:
The association of hallucinations and REM sleep both at night and during the day was examined in 10 consecutive nondemented patients with long-standing levodopa-responsive PD and hallucinations. Seven patients presented with paranoia and paranoid delusions. Overnight sleep recordings and standard multiple daytime sleep latency test were performed. The results were compared to those of 10 similar patients with PD not experiencing hallucinations.
RESULTS:
RBD was detected in all 10 patients with hallucinations and in six without. Although nighttime sleep conditions were similar in both groups, hallucinators tended to be sleepier during the day. Delusions following nighttime REM period and daytime REM onsets were observed in three and eight of the hallucinators, and zero and two of the others. Daytime hallucinations, coincident with REM sleep intrusions during periods of wakefulness, were reported only by hallucinators. Postmortem examination of the brain of one patient showed numerous Lewy bodies in neurons of the subcoeruleus nucleus, a region that is involved in REM sleep control.
CONCLUSION:
The visual hallucinations that coincide with daytime episodes of REM sleep in patients who also experience post-REM delusions at night may be dream imagery. Psychosis in patients with PD may therefore reflect a narcolepsy-like REM sleep disorder.
AD
Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U 289. isabelle.arnulf@psl.ap.hop.paris.fr
PMID
110
TI
Prevalence and clinical importance of sleep apnea in the first night after cerebral infarction.
AU
Iranzo A, Santamaría J, Berenguer J, Sánchez M, Chamorro A
SO
Neurology. 2002;58(6):911.
OBJECTIVE:
To determine the prevalence of sleep apnea (SA) during the first night after hemispheric ischemic stroke and its influence on clinical presentation, course, and functional outcome at 6 months.
METHODS:
The first night after cerebral infarction onset, 50 patients underwent polysomnography (PSG) followed by oximetry during the next 24 hours. Neurologic severity and early worsening were assessed by the Scandinavian Stroke Scale and outcome by the Barthel Index. Patients were evaluated on admission, on the third day, at discharge, and at 1, 3, and 6 months.
RESULTS:
There were 30 males and 20 females with a mean age of 66.8 +/- 9.5 years. Latency between stroke onset and PSG was 11.6 +/- 5.3 hours. Thirty-one (62%) subjects had SA (apnea-hypopnea index [AHI]>or = 10). Of these, 23 (46%) had an AHI>or =20 and 21 (42%) an AHI>or =25. Sleep-related stroke onset occurred in 24 (48%) patients and was predicted only by an AHI>or =25 on logistic regression analysis. SA was related to early neurologic worsening and oxyhemoglobin desaturations but not to sleep history before stroke onset, infarct topography and size, neurologic severity, or functional outcome. Early neurologic worsening was found in 15 (30%) patients, and logistic regression analysis identified SA and serum glucose as its independent predictors.
CONCLUSIONS:
SA is frequent during the first night after cerebral infarction (62%) and is associated with early neurologic worsening but not with functional outcome at 6 months. Cerebral infarction onset during sleep is associated with the presence of moderate to severe SA (AHI>or = 25).
AD
Services of Neurology, Hospital Clínic i Provincial de Barcelona, Barcelona, Spain. airanzo@clinic.ub.es
PMID
111
TI
Effects of deep brain stimulation of the subthalamic nucleus on sleep architecture in parkinsonian patients.
AU
Cicolin A, Lopiano L, Zibetti M, Torre E, Tavella A, Guastamacchia G, Terreni A, Makrydakis G, Fattori E, Lanotte MM, Bergamasco B, Mutani R
SO
Sleep Med. 2004;5(2):207.
Patients affected by Parkinson's disease (PD) often complain of disturbed sleep resulting from nighttime motor disabilities such as nocturnal akinesia, tremor and rigidity, motor behaviour during REM sleep or periodic leg movements (PLM) during sleep. Sleep may also be affected by dopaminergic and anticholinergic drugs or coexisting depressive syndrome. Deep brain stimulation (DBS) of subthalamic nucleus (STN) effectively reduces PD motor disability. The aim of this study is to evaluate the sleep architecture modifications after STN DBS. We assessed five patients (two men and three women, mean age 63.8+/-3.3 years, with a mean history of PD of 13.8+/-4.9 years) who underwent STN DBS. The mean levodopa equivalent dosage (LED) was 1010+/-318 mg before surgery and 116+/-93 mg 3 months after surgery. Polysomnography (PSG) with audiovisual recordings was performed on two separate nights, the first assessment in the week before surgery and the second 3 months after surgery. Three months after surgery, PSG showed an increase in total sleep time, in the longest period of uninterrupted sleep, and in the percentage of stage 3-4 NREM sleep, while there was a reduction of wakefulness after sleep onset. PLM, apnea-hyopnea index and REM sleep behaviour disorder were unaffected by STN DBS. STN DBS seems to be an effective therapeutic option for the treatment of advanced Parkinson's disease because it improves the cardinal symptoms and also seems to improve sleep architecture.
AD
Sleep Medicine Center, Neurologic Clinic II, Department of Neurosciences, University of Torino, Torino, Italy. alessandro.cicolin@unito.it
PMID
112
TI
The Impact of Subthalamic Deep Brain Stimulation on Sleep-Wake Behavior: A Prospective Electrophysiological Study in 50 Parkinson Patients.
AU
Baumann-Vogel H, Imbach LL, SürücüO, Stieglitz L, Waldvogel D, Baumann CR, Werth E
SO
Sleep. 2017;40(5)
Study Objectives:
This prospective observational study was designed to systematically examine the effect of subthalamic deep brain stimulation (DBS) on subjective and objective sleep-wake parameters in Parkinson patients.
Methods:
In 50 consecutive Parkinson patients undergoing subthalamic DBS, we assessed motor symptoms, medication, the position of DBS electrodes within the subthalamic nucleus (STN), subjective sleep-wake parameters, 2-week actigraphy, video-polysomnography studies, and sleep electroencepahalogram frequency and dynamics analyses before and 6 months after surgery.
Results:
Subthalamic DBS improved not only motor symptoms and reduced daily intake of dopaminergic agents but also enhanced subjective sleep quality and reduced sleepiness (Epworth Sleepiness Scale: -2.1±3.8, p<.001). Actigraphy recordings revealed longer bedtimes (+1:06±0:51 hours, p<.001) without shifting of circadian timing. Upon polysomnography, we observed an increase in sleep efficiency (+5.2±17.6%, p = .005) and deep sleep (+11.2±32.2 min, p = .017) and increased accumulation of slow-wave activity over the night (+41.0±80.0%, p = .005). Rapid eye movement sleep features were refractory to subthalamic DBS, and the dynamics of sleep as assessed by state space analyses did not normalize. Increased sleep efficiency was associated with active electrode contact localization more distant from the ventral margin of the left subthalamic nucleus.
Conclusion:
Subthalamic DBS deepens and consolidates nocturnal sleep and improves daytime wakefulness in Parkinson patients, but several outcomes suggest that it does not normalize sleep. It remains elusive whether modulated activity in the STN directly contributes to changes in sleep-wake behavior, but dorsal positioning of electrodes within the STN is linked to improved sleep-wake outcomes.
AD
Department of Neurology, University Hospital Zurich, University of Zurich, Zürich, Switzerland.
PMID
