Association of restless legs syndrome with nocturnal eating: A case‐control study

Provini, Federica; Antelmi, Elena; Vignatelli, Luca; Zaniboni, Alberto; Naldi, Giulia; Calandra-Buonaura, Giovanna; Vetrugno, Roberto; Plazzi, Giuseppe; Montagna, Pasquale

doi:10.1002/mds.22460

Cited by 82 publications

(71 citation statements)

References 17 publications

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“…Thus, the actual prevalence of the RLS clinical spectrum is likely larger than current estimates. These findings bear special significance for the obesity pandemic since according to this study and others, 4 the majority of RLS patients have NE, and more than a third have SRED. …”

Section: Epidemiology Of Ne/sred and Rlssupporting

confidence: 73%

“…In fact, subjects whose nocturnal eating symptoms were under control were more likely to be on these agents than subjects who continued to have nocturnal eating. 4 Further, a double-blind treatment trial of pramipexole for SRED demonstrated improved sleep and reduced nighttime activity, although, admittedly, nocturnal eating ingestions were not reduced in this small study. 34 In the series published here, we monitored therapy outcome in 44 RLS patients previously unexposed to dopaminergics with and without NE.…”

Section: Ne/sred In Rls Is Relieved By and Not Caused By Dopaminergicmentioning

confidence: 58%

“…Once food was ingested, the feeling abated and sleep was able to be reinitiated. 1,4,13 A more recent case noted a 74-year-old woman who originally presented 20 years prior with uncontrollable RLS and SRED. Both the nocturnal eating and RLS were well controlled with various combinations of opioids and dopaminergics.…”

Section: Similarities In Clinical Coursementioning

confidence: 99%

“…24,37 Only one study has looked into the incidence of both conditions among RLS patients and noted that compared to SRED (33%), NES was rare (3%). 4 However, this study utilized a now outdated definition of NES, excluding many NES patients under the revised criteria, particularly those whose predominant feature would be nocturnal eating. 38 One notable study 39 investigated NES patients with PSG and demonstrated an increased number of awakenings and reduced sleep duration, suggesting an underlying sleep disrupting process.…”

Section: Is Rls a Link Between Sred And The Night Eating Syndrome (Nes)?mentioning

confidence: 99%

“…This community-based case-control study found that 33 of 100 RLS patients met criteria for SRED compared to only 1% of normal population controls. 4 The authors pondered whether SRED was related to underlying RLS brain pathology or whether it was merely "killing time" during prolonged nocturnal awakenings, as previously suggested. 5 Conversely it has been suggested SRED in RLS may be due to anti-RLS dopaminergic agents.…”

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confidence: 96%

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Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

Howell

Schenck

2012

Journal of Clinical Sleep Medicine

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upon SRED. However, we have noticed subtler non-dysfunctional forms of NE, commonly in the setting of RLS. Also, we have noted that many cases of zolpidem-induced SRED had been originally misdiagnosed as having psychophysiological insomnia (INS), a condition for which a benzodiazepine receptor agonist was prescribed, but later noted to have underlying motor restlessness as the cause of their sleep diffi culties.To establish whether NE is common in RLS and whether NE is a product of frequent nocturnal awakenings, we compared the frequency of NE as well as SRED among patients presenting with RLS and INS, a distinct condition of cognitive hypervigilance that manifests with frequent nocturnal awaken- Measurements and Results:Patients presenting with RLS (n = 88) or INS (n = 42) were queried for the presence of NE and SRED. RLS patients described nocturnal eating (61%) and SRED (36%) more frequently than INS patients (12% and 0%; both p < 0.0001). These fi ndings were not due to arousal frequency, as INS patients were more likely to have prolonged nightly awakenings (93%) than RLS patients (64%; p = 0.003). Among patients on sedative-hypnotics, amnestic SRED and sleepwalking were more common in the setting of RLS (80%) than INS (8%; p < 0.0001). Further, NE and SRED in RLS were not secondary to dopaminergic therapy, as RLS patients demonstrated a substantial drop (68% to 34%; p = 0.0026) in the frequency of NE after dopamine agents were initiated, and there were no cases of dopaminergic agents inducing novel NE or SRED. Conclusion: NE is common in RLS and not due to frequent nocturnal awakenings or dopaminergic agents. Amnestic SRED occurs predominantly in the setting of RLS mistreatment with sedating agents. In light of previous reports, these fi ndings suggest that nocturnal eating is a non-motor manifestation of RLS with several clinical implications discussed here. S C I E N T I F I C I N V E S T I g A T I O N SR estless legs syndrome, or Willis-Ekbom Syndrome (labeled RLS), is characterized by an underlying discomfort, primarily in the lower extremities that compels the affl icted to move. These symptoms are relieved, although only momentarily, with movement and may interfere with sleep initiation or maintenance. 1 RLS has been associated with non-motor phenomena. In particular, patients with RLS often describe other comorbidities such as mood and anxiety disorders, 2 as well as other nocturnal compulsions such as nocturnal smoking that interfere with sleep.3 Further, patients with these non-motor manifestations of RLS have more severe motor restlessness as measured by the International RLS Rating Scale. Recently, an investigation demonstrated a high frequency of dysfunctional nocturnal eating (SRED) in patients with RLS. This community-based case-control study found that 33 of 100 RLS patients met criteria for SRED compared to only 1% of normal population controls. 4 The authors pondered whether SRED was related to underlying RLS brain pathology or whether it was merely "killing time" during prolonged nocturn...

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Section: Epidemiology Of Ne/sred and Rlssupporting

confidence: 73%

Section: Ne/sred In Rls Is Relieved By and Not Caused By Dopaminergicmentioning

confidence: 58%

Section: Similarities In Clinical Coursementioning

confidence: 99%

Section: Is Rls a Link Between Sred And The Night Eating Syndrome (Nes)?mentioning

confidence: 99%

mentioning

confidence: 96%

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Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

Howell

Schenck

2012

Journal of Clinical Sleep Medicine

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Reduced Interoception Abilities in Patients with Restless Legs Syndrome

Sandri

Mingolla

Camonita

et al. 2023

Movement Disord Clin Pract

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Background Restless legs syndrome (RLS) is a complex sensorimotor disorder occurring with a typical circadian fashion. Association with additional features, like alexithymia and nocturnal compulsive behaviors further complicates the framework. Objectives To assess interoception in RLS. Methods A total of 25 RLS patients and 28 controls underwent the heartbeat tracking task (interoceptive accuracy [IAC]). RLS symptoms’ frequency, disturbance and duration, nocturnal behaviors, interoceptive awareness (IAW), alexithymia, depressive and anxiety symptoms were also collected. Results RLS patients showed significant lower IAC (P = 0.0003) and IAW (P = 0.012), and reported more nocturnal eating behaviors (P < 0.001). IAC positively correlated with IAW (R = 0.32), and negatively correlated with age (R = −0.58). Nocturnal eating behavior negatively correlated with IAC (R = −0.44) and IAW (R = −0.50). Conclusions RLS patients presented reduced interoceptive abilities correlating with higher nocturnal eating behaviors. Future studies are needed to explore the role of interoception in RLS pathophysiology, also in relation to other sensorimotor aspects.

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Nocturnal eating in restless legs syndrome

Nirenberg

Waters

2010

Movement Disorders

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have to be congratulated for their hypothesis on PD pathogenesis. They suggest that the sequence of the brain changes in PD follows specific and repeatable patterns in all cases, as well as that a prion-like process underlies neurodegeneration. These ideas could explain several features of PD, such as the high prevalence of olfactory, autonomic, or sleep abnormalities. However, any pathogenic hypothesis should also explain:1. The variable rate of progression. 2. The heterogeneous presentation. 3. The persistent asymmetry of motor symptoms and signs. 4. The progressive worsening and somatotopic spreading of the same symptom, meaning that neurons displaying similar gene expression profile, intracellular enzymatic machinery, and signaling pathways are differentially affected by the process. 5. The case of young-onset cases: whereas they must have severe disease to present so early, disability progresses slowly.None of them are covered in the article. 1 Certainly, PD is a multisystem disorder. The view of PD resulting from the sequential pathological involvement of brain nuclei is based on the work by Braak, 2 which has received strong criticisms. 3 It relies on the presence of a-synuclein inclusions, Lewy bodies, and Lewy neurites in the brain of subjects' dead of different causes. However, clinical information was extremely limited, some of the subjects included did not develop neither motor nor cognitive symptoms during life, staging was independent of disease duration, and neuronal loss was not recorded. Despite these limitations, Braak's findings have been interpreted as an open door to presymptomatic diagnosis according to the presence of abnormalities resultant from this pattern of involvement (i.e., hyposmia, REM behavior disorder, constipation,. . .). Compelling evidence suggests that a-synuclein inclusions not closely correspond to the severity of neuronal loss, neuronal dysfunction, or clinical expression. There is a gap between pathology and clinical picture. Thus, even admitting that pathology could follow a predefined order, the view of PD as a disease that starts with hyposmia, sleep disturbances, and constipation, follows with motor symptoms and ends with dementia, is not always true. Thus, the predictive value of premotor symptoms is relative. The prevalence of a-synuclein inclusions in the brain of old individuals dead without any neurological dysfunction is around 30%, whereas the prevalence of PD in this group of age is 2%.Further arguments come from the development of nondopaminergic symptoms. A recent study showed that age and severity of PD but not duration of illness, act as independent risk factors for developing dementia. 4 Furthermore, the brain of the majority of parkinsonian patients displaying dementia presents abundant changes characteristic of Alzheimer's disease. The relationship between dementia, aging, PD, and associated pathologies needs clarification. Additionally, rate of progression is more determinant of PD outcome than its multisystemic nature. It is likely linked to compe...

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Association of restless legs syndrome with nocturnal eating: A case‐control study

Cited by 82 publications

References 17 publications

Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

Reduced Interoception Abilities in Patients with Restless Legs Syndrome

Nocturnal eating in restless legs syndrome

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