## 1 Introduction  
Chronic pain and sleep are linked by a complex bidirectional interplay. Although the underlying neuronal networks and mechanisms are not fully elucidated, a major role seems to be played by the periaqueductal gray, which modulates nociception and sleep stages [1], and by proinflammatory cytokines (e.g., interleukin-6) found at higher concentrations in some pain conditions but also during periods of sleep deprivation [2, 3]. Sleep disorders such as insomnia contribute to the increase in perceived pain by preventing adequate psychological and physiological rest [4, 5]. On the other hand, pain itself can intrude during sleep causing microawals and can disturb sleep initiation and maintenance [4, 5]. Consequently, there is evidence that disturbed nocturnal sleep increases the risk of pain occurrence and worsens the prognosis in cases of chronic pain by modulating circadian fluctuations of pain [4, 6]. Moreover, it should be considered that chronic pain and disturbed nocturnal sleep contribute to obesity, type 2 diabetes, and depression [4; 7]. Orofacial pain caused by temporomandibular disorders (TMDs) [8] is the second most common musculoskeletal disease, causing pain and disability [9; 10]. TMD is an umbrella term indicating disorders affecting the temporomandibular joint (TMJ), the masticatory muscles, or both [8]. There is evidence that poor sleep quality is a risk factor for orofacial pain [10], and it is also commonly reported by patients with chronic orofacial pain [11; 12; 13]. A higher prevalence of sleep disorders and a relationship between several sleep disorders (insomnia, restless legs syndrome, and obstructive sleep apnea syndrome) and a decrease in pain thresholds were found in a population of TMD patients [14; 15; 16; 17; 18; 19]. Therefore, disturbed nocturnal sleep can contribute to the central sensitization of pain, a common phenomenon in chronic TMD patients [14]. Central disorders of hyperosmnolence represent a group of disorders characterized by excessive daytime sleepiness (EDS) not linked to the impairment of nocturnal sleep or misaligned circadian rhythms. The main disorder of this group is narcolepsy type 1 (NT1) with a prevalence of 0.02% [20; 21]. Narcolepsy is a chronic sleep disorder predominantly characterized by EDS with repetitive sleep attacks, both during inactivity and at work, at school, and even while driving, making this condition socially disabling. These sleep episodes are irresistible, short lasting, caused by a deficiency in hypothalamic hypocretin-1/orexin-1 (<110 pg/mL) [22; 23], often associated with dreaming, for a premature occurrence of rapid eye movement (REM) sleep [24; 25]. The pathognonomic symptom of NT1 is cataplexy, characterized by a sudden and involuntary loss of muscle tone while awake [26]. Positive strong emotions generally trigger a cataplectic attack, which can last a few seconds to a few minutes with a variable frequency [26]. Sleep paralysis and hypnagogic hallucinations are described but are not specific to NT1 [27]. Non-sleep symptoms have also been described, such as obesity, mood disorders, and headache [28; 29; 30; 31]. Despite the little data available on the frequency of pain in NT1 patients, the results encourage further investigation into this correlation because one sample reported not only higher pain occurrence, but also a worse life quality compared to the controls [32]. Additionally, a second sample reported no differences in pain perception with the matched controls [33]. In addition, recent studies have been reported in which hypocretin-1 could have a role in central nociceptive processing [34; 35; 36]. An objective assessment of nocturnal sleep and of daytime sleep propensity is required to confirm the clinical diagnosis of NT1 [37]. Laboratory polysomnography (L-PSG) is the reference tool for studying sleep and its influence on physiologic functions.