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. Hypocretin deficiency is associated with autonomic disorders. This article summarizes the autonomic disorders and possible mechanisms associated with narcolepsy type 1. 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. Similar findings should strengthen the recognition and intervention of these disturbances in clinical practice. 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.

BACKGROUND: Vasovagal syncope (VVS) is the leading cause of syncope. The most frequent mechanism is that of a cardioinhibitory response, vasodepressor response, or mixture of both. Neural stimulation that negates or overcomes the effects of vagal tone may be used as a treatment strategy for VVS.
METHODS: Six male canines were studied. Stimulation (10-Hz, 2 ms pulse duration, 2 min duration) of the cervical vagus (CV), thoracic vagus (TV), and stellate ganglia (SG) was performed using needle electrodes at 3 V, 5 V, and 10 V output. SG stimulation at an output of 10 V overlaying TV stimulation at the same output was performed. Heart rate (HR), blood pressure (BP), and cardiac output (CO) were measured before, during, and after stimulation.
RESULTS: Right cervical vagal stimulation was associated with significant hemodynamic changes. HR, SBP, and DBP were reduced (107 ± 16 vs. 78 ± 15 bpm [P < 0.0001], 116 ± 24 vs. 107 ± 28 mmHg [P = 0.002] and 71 ± 18 vs. 58 ± 20 mmHg [P < 0.0001]), respectively, while left cervical vagal stimulation had minimal changes. CV stimulation was associated with greater hemodynamic changes than TV stimulation. Left and right SG stimulation significantly increased systolic blood pressure (SBP), diastolic blood pressure (DBP), and HR at 5 V and 10 V, which could be observed within 30 s after stimulation. An output-dependent increase in hemodynamic parameters was seen with both left and right SG stimulation. No difference between left and right SG stimulation was seen. SG stimulation overlay significantly increased HR, BP, and CO from baseline vagal stimulation bilaterally.
CONCLUSIONS: Stellate ganglia stimulation leads to increased HR and BP despite significant vagal stimulation. This may be exploited therapeutically in the management of vasovagal syncope.

Although sympathetic hyperactivity with preserved parasympathetic activity has been extensively recognized in fatal familial insomnia (FFI), the symptoms of parasympathetic nervous system failure observed in some patients are difficult to explain. Using heart rate variability (HRV), this study aimed to discover evidence of parasympathetic dysfunction in patients with FFI and the difference of parasympathetic activity between patients with FFI and Creutzfeldt-Jakob disease (CJD).
This study enrolled nine patients with FFI, eight patients with CJD and 18 healthy controls (HCs) from May 2013 to August 2020. All participants underwent a nocturnal video-polysomnography with lead II electrocardiography, and the data were analyzed using linear and nonlinear indices of HRV during both wake and sleep states.
Compared to the HC and CJD groups, the FFI group had a continuously higher heart rate with a lower amplitude of oscillations. The low frequency (LF)/high frequency (HF) ratio and ratio of SD1 to SD2 and correlation dimension D2 (CD2) were significantly different in the FFI group compared to the HC group. The root mean square of successive differences (RMSSD), HF and SD1 in the FFI group were significantly lower than in the HC group. RMSSD, SD1, and CD2 in the FFI group were all significantly lower than in the CJD group.
Cardiovascular dysautonomia in FFI may be partly attributable to parasympathetic abnormalities, not just sympathetic activation. HRV may be helpful as a noninvasive, quantitative, and effective autonomic function test for FFI diagnosis.

OBJECTIVE: Submandibular gland (SMG) regeneration depends on parasympathetic signals that modulate this process primarily by promoting ductal epithelial cell proliferation. The purpose of this study was to elucidate the mechanism underlying of parasympathetic regulation on salivary gland regeneration.
METHODS: We performed duct ligation/deligation with or without chorda lingual innervation in female Sprague-Dawley rats. Clodronate liposomes were administered retroductally and intravenously into the SMG to deplete macrophages. The proliferative ability and cell cycle-related genes of SMG were assessed using western blotting, quantitative real-time PCR, and immunohistochemical staining.
RESULTS: Parasympathetic stimulation boosted Interleukin-6 (IL-6) release by macrophage via muscarinic signalling. This process was suppressed by denervation, muscarinic blockade, or SMG macrophage depletion. SMG IL-6 release led to signal transducer and activator of transcription 3 (STAT3) phosphorylation in ductal epithelial cells to promote proliferation and regeneration by upregulating the expression of cell cycle-related genes. SMG parasympathetic denervation and macrophage depletion suppressed cell cycle-related genes upregulation and ductal cells proliferation.
CONCLUSIONS: These data indicated that the parasympathetic-macrophage-ductal epithelial cells axis promote SMG regeneration after duct ligation and deligation.

The autonomic nervous system regulates dynamic body adaptations to internal and external environment changes. Capitalizing on two different algorithms (that differ in empirical assumptions), we scrutinized the meta-analytic convergence of human neuroimaging studies investigating the neural basis of peripheral autonomic signal processing. Among the selected studies, we identified 42 records reporting 44 different experiments and testing 758 healthy individuals. The results of the two different algorithms converge in identifying the bilateral dorsal anterior insula and midcingulate cortex as the critical areas of the central autonomic system (CAN). Applying an unbiased approach, we were able to identify a single condition-independent functional circuit that supports CAN activity. Partially overlapping with the salience network this functional circuit includes the bilateral insular cortex and midcingulate cortex as well as the bilateral inferior parietal lobules. Remarkably, the critical regions of the CAN observed in this meta-analysis overlapped with the salience network as well as regions commonly reported across different cognitive and affective neuroimaging paradigms and regions being dysregulated across different mental and neurological disorders.

Atrial fibrillation (AF), one of the most common arrhythmias, is associated with chronic emotional disorder. Chronic pain represents a psychological instability condition related to cardiovascular diseases, but the mechanistic linkage connecting chronic pain to AF occurrence remains unknown. Wild-type C57BL/6J male mice were randomly divided into sham and chronic pain groups. Autonomic nerve remodeling was reflected by the increased atrial parasympathetic tension and muscarinic acetylcholine receptor M2 expression. AF susceptibility was assessed through transesophageal burst stimulation in combination with electrocardiogram recording and investigating AERP in Langendorff perfused hearts. Our results demonstrated the elevated protein expression of muscarinic acetylcholine receptor M2 in the atria of mice subjected to chronic pain stress. Moreover, chronic pain induced the increase of atrial PR interval, and atrial effective refractory periods as compared to the sham group, underlying the enhanced susceptibility of AF. Thus, autonomic cholinergic nerve may mediate mice AF in the setting of chronic pain.

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OBJECTIVE: Patients with psychiatric disorders have an increased risk of cardiovascular pathologies. A bidirectional feedback model between the brain and heart exists widely in both psychotic and nonpsychotic disorders. The aim of this study was to compare heart rate variability (HRV) and pulse wave velocity (PWV) functions between patients with psychotic and nonpsychotic disorders and to investigate whether subgroups defined by HRV and PWV features improve the transdiagnostic psychopathology of psychiatric classification.
METHODS: In total, 3448 consecutive patients who visited psychiatric or psychological health services with psychotic (N = 1839) and nonpsychotic disorders (N = 1609) and were drug-free for at least 2 weeks were selected. HRV and PWV indicators were measured via finger photoplethysmography during a 5-minute period of rest. Canonical variates were generated through HRV and PWV indicators by canonical correlation analysis (CCA).
RESULTS: All HRV indicators but none of the PWV indicators were significantly reduced in the psychotic group relative to those in the nonpsychotic group. After adjusting for age, gender, and body mass index, many indices of HRV were significantly reduced in the psychotic group compared with those in the nonpsychotic group. CCA analysis revealed 2 subgroups defined by distinct and relatively homogeneous patterns along HRV and PWV dimensions and comprising 19.0% (subgroup 1, n = 655) and 80.9% (subgroup 2, n = 2781) of the sample, each with distinctive features of HRV and PWV functions.
CONCLUSIONS: HRV functions are significantly impaired among psychiatric patients, especially in those with psychosis. Our results highlight important subgroups of psychiatric patients that have distinct features of HRV and PWV which transcend current diagnostic boundaries.

Congestive heart failure (CHF) is a cardiovascular disease associated with autonomic dysfunction, where sympathovagal imbalance was reported in many studies using heart rate variability (HRV). To learn more about the dynamic interaction in the autonomic nervous system (ANS), we explored the directed interaction between the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS) with the help of transfer entropy (TE). This article included 24-h RR interval signals of 54 healthy subjects (31 males and 23 females, 61.38 ± 11.63 years old) and 44 CHF subjects (8 males and 2 females, 19 subjects\' gender were unknown, 55.51 ± 11.44 years old, 4 in class I, 8 in class II and 32 in class III~IV, according to the New York Heart Association Function Classification), obtained from the PhysioNet database and then segmented into 5-min non-overlapping epochs using cubic spline interpolation. For each segment in the normal group and CHF group, frequency-domain features included low-frequency (LF) power, high-frequency (HF) power and LF/HF ratio were extracted as classical estimators of autonomic activity. In the nonlinear domain, TE between LF and HF were calculated to quantify the information exchanging between SNS and PNS. Compared with the normal group, an extreme decrease in LF/HF ratio (p = 0.000) and extreme increases in both TE(LF→HF) (p = 0.000) and TE(HF→LF) (p = 0.000) in the CHF group were observed. Moreover, both in normal and CHF groups, TE(LF→HF) was a lot greater than TE(HF→LF) (p = 0.000), revealing that TE was able to distinguish the difference in the amount of directed information transfer among ANS. Extracted features were further applied in discriminating CHF using IBM SPSS Statistics discriminant analysis. The combination of the LF/HF ratio, TE(LF→HF) and TE(HF→LF) reached the highest screening accuracy (83.7%). Our results suggested that TE could serve as a complement to traditional index LF/HF in CHF screening.

UNASSIGNED: Tinnitus can become a strong stressor for some individuals, leading to imbalance of the autonomous nervous system with reduction of parasympathetic activity. It can manifest itself as sleep disturbances, anxiety and even depression. This condition can be reversed by bioelectrical vagal nerve stimulation (VNS). Conventional invasive VNS is an approved treatment for epilepsy and depression. Transcutaneous VNS (taVNS) stimulating the auricular branch of the vagus nerve has been shown to activate the vagal pathways similarly as an implanted VNS. Therefore, taVNS might also be a therapeutic alternative in health conditions such as tinnitus-related mental stress (TRMS). This retrospective study in 171 TRMS patients reports the clinical features, psychophysiological characteristics, and results of the heart rate variability (HRV) tests before and after test-taVNS. This study also reports the therapy outcomes of 113 TRMS patients treated with taVNS, in combination with standard tinnitus therapy.
UNASSIGNED: Diagnostic tinnitus and hearing profiles were defined. To detect possible cardiac adverse effects, test-taVNS with heart rate monitoring as well as pre- and post-stimulation HRV tests were performed. Daily taVNS home therapy was prescribed thereafter. To assess therapeutic usefulness of taVNS, 1-year follow-up outcome was studied. Results of HRV tests were retrospectively analyzed and correlated to diagnostic data.
UNASSIGNED: The large majority of patients with TRMS suffer from associated symptoms such as sleep disturbances and anxiety. Baseline HRV data showed that more than three quarters of the 171 patients had increased sympathetic activity before test-taVNS. Test-taVNS shifted mean values of different HRV parameters toward increased parasympathetic activity in about 80% of patients. Test-taVNS did not cause any cardiac or other side effects. No significant adverse effects were reported in follow-up questionnaires.
UNASSIGNED: TRMS is an example of a stress condition in which patients may benefit from taVNS. As revealed by HRV, test-taVNS improved parasympathetic function, most efficiently in patients with a low starting HRV level. Our tinnitus treatment program, including taVNS, effectively alleviated tinnitus stress and handicap. For wider clinical use, there is a great need for more knowledge about the optimal methodology and parameters of taVNS.