Narcolepsy with Cataplexy Associated with Nocturnal Compulsive Behaviors: A Case-Control Study

Palaia, Vincenzo; Poli, Francesca; Pizza, Fabio; Antelmi, Elena; Franceschini, Christian; Moghadam, Keivan Kaveh; Provini, F.; Pagotto, Uberto; Montagna, Pasquale; Schenck, Carlos H.; Mignot, Emmanuel; Plazzi, Giuseppe

doi:10.5665/sleep.1280

Cited by 45 publications

(33 citation statements)

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“…We assume that smoking habits are similar in Slovakia. The proportion of smokers in our NC population is about 50% higher than in an Italian study where, however, was the same percentage of smokers in the control group as is reported for the Czech population, so also the Italian study has shown higher frequency of smoking among patients with NC, the authors explain this higher rate with the stimulatory action of nicotine (Palaia et al, 2011). Higher proportion of current smokers in NC than in controls (37.2% vs. 21.7%) was also reported in recent large French study (Barateau et al, 2016).…”

Section: Discussioncontrasting

confidence: 37%

Smoking Prevalence and Its Clinical Correlations in Patients with Narcolepsy-cataplexy

et al. 2016

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Narcolepsy-cataplexy (NC) is a chronic neurological disease with suggested autoimmune etiopathogenesis. Nicotine stimulates central nervous system and smoking increases the risk of autoimmune diseases. Assessment of smoking habits and its correlation to clinical parameters among 87 adult NC patients (38 male, 49 female) included night polysomnography and multiple sleep latency test. In our sample, 43.7% NC patients were regular smokers, and 19.5% former smokers compared to 22.2%, and 12.6%, respectively, in the general population. Patients started to smoke in the mean age of 20.0 (SD ±6.0) years. 72.2% of NC smokers started to smoke before the onset of NC and the mean of the delay between smoking onset and NC onset was 9.1 (±5. Report / Vol. 117 (2016) No. 2-3, p. 81-89 a direct correlation between smoking duration and the number of awakenings, duration of N1 sleep, REM sleep latency, and apnoea/hypopnoea index (AHI), and, on the contrary, indirect correlation between smoking duration and N3 sleep duration, showing that smoking duration consistently correlates with sleep macrostructure. Smoking is highly prevalent in NC and has relationship with clinical features of NC. 82) Prague Medical

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Section: Discussioncontrasting

confidence: 37%

Smoking Prevalence and Its Clinical Correlations in Patients with Narcolepsy-cataplexy

et al. 2016

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“…[16][17][18][19][20][21] In fact, even among SRED cases where RLS frequency was not addressed, there is a peculiar incidence of conditions frequently comorbid with RLS, such as Parkinson disease 22 and narcolepsy. 23 Like nondysfunctional nocturnal eating (a non-pathological variation of SRED), RLS may be mild or only minimally interfering with sleep onset. Further, RLS sensations are often difficult for patients to define, and current symptomatic criteria are not easily translated between languages.…”

Section: Epidemiology Of Ne/sred and Rlsmentioning

confidence: 99%

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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“…Although the obesity has been clearly linked to low cerebrospinal fluid (CSF) HCRT1 levels (Heier et al, 2011; Nishino et al, 2001; Poli et al, 2009) and abdominal fat deposits (Kok et al, 2003; Poli et al, 2009), the cause of the BMI increase in narcolepsy has been challenging to parse. Binge eating, irresistible food cravings, and sleep-related eating disorder have been reported in approximately a quarter of narcoleptic patients (Fortuyn et al, 2008; Palaia et al, 2011), but this population also has reduced daily caloric intake compared to healthy controls (Chabas et al, 2007; Lammers et al, 1996). Like other overweight people, patients with narcolepsy who are obese tend to have lower resting metabolic rates (Chabas et al, 2007).…”

Section: Overview Of Narcolepsymentioning

confidence: 99%

Challenges in the development of therapeutics for narcolepsy

Black

Yamanaka

Kilduff

2017

Progress in Neurobiology

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Narcolepsy is a neurological disorder that afflicts 1 in 2000 individuals and is characterized by excessive daytime sleepiness and cataplexy—a sudden loss of muscle tone triggered by positive emotions. Features of narcolepsy include dysregulation of arousal state boundaries as well as autonomic and metabolic disturbances. Disruption of neurotransmission through the hypocretin/orexin (Hcrt) system, usually by degeneration of the HCRT-producing neurons in the posterior hypothalamus, results in narcolepsy. The cause of Hcrt neurodegeneration is unknown but thought to be related to autoimmune processes. Current treatments for narcolepsy are symptomatic, including wake-promoting therapeutics that increase presynaptic dopamine release and anticataplectic agents that activate monoaminergic neurotransmission. Sodium oxybate is the only medication approved by the US Food and Drug Administration that alleviates both sleep/wake disturbances and cataplexy. Development of therapeutics for narcolepsy has been challenged by historical misunderstanding of the disease, its many disparate symptoms and, until recently, its unknown etiology. Animal models have been essential to elucidating the neuropathology underlying narcolepsy. These models have also aided understanding the neurobiology of the Hcrt system, mechanisms of cataplexy, and the pharmacology of narcolepsy medications. Transgenic rodent models will be critical in the development of novel therapeutics for the treatment of narcolepsy, particularly efforts directed to overcome challenges in the development of hypocretin replacement therapy.

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Narcolepsy with Cataplexy Associated with Nocturnal Compulsive Behaviors: A Case-Control Study

Cited by 45 publications

References 50 publications

Smoking Prevalence and Its Clinical Correlations in Patients with Narcolepsy-cataplexy

Smoking Prevalence and Its Clinical Correlations in Patients with Narcolepsy-cataplexy

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

Challenges in the development of therapeutics for narcolepsy

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