In summary, BP and HR were lower during resting wakefulness but higher during nighttime sleep in patients with NT1. ( 8) observed a significantly increased systolic BP in 10 untreated patients with NT1 vs. ( 13) reported a higher percentage of non-dipping BP in NT1 compared to healthy controls (31 vs. In addition, it is generally believed that patients with NT1 are prone to have non-dipping blood pressure, defined as a nocturnal BP decrease < 10% of the daytime BP ( 8, 11, 12). controls during wakefulness, and the non-rapid eye movement (NREM) and rapid eye movement (REM) stages ( 8– 10). In contrast, other studies found a significant increase in HR in patients with NT1 vs. ( 7) demonstrated lower heart rate (HR), blood pressure (BP), and resting muscle sympathetic nerve activity using direct microneurographic recordings in patients with NT1 during wakefulness. Several studies on cardiovascular changes have focused on daytime wakefulness, different sleep stages, and wake-sleep transitions. Autonomic disorders in the cardiovascular system may increase the risk of cardiovascular events and reduce the quality of life of patients with NT1. Previous studies suggested that 52% of adults with NT1 and 37% of children with NT1 and other hypersomnia disorders had the symptoms of orthostatic intolerance, indicating impairment of cardiovascular autonomic regulation ( 5, 6). Here, we review the autonomic disorders and their possible mechanisms in patients with NT1 ( Figure 1).ġ.1. However, autonomic symptoms are easily ignored compared with the typical symptoms in NT1. Clinically, autonomic dysfunction often affects visceral organs, vascular smooth muscle, myocardium, and glands activities ( 5). Hypocretin neurons have widespread projections to different areas involved in regulating the sleep-wake cycle, energy metabolism, neuroendocrine, body temperature, and cardiovascular functions, which are associated with changes in the autonomic nervous system ( 4). Patients with NT1 often have low levels of hcrt-1 in the cerebrospinal fluid. Hypocretin neuropeptides consisted of hypocretin-1 (hcrt-1) and hypocretin-2 (hcrt-2), and they modulate their actions via hcrt-1 and hcrt-2 receptors. The most significant neuropathological change is the selective and irreversible loss of hypocretin-producing neurons in the lateral hypothalamus ( 3). Patients can also present with multiple chronic comorbidities including obesity, depressive disorder, migraine, precocious puberty and other sleep disorders (such as rapid eye movement sleep behavior disorder and obstructive sleep apnea) ( 2). Narcolepsy type 1 (NT1) is a chronic sleep disorder with major clinical manifestations including excessive daytime sleepiness, cataplexy (a sudden loss of muscle tone triggered by strong, mainly positive, emotions), sleep paralysis, hypnagogic hallucinations, and nocturnal sleep disorder ( 1). In addition to hypocretin deficiency, current evidence also indicates that pharmacological therapy (including psychostimulants and anti-cataplectic drugs) and comorbidities may contribute to the alterations of autonomic system observed in narcolepsy type 1. Similar findings should strengthen the recognition and intervention of these disturbances in clinical practice. Patients with narcolepsy type 1 often have various systemic autonomic symptoms, including non-dipping blood pressure, reduced heart rate variability, dynamic cerebral autoregulation impairment, reduced gastric motility and emptying, sleep-related erectile dysfunction, skin temperature abnormalities, and blunted pupillary light reflex. This article summarizes the autonomic disorders and possible mechanisms associated with narcolepsy type 1. Hypocretin deficiency is associated with autonomic disorders. Narcolepsy type 1 is a kind of sleep disorder characterized by a specific loss of hypocretin neurons in the lateral hypothalamus and reduced levels of hypocretin-1 in the cerebrospinal fluid.
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