Nocturnal eating in restless legs syndrome

Abstract

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...

Parasomnias: An Updated Review

“…Interestingly, among RLS patients with nocturnal smoking, SRED was common (83%), and both phenomena often began simultaneously [94]. It has been debated whether SRED in RLS may be caused by dopaminergics because these agents are known to trigger daytime impulsive behaviors such as gambling [95][96][97][98][99]. However, through the preponderance of evidence, it is suggested that dopamine agents are not the cause of SRED.…”

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

“…13,15 It has been suggested that nocturnal eating in RLS patients may be caused by dopaminergic agents as these agents are known to trigger impulsive behaviors such as gambling. 6,7 Conversely, dopamine agents suppress feeding behavior in animal models. 32 This report, following up previous investigations, provides strong evidence that dopaminergic agents help treat, and are not the cause of NE.…”

“…5 Conversely it has been suggested SRED in RLS may be due to anti-RLS dopaminergic agents. 6,7 Most investigations of nocturnal eating (NE; eating after an arousal from sleep, prior to terminal awakening) have focused bRIEF SUMMARY Current knowledge/Study Rationale: This study compared the prevalence of NE and SRED in RLS to INS, a disorder with similar sleep disruption to determine whether nocturnal feeding behavior in RLS is merely "killing time." We then prospectively determined therapeutic response with dopaminergic and sedative medications.…”

Sleep-Related Eating Disorder in Two Patients with Early-Onset Parkinson’s Disease

“…Until now, the literature has not clearly discriminated BED from SRED in PD patients. Additionally, previous reports of nocturnal eating in PD patients with drug-related compulsive eating may have included unrecognized cases of SRED [16,19] .…”

“…However, this study did not enroll PD patients, and used small pramipexole doses (up to 0.36 mg/day) during a short (2 weeks) treatment period. Besides, a case control study comparing RLS and nocturnal eating showed that patients who received dopaminergic therapy for RLS presented a tendency to have a higher risk of developing SRED [10,19] .…”