Background
To investigate the effects of benzodiazepine receptor agonists on cognitive function in patients with chronic insomnia.
Method
According to the history of taking hypnotic drugs, they were ...divided into no medication group (n = 62), benzodiazepines group (n = 57) and non‐benzodiazepines group (n = 53); all subjects The Pittsburgh Sleep Quality Scale, the Epworth Scale, and the Insomnia Severity Index were used to evaluate their sleep quality, and the Hamilton Anxiety and Depression Scale to evaluate their anxiety and depression. The conversion test, the auditory word learning test was used to evaluate the memory function, and the Stroop color word test and the connection function test were used to evaluate the executive function.
Result
Compared with no medication, the non‐benzodiazepine group and the benzodiazepine group had longer sleep time throughout the night (P<0.05), and the non‐benzodiazepine group and the benzodiazepine group. The anxiety and depression scores of the drug group were lower than those of the non‐drug group (P<0.05), and the immediate memory and delayed memory scores of the benzodiazepine group and the non‐drug group were lower than those of the non‐benzodiazepine group (P<0.05). 0.05), the dose and duration of medication in the benzodiazepine group were negatively correlated with immediate memory (P<0.05), and the duration of medication in the benzodiazepine group was negatively correlated with prolonged memory (P<0.05). Regression analysis showed that the immediate memory score of taking benzodiazepines was 2.612 times lower than that of the non‐drug group, and the delayed memory score of taking non‐benzodiazepines was 1.439 times higher Regression analysis showed that the immediate memory score of taking benzodiazepines was 2.612 times lower than that of the non‐drug group, and the delayed memory score of taking non‐benzodiazepines was 1.439 times higher than that of the non‐drug group (P<0.05). The difference is statistically significant.
Conclusion
Benzodiazepines increase the risk of impaired immediate memory function in patients with chronic insomnia, and non‐benzodiazepines can improve their delayed memory function.
This study is aimed at investigating the features of fasciculation potentials (FPs) in amyotrophic lateral sclerosis (ALS) and peripheral nerve hyperexcitability syndromes (PNH). Needle ...electrophysiologic examination (EMG) was performed for 5-15 muscles in the ALS and PNH patients. The spontaneous activity of fasciculations and fibrillations/sharp-waves (fibs-sw) was recorded. The distribution, firing frequency, and waveform parameters of FPs in muscles were calculated and compared. In total, 361 muscles in ALS patients and 124 muscles in PNH patients were examined, with the FP detection rates of 45.1% and 53.2%. Moreover, the ALS patients with the upper limb onset had the highest FP detection rate. Fasciculations occurred more frequently in the upper limbs than in the lower limbs in ALS and PNH. The detection rate of fibs-sw in the bulbar muscle was relatively low, which could be elevated when combining fibs-sw and FPs. Benign FPs in PNH were of smaller amplitude, shorter duration, and fewer phases/turns, compared with malignant FPs in ALS. The FP area in PNH was significantly smaller than that in ALS. The incidence of polyphasic FPs in ALS was distinctly greater than that in PNH. The firing frequency of FPs in PNH was higher than that in ALS. There was no significant difference in the amplitude, duration, phases and turns, and area of FPs between groups with and without fibs-sw in the muscles of normal strength in ALS. Conclusively, it is necessary to detect the FPs in the thoracic and bulbar muscles of patients suspected having ALS. FP parameters in ALS are significantly different from PNH.
Sleep is considered closely related to cognitive function, and cognitive impairment is the main clinical manifestation of Alzheimer's disease (AD). Sleep disturbance in AD patients is more severe ...than that in healthy elderly individuals. Additionally, sleep deprivation reportedly increases the activity of the hypothalamic orexin system and the risk of AD. To investigate whether intervention with the orexin system can improve sleep disturbance in AD and its impact on AD pathology. In this study, six-month-old amyloid precursor protein/presenilin 1 mice were subjected to six weeks of chronic sleep deprivation and injected intraperitoneally with almorexant, a dual orexin receptor antagonist (DORA), to investigate the effects and mechanisms of sleep deprivation and almorexant intervention on learning and memory in mice with AD. We found that sleep deprivation aggravated learning and memory impairment and increased brain β-amyloid (Aβ) deposition in mice with AD. The application of almorexant can increase the total sleep time of sleep-deprived mice and reduce cognitive impairment and Aβ deposition, which is related to the improvement in Aquaporin-4 polarity. Thus, DORA may be an effective strategy for delaying the progression of AD patients by improving the sleep disturbances.
•Almorexant intervention can alleviate chronic sleep deprivation-induced AD learning and memory impairment and Aβ deposition.•The mechanism may be related to mitigating the damage to AQP4 polarity caused by sleep deprivation.•Orexin dual receptor antagonists can be an effective strategy for improving sleep in AD, and slowing pathological progression.
Obstructive sleep apnea (OSA) is closely associated with non-alcoholic fatty liver disease (NAFLD). The current definition of NAFLD cannot exclude the involvement of alcohol consumption in the ...development of fatty liver disease (FLD), but alcohol can aggravate OSA and participate in steatosis. There is limited evidence on the relationship between OSA and alcohol and its effect on FLD severity.
To determine the effect of OSA on FLD severity based on ordinal responses, and its relationship with alcohol consumption, in order to develop strategies for the prevention and treatment of FLD.
Patients with chief complaints of "snoring" who underwent polysomnography and abdominal ultrasound between January 2015 and October 2022 were selected. A total of 325 cases were divided into three groups according to abdominal ultrasound results: no FLD (n = 66), mild FLD (n = 116), and moderately severe FLD (n = 143) group. Patients were also categorized into alcoholic and nonalcoholic groups. Univariate analysis was used to examine the correlation between OSA and FLD severity. Multivariate ordinal logistic regression analysis was further used to identify the determinants of FLD severity and differences between the alcoholic and nonalcoholic groups.
A higher proportion of moderately severe FLD was observed in the group with an apnea/hypopnea index (AHI) > 30 compared to the AHI<15 group in all participants and in the nonalcoholic population (all p < 0.05). There was no significant difference among these groups in the alcoholic population. Ordinal logistic regression analysis found that in all participants, age OR = 0.966(0.947–0.986), BMI OR = 1.293 (1.205–1.394), diabetes mellitus OR = 1.932(1.132–3.343), hyperlipidemia OR = 2.432(1.355–4.464), severe OSA OR = 2.36(1.315–4.259) (all p < 0.05) were the independent risk factors for more severe FLD. However, different risk factors applied according to alcohol consumption. In addition to age and BMI, the independent risk factors for the alcoholic group also included diabetes mellitus OR = 3.323(1.494–7.834) while in the non-alcoholic group risk factors included hyperlipidemia OR = 4.094(1.639–11.137), and severe OSAOR = 2.956(1.334–6.664) (all p < 0.05).
Severe OSA is an independent determinant for developing more severe NAFLD in nonalcoholic population, and alcohol consumption may obscure the effect of OSA on the progression of FLD.
•Alcohol consumption influences the prevalence of fatty liver disease in the obstructive sleep apnea population.•Severe OSA is a risk factor for developing more severe non-alcoholic fatty liver disease in nonalcoholic population.•Risk factors that exacerbate Fatty liver disease include body mass index, diabetes mellitus, hyperlipidemia and severe OSA.
Purpose
The purpose of the study was to evaluate the quantitative relationship between Oxygen Desaturation Index (ODI) and sleep structure of obstructive sleep apnea (OSA) and cardiac remodeling.
...Methods
In this study, patients were enrolled from January 2015 to October 2022, and were divided into 3 groups according to AHI: patients with AHI < 15, patients with 15 ≤ AHI < 30, and 260 patients with AHI ≥ 30. Stratified linear regression was used to analyze independent risk factors for cardiac remodeling in OSA.
Results
A total of 479 patients were enrolled. We found that compared with AHI < 15 group (
n
= 120), the group with AHI > 30 (
n
= 260) had increased left atrial anteroposterior diameter, left ventricular end-diastolic internal diameter, left ventricular posterior wall thickness, right ventricular anteroposterior diameter, and interventricular septal thickness (
P
< 0.05). The group with 15 ≤ AHI ≤ 30 (
n
= 99) had increased left atrial anteroposterior diameter (
P
< 0.05). Multivariate linear regression revealed that N2 sleep was an independent risk factor for left ventricular posterior wall thickness, with positive correlation (
p
< 0.05). N3 sleep was an independent risk factor for transverse right atrial diameter and right ventricular anteroposterior diameter, with negative correlation (
P
< 0.05). ODI was an independent risk factor for interventricular septal thickness, with positive correlation (
P
< 0.05). The arousal index was an independent risk factor for increased left atrial anteroposterior diameter, with positive correlation (
P
< 0.05).
Conclusions
Increased ODI is an independent risk factor for interventricular septal thickness, while decreased slow wave sleep is an independent risk factor for right heart remodeling in OSA.
•Increase in plasma orexin-A level in patients with insomnia disorder.•The increased plasma orexin-A levels associated with the course and severity of insomnia.•Prepro-orexin and orexin receptor gene ...polymorphisms are not involved in insomnia.
Orexins, also known as hypocretins, play a regulatory role in the sleep-wake cycle by activating orexin receptors. Previous animal studies have shown that sleep deprivation can elevate orexinergic peptide levels. However, the relationship between insomnia disorder and orexin-A levels in humans has not been explored. In the current study, we examined plasma orexin-A levels in patients with insomnia disorder and in normal sleepers. We also studied the possible mechanisms underlying changes in orexin-A levels between the study groups; this included investigations of prepro-orexin and orexin receptor gene polymorphisms as well as exploration of other variables. We measured plasma orexin-A levels in 228 patients with insomnia disorder and 282 normal sleepers. The results indicated that the patients with insomnia disorder had significantly higher orexin-A levels than normal sleepers (63.42±37.56 vs. 54.84±23.95pg/ml). A positive relationship was detected between orexin-A level and age in patients with insomnia disorder. Orexin-A levels were elevated in relation to course of insomnia, as well as in relation to increased Insomnia Severity Index score. None of the evaluated prepro-orexin gene single nucleotide polymorphisms were informative between the two study populations. After sequencing all orexin receptor exons, one variation (rs2271933) in the OX1R gene and one variation (rs2653349) in the OX2R gene were found. However, no significant differences were found in either genotypic or allelic frequency distributions between the two study groups. It is suggested that the increased plasma orexin-A levels in patients with insomnia disorder are associated with the course and severity of insomnia, but not with prepro-orexin and orexin receptor gene polymorphisms.
Kennedy’s disease, resulted from the expansion of a CAG repeat in exon 1 of androgen receptor (AR) gene, is a motor neuron degenerative disease in the brainstem and spinal cord with the slow ...development of facial, bulbar, and limb muscle degeneration. To investigate the clinical manifestations and gene mutations in Han Chinese patients with Kennedy’s disease. The clinical manifestations of 5 male Han Chinese patients including 2 probands and their relatives from 2 families and 1 sporadic case were retrospectively studied. The CAG repeats in the first exon of AR were screened in 5 Han Chinese people including 2 probands and their healthy relatives from 2 families and 1 sporadic case by polymerase chain reaction (PCR) and direct sequencing. The average age at onset of Kennedy’s disease was 48.20 ± 8.70 (mean ± SD) years and the average duration was 7.60 ± 5.32 years. All the patients showed slow onset and progressive weakness, wasting, and fasciculations of the whole body. Four patients demonstrated decreased fertility and 1 patient showed mild gynecomastia. Serum creatine kinase and testosterone levels were elevated mildly in 2 and 1 patients, respectively. The electromyogram showed neurogenic abnormalities. Muscle magnetic resonance demonstrated reduced muscle volume and fatty infiltration. Three different enlarged CAG domains were discovered in the 2 families and 1 sporadic patient with Kennedy’s disease, and the CAG repeat number was 48, 43, and 44, respectively. The clinical manifestations of Kennedy’s disease in Han Chinese middle-aged men were progressive weakness and atrophy in the bulbar and spinal muscles, occasionally demonstrating incomplete androgen insensitivity syndrome. These patients were also characterized with enlarged CAG repeat number in the first exon of AR, indicating that CAG number could be used in the diagnosis of Han Chinese patients with Kennedy’s disease.
Abstract Cerebral ischemia is a major health crisis throughout the world, and the currently available thrombolytic therapy is unsatisfactory. Cell death following cerebral ischemia is mediated by a ...complex pathophysiological interaction of various mechanisms. During an ischemic insult, not only neurons but all of the components of the neurovascular unit, such as glia, endothelia, pericytes and basal membranes, are destroyed. Previous studies have shown that excessive stimulation of poly (ADP-ribose) polymerase (PARP-1) is crucial for cerebral injury after ischemic insult, which is an important cause of cell death in all cell types within the neurovascular unit. To investigate whether PARP-1 plays an important role in protecting the neurovascular unit following cerebral ischemia, we evaluated neurobehavioral deficits, PARP-1 activity, blood brain barrier (BBB) disruption and neurovascular unit deficits using Western blot analysis, TTC staining and electron microscopy in an MCAO rat model. The results revealed that PARP-1 enzymatic activity was dramatically increased after ischemia. Inhibition of PARP-1 significantly reduced the extent of both cerebral infarction and edema, improved neurological scores, and attenuated the damage to the neurovascular unit in cerebral ischemia. Collectively, these findings demonstrate that the down-regulation of PARP-1 activity contributes to reducing post-ischemic brain damage via protection of the neurovascular unit.
This study aimed to compare olanzapine and haloperidol efficacies in the treatment of acute psychiatric symptoms due to amphetamine-type stimulants (ATSs).
The Zelen II design method was used; 124 ...patients with acute mental disorders due to amphetamine were randomly divided into olanzapine group (n = 63) and haloperidol group (n = 61). Then, a 4-week open-label medical therapy was performed. Clinical Global Impression Scale Item 2 was employed to evaluate the onset time; meanwhile, Brief Psychiatric Rating Scale (BPRS) was used at baseline and at posttreatment weeks 1, 2, and 4. Moreover, adverse reactions during the treatment were recorded.
Onset time in the olanzapine group was significantly earlier than in the haloperidol group; BPRS scores in the olanzapine group were significantly lower than haloperidol group values at 1 and 2 weeks of treatment. The overall effective rates had no statistically significant difference.
Short-term olanzapine and haloperidol treatments had equivalent efficacies in the treatment of acute symptoms of mental disorders due to ATSs; however, olanzapine administration resulted in relatively earlier disease onset, with less adverse reactions.
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