The link between Parkinson's disease (PD) and certain primary sleep disorders has yet to be clarified. We performed a systematic review of case-control polysomnography studies to evaluate the relationship between PD and sleep disorders. A PubMed literature search and bibliography review yielded 15 case-control polysomnography studies in patients with PD. Studies differed by recruitment methods, duration of polysomnography monitoring, and sleep parameters measured. Subjective sleepiness was greater in patients than controls (50%-66% vs 2.9%-12%) despite lack of objective increase in daytime sleepiness by mean sleep latency testing. The 4 case-control polysomnography studies investigating rapid eye movement behavior disorder support a higher prevalence in PD (0%-47% vs 0%-1.8% in controls), although differences in diagnostic criteria hamper interpretation. The preponderance of evidence did not support an increased incidence of obstructive sleep apnea (27%-60% vs 13%-65%) or periodic leg movements of sleep in patients compared to controls. Adequately powered, prospective studies with uniform methodology and healthy controls are needed to further address the association and pathophysiological significance between PD and sleep problems.

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Restless legs syndrome (RLS) and Parkinson's disease (PD) are both common neurological disorders. There has been much debate over whether an etiological link between these two diseases exists and whether they share a common pathophysiology. Evidence pointing towards a link includes response to dopaminergic agents in PD and RLS, suggestive of underlying dopamine dysfunction in both conditions. The extrastriatal dopaminergic system, in particular altered spinal dopaminergic modulation, may be variably involved in PD patients with RLS symptoms. In addition, there is now evidence that the nigrostriatal system, primarily involved in PD, is also affected in RLS. Furthermore, an association of RLS with the parkin mutation has been suggested. The prevalence of RLS has also been reported to be increased in other disorders of dopamine regulation. However, clinical association studies and functional imaging have produced mixed findings. Conflicting accounts of emergence of RLS and improvement in RLS symptoms after deep brain stimulation (DBS) also contribute to the uncertainty surrounding the issue. Among the strongest arguments against a common pathophysiology is the role of iron in RLS and PD. While elevated iron levels in the substantia nigra contribute to oxidative stress in PD, RLS is a disorder of relative iron deficiency, with symptoms responding to replacement therapy. Recent ultrasonography studies have suggested that, despite overlapping clinical features, the mechanisms underlying idiopathic RLS and RLS associated with PD may differ. In this review, we provide a concise summary of the clinical, imaging and genetic evidence exploring the link between RLS and PD.

Multiple system atrophy (MSA) is a rare adult-onset synucleinopathy associated with dysautonomia and the variable presence of poorly levodopa-responsive parkinsonism and/or cerebellar ataxia. Other clinical symptoms that can be associated with MSA include hyperreflexia, stridor, sleep apnea, and rapid eye movement sleep behavior disorder (RBD). Mean survival from time of diagnosis ranges between 6 to 10 years, and definitive diagnosis is made on autopsy with demonstration of oligodendroglial cytoplasmic inclusions consisting of fibrillar α-synuclein. Magnetic resonance imaging (MRI) may be positive for cruciform T2 hyperintensity within the pons (the "hot cross bun sign"), volume loss in the pons and cerebellum, and T2 signal loss in the dorsolateral putamen with hyperintense rim on fluid attenuated inversion recovery (FLAIR) sequencing. Although most cases are sporadic, genetic polymorphisms have been identified both in familial and sporadic cases of MSA, and influence observed phenotypes. Treatment is symptomatic, with both pharmacological and nonpharmacological strategies. There are currently no consensus guidelines on management. Current and future research is aimed at identifying biomarkers and developing disease-modifying therapies.