The relationship between sleep disturbance, autonomic nerve dysfunction, and blood pressure in patients with major depressive disorder (MDD) was unclear. We studied 66 patients with MDD and 66 age-matched and sex-matched controls. Objective and subjective sleep were assessed using the polysomnography and Pittsburgh Sleep Quality Index, respectively. Autonomic nerve function was assessed using the heart rate variability (HRV). The averaged evening and morning systolic (SBP) and diastolic blood pressure (DBP) were analyzed. In patients with MDD, each 1 h reduction in an objective sleep duration was associated with 2.56-mmHg increase in SBP (p = 0.011) and 1.59-mmHg increase in DBP (p = 0.043). Increase in NREM-heart rate (HR), NREM-low frequency normalized unit (LFnu), and REM-HR and decrease in NREM-standard deviation of NN intervals, NREM-root mean square of successive differences, and NREM-LFnu were associated with shorter objective sleep duration (all p ≤ 0.043) and higher SBP and DBP (all p ≤ 0.037). These HRV mediated the association between objective sleep duration and BP with 17-79% mediating effects. No association was observed between subjective sleep duration and BP in patients with MDD or between objective/subjective sleep duration and BP in controls. In conclusion, objective, but not subjective short sleep duration, is associated with increased blood pressure in patents with MDD, that is mediated by autonomic nerve dysfunction.
Background: Emergence of periodic leg movements (PLM) on adaptive servo-ventilation (ASV) is well known in patients with chronic heart failure and reduced ejection fraction (HFrEF), but its clinical significance remains unclear. We investigated the effect of ASV on the emergence of PLM with arousal (PLMA) in HFrEF patients with obstructive or central sleep apnea (OSA or CSA) and determined whether emergent PLMA modifies the effect of ASV on fatigue and sleepiness.
Methods: Sixty stable HFrEF patients (ASV n = 29, control n = 31) with moderate to severe OSA or CSA were included. Polysomnography (PSG) was obtained at baseline and after 12 weeks.
Results: In HFrEF patients with OSA and CSA, ASV significantly increased PLMA-Index compared to control. ASV was associated with a significant reduction in Epworth sleepiness scale (ESS) and fatigue severity scale (FSS) in patients without emergent PLMA (52%) compared to those with emergent PLMA (48%; delta ESS: −3 (−3; 0) vs. 2 (−2; 4) p = 0.027; delta FSS: −1.3 (−2.1; 0.1) vs. −0.3 (−1.1; 1.7) p = 0.031) and compared to controls (0 (−1; 1) p = 0.039); (0.1 (−0.9; 0.4) p = 0.034).
Conclusion: ASV treatment increases PLMA in some HFrEF patients with OSA or CSA. On ASV treatment, patients reported only improved sleepiness and fatigue if no PLMA emerged.
Aims: Shangxia Liangji formula (SXLJF) is a traditional Chinese medicine formula used clinically for the treatment of insomnia. However, the exact mechanism of SXLJF remains unclear.
Methods and Results: A mouse insomnia model was established by intraperitoneal injection of p-chlorophenylalanine. Control, model, low/medium/high-dose SXLJF (9.26, 18.72, and 37.44 g/kg/day), and diazepam (2 mg/kg) groups were treated with designated reagents for 7 days. Behavioral changes were assessed via open field and pentobarbital-induced sleep tests. Hippocampal histopathology was evaluated using HE, Nissl, and TUNEL staining. Levels of serotonin (5-HT), 5-HIAA, dopamine (DA), norepinephrine (NE), IL-1β, IL-6, and TNF-α were measured using ELISA. RT-qPCR and immunofluorescence were used to analyze glial fibrillary acidic protein (GFAP), neuronal nuclei (NeuN), and brain-derived neurotrophic factor (BDNF) expression. Behavioral tests showed that SXLJF reduced mouse total distance traveled, average velocity, central distance, and sleep latency but increased sleep duration. It also attenuated expression of IL-1β, IL-6, and TNF-α, modulated levels of the monoamine neurotransmitters 5-HT, 5-HIAA, NE, and DA, upregulated NeuN and BDNF expression, downregulated GFAP expression, inhibited astrocyte activation, and mitigated neuronal apoptosis.
Conclusion: The mechanism underlying SXLJF’s anti-insomnia effect may be related to the regulation of monoamine neurotransmitters, inhibition of astrocyte activation and inflammatory factors, and suppression of neuronal apoptosis.
Background: Previous studies have shown that rapid eye movement (REM) sleep is important for promoting dendritic spine elimination after fear learning as well as for selectively maintaining new dendritic spines after motor learning. These REM sleep-dependent synaptic changes were measured on apical dendrites of layer 5 pyramidal neurons. Whether and how REM sleep affects synaptic structural plasticity on other cell types in the cortex remain unclear.
Methods: Used transcranial two-photon microscopy, we examined the effects of auditory cued fear conditioning (FC) and REM sleep on changes of dendritic spines of layer 2/3 pyramidal neurons in the mouse primary motor cortex.
Results: Auditory cued FC induced significantly higher elimination and formation of dendritic spines of layer 2/3 pyramidal neurons in the primary motor cortex over 4 hours. The degree of spine elimination rate was correlated with the freezing response during the 24 hour-recall test. Notably, REM sleep deprivation after FC prevented dendritic spine elimination, but not formation, of layer 2/3 pyramidal neurons. Furthermore, Ca2+ activity of layer 2/3 pyramidal neurons significantly increased during REM sleep, and that optogenetic blockade of Ca2+-CaMKII signaling during REM sleep prevented FC-induced spine elimination.
Conclusion: These findings reveal an important role of REM sleep in FC-induced pruning of dendritic spines of layer 2/3 pyramidal neurons in the motor cortex.
Narcolepsy is a chronic neurological disorder characterized by excessive daytime sleepiness and associated symptoms, including cataplexy, sleep paralysis, hypnagogic/hypnopompic hallucinations, and disrupted nocturnal sleep. It is classified into two subtypes: narcolepsy type 1 (NT1), which involves cataplexy and/or low cerebrospinal fluid (CSF) hypocretin-1 levels, and narcolepsy type 2 (NT2), which lacks cataplexy and has normal or intermediate CSF hypocretin-1 levels. Diagnosis is often delayed or missed due to symptom overlap with other sleep disorders, limited access to specialized testing, and low clinician awareness. Current diagnostic methods include the presence of cataplexy (specific to NT1), sleep-onset rapid eye movement periods (SOREMPs) detected through polysomnography (PSG) and multiple sleep latency tests, and low CSF hypocretin-1 levels (primarily for NT1). However, these methods have limitations, such as the invasiveness of CSF testing, variability in SOREMPs, and the absence of specific biomarkers for NT2. Emerging research suggests that electromyographic (EMG) activity during routine PSG, particularly elevated REM sleep without atonia, could serve as an alternative diagnostic marker for narcolepsy. This review explores the potential of EMG activity during REM sleep and the procedure of quantification in routine PSG, with the aim of improving early detection and reducing diagnostic delays in narcolepsy.