REM sleep behavior disorder in sleep-disordered patients with versus without Parkinson's disease: is there a need for polysomnography?
Introduction
Polygraphic sleep recordings of patients with Parkinson's syndrome found decreased sleep efficiency, increased wake after sleep onset, and sleep fragmentation [1], [2], [3], [4], [5]. Sleep disorders in Parkinson's disease (PD) are either based on the neurodegenerative process or they may result from nocturnal bradykinesia and rigidity, medication, psychiatric disorders, circadian rhythm disturbance, or rapid eye movement sleep behavior disorder (RBD) [6], [7], [8], [9], [10], [11].
RBD involves a complex behavior and the absence of skeletal muscle atonia during rapid eye movement (REM) sleep. Patients often recall violent dreams and sometimes injure themselves or their bedpartner during episodes of RBD. The minimal diagnostic criteria for RBD, as defined in the International Classification of Sleep Disorders (ICSD), include movements of limbs or body associated with dream mentation and at least one of the following: potentially harmful sleep behavior, dreams that appear to be “acted out”, or sleep behavior that disrupts sleep continuity [12]. The underlying cause of RBD is still unknown. Experimental lesions of the dorsolateral pontine tegmentum in animals cause the absence of physiological REM muscle atonia [13]. Findings from experimental lesion studies in animals and MRI studies suggest that degenerated or lesioned brainstem nuclei are the anatomic bases for RBD [14], [15]. Recent studies have shown that a considerable number of patients with RBD eventually developed PD (38%) [16]. RBD is frequent in multiple system atrophy (MSA) (90%) [11], [17]. The striatal presynaptic dopamine transporters have been demonstrated recently to be reduced in idiopathic RBD as in PD [18]. Fifteen percent of patients with PD and their caregivers report the clinical symptoms of RBD [10]. Another study, which does not include polysomnograms (PSGs), have shown that clinical symptoms of RBD preceded the onset of MSA by more than 1 year in 44% of the MSA patients [11]. We evaluated the sensitivity and specificity of specialized clinical interviews for diagnosis of RBD in a population of sleep-disordered patients with PD versus a population of patients without PD.
Section snippets
Study population
We reviewed all PSGs performed in our sleep laboratory within the last 3 years. This yielded 19 patients with PD and 273 patients without PD or any other neurodegenerative disease (for diagnoses of these patients, see Section 3). We excluded from the study patients with impaired cognitive function or mental deficits, and patients taking medication known to induce sleep alteration, but tolerated dopaminergic medication in PD patients. Every patient had at least two nights of PSGs, and the time
Study population
All patients who underwent the sleep interview and were advised to have a PSG, subsequently accepted and had a PSG. Age and sex distributions of the patients are summarized in Table 1. Patients with PD were significantly older than non-PD patients (67.7 versus 55 years, p=0.001). PD and non-PD patients were similar in their sex distribution.
The clinical and PSG diagnoses of the patients without PD included, mainly, obstructive and central sleep apnea syndrome (SAS), restless legs syndrome
Discussion
The sensitivity of specialized interviews for diagnosing PSG-confirmed RBD was excellent (100%) in non-PD patients, but was poor (33%) in PD patients. The specificity was good in both groups. This might be due to the fact that patients with PD often complain about sleep disturbances. Akinesia upon awakening or difficulties in maintaining sleep occurs frequently. A considerable number of drugs such as levodopa and dopamine agonists administered in PD may cause sleep disturbance. Violent
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